Clinical Examination in Cardiology [1 ed.] 9788131209646

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Clinical Examination in

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B.N. Vijay Raghawa Rao

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CLINICAL EXAMINATION IN CARDIOLOGY

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CLINICAL EXAMINATION IN CARDIOLOGY

B.N. Vijay Raghawa Rao MD, DM (CARDIOLOGY), DHA, FCCP, FICC, MBA (HM)

Formerly Addl. Director, Professor & HOD Gandhi Medical College/Gandhi Hospital, Secunderabad, Hyderabad, India Presently Consultant Interventional Cardiologist Vijay Marie and Yashoda Superseciality Hospitals, Hyderabad, India

ELSEVIER A division of Reed Elsevier India Private Limited

Clinical Examination in Cardiology B.N. Vijay Raghawa Rao ELSEVIER A division of Reed Elsevier India Private Limited Mosby, Saunders, Churchill Livingstone, Butterworth Heinemann and Hanley & Belfus are the Health Science imprints of Elsevier. © 2007 Elsevier First Edition 2007 All rights are reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission of the publisher. ISBN-13: 978-81-312-0964-6 Medical knowledge is constantly changing. As new information becomes available, changes in treatment, procedures, equipment and the use of drugs become necessary. The authors, editors, contributors and the publisher have, as far as it is possible, taken care to ensure that the information given in this text is accurate and up-to-date. However, readers are strongly advised to confirm that the information, especially with regard to drug dose/usage, complies with current legislation and standards of practice. Published by Elsevier, a division of Reed Elsevier India Private Limited Sri Pratap Udyog, 274, Captain Gaur Marg, Sriniwaspuri New Delhi – 110 065, India. Publishing Director: Sanjay K Singh Commissioning Editor: Sonali Dasgupta Developmental Editor: Dr Shelley Narula Manager (Editorial Projects): Dr Radhika Menon Production Executive: Ambrish Choudhary Typeset by Olympus Infotech Pvt. Ltd, Chennai, India. Printed and bound at Nutech Photolithographer, New Delhi.

Dedicated to my parents, Shri B. Narsimha & Smt B. Laxmamma, my wife Dr Shashikala, my daughters Dr Visha Rao & Vishala Rao and my teachers, students & patients who constantly encouraged to write & revise this clinical treatise.

P REFACE

TO

R EVISED R EPRINT

First Edition of Clinical Examination in Cardiology was published in 2007 by Elsevier India Pvt. Ltd which was well received and appreciated by PG students of Gen. Medicine, Pediatrics and Cardiology as well as by the practicing physicians, besides being a great helpful to undergraduate students. However there were some printing errors which were overlooked inadvertently. These errors have been corrected and even some figures, graphs, photographs and tables have been revised and updated in this revised reprint which will be an asset to clinical decision making. I am thankful to Elsevier India Pvt. for their keen interest shown in revising and reprinting this clinical text book.

Dr B.N. Vijay Raghawa Rao MD, DM (CARDIOLOGY), DHA, FCCP, FICC, MBA (HM)

P REFACE

TO THE

E ARLIER E DITION

“It is man’s mission to learn to understand”

Clinical Examination in Cardiology is primarily a clinical treatise. It provides a simple, lucid and comprehensive description of “Basic Anatomy and Physiology of Cardiovascular Medicine, Clinical Cardiology, and Basic Bedside Investigations (Electrocardiogram and X-ray Chest)” in a single book. It is the first of its kind in the present millennium highlighting the forgotten “Clinical Cardiology, in a scenario” where cardiovascular disease is now a global problem with enormous economic consequences. Besides index, this book consists of six parts with 34 chapters. Part 1 deals with “Basic Anatomy and Physiology of Cardiovascular Medicine” with ten chapters comprehensively described for better understanding of clinical cardiology. Part 2 follows the initial chapters which deal with “Cardiac Symptomatology” in two chapters. Part 3 with three chapters consists of “General Physical Examination, Arterial Pulse and Blood Pressure” described in detail. Part 4 has two chapters describing “Jugular Venous Pulse and Jugular Venous Pressure” in detail. Part 5 follows with five chapters which describe cardiovascular examination–“Inspection, Palpation, Percussion and Precordium in Common Heart Diseases, and Auscultation”. Finally, basic investigations are described in two portions, which are essential for comprehensive discussion of diagnosis and management of a cardiovascular disease. This Part 6 includes, Part 6a: “Clinical Electrocardiography” with nine chapters, which include basic concepts, normal ECG, common disease conditions, drugs effects, arrhythmias and prediction of coronary artery occlusion in a patient of acute myocardial infarction. Part 6b: “Radiology of the Heart and Great Vessels” includes four chapters, describing introduction, technical facts, routine reporting of an x-ray chest, calcifications and other views. Each chapter has adequate figures, tables and references, which can be used for rapid review of the material described. In total, there are 749 figures, 245 tables, and 675 references. This book is primarily focused for postgraduate students of “General Medicine, Cardiology and Paediatrics”. However, it will also be useful for the undergraduate students for better understanding of clinical cardiology, which is a part of general medicine. It may also prove useful to those who wish to broaden their knowledge of clinical cardiology and will aid in their day-to-day practice of cardiology. Besides my teaching experience of undergraduate and postgraduate medical students, I have also used standard textbooks and journals of Cardiovascular Medicine as references in compiling this clinical entity. I am thankful to my postgraduates, Dr Pramod, Dr Rajkiran and Dr Narender for providing beautiful photographs. I am indebted to my patients at my clinic, Remedy Superspeciality Hospital and Gandhi Medical College & Hospital for their immense cooperation. My special thanks to Mr Sanjay Singh and Dr Shelley Narula of Elsevier India Pvt. Ltd. for their constant encouragement and keen interest shown in completing this clinical treatise.

Dr B.N. Vijay Raghawa Rao MD, DM (CARDIOLOGY), DHA, FCCP, FICC, MBA (HM)

C ONTENTS Preface

vii

Abbreviations

xi

PART I

BASIC ANATOMY AND PHYSIOLOGY

1

Chapter 1

Anatomy of the heart

3

Chapter 2

Lymphatic system of the heart

28

Chapter 3

Venous drainage of the heart

31

Chapter 4

Arterial supply of the heart

34

Chapter 5

Nerve supply of the heart

40

Chapter 6

The conduction system of the heart

47

Chapter 7

Ultrastructure of the myocardium

54

Chapter 8

Basic electrophysiological principles

66

Chapter 9

Molecular basis of muscle contraction

73

Chapter 10

The cardiac cycle

77

PART 2

THE HISTORY AND SYMPTOMATOLOGY

83

Chapter 11

Cardinal symptoms

85

Chapter 12

Other symptoms

144

PART 3

GENERAL PHYSICAL EXAMINATION

159

Chapter 13

General examination

161

Chapter 14

Arterial pulse

225

Chapter 15

Measurement of the blood pressure

249

PART 4

JUGULAR VENOUS PULSE

269

Chapter 16

Introduction and jugular venous pulse waves

271

Chapter 17

Estimation of venous pressure and JVP in diseased conditions

283

PART 5

CARDIOVASCULAR SYSTEM EXAMINATION

297

Chapter 18

Inspection of the precordium

299

Chapter 19

Palpation of the precordium

315

x

CONTENTS

Chapter 20

Percussion of the precordium and precordial findings in common heart diseases

333

Chapter 21

Cardiac auscultation

354

PART 6A

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAM

457

Chapter 22

Introduction and basic concepts

459

Chapter 23

The normal electrocardiogram

474

Chapter 24

Abnormal P, T and U waves

490

Chapter 25

Ventricular hypertrophy

500

Chapter 26

Intraventricular conduction defects

516

Chapter 27

Myocardial infarction and ischemia

533

Chapter 28

Pericarditis and myocarditis

560

Chapter 29

Drug effects and electrolyte abnormalities

568

Chapter 30

Arrhythmias

580

PART 6B

BASIC INVESTIGATIONS: RADIOLOGY OF THE HEART AND GREAT VESSELS

659

Chapter 31

Introduction and evaluation of heart

661

Chapter 32

The pulmonary vasculature

684

Chapter 33

Cardiac calcification

693

Chapter 34

Evaluation of extracardiac structures and chest X-ray in other views

701

Index

708

A BBREVIATIONS PART 1 ADP: adenosine diphosphate AHA: american heart association AJR: abdominal jugular reflux AML: anterior mitral leaflet ANP: atrial natriuretic peptide ATP: adenosine triphosphate AV node: atrio ventricular node AV: atrioventricular AVT: anterior interventricular trunk CICR: calcium induced calcium release CLN: cardiac lymph node CT: chordae tendinae CVA: cerebrovascular accident CVC: cardiac vagal center IVC: inferior vena cava JSR: junctional sarcoplasmic reticulum LA: left atrium LAD: left anterior descending LBB: left bundle branch LCx: left circumflex LCC: left coronary channel LMCA: left main coronary artery LV: left ventricle MHC: myosin heavy chain MLC: myosin light chain MSC: main supracardiac channel OM: obtuse marginal OMT: obtuse marginal trunk PDA: patent ductus arteriosus PFO: patent foreman ovale PML: posterior mitral leaflet PM: papillary muscle pCO2: partial pressure of carbon dioxide pO2: partial pressure of oxygen PVT: posterior interventricular trunk RA: right atrium RBB: right bundle branch RCA: right coronary artery RCC: right coronary channel

RFW: rapid filling wave RLD: right lymphatic duct RV: right ventricle SA node: Sinoatrial node SERCA: sarco endoplasmic reticulum calcium ATPase SFW: slow filling wave SL: semilunar SVC: superior vena cava VMC: vasomotor center PART 2 Af: atrial fibrillation ALCAPA: anomalous left coronary artery from pulmonary artery AMI: acute myocardial infarction AP: angina pectoris AR: aortic regurgitation ARVD: arrhythmogenic right ventricular dysplasia AS: aortic stenosis ASD: atrial septal defect AVRT: atrioventicular reciprocating tachycardia BBB: bundle branch block CAD: coronary artery disease CCS: Canadian cardiovascular society CHF: congestive heart failure CHD: congenital heart disease CHB: complete heart block CM: cardiomyoapthy COA: coarctation of aorta COPD: chronic obstructive pulmonary disease CRF: chronic renal failure CT: cardiac tamponade CVA: cerebrovascular accident DCM: dilated cardiomyoapthy DORV: doublet outlet right ventricle HCM: hypertrophic cardiomyopathy HOCM: hypertrophic obstructive cardiomyopathy LAD: left anterior descending LAHB: left anterior hemi block LBBB: left bundle branch block

xii

ABBREVIATIONS

LCA: left coronary artery LVF: left ventricular failure LVOTO: left ventricular outflow tract obstruction MI: myocardial infarction MR: mitral regurgitation MS: mitral stenosis MVP: mitral valve prolapse MVV: maximum voluntary ventilation NYHA: New York heart association PAPVC: partial anomalous pulmonary venous connection PAT: paroxysmal atrial tachycardia PDA: patent ductus arteriosus PE: pulmonary embolism PND: paroxysmal nocturnal dyspnea PS: pulmonary stenosis PVR: pulmonary vascular resistance PTCA: percutaneous transluminal coronary angioplasty RBBB: right bundle branch block RVOTO: right ventricular outflow tract obstruction SAC: specific activity scale SLE: systemic lupus erythematosus SSS: sick sinus syndrome SV: single ventricle SVR: systemic vascular resistance SVT: supraventricular tachycardia TAPVC: total anomalous pulmonary venous connection TGA: transposition of great arteries TOF: tetralogy of Fallot TV: tidal volume, tricuspid valve VC: vital capacity VSD: ventricular septal defect VT: ventricular tachycardia PART 3 ABPM: ambulatory blood pressure monitoring AD: autosomal dominant inheritance AP window: aortopulmonary window AS: aortic stenosis ASD: atrial septal defect AR: aortic regurgitation AR: autosomal recessive inheritance BMI: basal metabolic index CAD: coronary artery disease CHF: congestive heart failure CO: cardiac output COA: coarctation of aorta

CT: cardiac tamponade CT: computed tomography DCM: dilated cardiomyopathy DM: diabetes mellitus HCM: hypertrophic cardiomyopathy HOCM: hypertrophic obstructive cardiomyopathy MI: myocardial infarction MRI: magnetic resonance imaging MS: mitral stenosis MVP: mitral valve prolapse PAPVC: partial anomalous pulmonary venous connection PDA: patent ductus arteriosus PR: peripheral resistance, pulmonary regurgitation PS: pulmonary stenosis PVC: premature ventricular contraction PVR: pulmonary vascular resistance RSOV: rupture of sinus of Valsalva SLE: systemic lupus erythematosus SVC: superior vena cava SV: stroke volume TAPVC: total anomalous pulmonary venous connection TGA: transposition of great arteries TOF: tetralogy of Fallot TR: tricuspid regurgitation TS: tricuspid stenosis VSD: ventricular septal defect PART 4 AJR: abdominal jugular reflux ASD: atrial septal defect CHB: complete heart block CHF: congestive heart failure COPD: chronic obstructive pulmonary disease CVP: central venous pressure EJV: external jugular vein EMF: endomyocardial fibrosis IJV: internal jugular vein LVF: left ventricular failure MR: mitral regurgitation MS: mitral stenosis PE: pulmonary embolism PS: pulmonary stenosis RVF: right ventricular failure RVEDP: right ventricular end diastolic pressure SVT: supraventricular tachycardia TR: tricuspid regurgitation

ABBREVIATIONS

TS: tricuspid stenosis TV: tricuspid valve VT: ventricular tachycardia PART 5 ACG: apex cardiogram AFM: Austin Flint murmur ALCAPA: anomalous left coronary artery from pulmonary artery AML: anterior mitral leaflet AP window: aortopulmonary window AR: aortic regurgitation AS: aortic stenosis ASD: atrial septal defect BVH: biventricular hypertrophy CAD: coronary artery disease CC: closing click CHD: congenital heart disease CHF: congestive heart failure COA: coarctation of aorta COPD: chronic obstructive pulmonary disease DM: diastolic murmur DORV: double outlet right ventricle EDM: early diastolic murmur ES: ejection sound ESM: ejection systolic murmur HCM: hypertrophic cardiomyopathy HOCM: hypertrophic obstructive cardiomyopathy ICS: intercostal space LAP: left atrial pressure LVF: left ventricular failure LBBB: left bundle branch block LPSA: left para sternal area LVH: left ventricular hypertrophy LVD: left ventricular dysfunction LVED: left ventricular end diastolic LVEDP: left ventricular end diastolic pressure LVOT: left ventricular outflow tract LVOTO: left ventricular outflow tract obstruction MDM: mid diastolic murmur MR: mitral regurgitation MRI: magnetic resonance imaging MS: mitral stenosis MSM: mid systolic murmur MVP: mitral valve prolapse NES: non ejection sound OC: opening click

OS: opening snap PADP: pulmonary artery diastolic pressure PBF: pulmonary blood flow PDA: patent ductus arteriosus PH: pulmonary hypertension PSM: pan systolic murmur PSL: para sternal lift PVC: premature ventricular contraction RSOV: rupture of sinus of Valsalva RVF: right ventricular failure RVEDP: right ventricular end diastolic pressure RVH: right ventricular hypertrophy RVOT: right ventricular outflow tract SM: systolic murmur TAPVC: total anomalous pulmonary venous connection TB: tuberculosis TGA: transposition of great arteries TOF: tetralogy of Fallot TR: tricuspid regurgitation TS: tricuspid stenosis TV: tricuspid valve VSD: ventricular septal defect PART 6A Af: atrial fibrillation Afl: atrial flutter AHA: American Heart Association AIVR: accelerated idioventricular rhythm AMI: acute myocardial infarction ARVD: arrhythmogenic right ventricular dysplasia AR: aortic regurgitation AS: aortic stenosis ASD: atrial septal defect AT: atrial tachycardia AVC: aberrant ventricular conduction AVNRT: atrioventricular nodal reciprocating tachycardia AVRT: atrioventricular reentry tachycardia BBB: bundle branch block CAD: coronary artery disease CABG: coronary artery bypass graft CHF: congestive heart failure COA: coarctation of aorta COPD: chronic obstructive pulmonary disease CP: constrictive pericarditis CT: cardiac tamponade CTI: cavo tricuspid isthmus

xiii

xiv

ABBREVIATIONS

DAD: delayed after depolarization GUSTO: global utilization of streptokinase and tissue plasminogen activator for occluded coronary arteries HTN: hypertension ICS: intercostal space IVC: inferior vena cava LAA: left atrial abnormality LAE: left atrial enlargement LAD: left anterior descending, left axis deviation LAFB: left anterior fascicular block LBBB: left bundle branch block LCx: left circumflex LGL: Lown Ganong Levine LPFB: left posterior fascicular block LVH: left ventricular hypertrophy LVOT: left ventricular outflow tract MAT: multifocal atrial tachycardia MI: myocardial infarction MR: mitral regurgitation MVP: mitral valve prolapse NCTI: non cavo tricuspid isthmus PAPVC: partial anomalous pulmonary venous connection PAC: premature atrial contraction PAT: paroxysmal atrial tachycardia PDA: patent ductus arteriosus PES: preexcitation syndromes PH: pulmonary hypertension PJRT: permanent form of AV junctional reciprocating tachycardia POTS: postural orthostatic tachycardia syndrome PS: pulmonary stenosis PTCA: percutaneous transluminal coronary angioplasty PVC: premature ventricular contraction RAD: right axis deviation RAA: right atrial abnormality RAE: right atrial enlargement RBBB: right bundle branch block RCA: right coronary artery RVH: right ventricular hypertrophy RVOT: right ventricular outflow tract

SVC: superior vena cava SVT: supraventricular tachycardia TDP: torsades de pointes TGA: transposition of great arteries TOF: tetralogy of Fallot TR: tricuspid regurgitation Vf: ventricular fibrillation Vfl: ventricular flutter VPC: ventricular premature contraction VT: ventricular tachycardia WPW: Wolffe Parkinson White PART 6B AP view: anteroposterior view ASD: atrial septal defect CAD: coronary artery disease CHF: congestive heart failure COPD: chronic obstructive pulmonary disease CT: computed tomography CT ratio: cardiothoracic ratio IVC: inferior vena cava LAE: left atrial enlargement LAO: left anterior oblique LPA: left pulmonary artery LVE: left ventricular enlargement LVF: left ventricular failure MRI: magnetic resonance imaging PAPVC: partial anomalous pulmonary venous connection PA view: posteroanterior view PBF: pulmonary blood flow PDA: patent ductus arteriosus PNS: paranasal sinuses RAO: right anterior oblique RDPA: right descending pulmonary artery RVF: right ventricular failure RVOT: right ventricular outflow tract SVC: superior vena cava TAPVC: total anomalous pulmonary venous connection TGA: transposition of great arteries TOF: tetralogy of Fallot VSD: ventricular septal defect

BASIC ANATOMY AND PHYSIOLOGY 1. Anatomy of the heart

3

2. Lymphatic system of the heart

28

3. Venous drainage of the heart

31

4. Arterial supply of the heart

34

5. Nerve supply of the heart

40

6. The conduction system of the heart

47

7. Ultrastructure of the myocardium

54

8. Basic electrophysiological principles

66

9. Molecular basis of muscle contraction

73

10. The cardiac cycle

77

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A NATOMY 1. GROSS ANATOMY OF THE HEART 2. EXTERNAL FEATURES OF THE HEART i. The Sulci of the Heart ii. The Surfaces of the Heart iii. The Borders of the Heart 3. THE CHAMBERS OF THE HEART i. Right Atrium ii. Right Ventricle iii. Left Atrium iv. Left Ventricle

3 4 4 5 6 7 7 10 12 13

CHAPTER 1

OF THE

H EART

4. THE FIBROUS SKELETON OF THE HEART i. Components and Attachments ii. Extensions iii. The Bundle of His 5. THE VALVES OF THE HEART General Description i. Mitral Valve ii. Tricuspid Valve iii. Semilunar (SL) Valves REFERENCES

16 16 17 17 17 17 18 22 24 27

1. GROSS ANATOMY OF THE HEART The heart is a conical, hollow muscular organ situated in the middle mediastinum behind the sternum and costal cartilages of the 3rd, 4th & 5th ribs. It lies obliquely so that 2/3 of the heart is to the left of the midline. The heart rests upon the diaphragm and is tilted forward and to the left so that the apex is anterior to the rest of the heart. The size and weight of the heart may vary depending upon the age, sex, body length, epicardial fat, and general nutrition. The average human adult heart measures about 12 cm  9 cm and weighs about 325  75 g in males and 275  75 g in females1 (see Table 1.1). It is described as follows: 1. External features 2. Chambers of the heart Table 1.1 Gross anatomy of the heart Features

Description

1. Shape 2. Location

Conical hollow muscular organ Middle mediastinum behind the sternum and costal cartilages of 3rd–5th ribs 12 cm  9 cm 325  75 g in males 275  75 g in females

3. Average size 4. Average weight

4

BASIC ANATOMY AND PHYSIOLOGY

3. The fibrous skeleton of the heart 4. The valves of the heart

2. EXTERNAL FEATURES OF THE HEART The heart has four chambers, right and left atria, and right and left ventricles, which are separated from each other by sulci and consist of surfaces and borders. The atria lie above and behind the ventricles (see Table 1.2). i. The Sulci of the Heart The atria are separated from the ventricles externally by the coronary (atrioventricular) sulci and from each other by an interatrial groove, which is faintly visible posteriorly and hidden by the aorta and pulmonary trunk anteriorly. The two ventricles are separated from each other by the interventricular sulci (grooves), which descend from the coronary sulcus toward the apex: ●

●

The anterior interventricular sulcus contains the left anterior descending coronary artery which courses over the muscular ventricular septum between the right and left ventricles to the apex (see Figs 1.1 and 1.2). The posterior interventricular sulcus which is situated on the diaphragmatic surface of the heart is the pathway for the posterior descending coronary artery, which is usually the terminal branch of the right coronary artery or less frequently of the left circumflex artery.

The right coronary artery travels in the right coronary sulcus between the right atrium and right ventricle until it descends on the posterior surface of the heart while the left circumflex artery runs in the left coronary sulcus between the left atrium and left ventricle. The crux of the heart is the area on the posterior basal surface: ● ●

●

Where the coronary sulcus meets the posterior interventricular sulcus. The coronary artery which crosses the crux (usually the right coronary artery) gives a small branch to the nearby AV node and Internally, the atrial septum joins the ventricular septum at this junction. Table 1.2 External features of the heart Features

Description

1. Chambers 2. Sulci

RA, RV, LA and LV Right and left coronary sulci, interatrial groove and anterior and posterior interventricular sulci Diaphragmatic or inferior, anterior or sternocostal and left surfaces Right border formed by: SVC and RA Left border formed by: LV and left auricle Inferior border formed by: RV

3. Surfaces 4. Borders

RA: right atrium, RV: right ventricle, LA: left atrium, LV: left ventricle, SVC: superior vena cava

ANATOMY OF THE HEART Brachiocephalic artery

5

Left common carotid artery Left brachiocephalic vein

Right brachiocephalic vein Superior vena cava

Right pulmonary artery

Left subclavian artery Arch of aorta Left pulmonary artery Left auricle Left ventricle

Right atrium

Anterior interventricular groove

Coronary sulcus Posterior interventricular groove Inferior vena cava

Apex of heart Right ventricle

Fig. 1.1

| External features of the heart—anterior view (diagrammatic). Aorta

Superior vena cava

Ligamentum arteriosum Left pulmonary artery Pulmonary trunk Left atrial appendage

Right atrial appendage Right atrium Right coronary artery in atrioventricular groove (coronary sulcus)

Left anterior descending coronary artery in interventricular groove Left ventricle

Right ventricle Apex

Fig. 1.2

| External features of the heart—anterior view.

ii. The Surfaces of the Heart ●

●

The area below the crux is known as the diaphragmatic or inferior surface of the heart. The diaphragmatic surface of the heart is formed in its left 2/3rd by the left ventricle and its right 1/3rd by the right ventricle. The anterior or sternocostal surface of the heart is formed mainly by the right atrium and right ventricle and partly by the left ventricle and left auricle.

6

BASIC ANATOMY AND PHYSIOLOGY

Arch of aorta

Left pulmonary artery

Superior vena cava

Right pulmonary artery

Left pulmonary veins Left auricle

Coronary sulcus Left ventricle Posterior interventricular groove Apex of heart

Fig. 1.3

Right pulmonary veins

Right atrium Left atrium

Inferior vena cava Right ventricle

| External features of the heart—posterior view (diagrammatic). Aorta

Left pulmonary artery

Right pulmonary artery Superior vena cava Pulmonary veins

Pulmonary veins Left atrium Coronary sinus and circumflex coronary artery Crux of the heart Left ventricle

Right atrium Inferior vena cava

Posterior descending coronary artery in posterior interventricular groove Right ventricle

Fig. 1.4

●

| External features of the heart—posterior view.

The left surface of the heart is mostly formed by the left ventricle and at the upper end by the left auricle (see Figs 1.3 and 1.4).

iii. The Borders of the Heart ●

The right border is more or less vertical which is formed by superior vena cava and the right atrium.

ANATOMY OF THE HEART ●

●

7

The left border is oblique and curved, mainly formed by the left ventricle and partly by the left auricle. The inferior border is nearly horizontal and is formed mainly by the right ventricle.

3. THE CHAMBERS OF THE HEART i. Right Atrium (RA) It receives venous blood from whole of the body via the superior vena cava (SVC) at its upper end and inferior vena cava (IVC) at its lower end and pumps it into the right ventricle through the right atrioventricular (tricuspid) valve during the ventricular diastole. a) External Features ●

●

●

It is a somewhat quadrilateral chamber situated behind and to the right side of the right ventricle, externally separated by the right coronary sulcus. A hollow conical muscular projection, the right auricle (right atrial appendage) arises from the antero-superior part of the right atrium and extends upwards and to the left of the ascending aorta. Along the right border of the right atrium, there is a shallow vertical groove, the sulcus terminalis which extends between the orifices of the superior vena cava and inferior vena cava which is produced by an internal muscular ridge called the crista terminalis. The upper part of the sulcus contains the SA node at the lateral margin of the junction of the superior vena cava with right atrium and the atrial appendage (see Table 1.5).

b) Internal Features The right atrial wall measures about 2 mm in thickness. The interior of the right atrium is broadly divided into three parts (see Figs 1.5, 1.6 and Table 1.3): ● ● ●

The smooth posterior part or sinus venarum The rough anterior part or pectinate part (atrium proper) and The septal wall.

(1) The smooth posterior part or sinus venarum ● ●

●

●

Developmentally, this portion is derived from the right horn of the sinus venosus. Superior vena cava opens at the upper end, inferior vena cava opens at the lower end and the coronary sinus opens between the opening of the inferior vena cava and the right atrioventricular (AV) orifice. The orifice of the superior vena cava has no valve while the orifice of the inferior vena cava is guarded by a rudimentary valve, the Eustachian valve. The Thebesian valve guards the orifice of the coronary sinus (see Table 1.4). The caval orifices vary in shape and size depending upon the phase of respiration, the cardiac cycle and contraction or relaxation of the surrounding muscle bands which play a role in promoting venous return and preventing atrial reflux.

8

BASIC ANATOMY AND PHYSIOLOGY

Superior vena cava

Aorta Right atrial appendage Pulmonary trunk

Right pulmonary artery

Pulmonary veins Right ventricle Fossa ovalis

Tricuspid valve

Orifice of coronary sinus Inferior vena cava

Fig. 1.5

| Interior of right atrium. Crista terminalis

Superior vena cava

Musculi pectinati

Openings of venae cordis minimae Right auricle Annulus ovalis

Fossa ovalis Valve of coronary sinus

Valve of inferior vena cava

Septal cusp of tricuspid valve

Inferior vena cava

Fig. 1.6

| Interior of the right atrium (diagrammatic).

Table 1.3 Development of the right heart Fetal structures

Portion developed

1. 2. 3. 4. 5.

Sinus venarum Atrium proper Atrial septal wall Inflow tract and body of right ventricle Infundibulum of right ventricle

Right horn of sinus venosus Primitive atrial chamber Septum primum and septum secundum Primitive ventricle Right part of the bulbus cordis

ANATOMY OF THE HEART

9

Table 1.4 Openings into the right atrium 1. Superior vena cava 2. Inferior vena cava 3. Coronary sinus

It has no valves It has rudimentary Eustachian valve It has Thebesian valve

Table 1.5 Nodes of the heart Node

Location

1. SA node

In sulcus terminalis at the lateral margin of the junction of SVC with right atrium In the triangle of Koch, anterior and medial to the coronary sinus just above the septal tricuspid leaflet

2. AV node

(2) The rough anterior part or atrium proper ● ●

●

Developmentally, this portion is derived from the primitive atrial chamber. Crista terminalis, remnant of the upper part of the right venous valve is a smooth muscle ridge which extends from the upper part of the atrial septum between the orifices of SVC and IVC. A series of transverse muscular ridges called muscular pectinati arise from the crista terminalis, run forwards and downwards towards the TV orifice, giving the appearance of the teeth of a comb. The muscles are interconnected to form a reticular network in the auricle.

(3) The septal wall ● ●

●

●

Developmentally, it is derived from the septum primum and septum secundum. An oval depression above and to the left of the opening of the inferior vena cava called fossa ovalis is formed by the septum primum. A sickle shaped sharp margin that surrounds the upper, anterior, and posterior margins of the fossa ovalis is the limbus fossa ovalis, developed from the lower free margin of septum secundum. The anterior limb of the limbus is continuous with the left horn of the valve of inferior vena cava. The remains of the foramen ovale is a small slit like valvular opening (patent foramen ovale, PFO) between the upper part of the fossa and the limbus which is normally occluded after birth and is occasionally present (see Table 1.6). The triangle of Koch, a triangular area bounded in front by the base of the septal leaflet of tricuspid valve, behind by the antero-medial margin of the opening of coronary sinus and above by the tendon of Todaro, which is a subendocardial ridge extending dorsally from the central fibrous body to the left horn of the valve of inferior vena cava. The AV node is located in this triangle anterior and medial to the coronary sinus, just above the septal leaflet of the tricuspid valve. The torus aorticus is a slight bulge in the antero-superior part of the septum and is caused by the bulging of the right posterior aortic (non-coronary) cusp and the right coronary cusp of the aortic root. The proximity of the aortic root to the

10

BASIC ANATOMY AND PHYSIOLOGY

Table 1.6 Description of the inter-atrial septum Features

Description

1. Fossa ovalis

Oval depression above and to the left of the opening of the superior vena cava Sickle shaped sharp margin that surrounds upper, anterior and posterior margins of the fossa ovalis Small slit like valvular opening between upper part of fossa ovalis and limbus Bulge in antero-superior part of the septum due to bulging of the right posterior and right coronary cusps of aorta

2. Limbus fossa ovalis 3. PFO (normally occluded after birth) 4. Torus aorticus

Table 1.7 Description of right heart Features

Description

1. Shape of the right atrium (RA) 2. Verticle groove on the RA 3. Wall thickness of the RA 4. Internal portions of RA

Quadrilateral chamber Sulcus terminalis: contains SA node 2 mm (i) Smooth sinus venarum (ii) Rough pectinate (atrium proper) (iii) Atrial septal wall Triangle or crescent 4–5 mm (i) Rough inflow tract (ii) Smooth infundibulum (iii) Body of the RV

5. Shape of the right ventricle (RV) 6. RV wall thickness 7. Portions of RV

●

right atrium permits an aneurysm of the sinus of Valsalva to rupture into the right atrium. The proximal right coronary artery is in immediate vicinity of the septum as it enters the coronary sulcus.

ii. Right Ventricle (RV) It is a triangular or a crescent shaped chamber, which receives the venous blood from the right atrium during ventricular diastole and pumps it into the pulmonary circulation during ventricular systole (see Table 1.7). a) External Features ●

●

The right ventricle is normally the most anterior cardiac chamber, lying directly beneath the sternum. It is partially below, in front of, and medial to the right atrium but anterior and to the right of left ventricle. It forms 2/3rd of the sterno-costal surface, most of the inferior surface and 1/3rd of the diaphragmatic surface of the heart.

ANATOMY OF THE HEART

11

Aorta Pulmonary trunk Superior vena cava Pulmonary valve Right atrial appendage

Infundibulum

Right atrium

Crista supraventricularis

Parietal band

Septal band Tricuspid valve Left ventricle

Inferior vena cava

Moderator band

Fig. 1.7

| Interior of the right ventricle

Pulmonary valve

Supraventricular crest Anterior cusp of tricuspid valve Chordae tandinae Moderator band Anterior papillary muscle

Fig. 1.8

| Interior of the right ventricle (diagrammatic)

b) Internal Features The right ventricular wall measures 4–5 mm in thickness,2 thinner than that of left ventricle in the ratio of 1:3. The interior of the right ventricle consists of three portions (see Figs 1.7 and 1.8): ● ● ●

The rough inflow tract The smooth outflow tract or infundibulum and The apical trabecular portion or body of the RV.

12

BASIC ANATOMY AND PHYSIOLOGY

(1) The rough inflow tract ●

●

●

Develops from the primitive ventricle of the heart tube, and consists of: (i) Tricuspid valve and (ii) The trabecular muscles of the anterior and inferior walls which direct the blood anteriorly, inferiorly, and to the left at an angle of 60 to the outflow tract. The trabecular carnae (muscles) are arranged into ridges, bridges and pillars (papillary muscles). The septomarginal trabecula is a muscular ridge extending from the ventricular septum to the base of the anterior papillary muscle. It contains the right branch of the AV bundle and is presumed to prevent the over-distension of the right ventricle, hence also called as the moderator band. The supraventricular crest, a muscular ridge situated between the tricuspid and pulmonary orifices separates the inflow and outflow tracts.

(2) The smooth outflow tract or infundibulum ●

●

●

Develops from the right part of the bulbus cordis, forms the superior portion of the right ventricle and gives rise to the pulmonary trunk. The apex of the conical shaped infundibulum has pulmonary orifice guarded by three semilunar cusps. The blood entering the infundibulum is ejected superiorly and posteriorly into the pulmonary trunk.

(3) The apical trabecular portion or body of the RV: It is also derived from the primitive ventricle of the heart tube, and is much coarser than that of the left ventricle. iii. Left Atrium (LA) It is a quadrangular chamber situated posteriorly, behind and to the left of the right atrium, and forms 2/3rd of the base of the heart. ●

●

The left atrium receives the oxygenated blood from the pulmonary veins and serves as a reservoir during left ventricular systole and pumps the blood into the left ventricle through the left atrio-ventricular (mitral) orifice during the left ventricular diastole. The posterior part is derived from the incorporation of the single pulmonary vein while the anterior part including the left auricle is developed from the left half of the primitive atrium (see Table 1.8). Table 1.8 Development of the left heart Fetal structures

Portion developed

1. Incorporated pulmonary veins 2. Left half of primitive atrium

Posterior portion of left atrium (LA) (i) Anterior portion of LA and (ii) Left auricle Outflow of left ventricle (LV) (i) Free wall, apex of LV (ii) Inflow tract of LV

3. Left part of bulbus cordis 4. Left part of primitive ventricle

ANATOMY OF THE HEART

13

a) External Features ●

●

The anterior wall of the left atrium is formed by the interatrial septum while the posterior surface of the left atrium forms the anterior wall of the oblique sinus of the pericardium. Its appendage, the left auricle projects anteriorly to overlap the infundibulum of the right ventricle.

b) Internal Features ●

●

●

The wall of the left atrium is 3 mm thick, slightly thicker than that of the right atrium. Most of the wall is smooth and only a network of muscular pectinati is present within the left auricle. Two pulmonary veins open into the left atrium on each side of the posterior wall. There are no true valves at the junction of the pulmonary veins and the left atrium, but the ‘sleeves of the atrial muscle extend from the left atrial wall around the pulmonary veins for 1 or 2 cm and may exert a partial sphincter-like influence, tending to lessen the reflux during atrial systole or mitral regurgitation. The atrial septum is also smooth and shows the fossa lunata corresponding to the fossa ovalis of the right atrium.

iv. Left Ventricle (LV) The left ventricle is roughly bullet-shaped with blunt tip directed anteriorly, inferiorly and to the left where it forms the apex of the heart with the lower ventricular septum. The left ventricle receives blood from the left atrium during ventricular diastole and ejects blood into the systemic circulation during ventricular systole. a) External Features The left ventricle forms: ● ● ● ●

the apex (with lower ventricular septum) 1/3rd of the sterno-costal surface most of the left surface and 2/3rd of the inferior surface of the heart.

The left ventricle is posterior and to left of the right ventricle and inferior, anterior and to the left of the left atrium. b) Internal Features The left ventricular chamber is approximately an ellipsoidal in shape and its walls measure 8–15 mm thick. However the tip of the LV apex is often thin, measuring 2 mm or less. The left ventricle consists of (see Fig. 1.9): ● ●

The ventricular septum The free wall of the left ventricle

14

BASIC ANATOMY AND PHYSIOLOGY Ascending aorta Pulmonary trunk

Pulmonary valve

Transverse atrium

Right ventricle

Aortic valve Left atrium

Interventricular septum

Left ventricle

Diaphragm Posterior cusp of mitral valve

Fig. 1.9

| Interior of the left ventricle (diagrammatic).

Table 1.9 Development of ventricular septum Portion of the ventricular septum 1. Muscular portion

2. Membraneous portion

● ● ●

Developed from Trabeculae and medial walls between the primitive LV and RV, appose and fuse together to form incomplete muscular septum at 3 mm stage Lower edge of conal septum and inferior endocardial cushion at 6 mm stage

The inflow tract The outflow tract The apical portion of the left ventricle.

(1) Ventricular septum ● ●

●

The medial wall of the left ventricle is the ventricular septum. It is roughly triangular in shape, with the base of the triangle at the level of the aortic cusps. It is entirely muscular but a small portion located superiorly just below the right coronary and posterior coronary cusps, is membranous (see Table 1.9). The upper 1/3rd of the septum is smooth endocardium while the remaining 2/3rd of the septum and remaining LV walls are ridged by interlacing muscles, the trabeculae carneae.

(2) The free wall of the left ventricle: The ridged trabeculae carneae excluding the ventricular septum is the free wall of the left ventricle (see Fig. 1.10).

ANATOMY OF THE HEART

15

Aorta

Pulmonary trunk Left atrial appendage

Fossa lunata Aortic valve Pulmonary veins

Left ventricle

Left atrium Trabeculae carneae cordis

Inferior vena cava Coronary sinus

Fig. 1.10

| Interior of the left heart with LV free wall and mitral valve removed.

Table 1.10 Description of the left heart Features

Description

1. Shape of the left atrium (LA) 2. LA wall thickness 3. Portions of LA

Quadrangular chamber 3 mm (i) Auricle: has musculi pectinati (ii) Smooth walled body (iii) Smooth interatrial septum with fossa lunata Bullet shaped with ellipsoidal chamber 8–15 mm, while apex is 2 mm thick (i) Triangular ventricular septum (ii) Free wall is ridged with trabeculae carnae (iii) Funnel shaped inflow (iv) Smooth conical shaped out flow

4. Shape of the left ventricle (LV) 5. LV wall thickness 6. Portions of LV

(3) The inflow tract ●

●

The anteromedial leaflet of the mitral valve (MV) extending from the top of the posteromedial septum to the anterolateral ventricular wall separates the LV cavity into an inflow tract and an outflow tract. The funnel shaped inflow tract is developed from the left part of the primitive ventricle and consists of mitral orifice with its mitral valve apparatus, which directs the atrial blood inferiorly, anteriorly and to the left towards the LV apex.

(4) The outflow tract ●

● ●

The conical smooth walled outflow tract is situated above, in front of and slightly to the right of the mitral orifice. It is developed from the left part of the bulbus cordis. It is surrounded by the inferior surface of the anteromedial mitral leaflet, the ventricular septum and the left ventricular free wall.

16

BASIC ANATOMY AND PHYSIOLOGY ●

●

It orients the blood flow from the LV apex to the right and superiorly at an angle of 90 to the inflow tract3 ejecting the blood into the ascending aorta through the aortic orifice during ventricular systole. The summit of the aortic vestibule is occupied by the aortic annulus guarded by three semilunar cusps.

(5) The apical portion of the left ventricle is characterized by fine trabeculations, also developed from the primitive ventricle (see Table 1.10).

4. THE FIBROUS SKELETON OF THE HEART i. Components and Attachments ●

The fibrous skeleton of the heart is made up of four fibrous rings (mitral, tricuspid, pulmonary and aortic) (see Fig. 1.11 and Table 1.11) at the bases of both ventricles around the mitral, tricusid, pulmonary and aortic orifices, which provide the attachment to: (i) Atrial and ventricular musculature (ii) Valves of the heart and (iii) Roots of the aorta and pulmonary trunk. Pulmonary valve Aortic valve Origin of right coronary artery

Tendon of infundibulum Trigonum fibronum sinistrum

Mitral valve

Tricuspid valve Trigonum fibrosum dextrum

Fig. 1.11

| Fibrous skeleton of the heart (diagrammatic). Table 1.11 Fibrous skeleton of the heart Features

Description

1. Four fibrous rings

(i) Pulmonary (ii) Aortic (iii) Mitral (iv) Tricuspid (iii  iv form central fibrous body) Right fibrous trigone Left fibrous trigone

2. Two trigones

ANATOMY OF THE HEART ●

●

●

●

17

The pulmonary ring lies above, in front of and slightly to the left of the aortic ring. Both the rings are set at right angles to each other and connected by a fibrous septum known as tendon of infundibulum. The medial aspects of mitral and tricuspid rings are fused by the central fibrous body known as trigonum fibrous dextrum or right fibrous trigone. The left margin of the trigone connects aortic and mitral rings, which is named as trigonum fibrosum sinistrum or left fibrous trigone. The right and left fibrous trigones which partially encircle the mitral and tricuspid orifices are the mitral and tricuspid annuli that give attachment to the mitral and tricuspid valves, atrial and ventricular muscle.

ii. Extensions ●

●

An important extension of the fibrous skeleton is the membranous ventricular septum, which extends inferiorly and anteriorly from the right fibrous trigone. It is located at the summit of the muscular septum, and provides support for the right coronary and noncoronary aortic cusps. A portion of the membranous septum extends slightly above the tricuspid valve, forming a small portion of the medial wall of the right atrium.

iii. The Bundle of His It penetrates the central fibrous body and travels along the inferior margin of the membranous ventricular septum. At the crest of the muscular septum, above the level of junction of the right coronary and noncoronary (posterior) aortic cusps, the His bundle divides into a left bundle branch and a right bundle branch. The right fibrous trigone is sometimes calcified in old age while this a constant feature in sheep’s heart.

5. THE VALVES OF THE HEART There are two pairs of valves in the heart (see Fig. 1.12). ● ●

A pair of atrioventricular valves: mitral and tricuspid and A pair of semilunar valves: aorta and pulmonary.

General Description ●

●

●

They maintain unidirectional flow of the blood and prevent its regurgitation in the opposite direction. The anatomy of the atrioventricular (AV) valves is more complex than that of the semilunar (SL) valves. Each cardiac valve has a central spongiosa (collagenous core) and a peripheral fibrosa. Both the sides of the fibrosa are covered by a loose fibroelastic tissue usually containing mucopolysaccharides and the entire valve is covered by endothelium.

18

BASIC ANATOMY AND PHYSIOLOGY Pulmonary orifice Aortic orifice Right ventricle Left ventricle

Septal papillary m.

Anterior papillary m.

Tricuspid orifice Anterior papillary m.

Mitral orifice Posterior papillary m.

Posterior or inferior papillary m. Interventricular septum

Fig. 1.12

section through the ventricles showing the valves of the heart | Transverse (diagrammatic).

Table 1.12 Valve leaflet surfaces

●

●

●

Surface

Description

1. Atrialis 2. Ventricularis 3. Arterialis

Atrial surface of atrioventricular valve leaflets Ventricular surface of all leaflets Arterial surface of the semilunar valve leaflets

The loose fibroelastic tissue on the atrial aspect of the AV valves is known as atrialis, ventricular surface of all four valves (AV & SL), the ventricularis, and aortic and pulmonary surfaces of SL valves are known as arterialis4 (see Table 1.12). The endothelium and loose connective tissue of the AV valves are continuous with the atrial and ventricular endothelium and those of the SL valves are continuous with the aortic and pulmonary intima. Smooth striated cardiac muscle may extend onto the proximal 1/3rd of the atrialis in the AV valves and often contain blood vessels. The distal 2/3rd of AV valves and both SL valves are avascular.4–8

i. Mitral Valve Mitral valve develops primarily from (see Table 1.13): ●

●

LV muscle wall: predominantly by delamination of the muscular ventricular wall,9 hence valve cusps initially are thick and fleshy.10 Endocardial cushions: (i) anterior mitral leaflet  from superior and inferior endocardial cushions (ii) posterior mitral leaflet  from left lateral endocardial cushion.

The mitral valve consists of six major anatomic components: annulus, leaflets, chordae tendinae, papillary muscles, posterior left atrial wall and left ventricular free wall (see Fig. 1.13 and Table 1.14).

ANATOMY OF THE HEART

19

Table 1.13 Development of the valves Part

Developed from

1. Mitral Anterior mitral leaflet Posterior mitral leaflet 2. Tricuspid Anterior leaflet Posterior leaflet Septal leaflet 3. Semilunar valves

Superior and inferior endocardial cushions Left lateral endocardial cushion Right lateral and dextro dorsal endocardial cushions Right lateral endocardial cushion Inferior endocardial cushion Truncus arteriosus Truncal and intercalated valve cushions

Posterior leaflet Median scallop

Middle scallop

Lateral scallop

Anterior leaflet

Mitral annulus

Basal zone

Clear zone Cuspal chordae Ventricular wall

Cuspal chordae

Rough zone Commissural chordae

Cuspal chordae Papillary muscle

Fig. 1.13

| Mitral valve complex (diagrammatic).

Table 1.14 Structure of the mitral valve Features

Description

1. Annulus

Saddle shaped; 4–6 cm2 in size; fibrous anteromedial portion and muscular posterolateral portion Sail shaped AML C shaped scalloped PML Anterolateral PM at 4o clock position Posteromedial PM at 7o clock position 120 in number Cuspal: primary, secondary and tertiary Commissural: anterolateral and posteromedial

2. Leaflets 3. Papillary muscles 4. Chordea tendinae

20

BASIC ANATOMY AND PHYSIOLOGY

a) Mitral Annulus ●

●

●

●

Shape of the mitral annulus is catenoid or saddle shaped in the embryo as well as in the adults. The size of the annulus is 4–6 cm2 (corresponds to mitral valve area–MVA) and the circumference of the valve (not really that of the annulus) is 8–10.5 cm with a mean of 9.4 cm.11–13 Anteromedial portion is formed from the fibrous trigone and collagen fibers which encircle 1/2 or 2/3rd of the annulus while rest of the annulus (posterolateral portion) is devoid of fibrous tissue and formed by the myocardium of the LV and left atrium. The decrease in annular size during ventricular systole is due to contraction of this posterolateral portion.

b) Leaflets Mitral valve has two leaflets: anterior mitral leaflet (AML) and posterior mitral leaflet (PML). However, it can have two small minor commissural cusps which are normally incomplete.14 (i) AML rd ● AML is sail shaped and is attached in a hinge like to 1/3 of the anteromedial portion of the annulus. ● It is directly continuous with 1/2 of the non-coronary (posterior) cusp and most of the left coronary cusp of aorta. ● It forms the semicircular posterior border of the LV outflow tract. (ii) PML rd ● PML is ‘C’ shaped, hinges on the posterolateral 2/3 of the annulus. ● It is longer at its base (6 cm of circumference) and shorter in its basal to apical length (1.2 cm) than AML (3 cm of circumference and 2.3 cm of basal to apical length)15 however both have similar surface area.11,12 16 ● The surface area of both leaflets is about 2½ times that of the orifice area, while the cross sectional area of both leaflets is 20% more than the mitral orifice. ● PML is sub-divided by medial and lateral clefts into three scallops-posteromedial, middle and anterolateral portions with middle being the largest (1.3 cm width compared to 1.0 cm for other two).15 (iii) Surface of the leaflets ● The atrial surface of the cusps is generally smooth except near the free edge where chordae tendinea are attached. Slightly away from the free edge on the atrial surface are fine nodules called the noduli Albini. ● The ventricular surface of the cusps is irregular due to insertion of the chordae tendinae. (iv) Commissures: The leaflets are connected to each other at junctions called commissures (SL valve commissures are ‘spaces’), anterolateral and posteromedial commissures.

ANATOMY OF THE HEART

21

c) Papillary Muscles (PM) There are two papillary muscles: anterolateral and posteromedial, located below the commissures projecting from the trabeculae carneae. Interpapillary muscle distance is relatively constant. Each PM has six heads.14 (i) Anterolateral PM: It is situated at 4o clock position and is supplied by a diagonal branch of left anterior descending) artery and obtuse marginal of left circumflex artery. (ii) Posteromedial PM: It is situated at 7o clock position and is supplied by posterior descending artery of right coronary artery in 85%, left circumference artery in 7% and by both in 8% (co-dominant) of individuals. d) Chordae Tendinae (CT) These are complex network of flexible cord like structures primarily made of collagen. They are of two types: cuspal (leaflet) chords and commissural chords. There are about 12 chordae attached to each of the six heads of each PM. These chordae divide about three times before their ultimate attachment. In total, there are about 120 chordae attached to both mitral leaflets.17 (i) Cuspal (leaflet) chords are classified into three groups: primary, secondary and tertiary. ●

●

●

Primary group originate near the PM apices, divide into a number of finer strands that insert at the extreme edge of the cusps. These chordae prevent the cusp inversion into the left atrium during ventricular systole. Secondary group of chordae also originate near the PM apices, are thicker in diameter, but less in number as compared to the first group and tend to insert on the ventricular surface of the cusps. They serve to anchor the valve. Tertiary group of chordae originate from the ventricular wall, may actively contain muscle and are attached to the ventricular aspect of posterior leaflet. These chords are specific to the PML.14,18

(ii) Commissural chords arise from the anterolateral and posteromedial PM and branch in a fan-like manner to be inserted on to both commissures. e) Mitral Valve Closure The closure of mitral valve involves a complex interplay of active and passive processes. It consists of three phases: initial leaflet phase, annular phase and ventriculogenic phase. (i) Initial leaflet phase: At the end of the rapid filling phase, the leaflets gradually move passively towards the closed position due to vortex currents generated under their ventricular surfaces. (ii) Annular phase: With the onset of atrial contraction, annular contraction begins which continues throughout the ventricular systole. The annular contraction is an important phase in MV closure and causes 20–40% decrease in annular orifice. Non-homogenous structure of the annulus produces an eccentric narrowing of the orifice during annular contraction.

22

BASIC ANATOMY AND PHYSIOLOGY

(iii) Ventriculogenic phase: With isometric contraction, the contraction of intravalvular muscle fibers occurs and leaflets become concave in shape which opposes leaflet eversion during ventricular systole. The large sail shaped AML swings and is engulfed by Gusset like C shaped PML causing closure of mitral valve. Leaflets are further sealed together by the opposing effect of intraluminal pressures. Papillary muscles and chordae maintain isometric tension and thereby stabilizes the leaflets during ventricular systole. ii. Tricuspid Valve The tricuspid valve develops from: (see Table 1.13) (i) RV muscle wall  by delamination of muscle wall (ii) endocardial cushion: ● Anterior leaflet from right lateral and dextro-dorsal endocardial cushions ● Posterior leaflet from right lateral endocardial cushion and ● Septal leaflet from inferior endocardial cushion. The tricuspid valve like mitral valve also consists of six major anatomic components: right atrial wall, annulus, leaflets, papillary muscles, chordae tendineae and right ventricular free wall (see Fig. 1.14 and Table 1.15).

Postero-septal commissure

Septal leaflet

Antero-septal commissure Anterior leaflet

Posterior leaflet

Basal zone Tricuspid annulus Clear zone

Basal chordae

Deep chordae

Ventricular wall Rough zone Commissural chordae

Chordae Free chordae Papillary muscle

Fig. 1.14

Rough zone chordae

| Tricuspid valve complex (diagrammatic).

Table 1.15 Structure of the tricuspid valve Features

Description

1. 2. 3. 4.

Circumferential in shape, 5–8 cm2 in size-anterior, posterior and septal portions Largest anterior, smallest medial or septal and scalloped posterior Anterior (largest), posterior (usually multiple) and septal (may be rudimentary) Five types: fan shaped, rough, deep, basal and free edged (deep and free edged are unique to TV)

Annulus Leaflets Papillary muscles Chordae tendinae

ANATOMY OF THE HEART

23

a) Tricuspid Annulus ●

●

●

It is nearly circumferential, larger than mitral annulus but lies at a lower level than the mitral annulus. The size of the tricuspid annulus is 5–8 cm2 with a mean of 7 cm2 (tricuspid valve area-TVA) and circumference of 11.4 cm  1.1 in males and 10.8  1.3 in females. The posterior leaflet makes up the largest portion of the annulus (7.5 cm), followed by the anterior (3.7 cm), and septal (3.6 cm) leaflets.19

b) Leaflets Tricuspid valve has three leaflets: anterior, posterior and septal. ● ● ●

Anterior leaflet is the largest with a width of 2.2 cm.19 Septal (medial) leaflet is the smallest with a width of 1.5 cm.19 The posterior leaflet measures 2.0 cm in width19 and may have 1–3 scallops produced by small clefts.

There are three commissures: ● ● ●

Anteroposterior with a size of 1.1 cm Posteroseptal with 0.8 cm size and Anteroseptal commissure with a size of 0.5 cm.

c) Papillary Muscles (PM) TV has three papillary muscles: anterior, septal (medial) and posterior. ●

●

●

The anterior PM is the largest, located below the anteroposterior commissure originating from the moderator band as well as from the anterolateral ventricular wall. The posterior PM lies beneath the posteroseptal commissure attached to the posterior wall of the RV and receive chordae from posterior and septal leaflets. It is usually multiple. The septal PM is small originating from the wall of the infundibulum. It has extensive attachments to the ventricular septum and receives chordae from the anterior and septal leaflets. At times, septal PM is rudimentary, absent, double or multiple.

d) Chordae Tendineae It may arise from the papillary muscles or from the muscle of the posterior or septal walls of the RV. On an average, there are 25 chordae inserted into the tricuspid valve: ● ● ● ●

7 chordae are inserted into the anterior leaflet 6 into the posterior leaflet 9 into the septal leaflet and 3 into the commissures.

TV has 5 types of chordae tendinea:19 ● ● ●

Fan shaped Rough Deep

24

BASIC ANATOMY AND PHYSIOLOGY ● ●

Basal and Free-edge.

The deep and free-edge are unique to the tricuspid valve.19 Deep chordae provide a second arcade for leaflet attachment, while free-edge are single and inserted into the leaflet’s free edge. Fan shaped chordae are inserted into the three commissures while basal chordae are the shortest and measure an average of 0.6 cm. Rough and deep chordae may be as long as 2.2 cm. iii. Semilunar (SL) Valves ●

●

●

●

Semilunar valves are derived from: (i) the truncus arteriosus and (ii) truncal and intercalated valve cushions. The aortic and pulmonary valves are called semilunar valves because their cusps are semilunar in shape. They are situated at the summit of the outflow tract of their corresponding ventricle, the pulmonary valve is anterior, superior and slightly to the left of the aortic valve. Each semilunar valve consists of an annulus, three equal-sized semicircular cusps, three equal spaced commissures and three sinuses of Valsalva (see Table 1.16).

a) Annulus Unlike aortic valve the pulmonary valve has no discrete annulus or fibrous ring. The apex of the infundibulum presents the pulmonary orifice which is circular and guarded by three semilunar cusps. The pulmonary valve annulus is about 1.5 cm above the level of the aortic valve annulus, but its circumference is similar: 7–9 cm. The average size of the aortic annulus is 2.5 cm2.

Table 1.16 Structure of the semilunar valves Features

Description

1. Annulus

PV: 7–9 cm in circumference AV: 2.5 cm2 in area AV: 2 anterior: right and left coronary cusps 1 posterior or noncoronary cusp PV: 2 posterior: right and left cusps 1 anterior cusp AV: 2 anterior: right and left 1 posterior PV: 2 posterior: right and left 1 anterior

2. Leaflets

3. Sinuses of Valsalva

PV: pulmonary valve; AV: aortic valve.

ANATOMY OF THE HEART

25

b) Leaflets (Cusps) ●

●

●

●

●

Each cusp is attached by its semicircular border (lower edge) to the wall of the aorta or pulmonary trunk while the upper free edges project into the lumen. The aortic and pulmonary valves are similar in configuration except that the aortic cusps are slightly thicker.5 The three aortic valve cusps: two anterior-right and left coronary cusps; one posterior or noncoronary cusp, while the pulmonary valve has two posterior cusps-right and left and one anterior cusp (see Figs 1.15 and 1.16). The aortic left and noncoronary cusps are continuous with AML of the mitral valve. The free margin of each cusp contains a central fibrous nodule on its ventricular surface called noduli Arantii which marks the contact sites of closure. From each side of the nodule, a thin smooth margin (lunule) extends to the base of the cusp, which is less prominent in the pulmonary valve (see Fig. 1.17). There may be variation in the cusps and commissural sizes and positions of the sinuses of Valsalva which result in asymmetric lines of closure and may accelerate ‘wear and tear’ (aging) of the valve structure especially of that of the aortic valve. Normal aortic valve Aorta

AORTA R

N

N

L Left cusp R

Anterior mitral leaflet

AML

Fig. 1.15

L

Ventricular diastole

of the aortic valve (diagrammatic)—N: noncoronary cusp, R: right | Structure anterior cusp, L: left anterior cusp, AML: anterior mitral leaflet.

R

L

R

A

L

Pulmonary trunk A RV free wall

Ventricular diastole

Right ventricular (RV) outflow

Fig. 1.16

of the pulmonary valve (diagrammatic)—R: right posterior cusp, | Structure L: left posterior cusp, A: anterior cusp.

26

BASIC ANATOMY AND PHYSIOLOGY Ascending aorta Left coronary artery

Nodule Lunule Anterior aortic sinus Right coronary artery

Fig. 1.17

| Structure of the aortic valve (diagrammatic).

Because of less systolic pressure in RV, these acquired senile (aging) changes in pulmonary valve do not occur. c) Commissures ●

●

●

●

Each semilunar valve has equally spaced three commissures i.e. the small space between the attachments of the adjacent cusps (vs. AV valves). The circumference connecting these points is termed as the sinotubular junction, which separates the sinuses of Valsalva from the adjacent tubular portion of the vessel. In aorta, a distinct hump or line marks this junction which was originally described by Leonardo da Vinci as the ‘supra-aortic ridge’. The circumference is measured at this sinotubular junction with echocardiography and at necropsy. While the lowermost portion of aorta (at the junction of the aortic valve with the ventricular septum) which is referred as the aortic ring, is measured by the surgeons to determine the size of the aortic prosthetic valve.

d) Sinuses of Valsalva A pouch-like dilatation above each cusp is known as sinus of Valsalva. The aortic right and left sinuses of Valsalva give rise to right and left coronary artery respectively. The aortic sinuses of Valsalva have close relation with right and left sided chambers. Hence, rupture of the right and non-coronary sinuses of Valsalva may communicate with right sided chambers (outflow tract RV and RA) while rupture of left sinus of Valsalva communicates with left sided chambers (LA or LV outflow tract). With age, ● ● ● ●

The aortic cusps thicken Nodules thicken and enlarges Sinuses of Valsalva calcify and dilate and Lunules develop fenestrations.

With age, the pulmonary valve cusps also thicken slightly but rest of the changes are less prominent. e) SL Valve Closure During ventricular systole, the cusps are passively thrust upward away from the center of the lumen. During ventricular diastole, the cusps fall passively into the lumen of the

ANATOMY OF THE HEART

27

vessel as they support the column of blood above while the nodules meet in the center which contributes to the support of the leaflets, thus preventing the regurgitation of blood.

REFERENCES 1. Edwards WD. Applied anatomy of the heart. In: Brandenburg RO, Fuster V, Giuliani ER, et al. eds. Cardiology: Fundamentals and Practice. Chicago: Year Book 1987:47–109. 2. Prakash R. Determination of right ventricular wall thickness in systole and diastole. Electrocardiographic and necroscopy correlation in 32 patients. Br Heart J 1978;40:1257–1261. 3. Walmsley R, Watson H. Clinical Anatomy of the Heart. New York. Churchill Livingstone 1978:1–22. 4. Gross L, Kugel MA. Topographical anatomy and history of the valves in the human heart. Am J Pathol 1931;7:445–474. 5. Waller BF. Morphological aspects of valvular heart disease. Part I. Curr Probl Cardiol 1984;9(7):1–66. 6. Clarke JA. An X-ray microscopic study of the blood supply to the valves of the human heart. Br Heart J 1965;27:420–423. 7. Duran CM, Gunning AJ. The vascularization of the heart valve: A comparative study. Cardiovasc Res. 1968;2(3):290–296. 8. Montiel MM. Muscular apparatus of the mitral valve in man and its involvement in left sided cardiac hypertrophy. Am J Cardiol 1970;26(4):341–344. 9. Dox X, Corone P. Embriologie cardiaque: Malformations (1). In: Embryologie Cardioaque-Editions Techniques Paris. Encyclopedie Medico-Chirurgicale. 1992:1–20. 10. Streeter GL. Developmental horizons in human embryos: Description of age groups XI. 13–20 somites and age group XII. 21–29 somites. Contrib embryol 1942;30:211–245. 11. Perloff JK, Roberts WC. The mitral apparatus: Functional anatomy of mitral regurgitation. Circulation. 1972;46(2):227–239. 12. Waller BF, Morrow AG, Maron BJ, Del Negro AA, Kent KM, McGrath FJ, et al. Etiology of clinically isolated, severe, chronic, pure mitral regurgitation: Analysis of 97 patients over 30 years of age having mitral valve replacement. Am Heart J. 1982;104(2 Pt 1):276–288. 13. Roberts WC. Morphologic features of normal and abnormal mitral valve. Am J Cardiol 1983;51(6): 1005–1028. 14. Netter FH. CIBA collection of medical illustration: Heart vol 5. Summit NJ: CIBA pharmaceutcal. 1987:9–112. 15. Ranganathan N, Lam JHC, Wigle ED, Silver MD. Morphology of human mitral valve: II. The valve leaflets. Circulation 1970;41:459–467. 16. Brock RC. The surgical and pathological anatomy of the mitral valve. Br Heart J 1952;14(4):489–513. 17. Constant J. Bedside Cardiology. 3rd. Boston, Mass: Little, Brown and Company; 1985. pp. 38–39. 18. Carbello BA. Mitral valve disease. Curr Probl Cardiol. 1993;18(7):423–478. 19. Silver MD, Lam JHC, Ranganathan N, Wigle ED. Morphology of human tricuspid valve. Circulation 1971;43(3):333–348.

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LYMPHATIC SYSTEM 1.

FORMATION OF RIGHT CORONARY CHANNEL 28 2. FORMATION OF LEFT CORONARY CHANNEL 28 3. FORMATION OF MAIN SUPRACARDIAC CHANNEL 29

CHAPTER 2

OF THE

4. FORMATION OF RIGHT LYMPHATIC DUCT REFERENCES

H EART 30 30

The lymphatic drainage of the heart flows from subendocardial vessels to an extensive capillary plexus lying throughout the subepicardium.1,2 These capillaries converge in collecting lymphatic channels which run alongside the coronary vessels which form the right lymphatic duct (see Figs 2.1 and 2.2). There are two main lymphatic channels: ● ●

Right coronary channel (RCC) and Left coronary channel (LCC).

1. FORMATION OF RIGHT CORONARY CHANNEL The posterior interventricular trunk (PVT) runs along with the posterior descending artery (PDA) in the posterior interventricular sulcus up to the crus of the heart, and then encircles around to the right from posterior to anterior in the right coronary sulcus to become the right coronary channel.

2. FORMATION OF LEFT CORONARY CHANNEL The two major LV channels are: anterior interventricular trunk and obtuse marginal trunk. ●

●

The anterior interventricular trunk (AVT) ascends from apex to base along with left anterior descending artery (LAD) in the anterior interventricular sulcus. The obtuse marginal trunk (OMT) runs alongside the left circumflex artery in left coronary sulcus.

LYMPHATIC SYSTEM OF THE HEART

29

IJV RLD Sci v CLN MSC

RCC

LCC OMT

PVT

Fig. 2.1

AVT

| Lymphatic drainage of the heart. Right lymphatic duct

Cardiac lymph node

Right coronary channel

Main supra-cardiac channel

PVT

Fig. 2.2

●

Left coronary channel

AVT

OMT

drainage of the heart (diagrammatic)—PVT: posterior interventricular | Lymphatic trunk, AVT: anterior interventricular trunk, OMT: obtuse marginal trunk.

Near the base of the pulmonary artery; the two LV channels, anterior interventricular trunk and obtuse marginal trunk join together to form left coronary channel.

3. FORMATION OF MAIN SUPRA-CARDIAC CHANNEL The right coronary channel unites with the left coronary channel to become main supra-cardiac channel (MSC), which passes upward beneath the left atrial appendage,

30

BASIC ANATOMY AND PHYSIOLOGY

behind the pulmonary artery to enter a pretracheal lymph node (cardiac lymph node; CLN) between the arch of aorta and the pulmonary artery.

4. FORMATION OF RIGHT LYMPHATIC DUCT From the CLN, the right lymphatic duct (RLD) arises which runs cephalad in the mediastinum to drain into the junction of the internal jugular vein (IJV) and right subclavian vein (Sci v). The thoracic duct, the largest lymphatic vessel of the body, extends from the upper part of the abdomen to the lower part of the neck crossing the posterior and superior mediastinum and drains into the junction of the left subclavian and left internal jugular veins or left brachiocephalic vein. On the right side of the thorax, there are three main lymphatic ducts: ● ● ●

Right jugular lymphatic duct drains into the right jugular vein. Right subclavian lymphatic duct drains into right subclavian vein and Right mediastinal lymphatic duct drains into right brachiocephalic vein.

Occasionally, the right jugular and right subclavian lymphatic ducts unite to form right lymphatic duct. The lymph vessels like veins contain valves to prevent backward flow.

REFERENCES 1. 2.

Feola M, Merklin R, Cho S, Brockman SK. The terminal pathway of the lymphatic system of the human heart. Ann Thorax Surg 1977;22:531–536. Miller AJ. Lymphatics of the Heart. New York: Raven press: 1982.

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V ENOUS D RAINAGE 1.

CORONARY SINUS i) Great Cardiac Vein ii) Oblique Vein of Left Atrium (or Oblique Vein of Marshall) iii) Posterior Vein of the LV iv) Middle Cardiac Vein (or Posterior Interventricular Vein)

32 33 33 33

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H EART

v) Small Cardiac Vein 2. ANTERIOR CARDIAC VEINS 3. THEBESIAN VEINS (VENAE CORDIS MINIMI) REFERENCE

33 33 33 33

33

There are three venous drainage systems:1 ● ● ●

Coronary sinus Anterior cardiac veins and Thebesian veins.

About 60% of the venous blood of the heart drains into the right atrium via the coronary sinus and remaining 40% drains into the different chambers of the heart via anterior cardiac veins and Thebesian veins (see Fig. 3.1 and Table 3.1). Coronary sinus conveys the greater part of the blood from the left coronary artery territory while the anterior cardiac veins drain most of the blood from the right coronary artery territory (see Fig. 3.2). Left brachio-cephalic vein Left superior intercostal vein

Superior vena cava

Ligament of left vena cava Oblique vein of left atrium

Anterior cardiac veins Right atrium Coronary sinus

Left marginal vein Posterior vein of left ventricle Great cardiac vein

Middle cardiac vein Small cardiac vein

Fig. 3.1

| Venous drainage of the heart (diagrammatic).

Right marginal vein

32

BASIC ANATOMY AND PHYSIOLOGY

Table 3.1 Venous drainage of the heart Coronary sinus

Anterior cardiac veins

Thebesian veins

1. Drains: LCA territory

Drains: RCA territory

2. Branches: 5 in number Great cardiac vein Oblique vein of left atrium Posterior vein of LV Middle cardiac vein Small cardiac vein

Branches: 1–4

Drains: Both the territories, but primarily RCA territory Branches: Small and numerous

Right ventricle

Thebesian veins

Right atrium

Anterior cardiac veins

CORONARY SINUS Great cardiac vein

OV of LV

LMV

Fig. 3.2

PV of LV

Middle cardiac vein

Small cardiac vein RMV

drainage of the heart (diagrammatic)—OV of LV: obtuse vein of left | Venous ventricle, PV of LV: posterior vein of left ventricle, LMV: left marginal vein, RMV: right marginal vein.

1. CORONARY SINUS ●

●

●

●

Coronary sinus is about 2–3 cm long situated in the posterior part of the atrioventricular groove (coronary sulcus) near the crux of the heart. It begins in the left part of the AV groove where it receives the great cardiac vein and oblique vein of left atrium at its left end, then passes downwards and to the right along the posterior part of the AV groove receiving posterior vein of left ventricle in its middle part and middle cardiac vein and small cardiac vein at its right end. Finally, the coronary sinus opens into the inferoposteromedial aspect of the right atrium between the orifice of the IVC and septal leaflet. The AV node lies just above its opening. A crescent shaped rudimentary valve, the Thebesian valve guards the opening of the coronary sinus. All the tributaries of coronary sinus are provided with valves except the oblique vein of left atrium. It is developed from the left horn and body of the sinus venosus. The Thebesian valve is derived from the lower part or the venous valve.

VENOUS DRAINAGE OF THE HEART

33

i) Great Cardiac Vein ●

●

It begins near the apex of the heart as anterior interventricular vein in the anterior interventricular sulcus, runs upwards along with left anterior descending artery, and turns leftward near the bifurcation of the left coronary artery to circle posteriorly under the left atrium in the left AV sulcus to become great cardiac vein. It receives the left marginal vein near its termination in the coronary sinus.

ii) Oblique Vein of Left Atrium (or Oblique Vein of Marshall) ●

●

It drains the posterior surface of the left atrium, runs on the posterior surface of the left atrium and terminates in the left of the coronary sinus. It develops from the left common cardinal vein (duct of Cuvier) which may sometimes form a large left superior vena cava.

iii) Posterior Vein of the LV ●

It drains the inferior surface of the left ventricle, runs on the diaphragmatic surface of the LV and ends in the middle of the coronary sinus on the left side of the middle cardiac vein.

iv) Middle Cardiac Vein (or Posterior Interventricular Vein) ●

It arises near the posterior aspect of the cardiac apex and ascends in the posterior interventricular sulcus along with the posterior descending artery and terminates into the right end of the coronary sinus or may sometimes directly drain into the right atrium.

v) Small Cardiac Vein ●

It lies in the right coronary sulcus accompanying the right coronary artery, receives the right marginal vein draining the RV and RA and terminates in the right end of the coronary sinus or sometimes directly into the right atrium.

2. ANTERIOR CARDIAC VEINS There are 2–4 anterior cardiac veins which drain the anterior RV wall, run superiorly on the anterior wall of the RV and cross the right AV sulcus to terminate directly into the anterior part of the right atrium. 3. THEBESIAN VEINS (VENAE CORDIS MINIMI) These are small numerous veins draining the myocardium directly into the cardiac chambers, primarily into the right atrium and right ventricle (see Fig. 3.2). REFERENCE 1.

James TN. Anatomy of the Coronary Arteries. New York: Hoeber Medical Division. Harper & Row. 1961:1–77.

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ARTERIAL SUPPLY 1.

LEFT CORONARY ARTERY i) Left Anterior Descending Artery (LAD) ii) Left Circumflex Artery (LC or LCx) iii) Ramus Intermedius

34 35 35 37

CHAPTER 4

OF THE

HEART

2. RIGHT CORONARY ARTERY (RCA) 3. DIVERGENT CORONARY ANATOMY 4. MEASUREMENTS i) Length ii) Luminal Diameter REFERENCES

37 38 39 39 39 39

The heart is supplied by two coronary arteries: left coronary artery and right coronary artery (see Table 4.1).

1. LEFT CORONARY ARTERY The left main coronary artery (LM or LMCA) arises from left anterior coronary sinus, passes behind the pulmonary trunk (RVOT), runs forwards and to the left between the pulmonary trunk and left auricle where it bifurcates into left anterior descending (LAD) and left circumflex (LC or LCx) branches1 (see Fig. 4.1).

Table 4.1 Coronary artery (CA) distribution CA branch

Distribution

1. 2. 3. 4. 5. 6. 7. 8. 9.

Anterolateral portion of LV Anterosuperior 2/3rd of vent. septum Left atrium Lateral free wall of LV RVOT SA node (in 50–60%) AV node (in 85%) Posteroinferior 1/3rd of vent. septum Posterolateral LV (85%)

Diagonal branches Septal branches LA branch OM Conus branch SA nodal branch AV nodal branch PDA PLV branch

ARTERIAL SUPPLY OF THE HEART

35

Aortic valve NC

LM

Tubular portion

Coronary ostia

LC

Sinotubular junction

L R

R LAD

R

NC (P)

L Sinus portion

Sinotubular junction AV cusp

R

Pulmonic valve

Fig. 4.1

| Origin of the coronary arteries.

i) Left Anterior Descending Artery (LAD) It runs in the anterior interventricular groove towards the apex. LAD gives 2–6 diagonal (D) and 3–5 septal (S) branches. ●

●

In 90%, there are 1–3 diagonal branches and no diagonal branches are present in 1%. The diagonal arteries course laterally over the free wall of the left ventricle (LV) in the angle between the LAD and LCx and supply the anterolateral portion of the LV. The septal branches originate from the LAD at a right angle and supply anterosuperior 2/3rd portion of the ventricular septum.

LAD terminates: ● ●

Beyond the ventricular apex (type-III) along the diaphragmatic aspect in 78%. At the apex (type II) or before the apex (type-I) in 22%.

Angiographically, LAD is divided into three portions: Proximal, Mid and Distal (see Figs 4.2, 4.3 and 4.4). ●

●

●

Proximal LAD is the portion from its origin from the LMCA to its first diagonal (D1) branch. Mid LAD is the portion between first diagonal (D1) and second diagonal (D2) branches. Distal LAD is the portion of the LAD beyond (D2) branch.

ii) Left Circumflex Artery (LC or LCx) After its origin from the LMCA, LCx travels in the left AV groove (left coronary sulcus) and in the posterior part of AV groove; it anastomoses with the branches of right coronary artery (RCA).

36

BASIC ANATOMY AND PHYSIOLOGY

LCx

LAD

OMB

RAO caudal

Fig. 4.2

| Coronary angiogram of LCA-RAO caudal. LCx

LAO cranial

LAD

Fig. 4.3

| Coronary angiogram of LCA-LAO cranial. LCx D

LMCA

S

LAD AP cranial

Fig. 4.4

| Coronary angiogram of LCA-AP cranial. In right dominant coronary circulation (85%), LCx gives 1–2 left atrial branches which supply the left atrium and 1–3 obtuse marginal branches (OM) that supply lateral free wall of the LV. In left dominant coronary circulation (8%) in addition to left atrial and OM branches, it gives rise to posterolateral left ventricular (PLV) branch, posterior descending artery (PDA), AV nodal artery and sinus nodal artery (in 40–50%).

ARTERIAL SUPPLY OF THE HEART

37

Similarly, LCx is angiographically divided into three portions: Proximal, Mid, and Distal (see Figs 4.2, 4.3 and 4.4). ●

● ●

Proximal LCx is the portion from its origin from the LMCA to the origin of the first obtuse marginal branch. Mid LCx is the portion of LCx between the first OM and second OM branches. Distal LCx is the portion of the LCx beyond second OM branch.

iii) Ramus Intermedius In some patients, a large intermedius or ramus medianus branch may originate directly from the LMCA, bisecting the angle between the LAD and LCx, so that there is a trifurcation of the LMCA.

2. RIGHT CORONARY ARTERY (RCA) It arises from the right coronary sinus which is lower is position than that of the left coronary artery, passes forwards and to the right between the pulmonary trunk and right auricle, then runs downwards in the right anterior coronary sulcus, winds round the inferior border of the heart to reach the diaphragmatic surface of the heart. Here, it passes upwards and to the left in the right posterior coronary sulcus and reaches the crux of the heart and terminates by anastomosing with the branches of the LCx. In general, it gives rise to: ● ● ● ●

Conus artery SA nodal branch Right atrial branches RV and acute marginal branches which supply the free wall of the right ventricle.

(i) The conus artery: It is usually the first branch of RCA, which supplies the infundibulum of the RV (RVOT), but in 40–50% it may originate from a separate ostium in the right coronary sinus (third coronary artery). (ii) SA nodal artery: In 50–60%, SA nodal artery originates from the RCA, runs along the anterior right atrium to the superior vena cava, which it encircles in a clockwise or anticlockwise before it penetrates the SA node. However, when the SA nodal artery arises from the LCx (in 40–50%), it crosses behind the aorta and in front of the left atrium to reach the superior vena cava and penetrating the SA node.2 (iii) In right dominant coronary circulation (in 85%), RCA gives rise to AV nodal artery, PDA which supplies the postero-inferior 1/3rd of the ventricular septum and one or more posterolateral LV branches (PLV), which supply the posterolateral portion of LV. (iv) Co-dominant coronary circulation or balance system occurs in 7% where PDA and PLV may originate from both RCA and LCx.

38

BASIC ANATOMY AND PHYSIOLOGY LAO straight

PLV

RCA

AMB PDA

Fig. 4.5

| Coronary angiogram of RCA-LAO view. Conus branch

RCA PDA RAO straight

Fig. 4.6

| Coronary angiogram of RCA-RAO view. (v) In type-I LAD (where it terminates before the apex), the larger and longer PDA from RCA supplies the ventricular apex also, which is then described as Super dominant RCA. (vi) Angiographically, RCA is divided into three parts: Proximal, Mid, and Distal (see Figs 4.5 and 4.6). ●

● ●

Proximal RCA is the portion of the RCA from its origin from the right anterior coronary sinus to the origin of its RV branch. Mid RCA is the portion of RCA between its RV branch and its PDA branch. Distal RCA includes PDA and PLV branches.

3. DIVERGENT CORONARY ANATOMY In 1–2%, there may be divergent coronary anatomic features.3 These include: ● ● ●

Anomalous origin of LCx from RCA Separate ostia of LAD and LCx or Separate ostia of RCA and its conus branch

ARTERIAL SUPPLY OF THE HEART

39

Table 4.2 Coronary artery: Length and luminal diameters Coronary artery 1. 2. 3. 4.

●

LMCA LAD LCx RCA

Length (mm) 1–25 100–130 60–80 120–140

Luminal diameter (mm) 2–5.5 2–5.0 1.5–5.5 1.5–5.5

(4) (3.6) (3) (3.2)

Occassionally, the right or left coronary ostium arises 1 cm or more (usually 2.5 cm) above the sinotubular junction. This ostial dislocation is termed as a high-takeoff coronary artery.4

4. MEASUREMENTS i) Length (i) The LMCA usually ranges from 1–25 mm in length1 and it is termed as short LMCA if it is 1 cm (ii) The LAD measures 10–13 cm in length (iii) Non-dominant LCx is 6–8 cm in length, while (iv) RCA is 12–14 cm in length before it gives rise to PDA (see Table 4.2). ii) Luminal Diameter The luminal diameter of LMCA is 2.0–5.5 mm (mean of 4 mm), LAD: 2.0–5.0 mm (mean of 3.6 mm) and LCx: 1.5–5.5 mm (mean of 3 mm). RCA has a luminal diameter of 1.5–5.5 mm (mean of 3.2 mm).1 LAD and LCx generally taper in diameter as they extend from the LMCA, while RCA maintains a fairly constant diameter till it gives rise to PDA.

REFERENCES 1. 2. 3. 4.

Baroldi G. Diseases of the coronary arteries. In: Silver MD, Ed. Cardiovascular Pathology: I. New York, Churchill Livingstone. 1983:317–391. Anderson KR, Ho SY, Anderson RH. Location and vascular supply of sinus node in human heart. Br Heart J 1979;41:28–32. Click RL, et al. Anomalous coronary arteries, location, degree of atherosclerosis and effect on survival— A report from Coronary Artery Surgery study. J Am Coll Cardiol 1989;13:531. Spring DJ, Thomsen JH. Severe atherosclerosis in the “single coronary artery”—Report of a previously undescribed pattern. Am J Cardiol 1973;31(5):662–665.

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N ERVE S UPPLY 1.

CARDIAC PLEXUS i) Superficial Cardiac Plexus ii) Deep Cardiac Plexus iii) Both Sympathetic and Parasympathetic Fibers

40 40 41 43

CHAPTER 5

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H EART

2. BARORECEPTORS AND CHEMORECEPTORS i) Baroreceptors ii) Chemoreceptors REFERENCES

43 44 46 46

The nerve supply of the heart is derived from1,2 (see Tables 5.1 and 5.2): 1. The cardiac plexus formed by the sympathetic and parasympathetic (vagal) fibers (see Figs 5.1 and 5.2) and 2. Baroreceptors and chemoreceptors.

1. CARDIAC PLEXUS i) Superficial Cardiac Plexus It is situated below the arch of aorta and in front of the right pulmonary artery. It is formed by: (i) The superior cardiac branch of superior cervical ganglion of the left sympathetic chain and (ii) The superior cardiac branches (from superior and inferior cervical nerves) of the left vagus nerve. Table 5.1 Nerve supply of the heart Cardiac plexus 1. Superficial cardiac plexus (below the aortic arch)

Branches to ● ● ●

2. Deep cardiac plexus (behind the aortic arch)

● ● ●

RCA (through coronary plexus) Left anterior pulmonary plexus Deep cardiac plexus Both atria Both coronary arteries (through coronary plexus) Right and left anterior pulmonary plexus superficial cardiac plexus

NERVE SUPPLY OF THE HEART

41

The superficial cardiac plexus gives branches to (i) The deep cardiac plexus (ii) Right coronary artery (coronary plexus) and (iii) Left anterior pulmonary plexus. ii) Deep Cardiac Plexus It is situated in front of the bifurcation of the trachea and behind the arch of aorta. It is formed by: (i) The cardiac branches of superior, middle and inferior cervical ganglia (except the cardiac branch arising from superior cervical ganglion of left sympathetic chain, Table 5.2 Peculiarities of nerve supply to the heart Nerve supply

Features

1. 2. 3. 4.

More at the base than at the apex of the heart Greater in posterior ventricular myocardium Affect SA node  AV node Affect AV node  SA node

Sympathetic innervation Vagal activity Right sympathetic and vagus nerves Left sympathetic and vagus nerves

Superior cardiac branch of superior cervical ganglion

Right coronary artery Superficial cardiac plexus

Superior cardiac branches of left vagus

Left anterior pulmonary plexus

Cardiac branches of superior cervical ganglion

Cardiac branches of middle cervical ganglion

Cardiac branches of upper 4–5 thoracic ganglia Deep cardiac plexus

Cardiac branches of inferior cervical ganglion

Both coronary arteries

Both atria Left and right anterior pulmonary plexus

Fig. 5.1

Inferior cardiac branches of vagus/ recurrent laryngeal nerve

| Cardiac plexus (diagrammatic).

42

BASIC ANATOMY AND PHYSIOLOGY

Thalamus

Medulla

Cervical sympathetic ganglia and nerves Superior

s

s

u Vag

ve ner

Middle Inferior (Stellate ganglion)

T1

(Via superior and inferior cardiac branches, and thoracic cardiac branches of right and left vagus)

T1

Thoracic sympathetic ganglia and nerves

T2 T3 T4 T5

(Post-ganglionic)

(Pre-ganglionic)

To S-A node, A-V node, atrial and ventricular muscle

Cardiac plexus

Parasympathetic

Fig. 5.2

To S-A node, A-V node, atrial and ventricular muscle

Sympathetic

| Nerve supply of the heart.

which forms superficial cardiac plexus) and upper 4 or 5 thoracic ganglia of right and left sympathetic chain. The inferior cervical ganglion and first thoracic ganglion are fused together to form a Stellate ganglion. (ii) Inferior (thoracic) cardiac branches of vagus and/or recurrent laryngeal nerves of both sides except superior cardiac branches of left vagus (which form superficial cardiac plexus). The deep cardiac plexus gives branches to: ● ● ● ●

superficial cardiac plexus both atria both coronary arteries (coronary plexus) and right and left anterior pulmonary plexus.

NERVE SUPPLY OF THE HEART

43

iii) Both Sympathetic and Parasympathetic Fibers These influence the SA node, AV node, both the atrial and ventricular myocardium, although vagal fibers are sparse to the ventricles.3 (i) Sympathetic stimulation to the heart is largely mediated by the release of norepinephrine and parasympathetic stimulation by acetylcholine. (ii) The sympathetic innervation is more at the base than at the apex of the heart, while the vagal activity is greater in the posterior ventricular myocardium which accounts for the vagomimetic effect of the inferior myocardial infarction. (iii) The right sympathetic and vagus affect the SA node more than the AV node while the left sympathetic and vagus affect the AV node more than the SA node. (iv) Hence, stimulation of right stellate ganglion causes sinus tachycardia with less affect on AV nodal conduction. Whereas stimulation of left stellate ganglion shortens the AV nodal conduction time and refractory period and produces the shift in sinus pacemaker to an ectopic site. (v) Also, stimulation of right (cervical) vagus slows sinus node discharge rate (producing bradycardia) while the stimulation of left vagus prolongs the AV nodal conduction time and refractoriness. In general, right sympathetic chain shortens the refractoriness primarily of the anterior portion of the ventricles while the left sympathetic chain primarily affects the posterior surface of the ventricles.

2. BARORECEPTORS AND CHEMORECEPTORS The cardiovascular regulatory mechanisms includes4 (see Table 5.3 and Fig. 5.4): (a) Chemical Regulatory Mechanisms through circulating vasodilators (bradykinin) and circulatory vasoconstrictors (epinephrine, nor-epinephrine, angiotensin II and vasopressin) and (b) Neural Regulatory Mechanisms which consist of: ● Sympathetic and parasympathetic systems through superficial and deep cardiac plexus and ● Medullary vasomotor and cardiac vagal centers. The ventrolateral region of medulla (Pressor area) exerts excitatory effects (increase) on sympathetic activity while the medial and caudal parts of fourth ventricle in medulla (Depressor area) cause decrease of sympathetic activity. Cardiac vagal center consists of inhibitory vagal fibers originating from the neurons of vagal nuclei located in the medulla (dorso-motor nucleus, nucleus of tractus solitarius and nucleus ambiguous) to converge on: ●

The sympathetic pre-ganglionic neurons of spinal cord to decrease the sympathetic activity and

44

BASIC ANATOMY AND PHYSIOLOGY

Inferior colliculus Bronchium pontis Pressor area

Depressor area

Fig. 5.3

| Vasomotor center (diagrammatic).

Table 5.3 Baroreceptors and chemoreceptors Receptors Baroreceptors 1. Arterial baroreceptors (pressure receptors)

2. Cardiac baroreceptors i. Volume receptors ii. Pressure receptors

Chemoreceptors 1. Carotid bodies 2. Aortic bodies

●

Location

Carotid sinus Aortic arch Root of subclavian artery Pulmonary trunk Atriocaval receptors (RA) Pulmonary venoatrial receptors (LA) Atrial: RA, LA, interatrial septum Ventricular: LV, interventricular septum (Bezold-Jarisch reflex) Common carotid artery bifurcation Around aortic arch

The heart to decrease the heart rate and force of the cardiac contraction. The vasomotor and cardiac vagal centers are influenced by the afferent fibers from the baroreceptor and chemoreceptors (see Fig. 5.3).

i) Baroreceptors Since they are sensitive to stretch, they are also called as mechanoreceptors. All are innervated by vagus nerve except the carotid sinus baroreceptors which are supplied by

NERVE SUPPLY OF THE HEART

Cardiovascular and respiratory medullary center

IX nerve

Carotid body

45

Carotid sinus Common carotid artery

Right aortic nerve (branch of vagus)

Left aortic nerve (branch of vagus)

Right subclavian artery Left subclavian artery

Aortic bodies

Aorta

Fig. 5.4

| Baroreceptors (

) and chemoreceptors (

).

carotid sinus nerve, a branch of glossopharyngeal (IX cranial) nerve. Broadly, there are two types of baroreceptors: arterial and cardiac. (a) Arterial Baroreceptors ● ●

●

●

●

These are located in the walls of the blood vessels mainly in the adventitial layer. The afferent signals are mainly carried through vagus to the vasomotor center and the cardio-vagal center in medulla. The arterial baroreceptors are situated at: 1. Carotid sinus (dilated initial part of internal carotid) 2. Aortic arch 3. Root of subclavian artery 4. Junction of thyroid artery with common carotid artery and 5. Pulmonary trunk near its division. Increased aortic pressure causes reflex inhibition of vasomotor center (VMC) and stimulation of cardiac vagal center (CVC), thereby decreasing the heart rate and systemic vascular resistance, while lowering the aortic pressure results in stimulation of VMC and inhibition of CVC, thereby increasing the heart rate and systemic vascular resistance. The range of operation of these baroreceptors is between 60–200 mmHg of mean blood pressure.

(b) Cardiac Baroreceptors These are located in the walls of the heart i.e. subendocardial in distribution.

46

BASIC ANATOMY AND PHYSIOLOGY

The cardiac baroreceptors are: 1. Atrio-caval receptors located at the junction of right atrium with inferior vena cava and superior vena cava. 2. Pulmonary veno-atrial receptors located at the junction of pulmonary vein with left atrium. Both [1] and [2] are volume receptors i.e. increase blood volume causes distension of the atrial walls producing reflex tachycardia (Bainbridge reflex) and moderate diuresis due to the release of atrial natriuretic peptide (ANP). 3. Atrial receptors scattered throughout the atria and interatrial septum. Increase in atrial pressure increases their impulse activity (however their discharge is sparse and irregular) resulting in reflex vasodilatation especially in the renal vessels. 4. Ventricular receptors are scattered throughout the left ventricle and ventricular septum. They are stimulated (their discharges are also sparse and irregular) by the injection of veratridine, serotonin or nicotine into coronary artery (especially left) or pulmonary artery or by partial occlusion of aorta or coronary sinus, resulting in profound bradycardia and hypotension due to reflex sympathetic inhibition (Bezold-Jarisch reflex). ii) Chemoreceptors Chemoreceptors are sensitive to the changes in the blood chemistry. Their main function is to keep the alveolar pCO2 at a normal level of 40 mmHg and also to maintain arterial pO2, pCO2 and pH. The important chemoreceptors are: Carotid bodies and Aortic bodies (i) Carotid bodies: These are located near common carotid artery bifurcation and are innervated by carotid sinus nerve, a branch of glossopharyngeal nerve. (ii) Aortic bodies: These are scattered around aortic arch and are innervated by aortic nerve, a branch of vagus nerve. Afferent fibers from these chemoreceptors ascend to relay in the nucleus of tractus solitarius of medulla. Hypoxia, hypercapnia and acidemia stimulate these receptors which activates the vasomotor center and respiratory neurons in the medulla producing pressure effects with an increase in the rate and depth of respiration.

REFERENCES 1. 2. 3. 4.

Mitchell GAG. Cardiovascular Innervation. Baltimore: Williams & Wilkins: 1956. Janes RD, Brandys JC, Hopkins DA, Johnstone DE, Murphy DA, Armour JA. Anatomy of human extrinsic cardiac nerves and ganglia. Am J Cardiol 1986 1;57(4):299–309. Randall WC, ed. Nervous Control Cardiovascular Function. New York: Oxford University Press: 1982. Jain AK. Cardiovascular regulatory mechanisms. In: Text book of Physiology: I. New Delhi: Avichal Publishing Co 2001:324–328.

■ ■ ■ CHAPTER 6

THE CONDUCTION SYSTEM OF THE HEART 1.

SINOATRIAL (SA) NODE (PACEMAKER NODE OF KEITH–FLACK NODE, 1907) 47 P Cells (Pale/nodal cells) 48 Transitional Cells (T cells) 49 Internal Atrial Myocardium 49 2. ATRIOVENTRICULAR JUNCTIONAL AREA 50 Transitional Cell Zone 50 Atrioventricular (AV) Node (Tarawa, 1906) 50

The Bundle of His (AV Bundle, Common Bundle) 3. THE BUNDLE BRANCHES AND TERMINAL PURKINJE FIBERS The Left Bundle Branch (LBB) The Right Bundle Branch (RBB) The Terminal Purkinje Fibers REFERENCES

51

51 51 51 52 52

The conduction system of the heart consists of three major parts (see Fig. 6.1 and Table 6.1): 1. Sinoatrial (SA) node 2. AV junctional area and 3. The bundle branches and terminal Purkinje fibers.

1. SINOATRIAL (SA) NODE (PACEMAKER NODE OF Keith–Flack, 1907) SA node is spindle shaped, 10–12 mm long and usually 1 mm thick situated in the sub-epicardium (less than 1 mm from the epicardial surface) at the lateral junction of the superior vena cava and right atrium. Blood supply to the SA node is by the sinus nodal artery, which arises from proximal RCA in 55–60%, LCx in 40–45% and from both in 11%.1 Histologically, the sinus node has: ● ● ●

P cells Transitional cells and Atrial muscle cells.

48

BASIC ANATOMY AND PHYSIOLOGY Anterior internodal tract Middle internodal tract

Sinoatrial node

Membranous ventricular septum

Posterior internodal tract

Atrioventricular node

Muscular ventricular septum Atrioventricular bundle

Nodal fibers

Fig. 6.1

Septo-marginal trabecula

Transitional fibers

Purkinje fibers

| Conduction system of the heart.

Table 6.1 Conduction system of the heart Structures

Location

1. 2. 3. 4.

Lateral junction of SVC and RA At the apex of Koch’s triangle Chord-like distal continuation of AV node Forms a cascade down the left ventricular septal surface Beneath the non-coronary aortic cusp Direct continuation of His bundle along the right side of the ventricular septum On the endocardial surface of both ventricles

SA node AV node The bundle of His Left bundle branch (LBB)

5. Right bundle branch (RBB)

6. The terminal Purkinje fibers

P Cells (Pale/nodal cells) ●

●

●

● ●

P cells are ovoid, small (5–10 m in greatest diameter) and resemble the primitive myocardial cells. The nuclei are of normal size, but double or multiple nuclei in a single cell are not observed. There are fewer mitochondria in a P cell compared to the normal contractile cells. Myofibrils are few in number and rarely attached to the sarcolemma. The P cells are the source of normal impulse formation in the SA node. However, intercellular contact is direct plasma membrane to plasma membrane, a factor responsible for slow conduction within the sinus node.

THE CONDUCTION SYSTEM OF THE HEART

49

Transitional Cells (T cells) ●

●

●

●

T cells are intermediate between P cells and atrial myocardial cells (elongated than P cells but shorter and narrower than atrial myocardial cells).2 They are located at the margins of the sinus node, where nodal cells become contiguous with atrial myocardium. T cells provide a ‘functional pathway’ for the distribution of sinus impulses formed in the P cells to the rest of the atrial myocardium. The fibrous tissue and fat increase with advancing age and hence the fibrous tissue is predominant in adult sinus node as compared to that of an infant.3

Internal Atrial Myocardium Certain population of atrial myocardial cells have different electrophysiological properties, and James and Sherf 4 supported the concept of three specific internodal tracts between SA and AV nodes: ● ● ●

Anterior internodal tract Middle internodal tract and Posterior internodal tract.

i) The Anterior Internodal Tract (Bachmann–James) It leaves the antero-superior part of the SA node and curves around in front of the superior vena cava, divides into two bundles of fibers one entering the left atrium while the other coursing over the anterior portion of the interatrial septum and descending obliquely behind the root of the aorta to enter the anterosuperior margin of the AV node. ii) The Middle Internodal Tract (Wenckebach) It leaves the postero-inferior margin of the SA node, curves behind the SVC and course along the posterior margin of the interatrial septum to enter the superior margin of the AV node. iii) The Posterior Internodal Tract (Thoral) It leaves the postero-inferior margin of the SA node and follows the course of crista terminalis and eustachian ridge to enter the posterior margin of the AV node. The middle and posterior internodal tracts may also extend the fibers from the right atrium to the left atrium.5 All the three tracts anastomose with each other above the AV node and have transitional cells and common atrial myocardial cells. However, presently the evidence does not support the presence of specialized internodal tracts6 and preferential internodal conduction in some parts of the atrium may be due to atrial myocardial fiber orientation, size and geometry rather than specialized tracts between the nodes.2,7,8

50

BASIC ANATOMY AND PHYSIOLOGY

2. ATRIOVENTRICULAR JUNCTIONAL AREA It consists of three distinct areas: ● ● ●

Transitional cell zone AV node and His bundle.

Transitional Cell Zone It is the ‘outer layer’ of the AV node which connects the right atrial myocardium with the AV node.9,10 This area is sub-divided into three main groups: Anterior or superior, Middle and Posterior or inferior.11 Atrioventricular (AV) Node (Tarawa, 1906) ●

●

●

●

AV node is a small ovoid structure (smaller than SA node) measuring 1  3  5 mm, lies just beneath the right atrial posterior epicardium, anterior to the ostium of coronary sinus and directly above the insertion of the septal leaflet of tricuspid valve. It is located at the apex of the triangle of Koch formed above by the tendon of Todaro, in front by the base of the septal leaflet of tricuspid valve and base by the ostium of the coronary sinus.12 The tendon of Todaro originates from the central fibrous body and passes posteriorly through the atrial septum. The compact AV node becomes the penetrating bundle of His at the apex of the triangle of Koch and passes through the membranous ventricular septum below the point of attachment of the tendon of Todaro to the central fibrous body.

The blood supply is through the AV nodal artery, which is a branch of RCA in 85–90% and LCx in 10–15%. Histologically, it has four types of cells: P cells, transistional cells, atrial myocardial cells and Purkinje cells. Electrophysiologically, AV node is divided into three regions: ● ● ●

AN region N region and NH region.

AN region corresponds to the transitional cell groups in the upper posterior portion of the AV node. N region is a small enclosed region where transistional cells merge with mid nodal cells. NH region is the anterior portion of the bundle of lower nodal cells. The dead end pathways consist of groups of cells that form an apparent electrophysiological cul de sac that does not contribute to overall conduction in the AV node.

THE CONDUCTION SYSTEM OF THE HEART

51

The Bundle of His (AV Bundle, Common Bundle) It is a chord like distal continuation of the AV node measuring 20 mm in length and up to 2 mm in diameter. It is anatomically subdivided into three portions: ● ● ●

Proximal non-penetrating Middle penetrating and Distal branching portion.

Proximal non-penetrating portion is distal to AV node. Middle penetrating portion is the tunneled segment within the fibrous tissue of the central body and the membranous septum. Distal branching portion i) His bundle bifurcates at the crest of the muscular septum into right and left bundles, immediately distal to the membranous ventricular septum. ii) The blood supply is from both LAD and PDA and hence this portion of the conduction system is less subject to the ischemic damage.13 iii) Histologically, His bundle primarily consists of Purkinje cells.

3. THE BUNDLE BRANCHES AND TERMINAL PURKINJE FIBERS The Left Bundle Branch (LBB) It forms a cascade down the left ventricular septal surface beneath the noncoronary aortic cusp. The left bundle radiates in a fanlike fashion with two major divisions: thin anterosuperior and thick posteroinferior fascicles.14 However, Tarawa15 and recent studies indicated a trifascicular division of the left bundle branch.16,17 The Right Bundle Branch (RBB) It is the direct continuation of the His bundle positioned along the right side of the ventricular septum. The right bundle branch becomes a subendocardial structure in the middle lower thirds of the ventricular septum and remains unbranched to the apex of the right ventricle (see Fig. 6.2). Blood Supply The left bundle branch receives blood supply from both LAD and RCA (see Table 6.2). The anterosuperior fascicle is supplied by the septal branches of LAD and AV nodal branch of RCA in 50%; and only by the septal branches of LAD in the other 50%. The posteroinferior fascicle is supplied by the AV nodal branch of RCA in 50% and by both the AV nodal branch of RCA and the septal branch of LAD in the other 50%. The blood supply of right bundle branch is similar to that of the anterosuperior fascicle of the left bundle branch. Histologically, the bundle branches (LBB and RBB) mainly consist of Purkinje cells intermingled with ordinary contractile myocardial cells.

52

BASIC ANATOMY AND PHYSIOLOGY Bundle of His Left anterior fascicle Left septal fibers Left posterior fascicle Right bundle branch

Purkinje fibers

Fig. 6.2

| Bundle branches and Purkinje fibers.

Table 6.2 Blood supply of the bundle branches Structures

Arteries

1. LBB i. Anterosuperior fascicle

Both LAD and RCA 50% by septal branch of LAD and AV nodal branch of RCA 50% only by septal branch of LAD 50% only by the AV nodal branch of RCA 50% by both AV nodal branch of RCA and septal branch of LAD Similar to that of anterosuperior fascicle of LBB

ii. Posteroinferior fascicle

2. RBB

The Terminal Purkinje Fibers These fibers connect with the ends of the bundle branches to form interweaving networks on the endocardial surface of both ventricles. However, Purkinje fibers tend to be concentrated at tips of the papillary muscles rather than at the base of the ventricles. They are more resistance to ischemia than the common myocardial fibres.18

REFERENCES 1. Vieweg MVR, Alpert JS, Hagan DS. Origin of the sinoatrial node and atrioventricular node arteries in right, mixed and left inferior emphasis systems. Cathet Cardiovasc Diag 1975;1(4):361–73. 2. Davies MJ, Anderson RH, Becker AE. The Conduction system of the Heart. Butterworth. 1983:1–200. 3. Lev M. Aging changes in the human sinoatrial node. J Gerontol 1952;9(1):1–9.

THE CONDUCTION SYSTEM OF THE HEART

53

4. James TN, Sherf L. Specialized tissues and preferential conduction in the atria of the heart. Am J Cardiol 1971 Oct; 28(4):414–427. 5. James TN. Anatomy of the conduction system of the heart. In: Hurst JW. Logue RB, Rackley CE, Sonnennblick EH, Wallace AG, et al. The Heart, 5th ed. New York: McGraw-Hill, 1982:26–56. 6. Becker AE, Bouman LN, Janse MK, Anderson RH. Functional anatomy of the cardiac conduction system. In: Harrison DC, ed. Cardiac Arrhythmias: A Decade of Progress, Boston, Hall; 1981:1–18. 7. Anderson KR, Ho SY, Anderson RH. The location and vascular supply of the sinus node in the human heart. Br Heart J 1979;41(1):28–32. 8. Zipes DP. Genesis of cardiac arrhythmias: Electrophysiological consideration. In: Braunwald E,ed. Heart Disease: A Text book of Cardiovascular Medicine, 2nd ed. Philadelphia: Saunders, 1982: 581–620. 9. Tarawa S. Das Reizeitungs system des Saugetierkerzens. Jena: Gustav Fischer, 1906. 10. Anderson AH, Becker AE, Brechenmacher C, Davies MJ, Rossi L. The human atrioventricular junctional area: A morphological study of the AV node and bundle. Eur J Cardiol 1975;3(1):11–25. 11. James TN. The connecting pathways between the sinus node and AV node and human heart. Am Heart J 1963;66:498–508. 12. Franco PM. Recherches sur les faiseaux de connxion auriculaires dans condition normales et pathologies. Arch Mal Coer 1951;22:287–292. 13. Trautwein W, Uchizono K. Electron microscopic and electrophysiologic study of the rabbit heart. Z Zellforsch Mikrosk Anat 1963;61:96–109. 14. Rosenbaum MB, Elizari JO. The Hemiblocks Tampa FL: Tampa Tracings: 1970. 15. Rossi L. Histopathology of Cardiac Arrhythmias. 2nd ed. Milan: Casa Editrice Ambrosiana: 1970: 1–75. 16. Massing GK, James TN. Anatomical configuration of the His bundle and bundle branches n the human heart. Circulation 1976;53:609–621. 17. Demoulin JC, Kulbertus HE. Histopathological examination of concept of left hemiblocks. Br Heart J 1972;34:807–814. 18. Becker AE, Bowman LN, Janse MJ, Anderson RH. Functional anatomy of the cardiac conduction system. In: Harrison DC ed. Cardiac Arrhythmias. A Decade of Progress. Boston: Hall: 1981:3–24.

■ ■ ■ CHAPTER 7

U LTRASTRUCTURE OF THE M YOCARDIUM 1. 2. 3. 4. 5.

P CELLS TRANSITIONAL CELLS PURKINJE CELLS AMOEBOID CELLS CONTRACTILE OR WORKING MYOCARDIAL CELLS

54 54 55 55 56

a) Sarcolemma b) Intercalated Discs c) Sarcotubular System d) Diadic Cleft e) Contractile Proteins REFERENCES

The ultrastructure of the myocardium consists of (see Table 7.1 and Fig. 7.1):

1. P CELLS See chapter 6.

2. TRANSITIONAL CELLS See chapter 6.

Table 7.1 Ultra-structure of the myocardium Cells

Location

1. P cells 2. Transistional cells 3. Purkinje cells

SA node Margins of SA node Margins of SA node, inter nodal tracts, adjacent to AV node, in the His bundle, LBB and RBB Eustachian ridge Atrial and ventricular myocardium

4. Amoeboid cells 5. Contractile cells

57 58 59 60 61 65

ULTRASTRUCTURE OF THE MYOCARDIUM

55

Myofibrils

Sarcolemma

Transverse tubule

Contact of reticulum with T-tubules Z band I band

Sarcoplasmic reticulum

Mitochondrion A band Mitochondrion H zone M line T-tubule (sarcolemmal invagination)

T-tubule Z band Contact of reticulum with T-tubule

Fig. 7.1

| Ultra-structure of the myocardial fibers.

3. PURKINJE CELLS These cells are broader and shorter than contractile myocardial cells measuring 20–50 m in length and 10–30 m in cross section. They are found in the margins of SA node, internodal tracts, adjacent to the AV node, in the His bundle and in its bundle branches.

4. AMOEBOID CELLS The conduction system of the heart also consists of elongated, triangular, oval or nongeometric shaped amoeboid cells in the Eustachian ridge, which have multilobular nuclei, many mitochondria, myofibrils and granules (which give dark appearance to these cells) with pseudopodic prolongations that fill the spaces between the neighboring cells. They may act as an auxiliary pacemaker or may be a source of atrial natriuretic peptide (ANP).

56

BASIC ANATOMY AND PHYSIOLOGY

5. CONTRACTILE OR WORKING MYOCARDIAL CELLS ●

●

●

●

●

They are 10–20 m in diameter and 50–100 m in length surrounded by a cell membrane, known as sarcolemma. The sarcoplasm (cytoplasm) has many mitochondria and centrally located elongated nucleus and many (50–60) myofibrils which are inserted in the region of intercalated disc (see Fig. 7.2 and Table 7.2). Each myofibril is striated, 1–2 m in diameter and lie parallel to one another and composed of a series of sarcomeres, the basic contractile units. The cell membranes of some adjacent cells form close margins called intercalated discs or junctions. The contractile myocardial cells are similar whether they are from the atrial or ventricular myocardium. However, the contractile myocardial cells which contain an intricate sarcotubular system of tubules, vesicles and cisternae1,2 are absent or rare in atrial myocardium.

Fig. 7.2

and anastomosing myocardial fibers with faint striations. The fibers | Branching are made up of cells with centrally placed nucleus. Cells are separated from one another by intercalated discs (arrows).

Table 7.2 Contractile myocardial cell Features

Description

1. Size

10–20 m in diameter 50–100 m in length Bi-layered phospholipid with channels Macula adherens, fascia adherens, gap junction T system, longitudinal sarcoplasmic reticulum 10000 diadic clefts/cell; 11 L-type Ca2 channels and 100 feet/cleft Myosin, actin, titin, tropomyosin, troponin T, C and I

2. 3. 4. 5.

Sarcolemma Intercalated discs Sarcotubular system Diadic cleft

6. Contractile proteins

ULTRASTRUCTURE OF THE MYOCARDIUM ●

57

The myofibrils are made up of the contractile proteins (which give striated appearance) while each intercalated disc consists of three types of specialized junctions.

a) Sarcolemma (Sarco Flesh; Lemma Thin Husk) The cell membrane consists of a bi-layer boundary of phospholipid molecules (see Fig. 7.3). The tail end of the phospholipid molecule is non-polar and hydrophobic pointing toward the center of the cell membrane. The head end is polar and hydrophilic pointing toward the outer and inner layers of the cell membrane (see Fig. 7.4). At rest, the resistance to ions (both cations and anions) is greater across the cell membrane than in the cytoplasm especially in the non polar hydrophobic layer. The cell membrane has openings called channels that span the cell membrane and serve as conduits

Outer membrane protein

Inner membrane protein

Fig. 7.3

Transmembrane protein

Transmembrane protein forming a channel

| Bi-layered cell membrane showing opening (channel). Choline Phosphate Glycerol forming the head

Fatty acids forming the tail

Fig. 7.4

| Tail and head of a phospholipid molecule of the bi-layered cell membrane.

58

BASIC ANATOMY AND PHYSIOLOGY

through which ions move. These channels are broadly made up of two types of protein complexes: i) Type I Intrinsic Membrane Protein (Voltage Operated Channels) These protein molecules protrude through the entire cell membrane and have major part outside the cytoplasm i.e. they are anchored to the inner layer of the cell membrane e.g. Na, K, Ca channels, Na-K pump. ii) Type II Intrinsic Membrane Protein (Ligand Receptors or Receptor Operated Channels) These protein molecules have major part in the cytoplasm with a very small fraction penetrate: ●

●

Only the outer layer of the cell membrane and serve as receptor sites for neurotransmitters and hormones. The inner layer of the cell membrane and serve as receptors for adenylate cyclase.

b) Intercalated Discs Three types of specialized junctions make up each intercalated disc: ● ● ●

Macula adherens or desmosome (see Fig. 7.5) Fascia adherens and Nexus or gap junctions (see Fig. 7.6).

i) Desmosome and Fascia Adherens They form the areas of strong adhesions between the cells and may provide a linkage for the transfer of mechanical energy from one cell to next cell.

Cell membrane Intermediate filaments Gap junction (gap = 3 nm)

Normal intercellular gap (20 nm)

Intercellular gap

Fig. 7.5

| Intercalated discs—Desmosome.

Fig. 7.6

| Intercalated disc—Gap junction.

ULTRASTRUCTURE OF THE MYOCARDIUM

59

ii) The Gap Junctions The cells are separated only by about 10–20 A and are connected by a series of hexagonally packed subunit bridges but are in functional contact with each other. They provide: (i) A low resistance electrical coupling between adjacent cells that permit the movement of ions and other small molecules and (ii) A biochemical coupling that permit cell to cell movement of ATP and other high energy phosphates. ● The gap junctions permit the conduction velocity faster in the direction of the long axis of the fiber than transversely. However, the conduction delay or block occurs more commonly in the longitudinal direction. ● The gap junctions permit a multicellular structure like heart to function electrically like an orderly, synchronized and interconnected unit and are also responsible partly for the anisotropic type of conduction in the myocardium. ● Acidosis increases and alkalosis decreases gap junctional resistance. An increased gap junctional resistance slows the rate of action potential propagation which could lead to conduction delay or block.3 ● Connexins are the proteins that form the intercellular channels of gap junctions. c) Sarcotubular System It is a highly specialized system of internal conduction of depolarization within the muscle fiber. It is made up of T-system and longitudinal sarcoplasmic reticulum (see Fig. 7.7). i) T-system or Transverse Tubular System ● ●

●

The cell membrane invaginates to form the transverse tubular system. The transverse tubules are arranged perpendicular to the long axis of the cell but branch longitudinally and can directly connect with other transverse tubules.4 At the area of Z band/line the T tubules give off a cistern-like structure, the intermediary vesicle.5

Thin filaments Terminal cistern

Triad

Longitudinal sarcoplasmic reticulum Transverse tubule system (T tubule)

ECF

Fig. 7.7

| Sarcotubular system; ECF: extracellular fluid.

60

BASIC ANATOMY AND PHYSIOLOGY

ii) Longitudinal Sarcoplasmic Reticulum ●

●

●

●

●

Longitudinal sarcoplasmic reticulum is a plexiform labyrinth of vesicles and tubules oriented parallel to the myofibrils. At Z band, these have local dilatations, lateral sacs or terminal cisternae which are rich in glycogen and Ca2. So, a triad of an intermediary vesicle and two lateral sacs is formed at Z line which is known as sub-sarcolemma cisternae (cisternae baskets, Latin) and their function is to release calcium from the calcium release channels (ryanodine receptors) in the longitudinal sarcoplasmic reticulum to initiate the myocardial contraction. The impulse rapidly spreads down the transverse tubules and intermediary vesicles to stimulate the lateral sacs (Junctional sarcoplasmic reticulum [JSR]) to release calcium into the diadic cleft for the initiation of myofibrillar contraction.6 There is one triad per sarcomere (two in skeletal muscle). Hence, the sarcotubular system plays an important role both in the electrical impulse conduction7 and electromechanical coupling.5

d) Diadic Cleft ●

●

Diadic cleft is a cleft-like space between the lateral sac of sarcoplasmic reticulum i.e. JSR and T tubular sarcolemmal membrane (It is triadic in skeletal muscle) (see Fig. 7.8).6 The narrow space or cleft between the sarcolemma and JSR is bridged by structures called the ‘feet’ which serve as the sites for calcium release to the diadic cleft space.

“T” tubule 3Na

Anionic sites

Na Na Ca Channel Channel Channel

Exchanger

3Na Sarcolemma Exchanger

Ca

Ca

12 n

m

Foo t

Cleft

Foot



Ca 

Ca

0.2 

m

JSR

Fig. 7.8

| Diadic cleft; JSR: junctional sarcoplasmic reticulum, T tubule: transverse tubule.

ULTRASTRUCTURE OF THE MYOCARDIUM ●

●

●

61

The calcium pump in the longitudinal SR plays an important role in the delivery of calcium to the JSR at the diadic cleft. There are 11 L-type calcium channels and 100 feet within the cleft, one cleft per 2 half sarcomere and about 10000 diadic clefts in each cell. There is a preferential localization of Na/Ca exchangers in the sarcolemma at the cleft through which mainly calcium fluxes out of the cell, while the calcium from the extracellular space enters the diadic cleft via i) L-type Ca channels in the sarcolemma and ii) the release of calcium from the JSR via the feet into the cleft (i.e. calcium induced calcium release [CICR]) by the stimulation from the intermediary vesicles of T system.

e) Contractile Proteins The sarcomere, the basic contractile unit between two Z lines is made up of major and minor proteins organized into thick and thin filaments (A and I bands respectively) which give a pattern of dark and light bands under light microscope (see Fig. 7.9). ●

The A band (highly refractile material i.e. Anisotropic) is the wide dark area between two peripherally located light band, the I band (lower refractile material i.e. isotropic).

Myofibrils

Contact of reticulum with T-tubules Z band I band Mitochondrion A band H zone M line

T-tubule Z band

Fig. 7.9

| Bands in myofibril.

62

BASIC ANATOMY AND PHYSIOLOGY ●

●

●

●

The A band is about 1.5 m in length and consists of both thick myosin and thin actin filaments arranged in a hexagonal pattern with six actin filaments surrounding each myosin filament. The I band is about 1.0 m in length and consists of only thin actin filaments attached to the Z line (Zwischenscheibe i.e. between disc). The H zone (after the discoverer Hansen) is a lighter band in the center of the A band and consists of only myosin filaments. In the center of the H zone is a thin dark line, the M line to which the thick myosin filaments are attached. The M line is particularly pronounced during muscle contraction. The major contractile proteins are:

● ● ● ● ●

Myosin thick filament Titin Actin thin filament Tropomyosin and Troponin T, C and I. While the minor contractile proteins are:

● ● ●

Alpha actinin c-protein and Nebulin.

i) Myosin It consists of a short bilobular head and a long tail or shaft (see Fig. 7.10). (i) The short compact bilobular head is 30 nm in length and 4 nm in diameter. It has two types of chains (myosin heavy chain and myosin light chain) and two important sites. There are three chains around the base of each myosin head: ●

One myosin heavy chain (MHC) (i.e. 2 MHC/bilobed head), the motor of contraction and

Actin

ATPa

Tail (LMM): 100 nm 4 nm Head (HMM) 30 nm

Fig. 7.10

| Myosin bilobed head and tail; Actin: actin binding site, ATPa: ATPase site.

ULTRASTRUCTURE OF THE MYOCARDIUM ●

63

Two myosin light chains (MLC) (i.e. 4 MLC/bilobed head) which perhaps inhibit the contractile process by interaction with actin.8

The two important sites are: ● ●

Actin binding site, where myosin comes in contact with actin and ATPase site that hydrolysis (breaks) ATP.

(ii) The long tail or shaft is 100 nm in length and 2 nm in diameter. It carries the load during contraction. ii) Titin (Connectin) It is the largest, extraordinarily long, flexible and slender myofibrillar protein.9 ● ●

●

It is 0.6–1.2 m in length extending from Z line to just short of the M line. It has two distinct segments: (i) Inextensible segment and (ii) Extensible segment. Titin protein has two main functions:10 (i) Inextensible portion tethers the myosin molecule to the Z line. (ii) Extensible portion stretches as the sarcomere lengthens.

iii) Actin ●

●

●

The thin actin filaments are composed of two actin units, which interwine in a helical pattern, both being carried on a heavier backbone, the tropomyosin molecule. (see Fig. 7.11) The thin actin filament is anchored to the Z line by alpha actinin and stretches from the Z line to the edge of the H zone. It is 4–5 nm in diameter.

iv) Tropomysin–Troponin Complex ●

●

Tropomyosin is a continuous coil of long filaments located in the groove between the two chains (double helix) of actin (see Fig. 7.12). It covers the binding site of actin where the myosin head comes in contact with the actin i.e. it prevents the interaction between actin and myosin filaments. I

C

Troponin

T 4–5 nm Actin Tropomyosin

Fig. 7.11

| Actin and Tropomyosin–troponin complex.

64

BASIC ANATOMY AND PHYSIOLOGY Tropomysin

Troponin

T C I

Actin

Binding site for myosin isoforms

T C I

Fig. 7.12

●

●

| Actin, tropomyosin and troponin.

Located at regular intervals of 38.5 nm along the tropomyosin molecules are three small globular regulatory proteins, the troponins. The three regulatory troponins are: (i) Troponin T: binds other troponins to tropomyosin. (ii) Troponin I: inhibits the interaction of myosin with actin. (iii) Troponin C: contains binding sites for Ca2 that initiates the muscle contraction.

v) Myosin isoforms There are three myosin isoforms depending upon the electrophoretic mobility: V1, V2 and V3. ●

●

●

●

● ●

Each myosin isoform consists of two distinct types of MHC genes. (i) V1 consists of

MHCs (ii) V3 consists of  MHCs and (iii) V2 consists of  MHCs. Each myosin isoform is produced by different gene located on different chromosome (V1 on chromosome 3, V3 on chromsome 14). V1 myosin isoform has high ATPase activity with increased (fast) shortening velocity but low efficiency of force (tension) production, while V3 myosin isoform has low ATPase activity with decreased (slow) shortening velocity but high efficiency of force production. The characters of V2 myosin isoform are in between V1 and V3. In ventricles: In utero until late fetal life V3 myosin isoform is abundant and V1 myosin isoform predominates only transiently shortly after birth. But thereafter,  MHC becomes and remains as the most abundant with 3–10% being MHC. In atria: V1 myosin isoform is predominant throughout the life. With increased work load, the ventricles get switched to V2 myosin isoform (  MHC genes) and atria get switched to V3 myosin isoform ( MCH genes). Re-induction of fetal program is a general adaptative process to the hemodynamic stress (pressure overload/hypertrophy).

ULTRASTRUCTURE OF THE MYOCARDIUM

65

REFERENCES 1. Porter KR, Palade GE. Studies on the endoplasmic reticulum: III. Its form and distribution in striated muscle cells. J Biophys Biochem Cytol 1957;3(2):269–300. 2. Hoffman BF. Physiology of atrioventricular transmission. Circulation 1961;24:506–517. 3. Severs NJ. Pathophysiology of gap junctions in heart disease. J Cardiovasc Electrophysiol 1996;5(5): 462–475. 4. Fawcett DW, McNutt NS. The ultrastructure of the cat myocardium: I. Ventricular papillary muscle. J Cell Biol 1969;42:1–45. 5. Essner E, Novikoff AB, Quintana N. Nucleoside phosphatase activities in rat cardiac muscle. J Cell Biol 1965;25:201–215. 6. Langer GA, Peskoff A. Role of Diadic Cleft in myocardial contractile control. Circulation 1997;96: 3761–3765. 7. Huxley AF, Taylor RE. Local activation of striated muscle fibers. J Physiol 1958;144(3):426–441. 8. Morano I, Ritter O, Bonz A, et al. Myosin light chain–actin interaction regulates cardiac contractility. Cir Res 1995;76(5):720–725. 9. Wang K, Ramirez-Mitchell R, Palter D. Titin is an extraordinarily long, flexible and slender myofibrillar protein. Proc Natl Acad Sci 1984;81(12):3685–3689. 10. Trombitas K, Jin JP, Granzier H. The mechanically active domain of titin in cardiac muscle. Cir Res 1995;77(4):856–861.

■■■

CHAPTER 8

BASIC E LECTROPHYSIOLOGICAL P RINCIPLES SARCOLEMMA, INTERCALATED DISC 66 INTRACELLULAR AND EXTRACELLULAR ION CONCENTRATIONS IN CARDIAC MUSCLE 66 PROPERTIES OF TRANSMEMBRANE POTENTIALS 67

CARDIAC ACTION POTENTIALS i. Phases of the Cardiac Action Potential ii. Origin and Sequence of Cardiac Activation REFERENCES

67 67 71 72

SARCOLEMMA, INTERCALATED DISC See chapter 7.

INTRACELLULAR AND EXTRACELLULAR ION CONCENTRATIONS IN CARDIAC MUSCLE The ionic concentrations of sodium (Na) and chloride (Cl) are more in the extracellular fluid while that of potassium (K) and calcium (Ca) are more in the intracellular fluid (see Table 8.1). Most of the intracellular Ca is bound to or sequestered in intracellular organelles (mitochondria and sarcoplasmic reticulum).

Table 8.1 Intracellular and extracellular ion concentrations Ion

Extracellular concentration

Intracellular concentration

Ratio of extracellular to intracellular concentration

E1 (equilibrium potential for the ion)

Na K Cl Ca

145 mM 4 mM 120 mM 2 mM

15 mM 150 mM 5 mM 10 7 M

9.7 0.027 24 2  104

60 mV 94 mV 83 mV 120 mV

BASIC ELECTROPHYSIOLOGICAL PRINCIPLES

67

PROPERTIES OF TRANSMEMBRANE POTENTIALS The resting potential and action potential amplitude and its overshoot are low in SA and AV nodes than that of atrial and ventricular muscle cells and Purkinje fibers. The propagation velocity of the stimulus is fastest in the Purkinje fibers due to their large size (see Table 8.2).

CARDIAC ACTION POTENTIALS i. Phases of the Cardiac Action Potential The cardiac transmembrane potential consists of five phases: one phase of depolarization, three phases of repolarization and one phase of resting membrane potential and diastolic depolarization (see Fig. 8.1 and Table 8.3): Phase 0: the upstroke or rapid depolarization Phase 1: early rapid repolarization Phase 2: plateau phase Phase 3: final rapid repolarization Phase 4: resting membrane potential and diastolic depolarization. Phase 0: The Upstroke or Rapid Depolarization The action potential which is conducted throughout the heart and responsible for initiating each ‘heart beat’ is independent of the size of the depolarizing stimulus. However, when the stimulus reaches the threshold potential ( 70 to 65 mV for Purkinje fibers) upstroke or rapid depolarization occurs which lasts for 1–2 msec.

Table 8.2 Properties of transmembrane potentials Properties 1. Resting potential (mV) 2. Action potential Amplitude (mV) Overshoot (mV) Duration (ms) Vmax (V/s) 3. Propagation velocity (m/s) 4. Fiber diameter (m)

SA nodal cell

AV nodal cell

Atrial muscle cell

Ventricular muscle cell

Purkinje fiber

50 to 60

60 to 70

80 to 90

80 to 90

90 to 95

60 to 70 0 to 10 100 to 300 1 to 10

70 to 80 5 to 15 100 to 300 5 to 15

110 to 120 30 100 to 300 100 to 200

110 to 120 30 200 to 300 100 to 200

120 30 300 to 500 500 to 700

0.05

0.1

0.3 to 0.4

0.3 to 0.4

2 to 3

5 to 10

5 to 10

10 to 15

10 to 16

100

BASIC ANATOMY AND PHYSIOLOGY 25 Transmembrane potential, mV

68

1 2

0 25 50

3

75 4 100 Na Influx

Fig. 8.1

Ca2 Influx

K Efflux

Na K Efflux Efflux

| Phases of action potential.

Table 8.3 Phases of cardiac action potential Phase

Mechanism

1. Phase 0: rapid depolarization

 INa but ISi in SA and AV nodes

2. Phase 1: early repolarization

(i) Inactivation of INa (ii) Activation of Ito

3. Phase 2: plateau phase

(i) Fall of K conductance (ii) ISi and ICl

4. Phase 3: final rapid repolarization

(i) Inactivation of ISi and ICl (ii) Activation of Ik

5. Phase 4: (a) resting membrane potential

Iki and Ca

(b) diastolic depolarization

(i) Decay of Ik (ii) ISi and If

INa: inward sodium current, ISi: slow inward current, Ito: transient outward current, ICl: small inward current through chloride channel, Ik: outward potassium current, Iki: inward potassium current, If: pacemaker current.

Mechanism for phase 0 (i) The upstroke in atrial and ventricular muscle and Purkinje fibers is due to sudden increase in the membrane conductance to Na i.e. increased inward sodium currents (INa), which is brief (while it is long lasting during plateau phase). ● The rate at which depolarization occurs during phase 0 (V max) is reasonable approximation of the rate and magnitude of Na entry into the cell and when the equilibrium potential for Na (ENa 60 mV) is reached, Na no longer enters the cell.

BASIC ELECTROPHYSIOLOGICAL PRINCIPLES

Rest

Na m h

Activated

m h

Inactivated

m h

69

30 mV

60 90

Fig. 8.2

| Membrane conductance of Na . 

The membrane conductance of Na during phase 0 is hypothetically regulated by two types of gates—m and h (see Fig. 8.2). – Three ‘m’ (activation) gates on the extracellular side and – One ‘h’ (inactivation) gate on the intracellular side of the membrane, which modulate Na passage through the sodium channels. ● When the membrane is in a resting polarized state, the ‘m’ gates are almost completely closed and ‘h’ gate is open and hence, no Na can enter the cell. ● However, depolarization of the membrane opens the ‘m’ gates and closes the ‘h’ gate, ‘m’ gates opening faster than the ‘h’ gate closing i.e. activation of the Na channels proceeds faster than inactivation can occur and Na flows through for about 1–2 msec when both gates are simultaneously open.1 (ii) The upstroke in SA node and AV node is due to slow inward current (ISi) through Ca channels. ●

Phase 1: Early Rapid Repolarization Following phase 0, the membrane repolarizes rapidly and transiently to near 0 mV. Mechanism for phase 1: It is partly owing to the inactivation of inward current (INa) and the activation of a transient outward current (Ito) carried through K channels. Phase 1 is well defined in Purkinje fibers and some muscle fibers but is indistinct and not separated in SA and AV nodes. Phase 2: Plateau Phase During the plateau phase, the membrane voltage remains zero for more than 100 ms. Mechanism for phase 2: Plateau phase is due to: ● ● ●

Fall of K conductance Slow inward current (ISi) through Ca channels and Small inward Cl (ICl) flux through Cl channel.

70

BASIC ANATOMY AND PHYSIOLOGY

Phase 3: Final Rapid Repolarization During this phase, rapid repolarization occurs. Mechanism for phase 3: Final phase of rapid repolarization is due to: ●

●

Time dependent inactivation of slow inward currents ISi and ICl so that intracellular movement of positive charges decreases and Activation of outward K current (Ik).

The net membrane current becomes more outward and the membrane potential shifts in a negative direction. Phase 4: (a) The Resting Membrane Potential It is 50 to 95 mV depending on the cell type i.e. the inside of the cell is negative in relation to the outside of the cell owing to the distribution of ions: K, Na, Ca2, and Cl across the cell membrane. Mechanism for resting membrane potential ●

●

The resting negative membrane potential is mainly due to inward K current (IKi ). During diastole, the cell membrane is quite permeable to K and relatively impermeable to Na and the sodium pump (Na, K ATPase) pumps three Na out of the cell and two K into the cell which results in high intracellular K (150 mM) and low intracellular Na (15 mM). The Ca2 contributes little to the resting membrane potential although changes in the Ca2 concentration can affect the permeability of the cell membrane to other ions, i.e. an increase in Ca2 increases the K conductance. Besides under normal conditions, one internal Ca2 is exchanged for three external Na by the Na/Ca2 exchanger.

Phase 4: (b) Diastolic Depolarization ●

●

●

Under normal conditions, the membrane potential of the atrial and ventricular muscle cells remains steady throughout the diastole. However in SA node, distal portion of AV node, muscles of mitral and tricuspid valves and Purkinje fibers; the resting membrane potential does not remain constant in diastole but gradually depolarizes and when it reaches the threshold potential, it produces spontaneous action potential. This property possessed by the spontaneously discharging cells is known as phase 4 diastolic depolarization and automaticity results when it leads to the initiation of action potential.

Mechanism for automaticity (i) Normal automaticity by SA node: The discharge rate of SA node normally exceeds the discharge rates of other potentially automatic pacemaker sites (e.g. Purkinje fibers) and thus SA node maintains the dominance of the cardiac rhythm. The automaticity of the SA nodal cells is due:  ● mainly to the decay of K current (IK) ● long-lasting slow inward current (I ) while Si

BASIC ELECTROPHYSIOLOGICAL PRINCIPLES ●

71

Phase 4 pacemaker current (If ) contributes only 20%, which is an inward K current produced by the sodium (Na, K ATPase) pump.

(ii) Abnormal automaticity of the Purkinje fibers ● ●

It is mainly due to phase 4 pacemaker current (If)2 and Slow inward current (ISi).

ii. Origin and Sequence of Cardiac Activation a) Atrial Depolarization ●

●

●

●

The normal impulse originates in the SA node and traverses the atria in a wave like front with a velocity of about 1 m/s. As SA node is situated in right atrium, the impulse initially activates the right atrium in a right and anterior direction, thereafter activating the interatrial septum, and lastly, the left atrium in a left and posterior direction. The region of the left atrium to be activated last is the tip of the left atrial appendage or the posteroinferior portion of the left atrium underneath the left inferior pulmonary vein.3 The atrial depolarization is completed in about 0.1 s.

b) Decremental Conduction at the AV Node The impulse then arrives at the AV node through the preferential internodal pathways where it is delayed by about 0.1 s due to smaller size of the AV nodal tissue and slower conduction in the AV node (0.05–0.1 m/s) as compared to Purkinje fibers and other muscle fibers. c) Ventricular Depolarization4 ●

●

●

Ventricular depolarization starts with almost simultaneous activation of central left side of the ventricular septum, the high anterior and apical posterior paraseptal areas of left ventricle (within 5 msec) proceeding from the endocardial to the epicardial surface. At 5–10 ms, left and right ventricles are activated and at 12 ms, remainder of the septum is activated. Initial epicardial activation occurs in the anterior right ventricular epicardial surface near the apex followed by the activation of anterior and inferior left ventricle, continuing in the lateral and basal areas of the left ventricle. The last portion to be depolarized is the basal portion of the septum (at 18 msec).

d) The Atrial Repolarization It follows approximately the same path as atrial depolarization, with the polarity of repolarization opposite to that of depolarization. e) The Ventricular Repolarization It proceeds in a direction opposite to that of depolarization, so its polarity is same as that of depolarization.

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BASIC ANATOMY AND PHYSIOLOGY

REFERENCES 1. 2. 3. 4.

Wit AL, Bigger JT Jr. Possible electrophysiological mechanism for lethal arrhythmias accompanying myocardial ischemia and infarction. Circulation 1975;52(Suppl. 6):III96–115. Irisawa H, Hagiwara N. Ionic current in sinoatrial node cells. J Cardivasc Electrophysiol 1991;2:531–40. Bioneau JP, Canavan TE, Schuessler RB, et al. Demonstration of a widely distributed atrial pacemaker complex in human heart. Circulation 1988;77(6):1221–37. Durrer D, Van Dam RT, Freud GE, et al. Total excitation of the isolated human heart. Circulation 1970;41(6):899–912.

■ ■ ■ CHAPTER 9

M OLECULAR BASIS OF M USCLE CONTRACTION 1) MUSCULAR CONTRACTION Sliding Filament Theory of Huxley and Hanson 2) MUSCULAR RELAXATION 3) THE VELOCITY AND THE AMOUNT OF TENSION

73 74 74

The Bowditch, Staircase, or Treppe Phenomenon The Frank-Starling Law of the Heart REFERENCES

75 75 76

75

1) MUSCULAR CONTRACTION Na entry through Na channels (the influx of Na during exit of Ca by Na/Ca exchanger also generates a small electric current which is insufficient for generation of normal action potential) generates action potential and depolarizes sarcolemma which opens up the L-type Ca channels. The Ca spreads down the T tubules, intermediate vesicles and the lateral sacs (junctional sarcoplasmic reticulum, JSR) in the subsarcolemma cisternae (Triad at Z line) which in turn is taken up by the calcium pump in the sarcoplasmic reticulum (i.e. calcium pumping ATPase of sarcoplasmic reticulum, also called SERCA i.e. sarco-endoplasmic reticulum Ca ATPase) to deliver Ca to the JSR at the diadic cleft via the feet. The Ca released in the diadic cleft: ●

●

Binds to troponin C which weakens the binding of troponin I to actin. This permits tropomyosin to move laterally, uncovering the binding sites of actin (7 myosin sites for each molecule of troponin T that binds a Ca); increases the myosin head ATPase activity to hydrolyze ATP into ADP and P1 (produces energy) and increases the phosphorylation of myosin light chain (which increases the affinity of myosin to actin). It also stimulates myocardial energy production by activating glycogen phosphorylase (which results in increased glycogenolysis), phosphofructokinase (which increases glycolysis) and pyruvate dehydrogenase (which stimulates the citric acid cycle with production of ATPs). The myosin heads interact with actin filaments forming cross-bridges (cross-linkages between myosin and actin) resulting in contraction through sliding filament mechanism. As the actin filaments move towards the center of the sarcomere, drawing the Z line closer, there occurs the shortening of the sarcomere (see Fig. 9.1).

74

BASIC ANATOMY AND PHYSIOLOGY

Myosin head attached due to Ca2 release

Myosin head swivels (turns freely on a pivot)

Myosin head detaches ready for next move

Fig. 9.1

| Mechanism of formation of cross bridges.

Sliding Filament Theory of Huxley and Hanson1 The shortening of contractile elements in the muscle is brought about by the sliding of actin filaments over the thick myosin filaments. ●

●

The sliding of the filaments is brought about by formation of the cross-bridges between the myosin head and actin filament. Additional Ca2 enters the cytosol through Ca2 channels during the lateral portion of the plateau phase of the action potential and also a small amount of Ca2 enters by the Na/Ca2 exchanger. Neither contributes to the CICR (Ca induced Ca release) in the SR (which is initiated by Ca2 entry via L-type calcium channels) but are stored in the SR to provide Ca2 for the subsequent contraction.

2) MUSCULAR RELAXATION ●

●

●

The rise in cytosolic (diadic cleft) Ca increases uptake of Ca2 into the SR by the calcium pump (SERCA) which diffuses back to the lateral sacs (see Fig. 9.2). This causes Ca2 to dissociate from troponin C which initiates conformational changes in the toponin-tropomyosin complex that inhibits actin and myosin interaction thereby causing relaxation. The Ca2 in the subsarcolemmal cisternae is effluxed from the myocardial cell mainly by the Na/Ca2 exchanger in which one Ca2 leaves the cell in exchange for three Na which are subsequently pumped out of the cell by Na, K-ATPase (sodium pump) in exchange for two K.

MOLECULAR BASIS OF MUSCLE CONTRACTION

Action potential

Increased sarcoplasmic reticulum uptake of Ca2

↓

Depolarization of sarcolemma and transverse ‘T’ tubular system ↓

75

↓

Ca2 efflux→ sarcoplasmic Ca2 ↓

Influx of Ca2 ↓

Calcium-induced Ca2 release from sarcoplasmic reticulum ↓

Binding of Ca2 to troponin C

Ca2 binding to troponin C ↓

Troponin-tropomyosin complex inhibition of actin–myosin contraction

↓

↓

Release of inhibition of actin and myosin

Actin–myosin relaxation

↓

Actin–myosin contraction Fig. 9.2

| Myocardial contraction and relaxation.

3) THE VELOCITY AND THE AMOUNT OF TENSION The velocity and the amount of tension developed by the actin-myosin filaments are directly related to the amount of Ca2 available to induce contraction. ●

●

●

Hence, an increased iontropic effect is seen in the following conditions where Ca2 availblity for activation is increased: – Drugs such as digitalis, sympathomimetic amines, phosphodiesterase inhibitors – Conditions like increased heart rate, paired pacing, postextrasystolic potentiation. Similarly, the negative iontropic effect of acidosis is due to decreased amount of Ca2 availability and decrease in the Ca2 sensitivity of the troponin complex. So, also at shorter sarcomere lengths, the Ca2 sensitivity of troponin is reduced and developed force is decreased.

The Bowditch, Staircase, or Treppe Phenomenon Increased heart rate abruptly increases the contractile force (which is due to increased availability of Ca2).2 Whereas, a long pause decreases the strength of contraction and is known as the Woodworth or reverse staircase phenomenon.3 The Frank-Starling Law of the Heart4 The force of contraction of the muscle fiber is directly proportional to its initial length i.e. the larger the initial length of the cardiac muscle fibers (preload), greater will be the force of contraction. It is one of the major mechanisms by which the normal right and left ventricles maintain equal minute outputs but their stroke outputs may vary considerably during normal respiration.

76

BASIC ANATOMY AND PHYSIOLOGY ●

●

●

At sarcomere length of 2 m, the actin filaments bypass one another and developed tension is less and At 2.2 m length of sarcomere, actin and myosin filaments are optimally overlapped to provide greatest tension. However at  than 2.2 m sarcomere length, the developed tension decreases as myofilaments are partially or completely disengaged.

Theoretically, the normal ventricle may have an ejecton fraction (EF) of 55% with a shortening of individual sarcomere length of only 13%.5

REFERENCES 1. 2. 3. 4. 5.

Huxley HE, Hanson J. Changes in the cross-striations of muscle during contraction and stretch and their structural interpretation. Nature 1954 May 22;173(4412):973–6. Sonnenblick EH, Morrow AG, Williams JF Jr. Effects of heart rate on the dynamics of force development in the intact human ventricle. Circulation 2. 1966;33(6):945–951. Woodworth RS. Maximal contraction, staircase contraction, refractory period and compensatory pause of the heart. Am J Physiol 1902;8:213–249. Starling EH. The Linacre Lecture on the Law of the Heart. London: Longman. Green: 1918. Wiggers CJ. Determinants of cardiac performance. Circulation 1951;4:485–495.

■■■

CHAPTER 10

T HE CARDIAC CYCLE 1.

VENTRICULAR SYSTOLE 78 i. Isovolumic Contraction 79 ii. Rapid Ventricular Ejection Phase 79 iii. Slow or Reduced Ventricular Ejection Phase 79 2. VENTRICULAR DIASTOLE 79 i. Protodiastole 79 ii. Isovolumic Relaxation Phase 80 iii. Rapid Ventricular Filling Phase 80

iv. Slow Ventricular Filling Phase 3. ATRIAL SYSTOLE 4. ATRIAL DIASTOLE 5. THE DIFFERENCES IN THE EVENTS BETWEEN RIGHT AND LEFT SIDES OF THE HEART 6. ECG CHANGES DURING CARDIAC CYCLE REFERENCES

80 81 81

81 82 82

The sequence of changes in the pressure and flow in the cardiac chambers and blood vessels in between the two subsequent cardiac contractions is known as Cardiac cycle (see Table 10.1 and Fig. 10.1). The cardiac cycle was first described by Wiggers1 but was fully assembled by Lewis.2 Normal duration of the cardiac cycle is 0.8 sec at the heart rate of 75/min. It consists of: ● ●

Ventricular systole: 0.3 s Ventricular diastole: 0.5 s Table 10.1 The cardiac cycle Phase of cardiac cycle

Duration

1. Ventricular systole i. Isovolumic contraction ii. Rapid ventricular ejection phase iii. Slow ventricular ejection phase

0.3 s 0.05 s 0.10 s 0.15 s

2. Ventricular diastole i. Protodiastole ii. Isovolumic ventricular relaxation phase iii. Rapid ventricular filling phase iv. Slow ventricular filling phase (diastasis) v. Last rapid filling phase

0.5 s 0.04 s 0.08 s 0.10–0.12 s 0.18–0.20 s 0.06–0.10 s

3. Atrial systole

0.1 s

4. Atrial diastole

0.7 s

78

BASIC ANATOMY AND PHYSIOLOGY 120

Aorta

80

tricle

60

Left ven

Pressure (mmHg)

100

40

20

Pulmonary artery ventricle a z Left atrium

t ventricle Righ

v

Left atrium Right x atrium

c

Left atrium

y

Right

0

Right ventricle

PC TO

TC PO

Right

Valve motion

MC

MO

AC

AO

Left S4

Sounds Volume curve of left ventricle Jugular pulse

S2

‘CLICKS’ S1

c

a z

S3

OS

v y

x

E

a IC Apex cardiogram

SFW

IR P

ECG 0

Fig. 10.1

0.1

0.2

0.3

RFW

O

T

ORS

0.4

0.5

0.6

The cardiac cycle correlations—MC: mitral component of S , AC: aortic com| ponent of S , TC: tricuspid component of S , PC: pulmonary component 1

2

1

of S2, MO: mitral valve opening, AO: aortic valve opening, TO: tricuspid valve opening, PO: pulmonary valve opening.

● ●

Atrial systole: 0.1 s Atrial diastole: 0.7 s.

1. VENTRICULAR SYSTOLE It is associated with ejection of blood out of the ventricles. It consists of: ● ● ●

Isovolumetric (isovolumic or isochoric) contraction: 0.05 s Rapid ventricular ejection phase: 0.10 s Slow ventricular ejection phase: 0.15 s.

THE CARDIAC CYCLE

79

i. Isovolumic Contraction It is the first phase of ventricular systole. This phase begins with the rise of pressure in the ventricles after the Z point. Although ventricular contraction occurs during this phase, there is no ventricular emptying and hence this phase is known as isovolumic contraction. This phase is associated with: ●

●

Initial mitral component (M1) of the first sound as the ventricular pressure exceeds the atrial pressure causing closure of the atrioventricular (AV) valves and Beginning of the isovolumic contraction (IC) wave of the apex cardiogram.

ii. Rapid Ventricular Ejection Phase This phase begins with the opening of the semilunar valves (aortic and pulmonary) when the LV pressure exceeds the aortic pressure and RV pressure exceeds the pulmonary artery (PA) pressure. It is associated with: ●

● ● ●

Rise in arterial pressure (aorta and PA) as blood enters the great vessels much faster than it can escape into the peripheral branches Decrease in ventricular volume About 2/3rd of the stroke volume is ejected during this phase and Peak of ejection E wave of the apex cardiogram.

iii. Slow or Reduced Ventricular Ejection Phase This phase occurs before the closure of the semilunar (SL) valves and: ●

●

●

It is associated with decline in the ventricular pressure as ventricular contraction begins to subside with slow ejection of blood During this phase, blood flows out of the aorta and PA more rapidly than it enters from the ventricles The blood flow in the aorta is maintained by the aortic distensibility, known as Windkessel effect.3

2. VENTRICULAR DIASTOLE It consists of: ● ● ● ● ●

Protodiastole : 0.04 s Isovolumetric (isovolumic) ventricular relaxation phase : 0.08 s Rapid ventricular filling phase : 0.10–0.12 s Slow ventricular filling phase or diastasis : 0.18–0.20 s Last rapid ventricular filling phase (due to atrial systole) : 0.06–0.10 s.

i. Protodiastole At the end of ventricular systole, the ventricular pressure drops more rapidly but the pressure in the great arteries is sustained by the elastic recoil of the vessel wall which

80

BASIC ANATOMY AND PHYSIOLOGY

exceeds that in the ventricles, resulting in the closure of the SL valves producing second heart sound and incisura of the arterial pressure tracing. ii. Isovolumic Relaxation Phase It begins after the closure of the SL valves and the intraventricular pressure continues to decline rapidly and ventricular muscle continues to relax without any change in the ventricular volume. Hence, this phase is known as isovolumic relaxation phase. ●

●

It is associated with an inward isovolumic relaxation wave (IRW) of the apex cardiogram (see Fig. 10.2). It lasts until the ventricular pressure falls below the atrial pressure and AV valve opens.

iii. Rapid Ventricular Filling Phase It accounts for most of the ventricular filling. It begins with the opening of the AV valves when the intraventricular pressure falls below that of atrial pressure and blood begins to flow from the atria into the ventricles. It is characterized by: ● ●

●

●

An increase in the ventricular volume with a fall of intraventricular pressure. Initiation with O point of apex cardiogram followed by outward rapid filling wave (RFW) of the apex cardiogram (see Fig. 10.2). The rapid filling phase may cause the physiological third heart sound (S3) or ventricular gallop.4 It is associated with a y descent (atrial emptying) both in atrial pressure tracing and jugular venous pressure (JVP).

iv. Slow Ventricular Filling Phase During this phase, the intraventricular pressures slowly rises as the ventricles are passively filled from the atria with decreased rate. IVC: 0.05 s S1, IC of ACG

RVE: 0.10 s E of ACG

SVE: 0.15 s

Protodiastole: 0.04 s S2

LRF: 0.06 s a of ACG

Fig. 10.2

SVF: 0.18 s SFW of ACG

RVF: 0.10 s S3, RFW of ACG

IVR: 0.08 s IRW of ACG

cycle and correlations with heart sounds and apex cardiogram (ACG) | Cardiac (diagrammatic)—IVC: isovolumic contraction, RVE: rapid ventricular ejection, SVE: slow ventricular ejection, IVR: isovolumic relaxation, RVF: rapid ventricular filling, SVF: slow ventricular filling, LRF: last rapid filling (atrial systole), IRW: isovolumic relaxation wave, RFW: rapid filling wave, SFW: slow filling wave.

THE CARDIAC CYCLE ●

●

81

There is equalization of atrial and ventricular pressures and ventricular filling partially stops (diastasis separation). However, renewed ventricular filling (i.e. last rapid ventricular filling) occurs by atrial systole. This phase is characterized by slow filling wave (SFW) of apex cardiogram.

3. ATRIAL SYSTOLE It occurs following the impulse generation in the SA node. With atrial contraction (‘atrial kick’), the increased atrial pressure results in an increase in the ventricular volume i.e. the last rapid ventricular filling phase which constitutes about 30% of the ventricular filling. It produces: ● ● ●

a wave in the atrial pressure tracing and in JVP Outward a wave of apex cardiogram (see Fig. 10.2) There may be a fourth heart sound, S4 (atrial gallop) at the peak of the atrial a wave particularly if there is vigorous atrial contraction and relaxation.

At times, an h wave is present in late diastasis prior to the occurrence of an a wave in the left atrial pressure tracing.

4. ATRIAL DIASTOLE During this phase, atrial muscles relax (producing x descent wave in atrial pressure and JVP) and atrial pressure gradually increases due to the continuous venous return (producing v wave in atrial pressure and JVP) until the opening of the AV valves.

5. THE DIFFERENCES IN THE EVENTS BETWEEN RIGHT AND LEFT SIDES OF THE HEART i) The right atrial systole precedes left atrial systole and opening of the tricuspid valve occurs slightly before the opening of the mitral valve. ii) However, the LV systole precedes the RV systole although the RV ejection of blood into the PA begins before the LV ejection (of the blood into the aorta) since the PA pressure is lower than the aortic pressure and RV pressure does not have to increase to such a high level before the ejection commences. ● Besides, the RV ejection lasts beyond the LV ejection resulting in a normal gap between A2 and P2 of the second heart sound. ● The shorter duration of LV ejection is related to the greater contractile force of the LV and to the differences in the aorta and PA impedance and the compressionchamber (Windkessel) characteristics.

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BASIC ANATOMY AND PHYSIOLOGY

Table 10.2 The cardiac cycle and ECG changes Waves/intervals

Cause

1. P wave 2. QRS complex 3. T wave

Atrial depolarization Ventricular depolarization Ventricular repolarization and end of T wave coincides with SL valves closure Atrial depolarization and His bundle conduction Ventricular depolarization and repolarization Ventricular repolarization Polarized state of the whole myocardial segment Slow repolarization of the Purkinje fibers/M cells deep in the subepicardium

4. 5. 6. 7. 8.

PR interval QT interval ST segment TP segment U wave

6. ECG CHANGES DURING CARDIAC CYCLE ● ●

●

●

●

P wave is due to atrial depolarization and precedes atrial systole (see Table 10.2). QRS complex is due to ventricular depolarization, precedes ventricular systole and is completed before the opening of the SL valves. T wave is due to ventricular repolarization and end of the T wave coincides with the closure of the SL valves. PR interval represents the atrial depolarization and His bundle conduction. QT interval represents ventricular depolarization and repolarization. ST segment represents ventricular repolarization. TP segment from the end of T wave to the beginning of P wave of next cardiac cycle is the TP segment. It represents the polarized state of the whole segment. U wave is sometimes seen as a small positive wave (with 0.08 sec duration and 0.1 mV height) due to slow repolarization of Purkinje fibers,5 but is more recently found to be due to the repolarization of M cells in subepicardium6 (see Table 10.2).

REFERENCES 1. 2. 3. 4. 5. 6.

Wiggere CJ. Modern Aspects of the Circulation in Health and Disease. Philadelphia, Lea and Febiger, 1915:98. Lewis T. The Mechanism and Graphic Registration of the Heart Beat. London, Shaw and Sons, 1920:24. Belz GG. Elastic properties and Windkessel function of the human aorta. Cardiovasc Drugs Ther 1995;9(1):73–83. Glower DD, Murrah RL, Olsen CO, et al. Mechanical correlates of the third heart sound. J Am Coll Cardiol 1992;19(2):450–457. Surawicz B. U wave: Facts, hypothesis, misconceptions, and misnomers. J Cardiovasc Electrophysiol 1998;9(10):1117–1128. Antzelevitch C, Sicouri S. Clinical relevance of cardiac arrhythmias generated by after depolarizations: Role of M cells in the generation of U waves, triggered activity and torsades de pointes. J Am Coll Cardiol 1994;23:259–277.

THE HISTORY AND SYMPTOMATOLOGY 11. Cardinal symptoms 12. Other symptoms

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■ ■ ■ CHAPTER 11

CARDINAL SYMPTOMS IMPORTANCE OF HISTORY TAKING 1. CHEST PAIN Etiology 1. The Duration of Chest Pain 2. The Location and Radiation of Chest Pain 3. Character and Mode of Onset of Chest Pain 4. Aggravating and Relieving Factors 5. Patient’s Gestures During Chest Discomfort 6. Associated Symptoms 7. Non Cardiac chest pain

85 87 87 89 90 93 98 100 100 101

2. SHORTNESS OF BREATH (SOB)/DYSPNEA 1. Dyspnea 2. Pathogenesis of Dyspnea 3. Etiology 4. Evaluation 3. PALPITATION 1. Etiology 2. Evaluation 4. FATIGUE 5. SYNCOPE 1. Etiopathogenesis REFERENCES

101 101 101 104 105 112 112 114 119 119 119 142

IMPORTANCE OF HISTORY TAKING ●

●

A carefully obtained history and careful clinical examination remains the cornerstone of the assessment of the patients with known or suspected cardiovascular disease despite the availability of many specialized investigations. It is undesirable to subject the patients to unnecessary risks and expenses inherent in many specialized tests when a diagnosis can be made on the basis of: – – – –

●

●

●

An adequate history and clinical examination Chest roentgenogram ECG and Other routine laboratory tests.

Besides, the history and physical examination provide the critical information necessary for the intelligent selection of ever increasing array of these tests. It provides a glimpse of the patient’s responsibility, fears, and aspirations which help to assess patient’s personality, emotions and stability. It also establishes a bond with the patient that may be valuable in securing patient’s compliance in following a diagnostic workup and treatment plan.

86

THE HISTORY AND SYMPTOMATOLOGY ●

●

●

However, many patients with severe heart disease have no symptoms while others have many symptoms associated with minor or no heart disease. We also know that some patients deny the presence of any symptoms as they do not accept the reality of the situation while others may purposefully withhold the information and some others overstate their symptoms for personal gains. Hence, whenever possible the examiner should question the patient’s relatives or close friends in order to obtain a clearer understanding of the extent of patient’s disability and importance of the disease on both the patient and the family. However, the ‘important facts’ that are not elicited during the initial history taking are usually not detected later.

The cardinal symptoms of cardiovascular system involvement are (see Table 11.1): 1. 2. 3. 4. 5.

Chest pain. SOB/Dyspnea. Palpitation. Fatigue. Syncope.

Table 11.1 Cardiovascular causes of cardinal symptoms Chest pain

Dyspnea

1. CAD 2. AS, AR, HCM

1. Cardiomyopathy 2. Valvular heart disease 3. Aortic dissection 3. Pericardial disease 4. Pericarditis 4. CHF 5. MVP

6. Severe systemic hypertension

7. Pulmonary hypertension

5. Pulmonary vascular disease

Palpitation

Syncope

Fatigue

1. AR, MR, TR 2. PDA, VSD

1. LVOTO: AS, HCM 2. RVOTO: PS

1. AMI 2. HF

3. ARVH 4. Ebstein’s anomaly 5. Cyanotic CHD with  PBF: TAPVC, TGA without PS 6. Tachyarrhythmias bradyarrhythmias, pacemaker related

3. CAD 4. Aortic dissection

3. Diuretics 4. Beta blockers

5. Tachyarrhytmias bradyarrhythmias pacemaker related 6. During and following catheterization 7. Nitrate syncope

CAD: coronary artery disease, AS: aortic stenosis, AR: aortic regurgitation, HCM: hypertrophic cardiomyopathy, MVP: mitral valve prolapse, CHF: congenital heart failure; MR: mitral regurgitation, TR: tricuspid regurgitation, PDA: patent ductus arteriosus, VSD: ventricular septal defect, ARVH: arrhythmogenic right ventricular hyperplasia, CHD: congenital heart disease, LVOTO: left ventricular outflow tract obstruction, PBF: pulmonary blood flow, TAPVC: total anomalous pulmonary venous connection, TGA: transposition of great arteries, PS: pulmonary stenosis, RVOTO: right outflow tract obstruction, AMI: acute myocardial infarction, HF: heart failure.

CARDINAL SYMPTOMS

87

1. CHEST PAIN Etiology The etiology of the chest pain is extensive. The important causes are given below (see Fig. 11.1): i. Cardiovascular Causes 1. Coronary artery disease (CAD) ● ●

Angina pectoris (AP) Myocardial infarction (MI).

2. Other cardiovascular causes a) Likely ischemic in origin: ● ● ● ● ● ●

Aortic stenosis (AS) Aortic regurgitation (AR) Hypertrophic cardiomyopathy Severe systemic hypertension Severe pulmonary hypertension Severe anemia/hypoxia.

b) Non ischemic in origin: ● ● ●

Aortic dissection Pericarditis Mitral valve prolapse.

ii. Non Cardiovascular Causes 1. Gastrointestinal ● ●

Esophageal spasm Esophageal reflux

Ischemic chest pain

CAD: MI, Angina

Fig. 11.1

Valvular: 1. AS 2. AR

Cardiovascular chest pain

1. HCM 2. Severe systemic hypertension 3. Severe pulmonary hypertension

Non ischemic chest pain

1. Aortic dissection 2. Pericarditis 3. MVP

(CV) chest pain—CAD: coronary artery disease, MI: myocardial | Cardiovascular infarction, AS: aortic stenosis, AR: aortic regurgitation, HCM: hypertrophic cardiomyopathy, MVP: mitral valve prolapse.

88

THE HISTORY AND SYMPTOMATOLOGY ● ● ● ●

Esophageal rupture Acid peptic disorders Acute cholecystitis Acute pancreatitis.

2. Respiratory a) Pulmonary: pulmonary embolus with or without pulmonary infarction. b) Pleural: ● Pnuemothorax ● Pleurisy ● Pneumonia with pleural involvement. 3. Neuro-musculoskeletal ● ● ● ● ●

Thoracic outlet syndrome Costochondritis (Tietze’s syndrome) Herpes zoster Chest wall myalgias, trauma Cervicodorsal spine: i. Cervical spondylitis ii. Osteoarthritis of cervical and upper dorsal spine.

4. Psychogenic Anxiety Depression ● Cardiac psychosis ● Self gain. The history remains the most important and valuable mode of examination for distinguishing among the many causes of chest discomfort (see Table 11.2), and while obtaining the history the following has to be determined. ● ●

Table 11.2 Differential diagnosis of chest pain Features

Cardiac ischemic chest pain

Non cardiac chest pain

1. Duration 2. Location

2–5 min, 15–30 min Precordial or substernal and diffuse Left shoulder, ulnar aspect of arm and fore arm, neck Squeezing, choking, pressing or tightness Exertion and/or emotion

20 s, min to hrs More peripheral, epigastric and localized Left lower chest or others or no radiation Sharp, shooting, lancing, catching, or dull ache Not related to exertion, spontaneous or provoked by food, posture or respiration Food, lying on the same side or nitrates have some or no response Respiratory, gastrointestinal or psychological symptoms

3. Radiation 4. Character 5. Precipitating or aggravating factors 6. Relieving factors

Rest, nitrates

7. Associated symptoms

SOB, palpitation or syncope

CARDINAL SYMPTOMS

89

1. Duration, frequency, mode of onset and pattern of recurrences of chest discomfort if any. 2. Location, radiation and character of chest discomfort. 3. Setting in which it occurs i.e. aggravating and relieving factors. 4. Patient’s gestures to be observed during chest discomfort. 5. Associated symptoms. 1. The Duration of Chest Pain It helps in determining its etiology. a) The Chest Pain Lasting for a Few Seconds Chest pain lasting for 20 sec: Angina can be excluded and is usually due to ● ● ●

Musculoskeletal causes Hiatus hernia and Functional causes.

b) The Chest Pain Lasting for a Few Minutes ● ● ●

Chest pain in angina pectoris usually lasts for 2–5 min (not 15 min, see Fig. 11.2). Chest pain in unstable angina lasts for 20 min (see Fig. 11.3). Hyperventilation: functional chest pain is often preceded by hyperventilation which causes increased muscle tension which in turn is responsible for diffuse chest tightness which lasts for 2–3 min.

c) The Chest Pain Lasting for Minutes to Hours i) Cardiovascular causes ● In acute myocardial infarction, pain usually lasts for 15 min to 30 min. In 30% of the patients, it is painless or atypical especially in diabetic and elderly patients. ● Pericarditis

Unstable angina

Stable angina

Fig. 11.2

angina, chest pain | Inlastsstable for 2–5 min.

Fig. 11.3

angina, chest pain | Inmayunstable lasts for 20 min.

90

THE HISTORY AND SYMPTOMATOLOGY ● ●

Aortic dissection Mitral valve prolapse.

ii) Non cardiovascular causes ● ● ● ●

Neuro-musculoskeletal disorders, including herpes zoster Gastrointestinal: esophageal causes, acid peptic disorders Respiratory: pulmonary embolism, pneumothorax and pleurisy Psychogenic: anxiety.

2. The Location and Radiation of Chest Pain a) Cardiovascular Causes i) Cardiac ischemic chest pain: It is usually felt in precordium or substernally. ●

●

It is diffuse and eludes precise localization, often radiates or is referred to the same corresponding segmental dermatomes (C8-T4)1 i.e. left shoulder, ulnar aspect of left arm and forearm and neck, less often to jaws, epigastrium, right chest and right arm. There is some relationship between location of ischemic chest pain and site of coronary artery occlusion. Substernal or left chest pain with radiation to left arm usually involves left coronary artery, while epigastric pain radiating to the neck or jaw usually do not have the disease of left anterior descending artery2 (see Fig. 11.4).

ii) The chest pain in pericarditis: It is more left sided than central and is often referred to neck, may also radiate to left shoulder, left arm or jaw.

Fig. 11.4

| Usual distribution of chest pain in MI.

CARDINAL SYMPTOMS

91

iii) The chest pain in aortic dissection: It is acute, excruciating, may migrate from the anterior chest to the back and may radiate widely including the neck, arms and legs depending on its location and progression. ● Aortic dissection should be considered in the setting of severe hypertension or Marfan syndrome, chest trauma, direct trauma to aorta or iatrogenic trauma (intra-arterial catheterization and insertion of intraoartic balloon pump). 3 ● The location of pain is helpful in suggesting the location of aortic dissection. – When the location of the chest pain is anterior only, involvement of ascending aorta in 90% of cases (see Fig. 11.5). – When the chest pain is located in the interscapular region only, there is involvement of descending thoracic aorta in 90% of cases (i.e. De Bakey’s type I or III dissection.) (see Figs 11.6 and 11.7). Type II

Fig. 11.5

Type I

location of the chest pain | Anterior usually in type II (De Bakey’s)

Fig. 11.6

Type III

I & III (De Bakey’s) | Type aortic dissection.

aortic dissection.

Back

Fig. 11.7

chest pain in aortic dissection (DeBakey’s type I or III), but | Interscapular less commonly in MI.

92

THE HISTORY AND SYMPTOMATOLOGY

Fig. 11.8

spondylosis. In | Cervical this conditions, pain may

Fig. 11.9

radiate to left shoulder but usually from neck.

rib (complete on left side). | Cervical In this conditions, pain may radiate to left shoulder but usually from neck.

– The presence of any pain (or radiation) in the neck, throat, jaw or face, strongly predicts the involvement of ascending aorta whereas pain in the back, abdomen or lower limbs strongly predicts the involvement of descending aorta. b) Non Cardiovascular Causes i) The chest pain localized to left nipple or cardiac apex or that radiates to left lower chest is usually non cardiac in origin and could be due to: ● ● ●

cervicodorsal osteoarthritis acid peptic disorder, resulting in gaseous distention of the stomach functional causes (psychogenic chest pain).

ii) The pain due to disorders of cervical spine: and left arm (see Figs 11.8 and 11.9).

It can also radiates to left shoulder

iii) In Tietze’s syndrome: The pain is localized to the costochondral and costosternal joints (chest wall); while in herpes zoster, persistent pain is localized to a dermatome along the intercostal space. iv) In thoracic outlet syndrome: The pain is often associated with paresthesias along the ulnar nerve distribution and forearm. v) The pain is substernal or epigastric in location in esophageal disorders, acid peptic disorders and in acute pancreatitis (see Fig. 11.10).

CARDINAL SYMPTOMS

93

Epigastrium

Fig. 11.10

●

● ●

pain is usually due to esophageal disorders, acid peptic disease | Epigastric or acute pancreatitis, but less commonly due to MI.

The esophageal pain radiates more often to the back and less often to the left shoulder, left arm and forearm Vs the anginal chest pain. Also, the pain in acute pancreatitis is usually transmitted to the back. The pain in biliary colic is generally most intense in right upper abdomen but may be present in the epigastrium or felt in the precordium, often referred to the scapula, and may radiate to the back or shoulder (in case of diaphragmatic irritation).

3. Character and Mode of Onset of Chest Pain a) Cardiovascular Causes i) Angina: pertinent. ●

●

●

●

Heberdens4 initial description of chest discomfort is still remarkably

Angina means choking not pain and is often described as: (i) pressing (ii) vice like (iii) squeezing (iv) heaviness (v) constricting (vi) burning (vii) tightness (viii) bursting (ix) choking (suffocating) (x) or weight in the chest. However, the quality of chest pain described by the patient is greatly influenced by the patient’s intelligence, education and social cultural background. Hence, any other description should be noted and evaluated appropriately. Anginal discomfort is crescendo in nature rather than reaching peak intensity instantaneously as in aortic dissection. The anginal threshold is lower in the morning and the activities that cause angina in the morning do not do so later in the day. Anginal equivalents: Instead of chest pain, some patient may describe other symptoms/ discomfort e.g. a patient may describe: – The mid chest as the site of shortness of breath, whereas true dyspnea is not usually well localized. – Discomfort in sites of secondary radiation such as shoulders, ulnar aspect of left arm and forearm, lower jaw or neck.

94

THE HISTORY AND SYMPTOMATOLOGY

Dilated aorta

Aortic valve

Dilated left ventricle

Fig. 11.11

| Nocturnal angina is characteristic of severe chronic AR.

– Development of gas and belching, nausea, indigestion, dizziness or diaphoresis. However, anginal equivalents above the mandible or below the umbilicus are uncommon. ●

Nocturnal anginal pain occurs when the diastolic blood pressure decreases to lower levels in nights and is typically described in severe chronic aortic regurgitation and in unstable angina (rest angina) (see Fig. 11.11).

ii) In aortic dissection: The pain is sudden in onset, excruciating and persistent with radiation to the site depending upon its location and progression. iii) In acute pericarditis: The pain is sharper than angina, more left sided than central and often referred to the neck. iv) The chest pain in MVP: It varies considerably among the patients (see Fig. 11.12). It may be similar to that of classic angina pectoris or may resemble the chest pain of neurocirculatory asthenia (functional). b) Non Cardiovascular Causes i) Shooting or lancing pain of short duration usually suggests musculoskeletal or neural pain. ●

●

The chest pain in Tietze syndrome is associated with swelling and tenderness of costochondral and costosternal joints while in myositis, pain is associated with muscular tenderness. In both, pain is aggravated by moving or coughing. Herpes zoster mimics MI when the left chest is affected, however the persistence pain, its localization to a dermatome and appearance of characteristic vesicles allow its recognition (see Fig. 11.13).

CARDINAL SYMPTOMS

95

LA

LV

Fig. 11.12

pain in mitral valve prolapse (arrow) is variable-simulating angina to | Chest that of neurocirculatory asthenia.

Fig. 11.13

zoster, pain is persistent with characteristic skin lesions localized | Into herpes a dermatome.

ii) In GIT etiology 1. In esophageal spasm, substernal or epigastric pain is squeezing, burning or aching in quality which is brought by eating, during swallowing or by lying down after meals and may be relieved with antacids and nitroglycerine. ●

●

Barium studies may reveal motility problems. Esophageal manometry may show diffuse esophageal spasm and increased pressure at the lower esophageal sphincter. Provocative test with methacholine may provoke esophageal pain and manometric signs of spasm.

96

THE HISTORY AND SYMPTOMATOLOGY

UES

LES

Fig. 11.14

esophageal disorders, the esophageal spasm or reflux, substernal or epi| Ingastric pain may mimic angina—UES: upper esophageal sphincter, LES: lower esophageal sphincter.

2. The chest discomfort due to esophageal reflux less closely mimics angina and is of heart burn or burning sensation in quality which is most common after meals, occurs in supine position or on bending and is often relieved by antacids (see Fig. 11.14). ●

●

●

●

The presence of acid reflux into the mouth (water brash) and/or dysphagia is a useful diagnostic clue to the esophageal diseases. Besides, the esophageal disorder frequently coexist with angina pectoris, and esophageal reflux lowers the threshold for the development of angina. Bernstein test5 may be helpful to differentiate the esophageal reflux from angina: alternate infusions of dilute acid and normal saline by a nasogastric tube, placing the tip at the level of mid esophagus, produces pain in over 90% of patients with subjective and objective evidence of gastroesophageal acid reflux. Acid reflux can also be recognized by recording the pH from an electrode placed at the tip of a catheter inserted into the distal esophagus.

3. In acid peptic disorders, pain is more often burning in character with characteristic relationship to food ingestion and it is relieved by antacids or food (see Fig. 11.15). 4. Acute pancreatitis may mimic AMI. However, pain is predominantly in the epigastrium, it is position sensitive, usually transmitted to the back and may be partly relieved by leaning forward, with usual history of alcoholism or biliary tract disease (see Fig. 11.16). 5. Biliary colic usually caused by a rapid rise in biliary pressure due to obstruction of the cystic or bile duct. The pain is steady, lasts for 2–4 hrs and subsides spontaneously without any symptoms in between the attacks.

CARDINAL SYMPTOMS

Fig. 11.15

97

acid peptic disorders, the burning pain often has relationship to food | Iningestion. Right hepatic duct

Left hepatic duct

Liver

Common hepatic duct Common bile duct

Cystic duct

Duodenum Gallbladder Pancreas

Pancreatic duct

Fig. 11.16

pancreatitis mimics acute myocardial infarction, but pain is usually | Acute transmitted to the back, while the pain in biliary colic is usually felt in the right upper abdomen.

iii) Pulmonary/pleural ●

●

●

causes of chest pain:

Large pulmonary embolism can cause acute onset of chest pain that mimics AMI with severe dyspnea, hypotension, and arterial hypoxemia (see Fig. 11.17). However, a clinical setting of prior immobilization with bed rest, prolonged travel or deep venous thrombosis should increase the suspicion of pulmonary embolism. Pneumothorax can cause acute chest pain and is associated with dyspnea, decreased breath sounds and hyperresonance note on the affected side. Pleuritic chest pain associated with pleural rub, accentuated by inspiration/movement of the chest wall and relieved to a great extent on lying down on the same side or holding the breath in deep expiration.

98

THE HISTORY AND SYMPTOMATOLOGY

Aorta Pulmonary embolism

PA LA

RA LV RV

Fig. 11.17

pulmonary embolism chest pain mimics AMI with acute dyspnea, hypox| Inemia and hypotension.

iv) Functional or psychogenic chest pain (Da Costa’s syndrome or neurocirculatory asthenia): It is localized, dull, and persistent ache that may last for hours and often accentuated by or alternates with attacks of sharp lancinating stabs of 1–2 sec. 4. Aggravating and Relieving Factors a) Angina Pectoris It characteristically occurs on exertion, exercise or other forms of stress (emotional stress, cold weather, heavy meal) except in Prinzmetal’s angina and unstable angina where chest pain can occur at rest. i) Depending on the severity of the anginal pain, patients are functionally classified from class I to IV by three functional classifications: 6 ● NYHA functional classification. 7 ● Canadian cardiovascular society (CCS) functional classificaion. 8 ● Specific activity scale (SAC) functional classification. However, CCS functional classification of angina is more popular and appropriate clinically. CCS functional classification Class I: No limitation of ordinary physical activity. Ordinary physical activity such as walking and climbing stairs does not cause angina. Only strenuous or prolong exertion causes angina. Class II: Slight limitation of ordinary physical activity. Ordinary physical activity causes angina such as: ● ●

Walking or climbing stairs rapidly. Walking uphill.

CARDINAL SYMPTOMS ● ● ● ●

●

99

Walking or climbing stairs after meals. Walking in cold, in wind. Walking more than two blocks on the level (one block distance is 100 m). Climbing more than one flight of ordinary stairs at a normal pace and under normal conditions or When under emotional stress.

Class III: Marked limitation of ordinary physical activity. Less than ordinary physical activity causes angina such as: ● ●

Walking one to two blocks on the level or Climbing one flight of stairs under normal conditions.

Class IV: Inability to do any physical activity without discomfort and anginal syndrome may be present at rest. ii) Linked angina is an episode of angina in patients with established CAD caused by gastrointestinal factors not related to increase in cardiac work such as stooping or which occur after meals.9 iii) Anginal chest pain characteristically relieved by stopping the activity and taking nitroglycerine usually in 1–5 min. But if it takes more than 10 min for relief of the discomfort, it could be due to unstable angina, AMI or non ischemic pain. b) In MVP Chest pain is atypical, occurs spontaneously and is unrelated to exertion which is due to tension of the papillary muscles. c) In Acute Pericarditis Chest pain is characteristically relieved by sitting and leaning forward (Mohammedan’s prayer sign) while in acute pancreatitis, pain is partly relieved by leaning forward. It is aggravated by breathing, turning in bed and twisting the body. d) The Esophageal Pain Usually occurs on eating, during swallowing, or on lying down after meals and may be relieved with antacids and nitroglycerine. e) The Pain in Acid Peptic Disorders Its characteristic relationship to food ingestion and its relief by antacids or food help in its diagnosis. f) The Pleuritic Chest Pain It is associated with a pleural rub, accentuated by inspiration or movement of the chest wall and is relieved to a greater extent on lying down on the same side or holding the breath in deep expiration (inhibiting the friction between the pleural layers).

100

THE HISTORY AND SYMPTOMATOLOGY

Fig. 11.18

of the fist in front of the | Clenching chest while describing the chest

Fig. 11.19

discomfort (Levine’s sign) is typical of ischemic chest pain.

pointing to a small circumscribed | Finger area in the left inframammary region while describing the chest discomfort is usually of noncardiac origin—more of a psychogenic origin.

g) In Thoracic Outlet Syndrome Pain is often associated with paresthesias along the ulnar distribution of arm and forearm and is typically precipitated by abduction of the arm, lifting a weight or working the hands above the shoulder but not by walking as it occurs in angina pectoris. 5. Patient’s Gestures During Chest Discomfort ●

●

Clenching the fist in front of the chest while describing the chest discomfort is a strong indication of an ischemic origin of the chest pain (Levine’s sign,10 (see Fig. 11.18) than when a finger is pointed to a small circumscribed area in the left infra mammary region which more likely represents the chest pain of psychogenic origin (see Fig. 11.19). The patient is usually in agony in chest pain due to AMI.

6. Associated Symptoms Presence of other cardinal symptoms: SOB, palpitation and syncope accompanying chest pain should be noted which confirms the cardiovascular cause for the chest pain (see Table 11.3). ●

●

In AMI, the chest pain is often accompanied by profuse sweating and palpitation (due to sympathetic stimulation), syncope, nausea, vomiting or SOB. However, SOB accompanying chest pain can also occur in pneumothorax and pulmonary embolism (PE). In PE, the patient in addition has hypotension and arterial hypoxemia with clinical setting of prior immobilization, prolong travel or deep venous thrombosis; while in pneumothorax, there are also decreased breath sounds and hyper resonance note on the affected side.

CARDINAL SYMPTOMS

101

Table 11.3 Chest pain and associated symptoms Associated symptoms

Cause

1. 2. 3. 4. 5.

AMI: acute myocardial infarction, MVP: mitral valve prolapse Myocardial infarction, pulmonary embolism, pneumothorax Aortic dissection, AMI Pulmonary embolism, lung tumor Pericarditis, AMI (low grade), pneumonitis, pleurisy

Sweating and palpitation Shortness of breath (SOB) Syncope Hemoptysis Fever

●

● ●

●

The chest pain accompanied by hemoptysis suggests PE with pulmonary infarction or lung tumor. Fever accompanying chest pain occurs in pericarditis, pneumonitis and pleurisy. In MVP, symptoms of autonomic nervous system dysfunction occur and are associated with palpitation, fatigue, postural hypotension and other psychiatric symptoms. Functional chest pain is usually accompanied by numbness and tingling in the extremities, frequent sighing, dizziness, anxiety or depression.

Definite Typical Anginal Chest Pain (ACC/AHA 2002 Guidelines)10a It occurs when all the three following characteristics are present: 1. Substernal chest discomfort with a characteristic quality (squeezing, pressing, choking or tightness) and duration (2–5 min) that is 2. Provoked by exertion or emotional stress and 3. Relieved by rest or nitroglycerin. 7. Non Cardiac Chest Pain (ACC/AHA 2002 Guidelines)10a Meets 1 of the typical angina characteristics. The chest pain is described as atypical angina when 2 of the above characteristics are present.

2. SHORTNESS OF BREATH (SOB)/DYSPNEA 1. Dyspnea It is defined as [i] difficult or labored breathing or [ii] unpleasant awareness of ones own breathing. 2. Pathogenesis of Dyspnea Dyspnea occurs when (see Table 11.4) ● ● ●

Maximum ventilation volume (MVV) is lesser than normal or decreases, Vital capacity (VC) decreases which in turn decreases MVV or Pulmonary ventilation (PV) increases by 4–5 times the normal.

102

THE HISTORY AND SYMPTOMATOLOGY

Table 11.4 Pathogenesis of dyspnea: Dyspnea occurs when the dyspnea index becomes 60% which is due to following mechanisms Mechanism

Effects

1. Decreased vital capacity  2. Decreased maximum ventilation volume 3. Increased pulmonary ventilation

Affects respiratory muscles and compliance of lungs and thorax Affects respiratory muscles and compliance of lungs and thorax Stimulates J receptors, causes hypoxemia and acidosis

i.e. dyspnea usually occurs when pulmonary reserve percentage (% PR) or Dyspnea index (DI) is 60% (normally it is about 80–90%), i.e. DI or % PR MVV PV  100/MVV. a) Vital Capacity It is the maximum volume of air which can be expelled from the lungs by forceful effort following a maximal inspiration, i.e. VC tidal volume  inspiratory reserve volume  expiratory reserve volume (4.8 L in males, 3.2 L in females). VC provides information about: ● ●

The strength of the respiratory muscles and Elasticity of the lungs.

b) MVV (or Maximum Voluntary Ventilation or Maximum Breathing Capacity) It is the largest volume of air that can be moved into and out of the lungs in one minute by maximum voluntary effort (normally it is 90–100 L/min). MVV depends on the work done during breathing i.e. ● ● ●

Strength of the respiratory muscles Compliance (distensibility) of the thoracic wall and lungs and Airway resistance.

Normal total work done during quiet breathing is 0.3–0.8 kg-m/min. and a healthy adult spends 5% of O2 consumption on breathing. i) Respiratory muscles: To move air into the lungs through air passages, the muscles of respiration have to do work to overcome all forms of resistance (elastic resistance of lungs and chest wall 65%, viscous resistance 7% and airway resistance 28%). Dyspnea occurs due to: ● ● ●

Fatigue of respiratory muscles: due to decreased cardiac output. Weakness of respiratory muscles: deconditioning. Respiratory muscle diseases: neuromuscular disorder e.g. myasthenia gravis, poliomyelitis, phrenic nerve dysfunction.

CARDINAL SYMPTOMS

103

ii) Compliance (distensibility) of lungs and thorax: Normal compliance is 0.13 L/cm H2O i.e. when there is an increase of airway pressure by 1 cm H2O, then the volume of lungs inside the thoracic wall increases by 0.13 L. Dyspnea occurs when compliance decreases. The compliance in turn depends on: ● ●

●

Viscous resistance (7%): Work done in moving the viscous material of the lung tissue. Airway resistance (28%) which is the work done in moving the air through respiratory passages (N 1.5–2 cm H2O/L/s i.e. when there is a fall of pressure by 2 cm H2O, there is airflow of 1 L/s). 80% of the total airway resistance is offered by the trachea and bronchial divisions upto 7th generation. Alveolar surface tension that is kept low by surfactant secreted by type II pneumocytes in the alveolar lining thereby it prevents pulmonary edema and keeps the alveoli dry.

c) Pulmonary Ventilation (or Minute Ventilation) It is the volume of air expired or inspired by the lungs in one minute i.e. PV (TV)  RR/min. (TV tidal volume; RR respiratory rate). So normal PV is 500  12 6,000 ml or 6 L/min. Dyspnea occurs when PV increases which may due to: (i) Stimulation of Juxta-pulmonary capillary (J) receptors (which are non myelinated vagal afferent nerve endings, located in the alveolar wall and sensitive to the content of interstitial fluid between capillary endothelium and alveolar epithelium) due to pulmonary congestion, pulmonary edema or pulmonary emboli. (ii) Hypoxemia due to ●

●

Decreased V/P ratio (ratio of [V] alveolar ventilation [4 L/min] to [P] pulmonary blood flow [5 L/min] which is normally 4/5 0.8) (Alveolar ventilation is the amount of air ventilating the alveoli per minute i.e. V TV DS  RR/min. DS dead space). So, V (500–150)  12 4.2 L/min. Decreased V/P ratio occurs either due to (i) uneven V (as in bronchial asthma, pneumothorax, emphysema, pulmonary fibrosis, congestive heart failure) or (ii) due to non uniform pulmonary blood flow (as in shunts e.g. TOF,  pulmonary vascular resistance e.g. CHF, ⇓ pulmonary vascular bed e.g. emphysema). Hypoxemia due to ⇓ PO2: Arteriovenous (A-V) O2 difference less than 0.2 ml/ 100 mL stimulates the respiratory neurons in medulla (respiratory center) via the chemoreceptors (in carotid and aortic bodies) to increase PV.

(iii) Acidosis ●

●

Respiratory acidosis due to  PCO2 (as in emphysema, respiratory depression due to morphine) causes stimulation of respiratory neurons in medulla via chemoreceptors to  PV that causes CO2 washed out and thereby restoring H concentration of blood towards normal. Metabolic acidosis due to diabetic ketoacidosis, renal failure, starvation ketoacidosis and lactic acidosis due to severe muscular exercise stimulates respiratory medullary center via chemoreceptors to  PV which causes wash out of CO2 and restoration of blood H concentration.

104

THE HISTORY AND SYMPTOMATOLOGY

3. Etiology Dyspnea due to cadiovascular causes is usually due to: (i) ⇓ Cardiac output (leading to fatigue of respiratory muscles) or (ii) Pulmonary venous hypertension (which results in ⇓ compliance,  airway resistance and pulmonary congestion stimulating J receptors and thereby affecting MVV and PV) (iii) However, neural impulses generated in the underperfuse and metabolically abnormal respiratory muscles could be responsible to  ventilatory drive.11 Common Causes of Dyspnea a) Cardiovascular causes (see Fig. 11.20) ● ● ● ● ●

Cardiomyopathy: dilated, hypertrophic, infiltrative, ischemic Valvular heart disease Pericardial disease Pulmonary vascular disease and Congenital heart disease (CHD).

b) Non cardiovascular causes i) Pulmonary causes ● Airways: upper airway obstruction, asthma, emphysema, cystic fibrosis. ● Parenchymal lung: interstitial lung disease, pneumonia, malignancy (primary/ metastatic). ● Pleural: effusion, fibrosis, malignancy.

Cardiomyopathy: Dilated, HCM, restrictive, ischemic Valvular heart disease: MS, AS, PS

Pericardial: Effusion, CT, CP

Dyspnea of CV origin Pulmonary vascular: PH, PE

Heart failure: CHF, LVF

CHD: Acyanotic, cyanotic

Fig. 11.20

(CV) causes of dyspnea-CT: cardiac tamponade, CP: con| Cardiovascular strictive pericaditis, PH: pulmonary hypertension, PE: pulmonary embolism, CHF: congestive heart failure, LVF: left ventricular failure, CHD: congenital heart disease.

CARDINAL SYMPTOMS ●

●

105

Respiratory muscle: neuromuscular disorders e.g. myasthenia gravis, poliomyelitis phrenic nerve involvement. Respiratory muscle weakness: deconditioning.

ii) Chest wall involvement ● ●

Deformities e.g. kyphoscoliosis Abdominal ‘loading’ causes: ascites, pregnancy, obesity.

iii) Metabolic causes: metabolic acidosis due to: ● ● ● ●

Diabetic ketoacidosis Renal failure Starvation ketoacidosis Severe muscular exercise leading to lactic acidosis.

iv) Anemia (of any cause). v) Psychogenic: anxiety. 4. Evaluation The symptom of dyspnea should be evaluated to rule out the non cardiovascular etiology for: ● ● ● ● ●

Duration Mode of onset Severity/aggravating factors (functional classification) Relieving factors Associated symptoms.

a) Duration Longer duration of dyspnea usually seen in mitral stenosis (5 yrs) while it is of shorter duration in most of the diseases e.g. AS, cardiomyopathy, CAD. b) Mode of Onset i) In most cardiac disorders, it is usually gradual in onset. ii) Sudden onset of dyspnea occurs in: ● ● ● ● ●

Acute pulmonary edema (see Fig. 11.21), Pulmonary embolism, Pneumothorax, pneumonia (see Figs 11.22 and 11.23), Airway obstruction or Psychogenic.

Sudden occurrence of dyspnea in a patient of mitral stenosis suggests the development of atrial fibrillation, rupture of chordae tendinae, or pulmonary embolism. iii) Dyspnea is late in onset in the course of mitral regurgitation and aortic regurgitation (palpitation is the initial symptom); while in mitral stenosis, dyspnea occurs earlier and is the initial symptom.

106

THE HISTORY AND SYMPTOMATOLOGY

Fig. 11.21

| Sudden onset of dyspnea occurs in pulmonary edema.

Right upper lobe

Fig. 11.22

In this conditions | Pneumonitis. sudden onset dyspnea and chest pain occurs.

Fig. 11.23

In this conditions sudden | Pneumothorax. onset dyspnea and chest pain occurs.

(c) Severity/Aggravating Factors Depending upon the severity of dyspnea (as also chest pain, palpitation and fatigue), patients are classified from class I to IV by the following functional classifications. i) New York Heart Association (NYHA) functional classification.6 ii) Canadian Cardiovascular Society (CCS) functional classication.7 iii) Specific Activity Scale (SAC).8 However clinically, NYHA functional classification is usually followed even though this classification of the severity of symptoms is not applicable and useful for pediatric patients. NYHA functional classification6 Class I ● ●

Patients with cardiac disease but no limitations of physical activity. Ordinary physical activity does not cause dyspnea, palpitation, fatigue and chest pain.

CARDINAL SYMPTOMS

107

Class II ● ● ●

Patients with cardiac disease with slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in dyspnea, palpitation, fatigue and chest pain.

Class III ● ● ●

Patients with cardiac disease with marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes dyspnea, palpitation, fatigue and chest pain.

Class IV ●

●

●

Patients with cardiac disease with inability to carry out any physical activity without discomfort. Symptoms (dyspnea, palpitation, fatigue and chest pain) may be present even at rest. If any physical activity is undertaken, discomfort is increased.

Goldman et al’s SPECIFIC ACTIVITY SCALE8 (modified): This functional classification is based on the estimated metabolic cost of various activities and is more reproducible and better predictor of exercise tolerance than either NHYA functional classification or CCS functional classification. Class I: Patients can perform to completion any activity that requires 7 metabolic equivalents (MET) e.g. ● ●

●

●

Personal activities: can shower and dress, have normal sexual life. Indoor activities: can do routine household activity: washing clothes, cleaning windows and floor, cooking, bed making. Outdoor activities: can do gardening, work in the fields, shovel snow, spade soil, weight bearing (80 lb). Sports and recreational activities: dancing, skating, skiing, swimming, cycling (on flat surface: 15 kmph), running (10 kmph), jog/walk 5 mph (3.10 kmph).

Class II: Patients can perform to completion any activity that requires 5 MET but

7 MET, e.g. ● ● ●

Can do all personal and indoor activities normally as stated above. Outdoor activity: restricted outdoor activity, can only do gardening. Sports and recreational activities: restricted, can dance, do skating, cycling (on flat surface 10 kmph), walk: 4 mph.

Class III: Patients can perform to completion any activity that requires 2 MET but

5 MET, i.e. restriction of all activities. e.g. ●

Restricted personal and indoor activities: can only shower and dress, make bed, clean window.

108

THE HISTORY AND SYMPTOMATOLOGY ● ●

No out door activity. Restricted sports and recreational activities: can bowl, play golf, drive car, walk: 2.5 mph.

Class IV: Patients cannot perform to completion any activity that requires 2 MET, i.e. cannot carry out any activity listed above in Class III (1 MET 3.5 mL of O2/kg consumed). Joseph K Perloff 12 proposed a new functional classification for congenital heart disease (CHD) patients as NYHA functional classification is inappropriate especially for dyspnea symptom since ‘dyspnea’ is in fact, hyperventilation unrelated to heart failure and these subjects have a substantially greater increase in ventilation during isotonic exercise than do normal subjects and hence ‘dyspnea’ may be a prominent subjective complaint. In cyanotic CHD, shunting of venous blood into systemic circulation lowers arterial O2 tension which stimulates the medullary centers via carotid bodies that results in  ventilation. Following is the CHD functional classification: Functional classification for CHD12 Class I: Patients are asymptomatic at all levels of activity. Class II: Symptoms are present but do not curtail average every day activity. Class III: Symptoms significantly curtail most but not all average every day activities. Class IV: Symptoms significantly curtail virtually all average every day activities and may be present at rest. American thoracic society scale of dyspnea:13 (see Table 11.5).

It quantifies the severity of dyspnea

Dyspnea at rest: ● ● ● ●

Pulmonary edema of any cause Pulmonary embolism Pneumothorax Functional.

Table 11.5 Quantifying the severity of dyspnea Descriptions

Grade

Degree

1. Not troubled by SOB when hurrying on the level or walking on a slight hill 2. Troubled by SOB when hurrying on the level or walking upon a slight hill 3. Walks more slowly than people of the same age on the level because of breathlessness or has to stop for breath when walking at own pace on the level 4. Stops for breath after walking about 100 yards or after a few minutes on the level 5. Too breathless to leave the home; breathless on dressing or undressing

0

None

1

Mild

2

Moderate

3

Severe

4

Very severe

CARDINAL SYMPTOMS

109

Drugs aggravating dyspnea: ● ● ● ●

Beta-blockers (especially nonspecific): increase bronchospasm. Digoxin: in hypertrophic obstructive cardiomyopathy (HOCM). Diuretic: in pericardial disease and in patients with isolated diastolic dysfunction. Steroids: may aggravate heart failure and chronic renal failure.

d) Variants of Dyspnea i) Episodic dyspnea: orthopnea.

It consists of paroxysmal nocturnal dyspnea (PND) and

(a) Paroxysmal nocturnal dyspnea (PND): This is the occurrence of dyspnea during sleep, commonly 2–3 hrs after going to bed. It is often associated with sweating, wheezing, and coughing and is usually relieved by assuming upright position for 5–15 mins. ●

●

● ●

PND strongly suggests PVH. It is due to interstitial edema and sometimes due to intra alveolar edema usually secondary to the left ventricular failure. MS is the commonest cause for PND. Other valvular heart diseases, DCM and CAD may also give rise to PND but are often late in occurrence. Patients with PND are functionally classified into NYHA class III. Once right ventricular failure develops (CHF), PND disappears (see Table 11.6).

(i) Pathogenesis (mechanism) of PND ●

Absorption of edema fluid from the interstitial compartments of lower limbs during supine position increases the venous return to the right heart and subsequently increases right ventricle (RV) output which cause overfilling of the lungs leading to pulmonary interstitial edema. Other mechanisms which may play a part in the pathogenesis are: – Decreased sympathetic drive during sleep which may decrease left ventricular (LV) contractility. – Nocturnal arrhythmias and dreams may also precipitate PND.

(ii) Other conditions simulating PND ●

Nocturnal episodes of bronchial asthma (typically occurs in early mornings, 4–6 AM). Other COPDs may also wake up the patient in the night. However, cough and

Table 11.6 Variant forms of dyspnea Variant form

Description

Cause

1. 2. 3. 4. 5.

Dyspnea during sleep Dyspnea in supine position Dyspnea in upright position Dyspnea in lateral position Rapid breathing

Mitral stenosis LVF, COPD, large ascitis LA myxoma, ball valve thrombus LA myxoma, ball valve thrombus Any cause of dyspnea

Paroxysmal nocturnal dyspnea Orthopnea Platypnea Trepopnea Tachypnea

LVF: left ventricular failure, COPD: chronic obstructive pulmonary disease, LA: left atrium.

110

THE HISTORY AND SYMPTOMATOLOGY

Fig. 11.24

● ● ● ●

| Patient is orthopneic due to left ventricular failure.

expectoration precede dyspnea and SOB is often relieved when the patient rids himself/herself of secretions. Nocturnal episodes of recurrent pulmonary emboli. Post nasal discharge with associated severe cough. Anxiety with hyperventilation. Obesity sometimes mimics PND.

(b) Orthopnea: It is dyspnea that occurs in supine position and is promptly relieved by assuming upright position (sitting or standing). ● ●

Orthopneic patients are functionally graded to be in NYHA class IV. Similarly, it is related to an increased venous return to the right heart in supine position and subsequently to increased RV output which further increases the pulmonary venous congestion.

Etiology of Orthopnea: Orthopnea is a characteristic of left ventricular failure (see Fig. 11.24) but can also occur in ● ● ●

i)

ii)

iii) vi)

COPD Bilateral weakness or paralysis of diaphragm Large ascites often due to constrictive pericarditis, chronic renal failure and sometimes associated with congestive heart failure Platypnea is dyspnea that occurs in upright position and may be relieved in supine position. It may be related to LA myxoma or ball valve thrombus in LA which obstructs the left inflow (MV) in upright position and results in dyspnea (see Fig. 11.25) Trepopnea is dyspnea that occurs only in lateral position and similarly may be due to LA myxoma or ball valve thrombus in LA which obstructs mitral valve orifice in lateral position and causes dyspnea Tachypnea is rapid breathing of any cause Angina equivalent: See chest pain symptom.

CARDINAL SYMPTOMS

111

RV

LV

VS AMVL AO

PMVL MYXOMA LA

Fig. 11.25

echocardiogram showing left atrial myxoma—platypnea or tre| Transthoracic popnea can occur in a patient with myxoma—AMVL: anterior mitral valve leaflet, PMVL: posterior mitral valve leaflet, LA: left atrium, LV: left ventricle, RV: right ventricle, AO: aorta, VS: ventricular septum.

e) Relieving Factors The factors which relieve dyspnea should be evaluated. ●

●

Dyspnea (which is often due to cardiac cause) can be relieved by stopping exertion and taking rest. By taking drugs: – Nitroglycerine and beta-blockers: in ischemic heart disease presenting as shortness of breath (anginal equivalents). – Diuretics and digoxin: in HF. – Bronchodilators and steroids: in bronchospasm.

● ● ● ● ●

Assuming upright position: in PND, orthopnea. Squatting position: in cyanotic congenital heart disease e.g. TOF. Supine position: in platypnea due to LA myxoma or ball valve thrombus. By exertion or by sedation: in a psychogenic cause. Dyspnea present only at rest and absent on exertion: invariably of psychogenic etiology.

f) Associated Symptoms Presence of other cardinal symptoms such as chest pain, palpitation and giddiness, pinpoints to cardiovascular cause of dyspnea (see Table 11.7). ●

●

●

However, SOB and chest pain can also occur in pulmonary embolism and pneumothorax but other characteristic features help in the diagnosis. Associated productive cough usually indicates respiratory cause for SOB; however in the presence of secondary infection, productive cough could be present in cardiac pathology. In COPD, cough and expectoration precede dyspnea. Presence of fever usually occurs in respiratory causes (COPD, pneumonia, pleuritis/ pleural effusion), but may be associated with pericardial disease and due to infection

112

THE HISTORY AND SYMPTOMATOLOGY

Table 11.7 SOB and associated symptoms Associated symptoms

Cardiovascular cause

Non cardiovascular cause

1. Chest pain 2. Cyanosis 3. Cough 4. Fever

CAD, pericarditis, PE Cyanotic CHD (TOF) Secondary infection Secondary infection, pericarditis, myocarditis, MI (low grade) HF, CP

Pneumothorax, COPD COPD COPD, pneumonia, pleuritis, malignancy (low grade)

5. Edema

Large bilateral pleural effusion

SOB: Shortness of breath, CAD: coronary artery disease, PE: pulmonary embolism, CHD: congenital heart disease, TOF: tetralogy of Fallot, COPD: chronic obstructive pulmonary disease; MI: myocardial infarction, HF: heart failure, CP: constrictive pericarditis.

●

●

●

in cardiac pathology (bronchitis in MS, bacterial endocarditis in valvular heart disease/ CHD, pulmonary tuberculosis in CHD, low grade fever in malignancy and ischemic heart disease). Associated cyanosis usually in cyanotic CHD, but occurs in COPD (chronic bronchitis). Associated edema most frequently due to HF. However, dyspnea and edema can also be observed in patients with large bilateral pleural effusions and angioneurotic edema with laryngeal involvement. In functional etiology, claustrophobia or sighing respirations are relieved by exertion, by taking a few deep breaths or by sedation. Most often, these patients are associated with emotional instability.

3. PALPITATION It is an unpleasant awareness of the forceful or rapid beating of the heart. It is the increased motion of the heart within the chest that is perceived as palpitation rather than the increase in cardiac contractility which explains the absence of palpitation in conditions characterized by an increased force of cardiac contraction, such as AS, PS and severe systemic or pulmonary hypertension. 1. Etiology The important causes of palpitation are as follows: Cardiac Causes i) Valvular heart disease: Due to increased stroke volume: AR, MR, TR (see Fig. 11.26). ii) Acyanotic congenital heart disease: ● ●

With shunts: PDA, VSD, ASD (late onset) Arrhythmogenic: arrhythmogenic right ventricular dysplasia (ARVD).

CARDINAL SYMPTOMS

113

Cyanotic CHD: Ebstein anomaly TAPVC, TGA, DORV, SV Acyanotic CHD: PDA, VSD, ARVH

Valvular: AR, MR

Palpitation

MVP, HCM, CAD Prolong QT syndrome

Arrhythmias: VT, SVT, Af, PVC, PAT, CHB, SSS

Pacemaker related

Fig. 11.26

(CV) causes of palpitation—AR: aortic regurgitation, MR: | Cardiovascular mitral regurgitation, TAPVC: total anomalous pulmonary venous connection, TGA: transposition of great arteries with PS, DORV: double outlet right ventricle without PS, SV: single ventricle without PS, ARVH: arrhythmogenic right ventricular hyperplasia, VT: ventricular tachycardia, SVT: supraventricular tachycardia, PVC: premature ventricular contractions, PAT: premature atrial tachycardia, CHB: complete hart bock, SSS: sick sinus syndrome, MVP: mitral valve prolapse, HCM: hypertrophic cardiomyopathy, CAD: Coronary artery disease, Af: atrial fibrillation.

iii) Cyanotic congenital heart disease ● ●

With increased pulmonary blood flow: TAPVC, PAPVC, TGA with VSD without PS Arrhythmogenic: Ebstein anomaly, after Mustard operation.

iv) Arrhythmias ●

● ● ●

Tachyarrhythmias: VT, SVT, atrial fibrillation, atrial flutter, paroxysmal atrial tachycardia (PAT), premature atrial contractions (PAC) and premature ventricular contractions (PVC). Bradyarrhythmias: CHB, Sick sinus syndrome (SSS), Pacemaker malfunctioning, MVP, HCM, CAD, Prolong QT syndrome, prosthetic heart valves.

Non Cardiac Causes i) Hyperkinetic circulatory states ● ● ● ● ●

Anemia Arteriovenous fistula Fever Thyrotoxicosis Pheochromocytoma.

114

THE HISTORY AND SYMPTOMATOLOGY

ii) Arrhythmogenic ● ● ●

Thyrotoxicosis Hypoglycemia Orthostatic hypotension.

iii) Drugs ● ● ● ● ●

Caffeine, alcohol (holiday heart syndrome), nicotine, cocaine and amphetamines Sympathomimetic drugs Digitalis Vasodilators (Calcium blockers, nitrates) Tricyclic antidepressants.

iv) Psychiatric Anxiety, depression, panic disorders, bereavement and somatization. Psychiatric causes account for 31%14 to 41%.15 2. Evaluation The history remains the most important and valuable mode of examination to distinguish cardiac from non cardiac causes of palpitation. It has to be evaluated in the following way: i) ii) iii) iv) v)

Duration and frequency, Mode of onset, Nature/character, Relieving factors, Associated symptoms.

i) Duration and Frequency of Palpitation i) Acute or chronic ii) Persistent or non persistent iii) If it is non persistent, then how frequently it occurs. Persistent palpitations suggest volume overload conditions such as: ● ● ● ● ●

Valvular heart disease: AR, MR, TR (see Figs 11.27 and 11.28) Acyanotic CHD: PDA, VSD, ASD (see Figs 11.29–11.31) Cyanotic CHD: with  PBF: TAPVC, PAPVC, TGA with VSD without PS Persistent arrhythmia like atrial fibrillation Non cardiac causes: anemia, arteriovenous fistula, thyrotoxicosis, psychiatric illness.

In these conditions, exertion results in exaggeration, and some patients may not experience palpitations at rest but may manifest it on exertion. Patients with chronic atrial fibrillation may not experience palpitations at all. Non persistent or paroxysmal palpitations are usually of arrhythmogenic origin due to: ● ●

Arrhythmias (see Figs 11.32–11.35) Non cardiac causes: thyrotoxicosis, hypoglycemia, addictions and drugs (see Fig. 11.36). Psychiatric illness may also cause paroxysmal palpitations.

CARDINAL SYMPTOMS

Dilated left atrium

115

Dilated aorta

Aortic valve

Dilated left ventricle

Fig. 11.27

Dilated left ventricle

| Mitral regurgitation.

Fig. 11.28

regurgitation. Persistent palpi| Aortic tation occurs in both the conditions.

Ductus arteriosus Aorta

Aorta

PA (dilated)

PA (dilated)

LA (dilated)

LA (dilated)

RA

RA

LV (dilated)

RV

Fig. 11.29

LV (dilated)

ductus | Persistent In this acyanotic

arteriosus. congenital heart diseases, persistent palpitation occurs.

RV (dilated)

Fig. 11.30

septal defect. | Ventricular In this acyanotic congenital heart diseases, persistent palpitation occurs.

Frequency: Palpitations due to arrhythmias and psychiatric etiology may be paroxysmal in nature and can occur frequently in a given day. Similarly, recurrent palpitations with perspiration in a hypertensive patient suggest pheochromocytoma. ii) Mode of Onset i) Whether palpitation occurred spontaneously or was precipitated or exaggerated by exertion?

116

THE HISTORY AND SYMPTOMATOLOGY

Aorta

PA (dilated)

LA

RA

LV RV (dilated)

Fig. 11.31

Fig. 11.32

septal defect. In this acyanotic | Atrial congenital heart diseases, persistent

right ventricular | Arrhythmogenic dysplasia—palpitation is one of the presenting symptoms.

palpitation occurs.

Aorta PA LA

RA LV

Ventricular tachycardia

RV Left ventricular damage Myocardial infarction Myocarditis

Fig. 11.33

tachycardia (VT). Among arrhythmias VT and SVT are the com| Ventricular monest causes of palpitation.

ii) If it begins suddenly and ends abruptly: often due to paroxysmal atrial or junctional tachycardia, atrial flutter or atrial fibrillation. iii) Gradual onset and cessation of the palpitation suggests: sinus tachycardia or anxiety. iii) Nature/Character of Palpitation The patient may describe symptoms of palpitation as pounding, stopping, jumping, racing, floating or flopping sensation in the chest. Some patients perceive almost every premature

CARDINAL SYMPTOMS

117

Orthodromic tachycardia

Fig. 11.34

reciprocating tachycardia (AVRT) which is the commonest | Atrioventricular cause of supraventricular tachycardia (SVT). Among arrhythmias VT and SVT are the commonest causes of palpitation.

Fig. 11.36 Fig. 11.35

|

| Thyrotoxicosis.

Atrial fibrillation. Both atrial fibrillation and thyrotoxicosis can present as persistent or non persistent palpitation.

beat, while others are totally unaware of frequent or advanced arrhythmias. Patients often are unaware of palpitation when they first lie down on their sides to sleep, especially on their left side.16 When the atrial fibrillation becomes permanent, patient perceives the palpitation only on exertion or excitement i.e. when the ventricular rate increases. Generally, a thin tense individual is more likely to be aware of the cardiac activity than others.

118

THE HISTORY AND SYMPTOMATOLOGY

i) When palpitation lasts for an instant it is often described as skipped beats or flopping in the chest which is commonly due to premature beats. The premature beats may be perceived as floating sensation in the chest. ii) A pounding sensation in the chest occurs due to paroxysmal tachycardia. iii) The sensation that the heart has stopped beating correlates with the compensatory pause following a premature beat. iv) Regular rapid palpitation may be due to sinus tachycardia, SVT or paroxysmal atrial tachycardia. v) Irregular rapid palpitation may be due to atrial fibrillation, atrial flutter or atrial tachycardia with a varying block. vi) Slow palpitation i.e. with slow heart rate may suggest AV block or sinus node disease. iv) Relieving Factors/How it Stops? It stops spontaneously in most of the paroxysmal arrhythmias. However if it is relieved by vagal maneuvers such as by stooping, breath-holding, or inducing gagging or vomiting, it suggests a diagnosis of paroxysmal SVT. v) Associated Symptoms Presence of other cardinal symptoms suggests cardiac etiology (see Table 11.8). i) Syncope: occurrence of syncope does not indicate a good prognosis. An episode of syncope following palpitation suggests: – Stokes-Adams attack – Asystole or severe bradycardia following termination of a tachyarrhythmia – Hypoglycemia or – Pheochromocytoma. ii) Chest pain: palpitation followed by angina suggests myocardial ischemia (precipitated by ⇓ MVO2 due to rapid heart rate). iii) Dyspnea: HF/LVF, acute pulmonary embolism, severe bronchial asthma. iv) Polyuria: paroxysmal atrial tachycardia, paroxysmal atrial fibrillation. v) Throbbing in the neck: AR. Table 11.8 Palpitation and associated symptoms Associated symptoms

Causes

1. 2. 3. 4. 5. 6. 7.

Stokes-Adam attack, severe bradycardia, pheochromocytoma, hypoglycemia Myocardial ischemia HF, acute pulmonary embolism, bronchial asthma Paroxysmal atrial tachycardia, paroxysmal atrial fibrillation MI, most arrhythmias, pheochromocytoma, hypoglycemia Prolong QT syndrome Thyrotoxicosis, hypokalemia induced arrhythmias, irritable bowel syndrome

Syncope Chest pain Dyspnea Polyuria Sweating Deafness Diarrhoea

HF: heart failure, MI: myocardial infarction.

CARDINAL SYMPTOMS

119

vi) Sweating: MI, hypoglycemia, pheochromocytoma, most of the arrhythmias (with hypotension) or anxiety. vii) Anxiety and hyperventilation: psychogenic. viii) Deafness: prolonged QT syndrome. ix) Diarrhea: thyrotoxicosis, hypokalemia induced arrhythmias, irritable bowel syndrome. 4. FATIGUE It is the most common and non specific symptom (see Fig. 11.37). ● ●

● ● ●

However, extreme fatigue sometimes precedes or accompanies AMI. On exertion, severe fatigue may occur due to global myocardial ischemia. However, any condition that results in depressed cardiac output is associated with fatigue and muscular weakness. It may be due to drug intake such as beta-blockers, diuretics (excess). Diuretic induced hypokalemia also gives rise to fatigue. Anemia, thyrotoxicosis, anxiety, depression and other chronic medical diseases are common conditions associated with fatigue and weakness.

5. SYNCOPE It is a sudden and transient loss of consciousness associated with a loss of postural tone, with spontaneous recovery not requiring electrical or chemical cardioversion. It occurs in all age groups, increases with age and accounts for 3% in men and 3.5% in women.17 In pre-syncope, there is a transient episode of altered consciousness with a loss of postural tone, i.e. patient feels dizzy and weak without the loss of complete consciousness. 1. Etiopathogenesis The basic mechanism of syncope and pre-syncope is (see Table 11.9): i) Reduction in cerebral blood flow due to: ● ●

Fall in cerebral perfusion pressure, i.e. 60 mmHg of mean aortic pressure. Elevation in cerebrovascular resistance or intracranial pressure. ↓Cardiac output

Beta blockers diuretics global myocardial ischemia

Fig. 11.37

Fatigue

AMI Hypokalemia

Anemia Thyrotoxicosis Anxiety Depression Chronic medical diseases

| Causes of fatigue—AMI: acute myocardial infarction.

120

THE HISTORY AND SYMPTOMATOLOGY

Table 11.9 Etiopathogenesis of syncope Mechanism

Causes

1. cerebral blood flow

Mean aortic pressure 60 mmHg cerebrovascular resistance/intracranial tension Blood sugar 40 mg% (hypoglycemia) PO2 60 mmHg (hypoxia)

2. energy substrates

ii) Reduction of energy substrates: ● ●

Hypoglycemia, i.e. blood sugar 40 mg%. Hypoxia, i.e. PO2 60 mmHg.

Etiologically, syncope and pre-syncope are classified into: (1) Cardiac (2) Non cardiac and (3) Undetermined. 1) Cardiac Syncope 10–20% of all causes of syncope. i) Due to structural abnormalities (3–11%) leading to decreased cardiac output (CO): ● ● ● ● ●

Left ventricular outflow tract obstruction (LVOTO) Right ventricular outflow tract obstruction (RVOTO) Coronary artery disease (CAD) Cardiac tamponade (CT) Aortic dissection.

ii) Due to arrhythmias (5–30%): ● ● ●

Tachyarrhythmias Bradyarrhythmias Pacemaker related.

iii) Neurally mediated syncope ● ●

During and following catheterization Nitrate syncope.

(2) Non Cardiac Syncope 40–50% of all causes of syncope. Broadly, it is subclassified into four groups: 1) 2) 3) 4)

Vascular Neurological Metabolic and Psychogenic.

CARDINAL SYMPTOMS

121

1) Vascular causes: They are the most common causes of syncope and constitute more than 1/3rd of all the syncopal episodes. They consist of three subgroups: a) reflex mediated b) orthostatic and c) anatomical. a) Reflex mediated syncope: (i) Neurally mediated: Neurocardiogenic/vasovagal syncope (the commonest cause) (ii)Neurally induced: • Carotid sinus syncope/carotid sinus hypersensitivity: a. Cardioinhibitory b. Vasodepressor c. Mixed. • Situational syncope (1–8%): a. Micturition syncope b. Defecation syncope c. Cough syncope d. Swallowing syncope e. Divers f. Postprandial syncope g. Valsalva syncope. (iii) Neuralgias: – Glossopharyngeal – Trigeminal b) Orthostatic syncope (orthostatic hypotension) (4–12%): ● ● ●

Venous pooling or volume depletion Drug induced Neurogenic.

c) Anatomical: Subclavian steal syndrome is a rare cause (0.1%) of syncopal episodes. 2) Neurologic syncope: (neurological disorders causing syncope) (10%): i) Cerebrovascular syncope (6%): CVA, TIA. ii) Seizure disorders (2%). iii) Migraine (12–18%). 3) Metabolic syncope:

(5%).

4) Psychogenic syncope (3) Undetermined (Syncope of Unknown Causes) 13–41% of all causes of syncope. 1. Cardiac Syncope Severe obstruction to cardiac output or rhythm disturbance can lead to syncope (see Fig. 11.38).

122

THE HISTORY AND SYMPTOMATOLOGY

Structural abnormalities

1. LVOTO: AS, HCM 2. RVOTO: PH, PPH, PS 3. CAD 4. CT 5. Aortic dissection

Cardiac syncope

Neurally mediated

Arrhythmias

1. Tachyarrhymias: VT, SVT 2. Bradyarrhythmias: SSS, CHB, SB 3. Pacemaker related: malfunctioning, pacemaker syndrome

1. During and following cath 2. Nitrate

Fig. 11.38

syncope—LVOTO: left ventricular outflow tract obstruction, AS: | Cardiac aortic stenosis, HCM: hypertrophic cardiomyopathy, RVOTO: right ventricular outflow tract obstruction, PPH: primary pulmonary hypertension, PS: pulmonary stenosis, CAD: coronary artery disease, CT: cardiac tamponade, SSS: sick sinus syndrome, CHB: complete heart block, SB: sinus bradycardia, cath: cardiac catheterization.

Post-stenotic dilatation of aortic arch

Stenosed aortic valve

Left ventricular hypertrophy

Fig. 11.39

| Syncope occurs in 42% of severe AS.

a) Due to structural abnormalities leading to obstruction to flow: Exertional syncope is a common manifestation of all types of heart diseases in which cardiac output is fixed and does not rise or may even fall with exercise. i) LVOTO: Common conditions are AS, HCM. Other causes include prosthetic valve malfunction. Aortic stensis (AS): Syncope occurs in 42% of patients with severe AS, usually with exertion18 (see Fig. 11.39).

CARDINAL SYMPTOMS

123

Mechanism of syncope in AS: ●

●

●

Due to fixed CO, CO decreases on exertion due to reflex fall in peripheral vascular resistance. Exercise/exertion leads to marked increase in LV systolic pressure without a corresponding increase in aortic pressure, which results in excessive stimulation of LV mechanoreceptors (Bazold-Jarisch reflex) leading to inhibition of sympathetic but activation of parasympathetic tone through cardiac vagal afferent fibres.18 Myocardial ischemia contributes to vasodepressor syncope or depressed coronary artery perfusion due to hypotension and bradycardia.19 Occurrence of arrhythmias: Rarely, ventricular tachyarrhythmias, atrial fibrillation or paroxysmal AV block cause syncope due to loss of ‘atrial kick’.

Stages of syncope in AS: Syncope in AS has two stages. ●

●

First stage (20–40 sec) (due to vasodepression): There is a sudden fall of blood pressure, light headedness and pallor, followed by transient loss of consciousness. ECG may be normal and heart sounds are distant during this stage. Second stage is secondary to decreased coronary blood flow and is characterized by cyanosis, absent pulse and heart sounds, apnea, twitching of the body or seizures and abnormal ECG (ST, VT, Atrial fibrillation, AV block, ventricular fibrillation or asystole).

Prognostic importance: Survival is 3 yrs in AS with syncope unless valve replacement is done. Hypertrophic cardimyopathy (HCM): Mechanism of syncope in HCM ●

● ●

Syncope occurs in 30% (see Fig. 11.40).

Dynamic LVOTO is worsened by an increase in LV contractility (stimulating the LV mechanoreceptors), decrease in chamber size, or decrease in after-load. Hence, a Valsalva maneuver, severe cough or drugs (e.g. digitalis) precipitates hypotension and syncope. Myocardial ischemia.20 Ventricular arrhythmias especially VT reported in 25% of adult patients.21

Predictors of syncope include.22* age 30 yrs.* LVED volume index 60 mL/m2 and* unsustained VT. Prognostic importance: Extensive hypertrophy and VT are associated with poor prognosis. ii) LV inflow obstruction: LV inflow obstruction can also cause syncope. MS: ●

● ● ● ● ● ●

It rarely leads to syncope and the mechanism could be (see Fig. 11.41):

Severe inflow obstruction leads to decreased LV filling which in turn may lead to decreased cardiac output and syncope Atrial fibrillation with rapid ventricular rate PH Pulmonary embolism (PE) Cerebral embolic event Ball valve thrombus Associated AS or CAD.

124

THE HISTORY AND SYMPTOMATOLOGY Increased PA pressure

Dilated left atrium Stenosed mitral valve Normal left ventricle

ASH

Fig. 11.40

Right ventricular hypertrophy

SAM

occurs in 30% of hyper| Syncope trophic cardiomyopathy.

Fig. 11.41

mitral stenosis, syncope is not | Incommon.

RV

Aorta

VS AMVL LV

AO

PT

RA

LA

PMVL MYXOMA LA

LV RV

Fig. 11.42

can cause syncope when MV | Myxomas or TV is obstructed especially on change of posture.

Fig. 11.43

can occur in Eisenmenger | Syncope complex.

Atrial myxomas: It result in obstruction of MV or TV and may obstruct ventricular filling leading to decrease cardiac output and syncope especially with change in body position (see Fig. 11.42). iii) RVOTO: ●

●

Causes of syncope due to RVOTO are:

PH: secondary to congenital heart diseases (Eisenmenger complex and syndrome, TOF), primary pulmonary hypertension (PPH, upto 30%) (see Figs 11.43 and 11.44). PS

CARDINAL SYMPTOMS

125

Pulmonary embolism Aorta PA PT

LA

RA RA

RV

LV RV

Fig. 11.44

is reported upto 30% in | Syncope primary pulmonary hypertension. Fig. 11.45

occurs in 10–15% in pulmonary | Syncope embolism when 50% of pulmonary vascular bed is obstructed.

●

PE (syncope occurs in 10–15% especially with massive PE i.e. 50% obstruction of pulmonary vascular bed) (see Fig. 11.45).

Mechanism of syncope ●

●

●

Inability to increase CO in association with a reflex fall of peripheral resistance results in hypotension and syncope. Activation of cardiopulmonary mechanoreceptors in the setting of increased force of ventricular contraction. In congenital heart disease with right to left shunt as in TOF results in marked arterial hypoxia which may precipitate syncope (see Fig. 11.46).

iv) CAD: Syncope can occur in 5–12% in AMI especially in elderly patients, while syncope in unstable angina (USA) and coronary spasm is rare (see Fig. 11.47). Mechanism of syncope ● ● ●

●

Sudden pump failure producing hypotension and decreased perfusion of the brain. Arrhythmias: VT or bradyarrhythmias. Stimulation of LV baroreceptors during acute inferior wall MI or ischemia involving right coronary artery. Other possible mechanisms: – Acute mechanical complications: MR, VSD, ventricular wall rupture. – Drug induced: vasodilators (nitrates, Ca channel blockers, morphine); volume depletion due to diuretics. – CT: due to postinfarct pericarditis, thrombolysis, and anticoagulant therapy, during PTCA, perforation by pacemaker wire. – Acute PE. – Postural hypotension: after prolonged bed rest.

126

THE HISTORY AND SYMPTOMATOLOGY

Pulmonary stenosis (infundibular) Pulmonary stenosis (valvular)

Aorta PA LA

Overriding aorta

LV

Ventricular septal defect

RA

RV

Right ventricular hypertrophy

Fig. 11.47

myocardial infarction (AMI)— | Acute syncope occurs in 5–10% in AMI especially in elderly patients.

Fig. 11.46

|

TOF—syncope occurs due to arterial hypoxia.

Type I Aorta PA LA RA LV RV

Pericardial tamponade

Fig. 11.48

dissection—Syncope occurs | Aortic in 5%.

Fig. 11.49

can occur in pericardial | Syncope tamponade.

v) Aortic dissection: Syncope occurs in 5% (see Fig. 11.48). Mechanism of syncope: (a) sudden, CT (b) stroke. vi) Cardiac tamponade (pericardial tamponade): Which affects both right and left side of the heart, can rarely produce syncope more so if associated with arrhythmias (see Fig. 11.49). b) Syncope due to arrhythmias: Arrhythmias account for 5–30% of causes of syncope, and about 80% of cardiac causes.

CARDINAL SYMPTOMS

127

i) Tachyarrhythmias: VT, SVT, atrial fibrillation or atrial flutter with rapid ventricular response and AV nodal reentrant tachycardia are common causes of syncope. Ventricular tachycardia: (VT) is commonest arrhythmia producing syncope and accounts for 39% of cardiac causes of syncope. ●

●

●

VT generally occurs in the setting of known organic heart disease and long QT interval syndrome which could be congenital (with or without deafness) or acquired. The commonly associated ventricular arrhythmia is Torsades de pointes, and sometimes, polymorphic VT may also be associated. The most frequent causes of acquired long QT interval syndromes are antiarrhythmic drugs (quinidine, procainamide, disopyramide, flecainide, encainide, amidarone, and sotalol) and electrolyte imbalance (hypokalemia, hypomagnesemia).

Supraventricular tachycardia (SVT): It accounts for 8% of cardiac causes of syncope. In young individuals, paroxysmal SVT usually does not cause syncope. Predisposing factors for producing syncope in SVT are: ●

● ● ●

Most often, SVT occurs in the setting of known organic heart disease: AS, HCM, restrictive CM, PS, and LV dysfunction. Advanced age. Rate of SVT: 200/min. Underlying pre-excitation.

Syncope in WPW syndrome (pre-excitation) is related to rapid rate of reciprocating SVT or rapid ventricular response over the accessory pathway during atrial fibrillation and is also related to vasomotor factors as well.23 ii) Bradyarrhythmias and advanced AV block: It accounts for 31% of cardiac causes of syncope. Profound sinus bradycardia, SA exit block, high AV block and sick sinus syndrome (SSS) are the common causes. However, SSS and CHB account for majority of the cases. Sinus bradycardia (SB): It may be due to excessive vagal tone, decreased sympathetic tone or sinus node disease itself. ●

●

In young healthy individuals, sinus bradycardia is due to  vagal tone or ⇓ sympathetic tone and rarely results in syncope. However, sinus bradycardia due to eye surgery, intracranial or mediastinal tumors, myxedema and drugs, may cause symptomatic bradycardia that results in syncope.

Sick sinus syndrome (SSS): Syncope is reported in 25–70% of SSS patients which is characterized by the disturbances of SA impulse formation or conduction. ●

●

ECG manifestations include: sinus bradycardia, pauses, arrest or exit block. The appearance of alternating sinus bradycardia with paroxysmal SVT is common and is known as bradycardia–tachycardia syndrome. There may be associated atrial fibrillation with slow ventricular response, AV and intraventricular conduction defects. Thus, AV block, impaired junctional escape rhythm or ventricular arrhythmias may actually be responsible for syncope in the setting of SSS.

128

THE HISTORY AND SYMPTOMATOLOGY

Complete heart block (CHB): Syncope is common in Stokes-Adams syndrome but rare in patients with congenital CHB as ventricular rate is usually adequate. Progression to high grade AV block or CHB in patients with conduction defects: right bundle branch block with left anterior hemiblock (RBBB  LAH), RBBB  1 AV block, left bundle branch block (LBBB)  1 AV block, alternating bundle branch block (BBB), fascicular blocks with Mobitz type II AV block or with prolonged PR interval can occur, but not usually in patients with bifascicular block and normal PR interval. iii) Pacemaker related: Syncope in patients with pacemaker implantation is due to pacemaker malfunctioning or pacemaker syndrome. ●

●

Dual chamber pacemakers can induce pacemaker-mediated tachycardias when there is retrograde conduction of the ventricular impulse to the atria. However in the present scenario, this complication is almost eliminated due to improved technology.

Mechanism of syncope in arrhythmias (i) In tachyarrhythmias: Mild–moderate tachycardias increase output (CO), whereas marked tachycardia (140/min) leads to decrease in diastolic filling and CO (Raul’s effect) resulting in hypotension and syncope. Besides tachycardia results in vigorous ventricular contraction stimulating ventricular mechanoreceptors leading to hypotension and syncope. (ii)In bradyarrhythmias: Usually, bradycardia leads to prolonged ventricular filling resulting in increased stroke volume to maintain CO. However, severe bradycardia (30/min) may result in inadequate compensatory increase in stroke volume and leads to syncope. c) Neurally mediated syncope: i) During and following cardiac catheterization: Pain associated with femoral puncture and groin compression after sheath removal may produce vasovagal episode and result in syncope. Most common in anxious and fearful patients and should be suspected when the patient becomes restless, yawns or vomits, since it is potentially dangerous in the left main coronary artery (LMCA) disease, severe three vessel disease (TVD), severe AS and severe PH. Prophylactic measures to prevent vasovagal episodes include: ● ● ● ●

Adequate explanation of the procedure to the patient. Congenial atmosphere in the cath lab and friendly attitude of the staff. Intravenous atropine in anxious bradycardia patients prior to removal of the sheath. Patient should be monitored for rhythm and blood pressure during sheath removal and immediately afterwards.

ii) Nitrate syncope: Normally, the vasodilator drugs such as nitrates that cause marked venous dilatation, decreased venous return and decreased CO results in tachycardia and increased cardiac inotrophic state. However, in susceptible individuals and presence of predisposing factors lead to stimulation of cardiac mechanoreceptors and

CARDINAL SYMPTOMS

129

syncope.24 When stable angina progresses to USA or evolving MI, nitrate syncope occurs due to: ● ● ●

Unrelieved ischemia Additional area of ischemia and Bradycardia as in inferior wall MI. Hence, a new onset nitrate syncope in a stable angina patient, prompt hospitalization and further investigation is mandatory. Predisposing factors include:

●

Concomitant therapy with: – Beta-blockers (prevent reflex tachycardia) – Diuretics (hypovolemia with veno-dilatation) – Other vasodilators (additional vasodilatation).

●

Prolonged standing: causes venous pooling.

2) Non Cardiac Syncope The non cardiac causes of syncope include vascular, neurological, metabolic and psychogenic (see Fig. 11.50). (a) Vascular syncope The vascular syncope mainly includes reflex mediated (vasovagal,24 situational and carotid sinus syncope) and orthostatic syncope. (1) Reflex mediated: i) Neurocardiogenic syncope (vasovagal/vasodepressor syncope/common faint): is one of the most common causes of syncope. It is characterized by a sudden fall of blood pressure with or without bradycardia, often preceded by a constellation of prodromal symptoms such as nausea, headache, sweating, hyperventilation, paraesthesia chest pain and palpitation. However, these prodromal symptoms may persist for minutes or hours after the syncopal episode has resolved. It often occurs in young individuals in response to the facilitating factors and often in the presence of predisposing factors and it classically resolves spontaneously once the patient assumes supine position (see Fig. 11.51).

Vascular 1. Vasovagal 2. Carotid sinus 3. Situational

Non cardiac syncope

Orthostatic Neurological

Psychogenic

Metabolic

1. Hypoglycemic related 2. Hypoxia related: high altitude syncope, anemia

1. CVA, TIA 2. Subclavian steel syndrome 3. Neuralgias 4. Migraine related

Fig. 11.50

cardia syncope—CVA: cerebrovascular accident, TIA: transient ischemic | Non attack.

130

THE HISTORY AND SYMPTOMATOLOGY

Facilitating factors

1. Emotions 2. Pain 3. Posture 4. ↓Volume status

Fig. 11.51

Vasovagal syncope

Predisposing factors

1. Fatigue 2. Surgery 3. Heat

| Vasovagal syncope.

i) The facilitating factors which precipitate syncope include: – – – –

Emotions: grief, anger, humiliation, or death of the loved one Pain Prolonged standing Depleted volume status, venipuncture and blood donation.

ii) The predisposing factors include: fatigue, surgery (eye, dental)25 and heat. But it may occur without identifiable predisposing factors. iii) Phases: Vasovagal syncope has three phases: – First phase: During this period, the blood pressure and heart rate increases largely due to baroreceptor mediated rise in sympathetic tone. – Second phase: There is an abrupt fall of blood pressure and heart rate (occasionally, there may be asystole of 10–20 sec) with prodromal symptoms culminating in syncope. Atropine may prevent fall in heart rate but not hypotension. – Third phase consists of rapid recovery on assuming supine position. iv) Pathophysiology – Normal response to upright position (standing): The decrease in venous return, stroke volume and arterial pressure leads to compensatory responses mediated by baroreceptors and medullary centers to increase sympathetic and decrease parasympathetic activity, thereby maintaining blood pressure and heart rate. – In vasovagal syncope: Facilitating factors (such as prolonged standing or grief ) in susceptible individuals trigger baroreceptors and medullary centers through afferent C fibers, (see Fig. 11.52) activating the parasympathetic tone but inhibiting the sympathetic tone through vagal efferent fibers resulting in hypotension and bradycardia, and thereby syncopy. ii) Situational syncope: accounts for 1–8%, and occurs in association with various daily activities, e.g. micturition, defecation, swallowing, coughing, Valsalva maneuver. (i) Micturition syncope: It is often seen in young men after rising from the bed in early morning hours and in men who experience sudden loss of consciousness during or immediately following voiding. Elderly individuals with multiple medical problems may also experience micturition syncope often in association with orthostatic hypotension.26

CARDINAL SYMPTOMS

131

↓ Central venous volume (Orthostatic stress, ↓ blood volume)

Baroreceptors unloaded ↑ Adrenergic tone ↑Myocardial contractility and ↑ heart rate Activation of cardiopulmonary mechanoreceptors Central vasomotor activation

Parasympathetic activation

Sympathetic withdrawal and ↑ circulating epinephrine (from adrenals)

Bradycardia Vasodilation Hypotension

Syncope

Fig. 11.52

| Mechanism of neurocardiogenic syncope.

Mechanism: It is similar to vasovagal syncope. The mechanoreceptors in bladder are triggered in the presence of predisposing and facilitating factors, causing syncope. ●

Predisposing factors: – – – – –

●

Fatigue Decreased food intake Alcohol ingestion Recent urinary tract infection Bladder pathology, e.g. bladder neck obstruction, pheochromocytoma of bladder.

Facilitating factors: – Physiological changes during sleep i.e. decline of blood pressure and heart rate mediated by decreased peripheral vascular resistance (⇓ sympathetic activity) during sleep. – Changes during micturition, i.e. sudden decompression of bladder, and possible Valsalva maneuver. – Orthostatic hypotension especially in elderly individuals.

(ii) Defecation syncope most commonly occurs in the elderly individuals, usually after rising from the bed at night or during manual disimpaction of the rectum.27

132

THE HISTORY AND SYMPTOMATOLOGY

Mechanism: There occurs triggering of mechanoreceptors in the gut wall in the presence of predisposing and facilitating factors. ●

Predisposing factors: – Fatigue, – Decreased food intake, – Alcohol ingestion, – GIT pathology, e.g. Meckel’s diverticulum, ruptured appendix, foreign body in the rectum, – Other underlying medical conditions e.g. CAD, pulmonary embolism, transient ischemic attack (TIA).

●

Facilitating factors:

– Physiological changes during sleep. – Possible Valsalva maneuver during defecation. – Orthostatic hypotension. Syncope during rectal and pelvic examination or sigmoidoscopy: Similar mechanism for syncope. (iii) Swallowing/deglutition syncope: Mechanism: During or immediately following swallowing, syncope occurs in patients associated with structural abnormalities of esophagus or heart due to triggering of mechanoreceptors in upper GIT, especially esophagus. ●

Predisposing factors:

●

– Esophagus abnormalities include: diverticula, achalasia, stricture, tumor or diffuse spasm. – Cardiac: acute myocardial infarction, acute rheumatic carditis treated with digoxin or calcified mass over the aortic valve or septum. SB, sinus arrest or high degree AV block have been demonstrated during swallowing syncope. Similar mechanism is implicated in syncope associated with esophagoscopy.28

(iv) Cough syncope (tussive or post tussive syncope/laryngeal vertigo): Syncope following a paroxysm of severe cough usually occurs in the middle aged men who drink alcohol, smoke and have a chronic lung disease. It may occur in children but is rarely seen in women. Mechanism ● ●

●

Reflex triggering of pulmonary mechanoreceptors. Severe coughing increases intrathoracic pressure which decreases venous return and in turn cardiac output (CO). Transmission of high intrathoracic pressure to the subarachnoid space during coughing may increase the cerebrovascular resistance and reduce the cerebral blood flow.

Cough syncope is rarely associated with Mobitz II or complete heart block, obstructive cardiomyopathy, hypersensitive carotid sinus syndrome and severe cerebrovascular disease. Similar mechanism is implicated for syncope during endotracheal intubation or bronchoscopy and sneeze syncope associated with Arnold-Chiari malformation.

CARDINAL SYMPTOMS

133

(v) Valsalva syncope: Valsalva maneuver, usually in the presence of predisposing factors (such as cerebrovascular disease or sick sinus syndrome) causes syncope due to progressive fall in venous ruturn, arterial pressure and cardiac output as a result of prolonged increase in the intrathoracic pressure.27 (vi) Divers syncope: It may occur in underwater diving and may lead to sudden death. It could be a form of neurocardiogenic syncope and hypoxia and bradycardia of diving reflex may contribute.27 (vii) Postprandial syncope: Postprandial hypotension (usually 45–60 min after meals)29 due to splanchnic blood pooling and peripheral vasodilatation may lead to syncope especially in the elderly individuals (up to 36%). Impaired baroreflex function and thereby inadequate sympathetic activity and release of gastrointestinal peptides could be the contributing factors.30 iii) Carotid sinus hypersensitivity/carotid sinus syncope: Carotid sinus hypersensitivity is characterized by profound bradycardia and/or hypotension with compression of carotid sinus in susceptible individuals. It is reported in 5–25% of asymptomatic population especially in elderly males, while carotid sinus syncope is characterized by spontaneous fainting, occurs in 5–20% of the individuals with abnormal carotid sensitivity. i) Mechanism: Triggering of carotid sinus baroreceptors (located in the internal carotid artery just above the bifurcation of common carotid artery) and medullary centers via afferent fibers (glossopharyngeal and vagus nerves) activates parasympathetic and inhibits sympathetic tone via vagal and sympathetic efferent fibers respectively which further results in profound bradycardia and hypotension.31 ii) Types of carotid sinus hypersensitivity: Three types have been described:32 ●

●

●

Cardioinhibitory type is defined as cardiac asystole of 3 sec. It is the most common type accounting for 34–78% and is secondary to marked sinus bradycardia, SA block, and/or high degree AV block. Vasodepressor type is defined as a systolic blood pressure decline of 50 mmHg, in the absence of significant bradycardia. It accounts for 5–10%. Presyncopal symptoms and signs, such as nausea, sweating and pallor are not usually observed. Mixed type is the combination of cardioinhibitory and vasodepressor response, with bradycardia and hypotension. The vasodepressor component (hypotension) may not be evident until atropine blockade or during cardiac pacing. iii) Predisposing factors:

For carotid sinus syncope: – CAD and hypertension in majority. – Neck pathology: Enlarged lymph nodes, tissue scars, carotid body tumors, parotid tumors, thyroid tumors, head and neck tumors. – Possible associations with digitalis, alpha-methyl dopa and propanol intake have been reported. ● For carotid sinus hypersensitivity: Sinus node dysfunction and AV node conduction abnormalities are often noted in the patients. iv) Precipitating factors: Factors which exert pressure on the carotid sinus may precipitate syncope, e.g. tight collar, shaving, sudden turning of the head. ●

134

THE HISTORY AND SYMPTOMATOLOGY

(2) Orthostatic syncope (hypotension): A decline of 20 mmHg in systolic or 10 mmHg in diastolic blood pressur upon assuming upright posture is often defined as orthostatic hypotension. ●

●

●

●

●

It is a disorder in which assumption of upright posture results in hypotension associated with light-headedness, blurring of vision and a sense of profound weakness.27 If the fall in the perfusion pressure to the brain is profound, syncope occurs and if the individual assumes the recumbent posture, BP rapidly normalizes and consciousness is restored. These symptoms are often worst on arising in the morning or after meals or exercise. i) Mechanism Normally, upright posture results in pooling of 500–700 ml of blood in lower limbs and splanchnic circulation leads to decrease venous return and cardiac output, and triggering of aortic, carotid and cardiopulmonary baroreceptors. This reflexly increases sympathetic outflow and inhibit parasympathetic activity, resulting in increase in heart rate and vascular resistance to maintain systemic blood pressure on standing upright.33 Hence, orthostatic hypotension occurs when a defect exist in the regulation of systemic blood pressure in any element of this system.

ii) Etiology and classification: Etiologically, orthostatic hypotension is classified into three groups: Due to venous pooling and/or blood volume depletion: Prolonged bed rest Pregnancy Blood loss Prolonged standing Venous varicosities Dehydration Neurogenic causes ● General medical disorders: Diabetes mellitus, renal failure, amyloidosis, and alcoholic neuropathy. ● Autoimmune diseases: Mixed connective tissue disease, SLE, rheumatoid arthritis, Gullaine Barre syndrome, Eaton-Lambert syndrome. ● Central brain lesion: Multiple cerebral infarcts, multiple sclerosis, craniopharyngioma. ● Autonomic failure: Shy-Drager syndrome (multiple system atrophy), Parkinson’s disease. ● Tabes dorsalis, syringomyelia. ● Circulating endogenous vasodilators: Hyperbradykinism, carcinoid syndrome, mastocytosis. ● Idiopathic orthostatic hypotension. Drug induced: It accounts for 2–9%. ● Vasodilators: Ca channel blockers, nitrates, hydralazine, ACE inhibitors, and prazosin. ● Other antihypertensives: Methyldopa, clonidine, labetalol, and diuretics. ● Antidepressants: MAO inhibitors and tricyclic antidepressants. ● Tranquilizers: Phenothiazines and barbiturates. ● Antiparkinsonian drugs. iii) Idiopathic orthostatic hypotension is a rare disorder, common in males and is often associated with other autonomic disturbances such as impotence, impaired erection and ejaculation, impaired sweating and sphincter malfunction.

CARDINAL SYMPTOMS

b) Neurological syncope: (10%).

135

Neurological disorders are infrequent causes of syncope

i) Cerebrovascular syncope: associated with syncope.34

6% of cerebrovascular accidents (CVA) and TIA are

Vertebrobasilar system: In almost all the patients, atherosclerotic occlusive disease of vertebrobasilar system is involved in this type of syncope,34 with compromised perfusion to the medullary centers, which is usually preceded by symptoms of vertigo, diplopia, dysarthria and ataxia. Subclavian artery: Subclavian steal syndrome due to occlusive disease of the subclavian artery proximal to the origin of the vertebral artery may give rise to syncope.27 Brachiocephalic artery: In the occlusive disease of the origins of the brachiocephalic vessels e.g. aortic arch syndrome, Takayasu’s arteritis, syncope is not uncommon.26 Syncope is a rare manifestation: of SLE, giant cell arteritis, sickle cell disease, embolic complications of rheumatic heart disease and myxoma, dissection of extracranial arterics. Syncope may occur in the anomalies of cervical spine or cervical spondylosis. ii) Reflex mediated syncope: It includes neuralgias: Glossopharyngeal neuralgia: Severe unilateral paroxysmal pain in oropharynx, tonsillar fossa, base of the tongue, or ear precipitated by swallowing, chewing, or coughing, occasionally results in syncope and seizure during the attack. Syncope is mostly caused by asystole or bradycardia and rarely due to vasodepressor response. It is associated with neoplasms of neck or lymphomas with meningeal involvement in 1/6th of the patients with syncope. Trigeminal neuralgia: It may also be associated with syncope due to bradycardia asystole or vasodepressor response. iii) Seizure disorders: ●

●

2% of seizure patients have syncope.35

Temporal lobe syncope: Temporal lobe epilepsy is rarely associated with bradyarrhythmias and is the most likely form of epilepsy to masquerade as syncope. Hence, the term temporal lobe syncope is used for partial complex seizures when patients have drop attacks resembling syncope.36 Non convulsive seizures i.e. atonic seizures or epileptic drop attacks which are common with secondary generalized seizures or partial epilepsy affecting mesial frontal or central cortical regions may masquerade as syncope.

iv) Migraine related syncope: 12–18% of patients with migraine may have syncope and orthostatic hypotension due to hyperresponsiveness of dopamine receptors with the inhibition of vasomotor center and vasovagal reaction secondary to pain. ●

●

Syncope usually occurs in less form of migraine due to basilar arterial system involvement. This type of migraine usually afflicts young women and has a strong menstrual association.

136

THE HISTORY AND SYMPTOMATOLOGY

c) Metabolic syncope: i) Hypoglycemia related syncope is associated with weakness, sweating, sensation of hunger, confusion and altered consciousness, which are not related to posture and usually promptly respond to food ingestion or intravenous glucose administration. ●

●

Most common causes are: due to insulin or oral hypoglycemic drugs, alcohol, prolonged fasting and rarely, insulinomas. It is gradual in onset (circulatory cause) and is associated with sinus tachycardia and rarely, hypotension. However, hypoglycemia may trigger neurocardiogenic syncope.27

ii) Hypoxia related syncope: ●

High altitude syncope may occur in young healthy adults exposed to moderate to very high altitudes37 due to: – Reflex bradycardia, hyperventilation, and subsequent hypocapnia, resulting in reflex cerebral vasoconstriction which decreases cerebral oxygen delivery. – Mild volume depletion due to diuresis at high altitudes or due to physical activity may lead to vasovagal syncope.

●

●

In the presence of cardiovascular disease, pulmonary insufficiency and anemia; syncope may occur at lesser levels of oxygen deprivation. It is associated with sinus tachycardia while blood pressure is usually normal.

d) Psychogenic syncope: Syncope may be a manifestation of generalized anxiety disorder, major depression or panic disorder, especially in young females by precipitating vasovagal reactions.38 During hyperventilation seen in psychiatric patients, there is tachycardia and slight hypotension but no profound fall of blood pressure. Complete loss of consciousness rarely occurs. 3. Exercise Induced Syncope Syncope may occur during or immediately after exercise. The most common causes are: (1) Underlying cardiac diseases: ●

Structural abnormalities: – – – –

●

These are the most common causes:

LVOTO: AS, HCM RVOTO: PH Cardiomyopathy: DCM, HCM, RV dysplasia CAD: atherosclerotic, anomalous origin of coronary arteries (in young).

Arrhythmogenic: VT, SVT, accessory pathways, long QT syndrome. Underlying cardiac diseases have a potential for sudden cardiac death.

(2) Underlying neurological causes subclavian steal syndrome. (3) Neurocardiogenic: Exercise syncope without structural heart disease is due to the increase in catecholamines and force of ventricular contraction results in triggering of cardiac mechanoreceptors in the setting of mild volume depletion and shifts of blood flow to dissipate heat.

CARDINAL SYMPTOMS

Clinical history

ECG: Standard Signal averaged Holter monitoring

Evaluation of cardiac syncope

Clinical history

Structural heart

1. Chest X-ray and ECG 2. Echocardiogram

Arrhythmogenic Structural heart disease & ALCAPA

Electro-physiological studies

Fig. 11.53

137

Cath study and angiogram

Arrhythmogenic

of cardiac syncope—ALCAPA: anomalous left coronary artery from | Evaluation pulmonary artery. Evaluation of noncardiac syncope

BP measurementsupine and standing

Clinical history

Postural hypotension

Fig. 11.54

HUTT

CT scan, EEG, carotid doppler

Neurally mediated syncope

Neurological cause/ seizure disorder

Carotid massage

Carotid sinus syncope

of noncardiac syncope—HUTT: head up tilt test, CT: computer | Evaluation tomography, EEG: electroencephalogram.

Evaluation of Syncope A detailed clinical history from the patient and a witness if present is crucial for diagnosis of specific entities and to distinguish syncope from seizure. It is supplemented by physical examination and baseline investigations (see Figs 11.53 and 11.54). 1) Clinical history: While obtaining the history, the following have to be determined (see Table 11.10): ● ● ● ● ● ● ●

Mode of onset Duration of episode Precipitating factors (triggers) How was consciousness regained? Associated factors—before (prodromes, aura), during, and after (postictal) Predisposing factors Family history.

138

THE HISTORY AND SYMPTOMATOLOGY

Table 11.10 Clinical history in cardiac syncope vs seizure disorder Features

Cardiac syncope

Seizure disorder

1. 2. 3. 4.

Rapid

1 min Unrelated in arrhythmogenic Promptly

Rapid 5 min Unrelated Slowly

Exertion Sweating, nausea before the event (sometimes)

Nil (i) Aura

Mode of onset Duration Posture Restoration of consciousness 5. Triggering factors 6. Associations

7. Family history

In hypertrophic obstructive cardiomyopathy (HOCM)

(ii) Convulsive movements, frothing at the mouth, tongue bite (iii) Postictal confusion, sleep, aches Usual

i) Mode of onset ● Rapid/sudden onset in cardiac and vasovagal syncope and seizure disorder. Gradual onset in hypoglycemia, drug related syncope and hyperventilation. ● Unrelated to posture: Arrhythmogenic and seizure disorder. – Prolong standing: Prolonged standing facilitates vasovagal syncope. – After arising: In orthostatic hypotension. – Syncope on changing position (from sitting to lying, bending, turning over in bed): In atrial myxomas. ii) Duration of episode: In syncope, duration of the event is usually 1 min and duration of episode usually lasts 5 min; while in seizures, the duration of unconsciousness is usually 5 min. iii) Restoration of consciousness: Regained consciousness promptly in syncope (of cardiac origin); while in seizure disorder, it occurs slowly. iv) Triggering factors: (i) On exertion: On exertion, cardiac syncope occurs due to LVOTO (AS, HOCM), RVOTO (PH, PE), CAD and sometimes due to arrhythmias. ● With arm exercise: Subclavian steal syndrome. ● After exercise in well trained athletes: Exercise induced syncope. (ii) With head rotation/pressure on carotid sinus: Carotid sinus syncope/hypersensitivity. (iii) Pain, grief, emotional stress, unpleasant sight, sound or smell: Vasovagal syncope. (iv) During or immediately after micturition, defecation, swallowing, coughing: Situational syncope. v) Associations (i) Associated with aura: In seizure disorders. (ii) Prodromes of warmth, nausea, sweating, light headedness: They occur in vasovagal syncope.

CARDINAL SYMPTOMS ● ●

139

Sweating or nausea before the event (sometimes in): Cardiac syncope. Preceded by vertebrobasilar symptoms such as vertigo, diplopia, dysarthria, ataxia: CVA (in vertebrobasilar system).

(iii) Episode associated with blue face, frothing at the mouth, tongue biting, urinary incontinence, convulsive movements in seizure disorders. (iv) Postictal confusion state, sleepiness, aching muscles in seizure disorders. vi) Predisposing factors (i) Fatigue, surgery (eye, dental), exposure to heat: Vasovagal syncope. (ii) In situational syncope: – – – –

Fatigue, alcohol ingestion, UTI, bladder pathology (micturition syncope) Fatigue, alcohol intake, GIT pathology (defecation syncope) Esophageal pathology (swallowing syncope) Smoking, chronic lung diseases, alcohol intake (cough syncope).

(iii) Neck pathology, CAD, hypertension: Carotid sinus syncope. (iv) Concomitant use of drugs: Postural hypotension, nitrate syncope (diuretics, vasodilators, betablockers). (v) Head injury: Seizure disorders. vii) Family history: (i) Family history of epilepsy may be present in seizure disorders. (ii) Positive family history in HOCM, long QT syndrome. 2) Blood pressure measurement for detection of orthostatic hypotension: Supine BP and heart rate are measured after the patient has been lying down for at least for 5 min. Standing measurements should be obtained immediately and for at least 2 min., and should be continued for 10 min when there is a high suspicion of orthostatic hypotension. Sitting blood pressures is not reliable. 3) Carotid massage for the detection of carotid sinus syncope: Even though the technique is not standardized, carotid massage is done in supine position for 6–10 sec,39 with continuous ECG and blood pressure monitoring. ●

●

●

Simultaneous bilateral carotid massage should never be done, and at least 15 sec should be allowed to elapse between the massage from one side to the other. However, it may be done in sitting or standing positions if vasodepressor variety is suspected and the test is negative in supine position. Complications of carotid sinus massage are extremely low and include: prolonged asystole, transient or permanent neurological deficit, ventricular fibrillation and death.

4) Head up tilt test (HUTT):40 with syncope.

It is a standard diagnostic test for evaluating patients

(i) Indications40 ●

Recurrent syncope or a single syncopal episode in a high risk patient who either has no evidence of structural heart disease or in whom other causes of syncope have been excluded.

140

THE HISTORY AND SYMPTOMATOLOGY ●

●

Evaluation of patients in whom an apparent cause of syncope has been established (e.g. asystole, AV block) but in whom the presence of neurally mediated syncope would influence the treatment, and As a part of the evaluation of patients with exercise-related syncope.

(ii) Potential emerging indications ●

●

●

●

Recurrent idiopathic vertigo in whom neurally mediated bradycardia and hypotension may be the cause. Recurrent TIAs especially if Doppler ultrasound, carotid angiography and transesophageal echocardiogram (TEE) have failed to disclose an etiology for the symptoms. Chronic fatigue syndrome: In some, neurally mediated bradycardia and hypotension may contribute to the symptom complex. Sudden infant death syndrome: Since potentially neurally mediated hypotension may play a role in this syndrome, HUTT may help in better understanding of this problem.

(iii) Relative contraindications ● ● ● ●

Syncope with clinically severe LVOTO. Syncope in presence of critical mitral stenosis. Syncope in setting of known critical proximal coronary artery stenosis. Syncope in conjunction with known critical cerebrovascular stenosis.

(iv) Not warranted ●

●

●

Single syncopal episode which is highly typical of neurally mediated syncope without an injury and also not in a high risk setting. Syncope in which an alternative specific cause has been established and in which additional demonstration of a neurally mediated susceptibility would not alter the treatment plans. It is not useful in establishing a diagnosis of situational syncope.41

(v) Technique ●

Preparation – The test is performed in a quiet room/lab, minimizing the surrounding noise with ample lighting and comfortable temperature in a fasting state (75 mL of normal saline for each hour of fasting may be infused to decrease the possibility of false positive result). – All non essential and vasoactive drugs should be withheld for about 5 half-lives. – Tilt table with foot board support is used. – Simultaneous and continues monitoring of minimum 3 ECG leads and BP is done. Monitoring of BP is usually done non invasively (digital plethysmography) so as not to provoke the vasovagal reaction.

●

Procedure: 20–45 min supine equilibrium period before the start of the test. HUTT has two protocols. – Passive tilt testing: Table is tilted to an angle of 60–80 (usually 70) for 30–45 min. If there is no positive response i.e. syncope or pre-syncope in association with hypotension and/or bradycardia, proceed with pharmacological provocation.

CARDINAL SYMPTOMS

141

– Provocative tilt testing: Usually isoproternol, nitroglycerine or edrophonium are used as pharmacological provocation. 1 g/min of isoproternol infusion is started while the patient is in supine position and then the patient is tilted for 10–15 min and watched for any positive response. If there is no positive response, the patient is again brought to supine position and the procedure is continued with increasing dosage (infusion rate is increased by 1 g/min each time) and patient is tilted for similar duration till the positive response, or another end point (maximum dosage of 3–5 g/min or adverse effects or severe tachycardia) is reached. Alternatively, increasing bolus dosages (each increment of 1–2 g) may be given instead of continuous infusion. (vi) Positive response: Three types of positive responses have been described:42 mixed, cardioinhibitory and pure vasodepressor. Type 1: Mixed response ●

●

Heart rate initially rises and then falls, but the ventricular rate does not fall to 40/min or fall to 40/min for 10 sec with or without asystole for 3 sec. BP rises initially and then falls before heart rate falls.

Type 2: Cardioinhibitory response: Heart rate rises initially and then falls to a ventricular rate of 40/min for more than 10 sec or asystole occurs for 3 sec. ● ●

Type 2A cardioinhibitory: BP rises initially and then falls before heart rate falls. Type 2B cardioinhibitory: BP rises initially and only falls to 80 mmHg systolic at or after the onset of rapid and severe fall in heart rate.

Type 3: Pure vasodepressor response ●

●

Heart rate rises progressively and does not fall more than 10% from the peak at the time of syncope. BP falls to cause syncope.

The estimated sensitivity and specificity for passive tilt test is 65% and 90% respectively while with pharmacologic provocation, sensitivity is 75% and specificity 80%, with overall reproducibility of 67–85%. 5) ECG (i) Standard ECG: For diagnosis of syncope due to arrhythmias. (ii) Signal averaged ECG: For the detection of late potentials for prediction of inducible ventricular tachycardia in patients with syncope.43 (iii) Holter monitoring: It determines the presence or absence of arrhythmias in patients who develop symptoms during ambulatory monitoring. 6) Electrophysiological (EP) studies: It is indicated in patients with suspected structural heart disease and unexplained syncope and it should not be performed in patients with known cause of syncope for whom treatment will not be influenced by the findings of the test.44 EP studies are helpful in establishing a diagnosis of sick sinus syndrome, heart block, SVT or VT in patients with syncope. 7) CT scan, EEG, carotid duplex scan: These are helpful in establishing neurological causes of syncope and seizure disorders with careful history and neurological examination.

142

THE HISTORY AND SYMPTOMATOLOGY

8) Echocardiography: For detection of occult cardiac disease and impaired ventricular function to suggest a cardiac cause of syncope. 9) Stress testing ● It is reserved for patients in whom syncope or pre-syncope occurred during or immediately after exertion or in association with chest pain. ● It is indicated in young individuals with recurrent syncope during exertion when other causes of syncope have been excluded and to rule out anomalous coronary arteries. It is contraindicated in patients suspected of having severe AS or HOCM. 10) Cardiac catheterization: For establishing the diagnosis of structural heart diseases and anomalous coronary arteries with syncope. 11) Routine blood tests: Such as serum electrolytes, glucose and hematocrit levels may be helpful, but have a low diagnostic value in evaluation of the patient with syncope.

REFERENCES 1. 2. 3. 4. 5. 6. 7. 8.

9.

10. 10a. 11.

12. 13. 14. 15. 16.

Sampson JJ, Cheitlin MD. Pathophysiology and differential diagnosis of cardiac pain. Prog Cardiovasc Dis 1971;13(16):507–531. Lichstein E, Breitbart S, Shani J, et al. Relationship between location of chest pain and site of coronary artery occlusion. Am Heart J 1988;115(3):564–568. Spittell PC, Spittell JA Jr, Joyce JW, et al. Clinical features and differential diagnosis of aortic dissection: Experience with 236 cases (1980–1990). Mayo Clin Proc 1993;68:642–651. Heberden W. Some accounts of a disorder of the breast. Medical Trans 1772;2:59–67. Bernstein LM, Fruin RD, Pacini R. Differentiation of esophagus pain from angina pectoris: Role of the esophageal acid perfusion test. Medicine 1962;41:143–162. The Criteria Committee of the New York Heart Association: Diseases of the Heart and Blood Vessels Nomenclature and Criteria for Diagnosis. 6th ed Boston, Little Brown and Co., 1964. Campeau L. Grading of angina pectoris. Circulation 1976;54(3):522–523. Goldman L, Hashimoto B, Cook EF, and Loscalzo A. Comparative reproducibility and validity of systems for assessing cardiovascular functional class: Advantages of a new specific activity scale. Circulation 1981;64(6):1227–1234. Chauhan A, Mullins PA, Taylor G, Petch MC. Schofield PM. Cardioesophageal reflex: A mechanism for “linked angina” in patients with angiographically proven coronary artery disease. J Am Coll Cardiol 1996;27(7):1621–1628. Levine HJ. Difficult problems in the diagnosis of chest pain. Am Heart J 1980;100(1):108–118. ACC/AHA Guidelines update for the management of patients with chronic stable angina. Circulation 2003;107:149–158. Sullivan M, Higginbotham M, Cobb F. Increased exercise ventilation in patients with chronic heart failure: intact ventilatory control despite hemodynamic and pulmonary abnormalities. Circulation 1988;77:552–559. Joseph K Perloff. Congenital heart disease in adults. In: Braunwald E. ed. Heart Disease: A Textbook of Cardiovascular Medicine, 5th edn. Bangalore: Prism books Pvt Ltd; 1997:972. American Thoracic Society: Dyspnea: Mechanism, assessment and management. A consensus statement. Am J Respir Crit Care Med 1999;159(1):321–340. Weber BE, Kapoor WN. Evaluation and outcomes of patients with palpitations. Am J Med 1996; 100(2):138–148. Knudson MP. The natural history of palpitations in a family practice. J Fam Pract 1987;24(4):357–360. Vanden Belt RJ. The history. In: Chizner M, ed. Classic Teachings in Clinical Cardiology: A Tribute to W. Proctor Harvey. Cedar Grove, NJ: Laennac; 1996:41–54.

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17. Come PC, Pitt B. Nitroglycerine-induced severe hypotension and bradycardia in patients with acute myocardial infarction. Circulation 1976;54:624–628. 18. Grech ED and Ramsdale DR. Exertional syncope in aortic stenosis; evidence to support inappropriate left ventricular baroreceptor response. Am Heart J 1991;121(2 Pt 1):603–606. 19. Baltazar RF, Go EH, Benesh S and Mower MM. Case report: Myocardial ischemia: an overlooked substrate in syncope of aortic stenosis. Am J Med Sci 1992;303(2):105–108. 20. Dilsizian V, Bonow RO, Epstein SE and Fananapazir L. Myocardial ischemia detected by thallium scintigraphy is frequently related in to cardiac arrest and syncope in young patients with hypertrophic cardiomyopathy. J Am Coll Cardiol 1993;22:796–804. 21. Fananapazir L, Tracy CM, Leon MB, et al. Electrophysiologic abnormalities in patients with hypertrophic cardiomyopathy. Circulation 1989;80(5):1259–1268. 22. Nienaber CA, Hiller S, Spielmann RP, et al. Syncope in hypertrophic cardiomyopathy: Multivariate analysis of prognostic determinants. J Am Coll Cardiol 1990;15(5):948–955. 23. Leitch JW, Klein GJ, Yee R, Leather RA, Kim YH. Syncope associated with supraventricular tachycardia. Circulation 1992;85(3):1064–1071. 24. Raviele AN, Gasparini G, DiPede F, et al. Nitroglycerine infusion during upright tilt: A new test for the diagnosis of vasovagal syncope. Am Heart J 1994;127(1):103–111. 25. Boorin MR. Anxiety. Its manifestation and role in the dental patient. Dent Clin North Am 1995;39(3):523–539. 26. Kapoor WN, Peterson J and Karpf M. Micturition syncope. A reappraisal. JAMA 1985;253(6):796–798. 27. Schaal SF, Nelson SD, Boudoulas H, Lewis RP. Syncope. Curr Probl Cardiol 1992;17(4):205–264. 28. Ferrante L, Artico M, Nardacci B, Frajoli B, Cosentino R, Fortuna A. Glossopharyngeal neuralgia with cardiac syncope. Neurosurgery 1995;36(1):58–63. 29. Vaitkevicius PV, Esserwein DM, Maynard AK, et al. Frequency and importance of postprandial blood pressure reduction in elderly nursing-home patients. Ann Intern Med 1991;115(11):865–870. 30. Jansen RWMM, Lipsitz LA. Postprandial hypotension: Epidemiology, pathophysiology, and clinical management. Ann Intern Med 1995;122(4):286–295. 31. Strasberg B, Sagie A, Erdman S, et al. Carotid sinus hypersensitivity and the carotid sinus syndrome. Prog Cardiovas Dis 1989;31(5):379–391. 32. Weiss S, Baker JP. The carotid sins reflex in health and disease: Its role in the causation of fainting and convulsions. Medicine 1933;12:297–354. 33. Lipsitz L. Orthostatic hypotension in the elderly. N Eng J Med 1989;321(14):952–957. 34. Davidson E, Rotenbeg Z, Fuchs J, et al. Transient ischemic attack-related syncope. Clin Cardiol 1991;14(2):141–144. 35. Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69(3):160–175. 36. Jacome DE. Temporal lobe syncope: Clinical variants. Clin Electroencephal 1989;20:58. 37. Nicholas R, O’Meara PD, Calonge N. Is syncope related to moderate altitude exposure? JAMA 1992;268:904. 38. Kapoor WN, Fortunato M, Hanusa BH, and Schulberg. Psychiatric illness in patients with syncope. Am J Med 1995;99(5):505–512. 39. Brignole M, Oddone D, Cogorno S, et al. Long term outcome in symptomatic carotid sinus hypersensivity. Am Heart J 1992;123(3):687–692. 40. Benditt DG, Ferguson DW, Grubb BP, et al: Tilt table testing for assessing syncope. ACC Expert Consensus Document. J Am Coll Cardiol 1996;28:263–275. 41. Sumiyoshi M, Nakata Y, et al. Response to head-up tilt testing in patients with situational syncope. Am J Coll Cardiol 1998;82(9):1117–1118. 42. Sutton R, Peterson ME. The clinical spectrum of neurocardiogenic syncope. J Cardiovasc Electrophysiol 1995;6(7):569–576. 43. Steinberg JS, Prytowsky E, Freedman RA, et al. Use of the signal averaged electrocardiogram for predicting inducible ventricular tachycardia in patients with unexplained syncope: Relation to clinical variables in a multivariate analysis. J Am Coll Cardiol 1994;23(1):99–106. 44. Bradenburg RO. Syncope and sudden death in hypertrophic cardiomyopathy. J Am Coll Cardiol 1990;15(5):962–964.

■■■

CHAPTER 12

OTHER SYMPTOMS 1.

HEMOPTYSIS i. Etiology ii. Evaluation 2. HOARSENESS 3. CYANOSIS

144 144 144 146 147

i. Definition ii. Types iii. Evaluation of Cyanosis REFERENCES

147 148 156 158

1. HEMOPTYSIS It is defined as coughing of blood or sputum streaked or contaminated with blood. i. Etiology The cardiovascular causes of hemoptysis are as follows (see Table 12.1): ●

●

●

Acquired causes: MS, pulmonary edema (due to any cause), pulmonary embolism (PE) with pulmonary infarction, rupture of aortic aneurysm into bronchopulmonary tree, rupture of bronchopulmonary collaterals [due to pulmonary venous hypertension (PVH) as in MS] (see Figs 12.1, 12.2 and 12.3). Congenital heart diseases: Eisenmenger syndrome (see Fig. 12.4), rupture of pulmonary arteriovenous fistula, rupture of bronchopulmonary collaterals. Drug intake: Anticoagulants, immunosuppressive drugs, oral contraceptives (see Fig. 12.5). MS pulmonary edema and pulmoanry embolism are the commonest causes.

ii. Evaluation The history remains the most important and valuable mode of examination to distinguish cardiovascular causes of hemoptysis from other causes. While taking history the following has to be determined: ● ● ●

Duration, frequency and recurrence of hemoptysis. Quantity of the expectorant. Associations.

OTHER SYMPTOMS

145

Increased PA pressure

Dilated left atrium Stenosed mitral valve Normal left ventricle

Right ventricular hypertrophy

Fig. 12.1

Fig. 12.2

| Mitral stenosis.

| Pulmonary edema.

Ao Aorta Pulmonary embolism

PA

PT

RA

LA

LA

RA LV LV

RV

RV

Fig. 12.3

| Pulmonary embolism.

Fig. 12.4

syndrome—commonest cause | Eisenmenger of hemoptysis in congenital heart disease.

a) Duration, Frequency and Recurrence of Hemoptysis Recurrent episodes not uncommon in MS, other causes include: tuberculosis, chronic bronchitis and bronchiectasis. b) Quantity ●

●

●

Small: MS, pulmonary edema, pulmonary infarction, Eisenmenger syndrome, rupture of bronchopulmonary collaterals, due to drug ingestion. Large/massive: Rupture of pulmonary arteriovenous fistula, rupture of aortic aneurysm into the bronchopulmonary tree. Other causes: lung carcinoma, pulmonary tuberculosis.

146

THE HISTORY AND SYMPTOMATOLOGY

Drug intake Mitral stenosis

Pulmonary embolism with PI

Acquired causes Aortic aneurysm rupture into bronchopulmonary tree

Pulmonary edema Hemoptysis

Eisenmenger syndrome

Congenital heart diseases

Rupture of pulmonary AV fistula

Rupture of bronchopulmonary collaterals

Fig. 12.5

causes of hemoptysis—PI: pulmonary infarction, AV: arteriove| Cardiovascular nous. Drug intake includes anticoagulants, oral contraceptives and immunosuppressants.

c) Associations ●

●

●

Chest pain (pleuritic) in pulmonary embolism and infarction, rupture of aortic aneurysm. SOB: In MS, pulmonary edema, PE with infarction, rupture of aortic aneurysm/ pulmonary arteriovenous fistula, Eisenmenger syndrome. Sputum: – – – – – –

● ● ●

Blood tinged in MS, pulmonary embolism with infarction. Pink frothy sputum: Pulmonary edema. Grey sputum: COPD. Yellowish-green sputum: Pulmonary infections. Putrid sputum: Lung abscess. Large quantity: Bronchiectasis.

Weight loss and anorexia: Ca lung, chronic pulmonary infections Asymptomatic: Bronchial adenoma. Drug ingestion such as anticoagulants, immunosuppressive drugs, oral contraceptives.

2. HOARSENESS It is usually not related to cardiovascular diseases. However, hoarseness can occur in (see Table 12.1): ● ●

Aortic aneurysm involving recurrent laryngeal nerve (see Fig. 12.6). MS: Due to compression of the recurrent laryngeal nerve by the dilated pulmonary artery, or greatly enlarged left atrium.

OTHER SYMPTOMS

147

Table 12.1 Cardiovascular causes of other symptoms Hemoptysis

Hoarseness

1. Mitral stenosis (MS) 2. Pulmonary edema 3. Pulmonary embolism 4. Eisenmenger’s syndrome 5. Rupture of aortic aneurysm 6. Rupture of pulmonary arteriovenous (AV) fistula 7. Anticoagulants, immunosuppressive, drugs, oral contraceptives

1. 2. 3. 4.

Aortic aneurysm MS Pericardial effusion (myxedema related) Post cardiac surgery (intubation related)

Ascending aorta aneurysm

Fig. 12.6

aneurysm—hoarseness | Aortic occurs if recurrent laryngeal nerve is also involved.

●

●

Fig. 12.7

causes hoarseness of | Myxedema voice.

Pericardial effusion may be related to myxedema, which may be associated with hoarseness of voice (see Fig. 12.7). Hoarseness and loss of voice following intubation of endotracheal tube during cardiac surgery.

3. CYANOSIS Cyanosis, (a Greek word, kyanos blue, osis condition) is both a symptom and a physical sign. i. Definition Cyanosis is a bluish discoloration of skin and mucous membranes resulting from an increased quantity of reduced hemoglobin (Hb) (4 g/dl) or abnormal hemoglobin pigments in the blood perfusing these areas1 (0.5 g/dl of methemoglobin).

148

THE HISTORY AND SYMPTOMATOLOGY

Raynaud’s phenomenon

CHF, septicemia Peripheral

Peripheral vascular disease

Cold environment Cyanosis dTGA

Truncus arteriosus

TOF

Central

DORV

Single ventricle

TAPVC Eisenmenger syndrome

Fig. 12.8

of cyanosis—CHF: congestive heart failure, dTGA: dextro transposition | Causes of great arteries, DORV: double outlet right ventricle, TOF: tetralogy of Fallot, TAPVC: total anomalous pulmonary venous connection.

ii. Types Principally, there are three types of cyanosis: peripheral, central and mixed (see Fig. 12.8). a) Peripheral Cyanosis It is usually indicates stasis of blood flow in the periphery with normal arterial O2 saturation but widened arteriovenous (AV) O2 difference. The reduced hemoglobin in the capillaries of the skin exceeds 4 g/dl. (i) It is most prominent in the cool exposed areas that may not be well perfused, such as extremities particularly nail beds and nose, and the limbs are cold on palpation. (ii) Does not worsen on exertion. The resting peripheral cyanosis of CHF may be slightly accentuated during exertion. (iii) Immersion of the limbs in warm water for several minutes reverses the cyanosis. (iv) Etiology: Most commonly secondary to cutaneous vasoconstriction often due to: ● Low cardiac output as in: CHF, septicemia ● Exposure to cold environment ● Raynaud’s phenomenon (cyanosis localized to hands, see Fig. 12.9) ● In a new born, it is mostly acrocyanosis (autonomically controlled alterations in cutaneous distribution of exposed blood flow) ● Peripheral vascular disease (a localized arterial or venous obstruction) b) Central Cyanosis It usually becomes apparent at a capillary concentration of 4 g/dl of reduced Hb (1/3rd of Hb in reduced from) or 0.5 g/dl of methemoglobin.

OTHER SYMPTOMS

Fig. 12.9

phenomenon with digital ulcers | Raynaud’s and peripheral cyanosis.

Fig. 12.10

149

cyanosis often associated | Central with clubbing.

i) O2 saturation: The O2 saturation in normal arterial blood is 95% (i.e. 13.3 g of 14 g/dl is oxyhemoglobin, and 0.7 g/dl is reduced hemoglobin). The O2 saturation in normal mixed venous blood is 70% (i.e. 9.8 g of 14 g/dl is oxyhemoglobin, and 4.2 g/dl is reduced hemoglobin). The amount of reduced Hb in capillary blood is assumed to be the mean of reduced Hb in arterial and mixed venous blood i.e. 0.7  4.2/2 2.45 g/dl. Hence, the color of the normal skin and mucous membranes is pink, not blue. Cyanosis is apparent in Caucasians at arterial O2 saturation of 85% while in pigmented races, O2 saturation has to further drop to lower levels. Since it is the absolute quantity of reduced Hb in blood that is responsible for cyanosis, the higher the total Hb content, the greater is the tendency toward cyanosis. Thus, patients with marked polycythemia become cyanotic at higher levels of arterial O2 saturation than do patients with normal hematocrit values, and cyanosis may be absent in patients with severe anemia (Hb 33%) despite marked arterial O2 desaturation. ii) Associations: Central cyanosis in severe form is often associated with polycythemia and clubbing (see Fig. 12.10). iii) Site: It involves the entire body, including warm well perfused sites, such as conjunctiva and mucous membrane of the oral cavity, and limbs are warm on palpitation. iv) Etiology of central cyanosis ●

●

●

At birth: Apparent cyanosis at birth is due to dTGA and Admixture lesions e.g. TAPVC, single ventricle, DORV (subaortic VSD with PS), truncus arteriosus. Neonatal period: ASD with transient right to left shunt. However, cyanosis is more commonly due to pulmonary parenchymal disease or CNS depression. Infancy: Usually congenital heart disease, hereditary methemoglobinemia (a) 1–3 months of age: When spontaneous closure of PDA causes a reduction of pulmonary blood flow in the presence of right sided obstructive cardiac anomalies, most commonly Tetralogy of Fallot (TOF). Cyanosis in TOF may be apparent from days to 4–6 weeks of birth (see Fig. 12.11).

150

THE HISTORY AND SYMPTOMATOLOGY

Pulmonary stenosis (infundibular)

Ao Pulmonary stenosis (valvular)

Aorta PA

PT LA

Overriding aorta

LV

Ventricular septal defect

LA

RA

RA LV RV

RV

Right ventricular hypertrophy

Fig. 12.11

of Fallot (TOF)—commonest | Tetrology cause for cyanosis in children.

Fig. 12.12

syndrome—commonest | Eisenmenger cause of cyanosis in children as well as in adults.

●

(b) 6 months of age: Due to development or progression of RVOTO in patients with VSD. Childhood: Usually, CHD due to progressive increase in pulmonary vascular resistance and cyanosis secondary to pulmonary arteriovenous fistula. (a) 2–5 years of age: TOF, Eisenmenger complex due to VSD (see Fig. 12.12). (b) After 10 years of age: Eisenmenger complex due to VSD. (c) After 20 years of age: Eisenmenger syndrome due to ASD.

v) Pathogenesis of central cyanosis: Central cyanosis is due to three causes (see Fig. 12.13): ●

●

●

Decreased arterial O2 saturation due to inadequate oxygenation owing to impaired pulmonary function and pulmonary venous blood is not fully saturated. Inhalation of 100% oxygen may diminish or clear the cyanosis. This is known as Anoxemic cyanosis, e.g. pulmonary disorders. Decreased arterial O2 saturation due to intracardiac or extracardiac right to left shunt and pulmonary venous blood is fully saturated. Inhalation of 100% oxygen does not clear or decrease the cyanosis. This is known as Shunt or admixture cyanosis, e.g. cyanotic CHD. Decreased arterial O2 saturation due to replacement of normal by abnormal Hb. This is Replacement cyanosis, e.g. methemoglobinemia. There is a family history of cyanosis but absence of heart disease in hereditary methemoglobinemia.

vi) Factors influencing O2 saturation (thereby affecting the intensity of cyanosis): ●

Temperature and physical activity: Cyanosis appears or intensifies with physical activity as the oxygen saturation declines concurrently with an increase in right to left shunt across a defect as peripheral vascular resistance decreases.

OTHER SYMPTOMS

151

Central cyanosis Inadequate oxygenation

Abnormal Hbmethemoglobinemia ↓ Arterial O2 saturation

Intra or extra cardiac shunts

Fig. 12.13

●

●

●

Influencing factors ↑ Temperature and physical activity

↓ Blood PH

Large R-to-L shunt > 25% of LV output

↑ Fetal Hb

of central cyanosis—Hb: hemoglobin, R: right, L: left, LV: left | Pathogenesis ventricular.

Blood pH and 2-3 diphosphoglycerate: Oxygen transport to the tissues is affected by shifts in oxygen hemoglobin dissociation relation (curve) which may be affected by blood pH and levels of 2-3 diphosphoglycerate concentration. Ratio of fetal to adult Hb: Fetal Hb has a higher affinity for oxygen than adult Hb and would be more highly saturated at any given pO2. Degree of right to left shunt: Cyanosis occurs when the volume of blood of right to left shunt exceeds 25% of LV output.

Hence, determination of systemic arterial O2 tension may provide a more accurate picture of underlying pathophysiology than the measurement of O2 saturation alone. vii) Types of central cyanosis ● ● ● ●

●

Shunt or admixture cyanosis Anoxemic cyanosis Replacement cyanosis Cyanose tardive: Cyanosis in CHD as in Eisenmenger syndrome which first make its appearance in the second decade of life or later. Differential cyanosis is applied to the condition where some part of the body receives more hypoxic blood than others, and virtually always indicates the presence of CHD which can be brought about by exercise (see Table 12.2).

Differential cyanosis: Cyanosis confined to lower limbs with little or no cyanosis of arm and face, typically seen in ●

PH with right to left shunt through PDA (see Fig. 12.14). But if the ductus is proximal to left subclavian artery: then the right hand is less cyanosed than left hand and both the feet.

152

THE HISTORY AND SYMPTOMATOLOGY

Table 12.2 Types of central cyanosis Type of cyanosis

Example

1. Admixture cyanosis 2. Anoxemic cyanosis 3. Replacement cyanosis 4. Cyanosis tardive 5. Differential cyanosis 6. Reversed differential cyanosis

Cyanotic CHD Pulmonary disorders Methemoglobinemia Eisenmenger syndrome PDA PH with right to left shunt TGA and COA with retrograde flow through PDA

CHD: congenital heart disease, PDA: patent ductus arteriosus, PH: pulmonary hypertension, TGA: transposition of great arteries, COA: coarctation of aorta.

RCC Aorta

Ductus arteriosus

LCC RSA

LSA

PDA PA

LA COARC Ao

RA

RV

LV

PT

Fig. 12.15 Fig. 12.14

|

Differential cyanosis occurs in patent ductus arteriosus (PDA) with PH and right to left shunt.

●

cyanosis also occurs in | Differential coarctation of aorta (COARC) with PDA and right-to-left shunt—RSA: right subclavian, RCC: right common carotid, LCC: left common carotid, LSA: left subclavian.

Coarctation of aorta or interrupted aortic arch: oxygenated blood to upper part of the body and desaturated blood to lower part of the body by way of right to left shunt through PDA (see Fig. 12.15).

Cyanosis of the fingers exceeds that of the toes is known as Reversed differential cyanosis, seen in: ●

●

●

TGA with preductal narrowing of aorta (either coarctation or interrupted aortic arch) PH and reverse flow (i.e. from pulmonary artery to aorta) through PDA2 (see Fig. 12.16). DORV with subpulmonary VSD (Taussig-Bing anomaly), PH (pulmonary vascular disease) and reverse flow (i.e. from pulmonary artery to aorta) through PDA.3 TGA with intact ventricular septum, PH and reverse flow through PDA4 (see Fig. 12.17).

OTHER SYMPTOMS

Innom. a.

153

PDA

Interrupted arch LCA LSA

ASD

Ao

PDA

Asc. ao.

PT Desc. ao.

RA

PT RA

LA

LA

RV

Fig. 12.16

LV

LV

RV

cyanosis in inter| Differential rupted aortic arch with PDA

Fig. 12.17

and right-to-left shunt.

differential cyanosis occurs in transpo| Reverse sition of great arteries (TGA) with intact ventricular septum, PH and reverse flow through PDA.

viii) Differentiation of cyanosis of cardiac origin from that of pulmonary causes 1. Respiratory patterns • Tachypnea: – In CHD: Cyanosis, tachypnea but no other signs of respiratory distress. In upper or lower air obstruction: There may be cyanosis, tachypnea with flaring of alae nasi, chest wall retraction and grunting. • Apnea: Intermittent apneic episodes are rare in cardiac diseases but common in: – Premature infants with CNS immaturity or disease and – Intracranial diseases. • Cheyne stokes breathing can occur both in heart failure and respiratory failure. 2. Arterial blood gas analysis in patients with cyanosis (blood sample from radial or temporal artery) also helps in differentiating cyanosis of cardiac origin from that of respiratory cause (see Table 12.3). c) Mixed Cyanosis It is the presence of both peripheral and central cyanosis which occurs in conditions like chronic cor pulmonale due to chronic emphysema or fibrosis of lung. The lung lesion tends to produce central cyanosis while associated right heart failure tends to cause peripheral cyanosis. d) Methemoglobinemia i) Normal physiology ●

The major function of Hb is the transport of oxygen from the lungs to body tissues, which is mediated by reversible binding of molecular O2 to heme iron. The heme

154

THE HISTORY AND SYMPTOMATOLOGY

Table 12.3 Arterial blood gas analysis in infants with cyanosis PH (7)

PO2 (80–100 mmHg)

PCO2 (35–45 mmHg)

Response to O2 inhalation

1. Due to respiratory cause

⇓

⇓⇓



 PO2

2. Due to respiratory cause 3. Cardiac cause 4. Cardiac cause 5. Peripheral cyanosis

⇓

⇓



 PO2

_

⇓

_

 PO2

⇓

⇓⇓

_

_

⇓⇓⇓

⇓

_

_  PO2

Pattern

Suggested condition

Hyaline membrane disease or other pulmonary parenchymal disease often associated with  PVR and shunting across PFO or PDA Hypoventilation (CO2 retention) Obligatory venous admixture e.g. TAPVC ⇓ pulmonary blood flow e.g. TOF Systemic hypoperfusion

_: no effect, ⇓: decrease, : increase, PO2: partial pressure of oxygen, PCO2: partial pressure of carbon dioxide, PFO: patent foramen ovale, PDA: patent ductus arteriosus, TAPVC: total anomalous pulmonary venous connection, TOF: tetralogy of Fallot.

●

●

iron of deoxy Hb must be in the ferrous (Fe2) state to allow reversible binding with O2. This ferrous iron is continually subjected to oxidant stresses resulting in the formation of a stable ferric (Fe3) hemoglobin i.e. methemoglobin, which is incapable of reversible O2 binding. Hence, if the significant portion of total Hb exists in the ferric state, then fatal tissue hypoxia may develop. However; under normal circumstances, the rate of endogenous methemoglobin production is relatively constant at 3% per day, and RBCs are able to decrease methemoglobin 250 times of the rate at which it is normally formed by NADH dependent reductases. Consequently, normal individuals have a methemoglobin concentration of 1%. NADH dependent reductase, diaphorase I is absent in hereditary methemoglobinemia.

ii) Etiology of methemoglobinemia: Besides hereditary cause, other causes are: 1. 2. 3. 4.

Nitrites: Due to contaminated well water, food additives. Aniline dyes: Laundry dyes, shoe dyes, red crayons and disinfectant. Naphthalene and Drugs (see Tables 12.4 and 12.5).

iii) Presentation ●

Slate gray cyanosis is appreciated when methemoglobin exceeds 10%, but the levels between 20% and 25% are usually well tolerated.

OTHER SYMPTOMS

155

Table 12.4 Drugs causing methemoglobinemia 1. 2. 3. 4. 5. 6.

Anesthetics: Benzocaine, prilocaine Analgesics: Acetophenetidin, phenacetin Antimalarials Nitrates: Amylnitrate, nitroprusside, ammonium nitrate Sulfonamides Vitamin K analogues

Table 12.5 Etiology of cyanosis and methemoglobinemia Central cyanosis

Peripheral cyanosis

Mixed cyanosis

Methemoglobinemia

1. TOF

1. CHF

1. Chronic cor pulmonale

1. Hereditary

2. Eisenmenger syndrome 2. Septicemia 3. dTGA, TAPVC, DORV 3. Cold exposure 4. Truncus arteriosus 4. Peripheral vascular disease 5. Raynaud’s phenomenon

2. Nitrites 3. Aniline dyes 4. Drugs (antimalarials, analgesics, anesthetics)

TAPVC: total anomalous pulmonary venous connection, TOF: tetralogy of Fallot, dTGA: dextro transposition of great arteries, DORV: double outlet right ventricle, CHF: congestive heart failure.

● ● ●

At 30–40% levels, patient becomes irritable, lethargic and develop exercise intolerance. At 50% levels, severe CNS depression develops. At  70% levels, it is incompatible with life.

However, symptoms may appear earlier in the anemic individuals. iv) Diagnosis of methemoglobinemia ●

● ●

When a sample of venous blood is agitated in air for 15 min, a characteristic chocolate brown color is formed. Decreased O2 saturation despite normal levels of pO2. Measurement of methemoglobin levels with spectroscope. In drug-induced methemoglobinemia, sulfhemoglobin is also detected.

v) Treatment of methemoglobinemia ●

●

Slow IV infusion of 1–2 mg/Kg body wt. of 1% freshly prepared methylene blue in normal saline, which decreases methemoglobin levels (reduction via diaphorase II). If there is no adequate response with methylene blue, investigate for G-6 phosphate dehydrogenase deficiency. Withdrawal of the offending drugs.

156

THE HISTORY AND SYMPTOMATOLOGY

At 1–3 months TOF

Neonatal 1. ASD R-to-L 2. PPD 3. CNS

Age of appearance

At birth 1. TGA 2. Admixture lesions

 6 months ↑RVOTO in VSD (subpulmonary) Childhood 2 years 1. TOF 2. Eisenmenger VSD >20 years Eisenmenger ASD

Equal in UL and LL 1. Central cyanosis 2. Peripheral cyanosis 3. Methemoglobinemia

More in UL TGA and COA with PDA Distribution More in LUL and both feet PDA proximal to LSA with PH

More in LL 1. PDA with PH 2. COA with PH Exertion Cyanotic CHD

Aggravating factors

More in the morning TOF

Cold exposure Peripheral cyanosis

100% O2 inhalation Pulmonary disorders

Squatting TOF

Relieving factors

Beta blockers TOF

Hot bath Peripheral cyanosis

Central cyanosis 1. Clubbing 2. Polycythemia

Association

Peripheral cyanosis 1. Low cardiac output 2. Raynaud’s phenomenon

Methemoglobinemia 1. Hereditary 2. Drug exposure

Fig. 12.18

of cyanosis—ASD R-to-L: atrial septal defect with transient right to | Evaluation left shunt, PPD: pulmonary parenchymal disease, CNS: central nervous system depression, TGA: transposition of great arteries, TOF: tetralogy of Fallot, RVOTO: increasing right ventricular outflow tract obstruction, COA: coarctation of aorta, PH: pulmonary hypertension, LSA: left subclavian artery.

iii. Evaluation of Cyanosis Again, history plays a key role in differentiating cardiac cause of cyanosis from other causes (see Fig. 12.18). a) Duration at What Age Cyanosis Appeared/Notice ●

At birth: CHD like dTGA, admixture lesions.

OTHER SYMPTOMS ●

● ● ●

157

Neonatal period: ASD with transient right to left shunt, pulmonary parenchymal diseases, CNS depression. 1–3 months of age: TOF. 6 months of age: Progression of RVOTO in VSD (sub-pulmonary type). Childhood: CHD including pulmonary AV fistula: (i) 2–5 years of age: TOF, Eisenmenger syndrome due to VSD. (ii) After 10 years of age: Eisenmenger syndrome due to VSD. (iii) After 20 years of age: Eisenmenger syndrome due to ASD.

b) Distribution of Cyanosis Equal on both sides or differential cyanosis is present: ●

● ● ●

Equal in upper limb (UL) and lower limb (LL): Central/peripheral/mixed cyanosis/ methemoglobinemia. More in LL: PDA with PH, COA or interrupted aortic arch with PDA. More in UL (Reversed differential cyanosis): TGA and COA with PDA. More in left UL and both feet: If ductus is proximal to left subclavian artery in PDA with PH.

c) Aggravating Factors ● ● ● ●

●

On exertion/exercise/playing Eating Defecation More in the morning: Cyanotic congenital heart diseases especially in TOF, but not in peripheral cyanosis Swimming or cold exposure: Cyanosis appears or is aggravated in peripheral cyanosis, including Raynaud’s phenomenon.

d) Relieving Factors Cyanosis/cyanotic spells may decrease or get relieved by: ● ● ●

●

Squatting or squatting equivalents in TOF and other cyanotic CHDs as well. Beta-blockers in TOF. 100% O2 inhalation in central cyanosis, and the relief is more prominent in pulmonary disorders. After hot bath: Peripheral cyanosis may decrease or disappear.

e) Associations ● ● ● ● ● ● ●

Central cyanosis is most often associated with CHD. Central cyanosis is often associated with polycythemia and clubbing. Raynaud’s phenomenon in peripheral cyanosis. Low cardiac output in peripheral cyanosis. Hereditary disorder without cardiac ailment: Methemoglobinemia. Drug exposure in methemoglobinemia. Cor pulmonale: Mixed cyanosis.

158

THE HISTORY AND SYMPTOMATOLOGY

1

Fig. 12.19

2

3

4

5

and its equivalents adopted by the patients to alleviate the cyan| Squatting otic spells (line diagrams)—1: typical squatting, 2: sitting in a chair with legs drawn underneath, 3: legs crossed while standing, 4: mother holding an infant with its legs flexed upon its abdomen, 5: simply lying down.

vi. Squatting a) Squatting equivalents ● ● ● ● ● ● ●

Lying on left side. Sitting with legs closely drawn beneath the trunk. Sitting with legs drawn up on the seat of a chair. Prune knee chest position. Simply lying down (see Fig. 12.19). Crossed their legs and squeezed them together when asked to stand or sit. Babies sometimes soothed by being held with their legs flexed and knees squeezed well into their abdomen.

b) How squatting alleviates the symptoms ●

●

In normal: Squatting increases systemic BP, systemic vascular resistance (SVR) and venous return as well as an increase in O2 saturation. The increase in SVR is due to: – kinking of the iliac arteries. – squatting reduces the distending pressure of gravity on the lower limb vessels. In TOF: Squatting increases SVR with PS remaining constant which results in decrease of right to left shunt and increase in pulmonary blood flow with immediate improvement in arterial O2 saturation, thereby alleviating hypoxic/cyanotic spells.

REFERENCES 1. 2.

3. 4.

Braunwald E. Cyanosis. In: Isselbacher KJ, Braunwald E, et al. eds. Harrison’s Principles of Internal Medicine. 13th ed. New York, McGraw-Hill, 1994:178–182. Buckley MJ, Mason DT, Ross J Jr, Braunwald E. Reversed differential cyanosis with equal desaturation if the upper limbs. Syndrome of complete transposition of the great vessels with complete interruption of the aortic arch. Am J Cardiol 1965;15:111–115. Wedemeyer AL, Lucas RV, Castaneda AR. Taussig-Bing malformation, coarctation, and reversed patent ductus arteriosus. Circulation 1970;42(6):1021–1027. Waldman JD, Paul MH, Newfeld EA, Muster AJ, Idriss FS. Transposition of great arteries with intact ventricular septum and patent ductus arteriosus. Am J Cardiol 1977;39(2):232–238.

GENERAL PHYSICAL EXAMINATION 13. General examination

161

14. Arterial pulse

225

15. Measurement of the blood pressure

249

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■■■

CHAPTER 13

G ENERAL E XAMINATION 1.

2. 3. 4.

5.

GENERAL BUILD AND STATURE i) Tall Stature ii) Short Stature iii) Build POSTURE OR ATTITUDE GESTURES AND SIGNS FACIAL APPEARANCE i) Facial Dysmorphism ii) Facial Edema iii) Dull Expressionless Face with Periorbital Puffiness iv) Dull Expressionless Face with Ptosis v) Butterfly Rash on the Face vi) Malar Rash (Brownish Tint or Flush) vii) Flushing viii) Striking Premature Aging ix) Facial Expression of Fright and Anxiety x) Moon Face xi) Ape Like Appearance xii) Mongoloid Facies xiii) Grotesque Facial Features xiv) Elfin Facies xv) Distinctive Unilateral Lower Facial Weakness (7th Cranial Nerve Palsy) xvi) Midfacial Growth Deficiency EYES i) Hypertelorism ii) Exophthalmos iii) Enophthalmos iv) Nystagmus v) Eye Lids vi) Conjunctiva vii) Sclera viii) Cornea

162 163 165 166 169 170 172 172 172 173

6. 7.

8.

173 173 173 174 174 174 174 174 175 175 175

9.

10. 11.

175 176 176 176 176 177 177 177 177 178 178

12.

13.

ix) Iris x) Pupils xi) Lens xii) Retina NOSE EARS i) Ear Lobe Crease ii) Cauliflower (Floppy) Ear iii) Low Set Ears iv) Deafness ORAL CAVITY i) Lips ii) Mucous Membrane iii) Teeth iv) Gums v) Tongue vi) Palate NECK i) Short Neck ii) Webbed Neck iii) Low Hair Line iv) Lymphadenopathy v) Thyromegaly vi) Parotid Enlargement SPINE SKIN i) Pigmentation ii) Skin Texture iii) Xanthomas iv) Nodules v) Cyanosis, Icteru, and Pallor EXTREMITIES i) Digits ii) Nails iii) Feet iv) Joints PERIPHERAL EDEMA i) Pathogenesis

179 181 181 181 185 185 185 185 185 187 187 187 188 188 189 189 189 190 190 191 191 192 192 192 192 193 194 195 196 198 200 200 200 205 210 212 215 216

162

GENERAL PHYSICAL EXAMINATION

ii) Causes iii) Types and Site of Peripheral Edema

217 218

iv) Characteristics of Peripheral Edema REFERENCES

221 222

In the present-day ‘high tech’ practice of medicine, the physical examination remains a valuable and inexpensive tool for early detection of critical findings, which aid in the early diagnosis of the cardiovascular diseases. It helps in the intelligent selection of costly diagnostic tests, besides creating a closer bond with the patient at a time when the medical care system is becoming often impersonal, which may be valuable in securing patient’s compliance in following a diagnostic workup and treatment plan. Important information concerning the patient with definite or suspected heart disease is often obtained by a careful and deliberate physical examination from head-to-toe, which includes general examination, examination of arterial pulses, measurement of blood pressure and evaluation of the jugular venous pressure and pulsations, before thorough examination of the cardiovascular system systematically to arrive at a definitive diagnosis. An assessment of the patient’s general appearance begins with a detailed inspection while the history is being obtained.

1. GENERAL BUILD AND STATURE The general build and stature of the patient is usually assessed best by taking the following measurements (see Table 13.1): (i) Height of the patient: It includes upper and lower segments. ● The upper segment of the body is measured from the top of the head to pubic ramus, and the lower segment is measured from the pubic ramus to the floor, (Pubic bone has 3 parts—body, superior and inferior rami. Here, reference is to the superior remus which has 3 borders—obturator, pectineal and inferior. So, it is not appropriate to use top of the pubic ramus) ● Calculate the upper to lower segment ratio, which is equal after 10 yrs of age. (ii) Arm span: It is the distance between the tips of the middle fingers of one hand to the other. The arm span to height ratio is normally equal or 1.05. (iii) Body mass index (BMI): It is the body weight of the individual in kg/height in meters2 (wt/ht2). Normal BMI is 18.5–24.9 kg/m2.1 Table 13.1 Indices of build and stature 1. 2. 3. 4.

Height, lower and upper segments Arm span Body mass index Waist circumference

GENERAL EXAMINATION

163

(iv) Waist circumference: It is measured at midway between lowest rib and iliac crest. Normally, it should be 102 cm in males and 88 cm in females.2 i) Tall Stature When the height of an individual is far in excess of the average normal for the age and race (2 standard deviation of the mean height), the individual is considered to be tall in stature (in India usually 6 ft). Causes of tall stature are as follows: ●

●

Tall stature with equal upper and lower segments or equal arm span to height ratio: constitutional and pituitary giants. Tall stature with upper to lower segment ratio of 0.8 or arm span to height ratio of 1.05: Marfan syndrome (Fig. 13.1), homocystinuria, Klinefelters syndrome (see Fig. 13.2).

Marfan Syndrome Ghent diagnostic criterion for Marfan syndrome3 include (see Fig. 13.1 and Table 13.2): 1. With family history: 1 major criterion in an organ system  involvement of second organ system (11).

Fig. 13.1

stature | Tall syndrome.

with long extremities in Marfan

Fig. 13.2

stature with gynecomastia | Tall in Klinefelters syndrome.

164

GENERAL PHYSICAL EXAMINATION

Table 13.2 Syndromes with tall stature and cardivascular manifestations Syndrome

Diagnostic clinical features

Cardivascular manifestations

1. Marfan syndrome

Ghent diagnostic criteria3

2. Homocystinuria

Due to deficiency of cystathionine  synthase4 Tall, long extremities, other skeletal deformity, downward lens subluxation and mental retardation Tall, eunuchoid appearance, small testes, azoospermia, gynecomastia, mild mental retardation (see Fig. 13.2)

i. Dilatation of ascending aorta  AR ii. Dissection of ascending aorta iii. MVP  valvular mitral regurgitation iv. Calcification of mitral annulus in 40 yrs of age v. Dilatation of MPA in the absence of valvular or peripheral PS or any other obvious cause in 40 yrs of age vi. Dilatation or dissection of descending thoracic aorta or abdominal aorta in 50 yrs of age i. Aortic and pulmonary dilatation ii. Intravascular thrombosis which may cause MI, stroke or pulmonary embolism5

3. Klinefelters syndrome (47 XXX/XXY)6

i. Venous thromboebolism ii. Increased incidence of congenital heart diseases, especially ASD

AR: aortic regurgitation, MVP: mitral valve prolapse, MPA: main pulmonary artery, PS: pulmonary stenosis, MI: myocardial infarction, ASD: atrial septal defect.

2. With no family history: major criteria in 2 different organ system  involvement of third organ system (21). Usual organ systems involved are skeletal, ocular, cardiovascular system, lungs, skin and duramater. (1) Skeletal system: For major criterion in skeletal system, 4 major signs of the following should be present. (FEW TAP 2S) ● ● ● ●

● ● ● ●

Flat foot (medial displacement of medial malleolus causing pes planus) Reduced extension at the elbow (170) Wrist (Walker-Murdock) and thumb (Steinberg) signs (due to arachnodactyly) Tall stature (upper to lower segment ratio of 0.8 or arm span to height ratio of 1.05) (due to long arms and legs: dolichostenomelia) Protrusio acetbulae of any degree (confirmed by radiography) Pectus carinatum Pectus excavatum requiring surgery and Scoliosis of 20 or spondylolisthesis.

For organ involvement criterion: 2 major signs or 1 major sign  2 minor signs should be present.

GENERAL EXAMINATION

165

Minor signs include: ● ● ● ●

Pectus excavatum of moderate severity Joint hyper mobility High arched palate with crowding of teeth Abnormal facial appearance (due to dolichocephaly, malar hypoplasia, enophthalmos, retrognathia, down slanting palpebral fissures).

(2) Ocular system: For major criterion in ocular system, ectopia lentis is included. For organ involvement criterion: 2 of the following signs must be present. ● ● ●

Abnormally flat cornea Increased axial length of globe Hypoplastic iris or hypoplastic ciliary muscle causing decreased miosis.

(3) Cardiovascular system: For major criterion in cardiovascular system, atleast one of the following major signs should be present. ●

●

Dilatation of ascending aorta involving sinuses of Valsalva with or without aortic regurgitation Dissection of ascending aorta.

For organ involvement criterion: 1 major sign or 2 minor signs must be present. Minor signs include: ● ● ●

●

Mitral valve prolapse with or without mitral valve regurgitation Calcification of mitral annulus in 40 yrs of age Dilatation of main pulmonary artery in the absence of valvular or peripheral pulmonary stenosis (PS) or any other obvious cause in 40 yrs of age Dilatation or dissection of descending thoracic or abdominal aorta in 50 yrs of age.

(4) Lungs: Only organ involvement criterion: one of the following must be present. ● ●

Spontaneous pnuemothorax Apical blebs.

(5) Skin: Only organ involvement criterion: one of the following must be present. ●

●

Stretch marks not associated with marked weight gain, pregnancy or repetitive stress Recurrent or incisional herniae.

(6) Dura: For major criterion, lumbosacral dural ectasia confirmed by CT scan or MRI must be present. Also for organ involvement criterion, lumbosacral dural ectasia must be present. ii) Short Stature When the height of an individual is far shorter than the average normal for age and race (2 standard deviations of the mean height), the individual is considred to be

166

GENERAL PHYSICAL EXAMINATION

Table 13.3 Syndrome with short stature and cardiovascular manifestations Syndrome

Diagnostic clinical features

Cardiovascular manifestations

1. Turner syndrome (45X) (gonadal dysgenesis)

Short female, webbed neck, low hair line, low set ears, broad chest with widely spaced nipples, sexual infantalism, deafness, pigmented nevi, normal intelligence

Coarctation of aorta (post-ductal type), bicuspid aortic valve, PAVC7

2. Noonan syndrome8 (normal chromosomal pattern) (male Turner syndrome, but both sexes are affected) AD inheritance

Short, webbed neck, low hair line, hypertelorism, pectus excavatum, cubital valgus, ptosis, cryptorchidism, mental dullness

Dysplastic PS, HCM

3. Ellis-van Creveld syndrome.9 AR inheritance (common in Amish population)

Short limbs, polydactyly, dysplastic nails and teeth, genu valgum, lip tie due to multiple frenulum

Single atrium, ASD

AD: autosomal dominant, AR: autosomal recessive, PAVC: partial anomalous venous connection, PS: pulmonary stenosis, HCM: hypertrophic cardiomyopathy, ASD: atrial septal defect.

short in stature. In the Indian subcontinent, 4 ft of height is considered as short stature. Causes of short stature are (see Table 13.3): ●

●

●

●

●

Constitutional (hereditary): Gurkhas, African pygmies. The individuals are normal in all respects except the height. The growth hormone and gonodotropin levels are normal. Endocrine: Cretin (ratio between upper and lower segments is 1 with mental retardation, see Fig. 13.3), pituitary dwarf (short limbed, normal intelligence but may be associated with infantalism), Froehlich’s syndrome (obese, diabetes insipidus, hypogonadism), Cushing syndrome (obese, moon facies, abdominal striae, hypertension and impaired glucose tolerance, see Fig. 13.4). Genetic: Turner syndrome (phenotypic female: 45XO, see Fig. 13.5), Noonan syndrome (normal chromosomal pattern), Hurler’s syndrome, Morquio’s syndrome, Multiple lentigines syndrome. Skeletal: Ellis van Creveld syndrome (chondrodystrophic dysplasia, short arms, and legs see Fig. 13.6), achondroplasia (short and bowed legs and arms, waddling gait see Fig. 13.7), osteogenesis imperfecta (4 types, autosomal dominance [AD]/autosomal recessive [AR] inheritance). Acquired: Acquired skeletal causes include: rickets, Pott’s spine (in children).

iii) Built Excess fat lengthens the ‘waist line’ but shortens the ‘life line’ of an individual. Obesity predisposes or aggravates hypertension, hyperlipidemia, diabetes mellitus, atherosclerosis,

GENERAL EXAMINATION

Fig. 13.3

Fig. 13.5

dwarf— | Endocrine cretin.

dwarf—turner | Genetic syndrome with wide set nipples webbed neck and absent pubic hair.

Fig. 13.4

Fig. 13.6

167

dwarf—cushing syndrome with | Endocrine moon face, abdominal striae and obesity.

dwarf— | Skeletal Ellis-van Creveld syndrome.

Fig. 13.7

| Achondroplastic dwarf.

168

Fig. 13.8

GENERAL PHYSICAL EXAMINATION

obesity—mainly | Central abdominal giving rise to an apple shaped body and prone for coronary artery disease (CAD).

Fig. 13.9

obesity— | Generalized mainly on the hips and thighs giving rise to a pear shaped body.

Fig. 13.10

polydactyly | Obesity, and genu valgum in Laurence Moon Biedl syndrome.

restrictive lung disease, gout, cholelithiasis, infertility, and degenerative arthritis, besides increasing the morbidity and mortality. Obesity, which can be defined as an excessive accumulation of body fat, and since, it is difficult to determine the amount and location of body fat, body mass index (BMI) and waist circumference have been used as surrogate parameters. (i) Depending upon BMI, there are three grades of over weight:1 2 ● Grade 1 over weight with BMI of 25–29.9 kg/m . 2 ● Grade 2 over weight is known as ‘obese’ with BMI of 30–39.9 kg/m . 2 ● Grade 3 over weight is known as ‘morbidly obese’ with BMI of 40 kg/m . ● Obesity has been described as ‘enviable’ for grade 1, ‘regal’ for grade 2 and ‘pitiable’ for grade 3 over weight. (ii) Depending upon the waist circumference: The individuals with central (abdominal) obesity (as in metabolic syndrome, see Fig. 13.8) are more prone to coronary artery disease as compared to generalized obesity (see Fig. 13.9). In central obesity, the males have a measurement of 102 cm and females 88 cm of waist circumference.2 (iii) The conditions in which the patients are obese are (see Figs 13.4 and 13.10, Table 13.4): ● Metabolic syndrome ● Cushing’s syndrome

GENERAL EXAMINATION

169

Table 13.4 Syndromes with obesity and cardiovascular manifestations Syndrome

Diagnostic clinical features

Cardiovascular manifestations

1. Pickwickian syndrome10

Obese, somnolence, hypoventilation, cyanosis, secondary polycythemia (Dickens fat boy)

Increased PVR, pulmonary hypertension

2. Laurence-Moon-Biedl syndrome

Obese, retinitis pigmentosa, polydactyly and syndactyly, mental retardation, hypogonadism

Variable congenital heart disease11

3. Cushing’s syndrome12 (hypercortisolism)

Truncal obesity, moon face, buffalo hump abdominal striae, fatigue, hirsutism, osteoporsis, diabetes mellitus, acne

Hypertension, accelerated atherosclerosis (MI, CHF, stroke)

PVR: pulmonary vascular resistance, MI: myocardial infarction, CHF: congestive heart failure.

Table 13.5 Posture or attitude and cardiovascular manifestations Posture/attitude

Cause

1. Sitting quietly 2. Sitting up posture 3. Moving restlessly 4. Comfortable in sitting 5. Kneeling forward 6. Squatting

Angina pectoris Heart failure Acute myocardial infarction Left ventricular failure Pericarditis Cyanotic congenital heart disease

Pickwickian syndrome Laurence-Moon-Biedl syndrome, and ● Myxedema. (iv) An individual is described as underweight or thin with BMI of 18.5 kg/m2. Malnutrition and cachaxia occur in severe chronic heart failure, which may be confirmed usually by the tricep’s skin fold thickness (midway between the point of acromian and olecranon process) by Schofield’s calipers. ● ●

2. POSTURE OR ATTITUDE Posture or attitude of the patient can be observed on inspection which offers a great diagnostic value (see Table 13.5). (i) If the patient is in pain: ● If the patient is sitting quietly, it is typical of angina pectoris. ● If the patient is moving about, trying to find a more comfortable position, it is suggestive of acute myocardial infarction.

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GENERAL PHYSICAL EXAMINATION

Fig. 13.11

| Sitting up posture in left ventricular failure. ●

●

Fig. 13.12

posture in tetrology | Squatting of fallot.

If the patient is comfortable in sitting up posture (see Fig. 13.11), it is seen as in heart failure (LVF) (noncardiac conditions include: bronchial asthma, severe ascitis, massive abdominal tumor, late pregnancy) or kneeling forward (prayer posture) observed in pericarditis.

(ii) Squatting posture to get relief from dyspnea is seen in cyanotic congenital heart diseases (see Fig. 13.12).

3. GESTURES AND SIGNS Patient’s gestures while describing the symptoms should also be carefully observed (see Table 13.6). ●

●

●

●

●

Levine’s sign:13 Clenching of the fist in front of the chest while describing the chest discomfort is a strong indication of an ischemic chest pain (see Fig. 13.13). Finger pointed to a small circumscribed area in the left inframammary region, while describing the chest discomfort, is more likely of psychogenic origin (see Fig. 13.14). The cold sweaty palms with frequent sighing respirations are typical of neurcirculatory asthenia. Patient is dyspneic in heart failure, pericardial effusion (massive) (see causes of dyspnea in symptomatology). Gower’s sign: It is observed in Duchene muscular dystrophy which may be associated with cardiomyopathy (posterobasal LV wall is involved, see Fig. 13.15).

GENERAL EXAMINATION

171

Table 13.6 Gestures and diseases

Fig. 13.13

Gestures/signs

Cause

1. 2. 3. 4. 5.

Ischemic chest pain Muscular dystrophy  cardiomyopathy Psychogenic chest discomfort Neurocirculatory asthenia Heart failure, pericardial effusion

Levine’s sign Gower’s sign Localized chest discomfort Sighing respirations with sweating Dyspneic

of the fist in front of the | Clenching chest while describing the chest

Fig. 13.14

while describing the chest discomfort is usually of non-cardiac origin—more of a psychogenic origin.

discomfort (Levine’s sign) is typical of ischemic chest pain.

1

Fig. 13.15

pointing to a small circumscribed | Finger area in the left inframammary region

2

3

4

5

7

8

6

9

of rising from supine to erect position i.e. Gower’s sign in Duchene | Method muscular dystrophy which may be associated with cardiomyopathy.

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GENERAL PHYSICAL EXAMINATION

4. FACIAL APPEARANCE i) Facial Dysmorphism ●

●

●

Facial dysmorphism may be due to hypertelorism, epicanthic folds, broad flat nose, low set ears, thick lips, abnormal teeth, short and webbed neck, low hair line and mid facial hypoplasia. It occurs in disorders due to genetic abnormalities such as Down syndrome, Turner syndrome, Noonan syndrome (see Figs 13.16 and 13.17) and William’s syndrome which may be associated with cardiovascular manifestations. It may give rise to characteristic facies such as mongoloid facies of Down’s syndrome (see Fig. 13.18), elfin facies of William’s syndrome and grotesque facies of Hurler’s syndrome.

ii) Facial Edema ●

Figs 13.16 & 13.17

It may be present in the patients with tricuspid valve disease or constrictive pericarditis (see Table 13.7).

syndrome—showing facial dysmor| Noonan phism, low set ears hypertelorism and low

Fig. 13.18

syndrome—showing | Down facial dysmorphism.

hairline. Table 13.7 Abnormal facies and syndromes with cardiovascular manifestations Facial expression

Syndromes/cause

1. Hypertelorism, epicathic folds, broad flat nose, low set ears and short neck 2. Moon face 3. Ape like face 4. Senile face 5. Mongoloid facies 6. Grotesque facies 7. Elfin facies 8. Dull expression face 9. Frightened and staring

Turner and Noonan syndromes Cushing’s syndrome Acromegaly Werner’s syndrome Down syndrome Hurler’s syndrome William’s syndrome Myxedema; Myotonic dystrophy Thyrotoxicosis

GENERAL EXAMINATION ●

173

In SVC obstruction syndrome, upper part of the chest and face are involved with edema and engorged veins.

iii) Dull Expressionless Face with Periorbital Puffiness It is associated with loss of lateral eyebrows, large tongue, thickened skin and dry sparse hair, cold intolerance, lethargy, constipation, menorrhagia, hoarse voice, increase in weight, decreased intellectual and motor activity are characteristics of myxedema14 (which may have pericardial effusion and increased risk of atherosclerosis) (see Figs 13.19 and 13.20). iv) Dull Expressionless Face with Ptosis It is observed in myotonic dystrophy, which may be associated with cardiac manifestations (myocardial disease, conduction defects, arrhythmias).15 v) Butterfly Rash on the Face It is associated with malar depigmentation, seen in systemic lupus erythematosis (SLE) which may be associated with cardiovascular manifestations16 in 57% (see Fig. 13.21). ● ● ●

● ●

Pericarditis (up to 30%)17 Myocarditis (up to 10%)18 Libman-Sacks endocarditis (upto 50% in autopsy series, commonly leading to AR and MR, less frequently to AS, MS, TS and TR).19 Congenital heart blocks in offsprings of affected mother, and CAD (may be due to steroids or antiphosphlipid antibody syndrome).20

vi) Malar Rash (Brownish Tint or Flush) It is seen on face, cheeks, nose and ears, and is observed in patients with chronic MS (due to venocapillary stasis caused by low cardiac output, see Fig. 13.22).

Fig. 13.19

expressionless | Dull face in myxedema.

Fig. 13.20

edema in | Periorbital acute nephritis.

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GENERAL PHYSICAL EXAMINATION

Fig. 13.21

rash in systemic | Butterfly lupus erythematosis.

Fig. 13.22

flush in chronic | Malar mitral stenosis.

vii) Flushing It occurs in carcinoid syndrome (due to metastasizing carcinoid tumor of ileum), accompanied by facial and periorbital edema, diarrhea, bronchial constriction and valvular lesions (usually TR and PS/PR).21 viii) Striking Premature Aging It is often seen in Werner’s syndrome22 and is characterized by: ● ● ● ●

Loss of subcutaneous tissue (scleroderma-like changes) Graying of hair and baldness Cataract and leg ulcers It is often associated with severe coronary atherosclerosis.

ix) Facial Expression of Fright and Anxiety ●

●

Staring eyes (other ocular signs: lid lag, lid retraction, infrequent blinking, ophthalmplegia) and moist skin with fine and silky hair, Plummers nail especially in ring fingers (separation of nail from nail bed) seen in thyrotoxicosis (see Fig. 13.23). It is often associated with arrhythmias (sinus tachycardia, atrial fibrillation), wide pulse pressure, high output failure and Means-Lerman scratch, a to and fro high pitched sound in the pulmonary area, simulating pericardial rub.23

x) Moon Face Associated with central obesity and hirsutism is observed in Cushing’s syndrome12 (see Fig. 13.24). xi) Ape Like Appearance ●

Coarse features with broad nose, thick lips, prominent forehead and cheek bones, prognathism, enlarging hands and feet, hypertrichosis, and weight gain are charcteristic of acromegaly (see Fig. 13.25).

GENERAL EXAMINATION

Fig. 13.23

expression of | Facial fright and anxiety

Fig. 13.24

face of Cushing’s | Moon syndrome.

Fig. 13.25

with exophthalmos in hyperthyroidism. ●

175

like face | Ape with borad nose in acromegaly.

It is often associated with hypertension, cardiomyopathy, arrhythmias (premature ventricular contractions, atrial fibrillation, atrial flutter, interventiclar conduction defects), and atherosclerosis.24,25

xii) Mongoloid Facies ●

●

Broad flat nose, inner epicanthic folds, Brushfield’s spots in iris, lenticular opacities, low set ears, large protuberant tongue, mental retardation, broad and short hands with a single transverse palmar crease, short and incurved little fingers (clindactyly) are charcteristic of Down’s syndrome (trisomy 21) (see Fig. 13.18). It may be associated with endocardial cushion defect26, less frequently with TOF, ASD, PDA.27

xiii) Grotesque Facial Features ●

●

Prominent supraorbtal ridges, depressed nasal bridge, thick lips and peg shaped teeth, corneal clouding, hepatosplenomegaly and mental retardation, seen in Hurler’s syndrome [mucopolysaccharidosis (MPS)-I, autosomal recessive inheritance ]28 due to iduronidase deficiency and It is associated with CAD, AR, MR (mitral annulus calcification) and hypertrophic cardiomyopathy.

xiv) Elfin Facies ●

●

Hypertelorism, epicanthic folds, strabismus, low set ears, depressed nasal bridge, anomalies of dentition, hoarse voice and hypercalcemia are charcteristic of cardiofacial syndrome II (William syndrome, see Fig. 13.26).29 It is often associated with supravalvular AS and peripheral PS.

xv) Distinctive Unilateral Lower Facial Weakness (7th Cranial Nerve Palsy) In cardiofacial syndrome I, seventh cranial nerve palsy is associated with VSD.

176

GENERAL PHYSICAL EXAMINATION

Fig. 13.26

| Elfin facies with broad flat nose in William syndrome.

xvi) Midfacial Growth Deficiency ●

●

Hypoplastic upper lip, thin or absent philtrum, short palpebral fissures, micrognathia and microcephaly are charecteristic of fetal alcohol syndrome.30 It is associated with VSD and ASD.

5. EYES Eyes are examined for: i) Hypertelorism This refers to wide set eyes i.e. distance between the two eyes is more than the size of one eye. It is observed in: ● ● ● ● ● ●

Noonan syndrome often associated with PS (see Fig. 13.16). Turner syndrome often associated with coarctation of aorta. LEOPARD (multiple lentigines) syndrome often associated with PS and HCM. Hurler syndrome associated with arrhythmias and valvular regurgitation. William syndrome associated with nonfamilial supravalvular AS and PS. Klippel-Feil syndrome often associated with VSD (see Table 13.8).

ii) Exophthalmos ●

● ●

Exophthalmic ophthalmoplegia and staring with lid lag seen in thyrotoxicosis (see Fig. 13.23). Pulsatile exophthalmos31 and pulsating earlobes occur in severe TR.32 It is rarely seen in severe myopia, chronic cor pulmonale and in normal individuals as congenital anomaly.

GENERAL EXAMINATION

177

Table 13.8 Syndromes with cardiovascular manifestations Syndrome

Diagnostic clinical features

Cardiovascular manifestations

1. LEOPARD (multiple lentigenes) syndrome (AD inheritance)

Lentigines (basal cell nevi), ECG defects, broad facies with ocular hypertelorism, growth retardation, deafness, genital and rib anomalies

Pulmonary stenosis, hypertrophic cardiomyopathy, AV blocks, left axis deviation or superior axis

2. Klippel-Feil syndrome

Facial asymmetry with short webbed neck, low hairline, small jaw, cleft palate, torticollis, scoliosis, deafness and strabismus

Ventricular septal defect34 (most common, dextrocardia may also occur)

3. Kearns-Sayre syndrome35,36

Ptosis, progressive external ophthalmoplegia, pigmentary retinopathy, ataxia, deafness and diabetes mellitus

Progressive AV block, dilated cardiomyopathy, hypertrophic cardiomyopathy

iii) Enophthalmos It occurs in cachexia. iv) Nystagmus It may be noted in Friedrich’s ataxia33 (autosomal recessive inheritance of spinocerebellar degeneration) which is associated with kyphoscoliosis, HCM, SA node artery occlusion and arrhythmias. v) Eye Lids Examine lids for: ● ●

●

Lid lag with other signs in hyperthyroidism. Ptosis: It is often associated with external ophthalomoplegia, pigmentary retinopathy, myocardial diseases and complete heart block in Kearns-Sayre syndrome (see Fig. 13.27). Ptosis also occurs in Klippel-Feil syndrome and multiple lentigines syndrome. Xanthelasma (soft yellowish nodules of cholesterol) near inner canthus in dyslipidemia (other signs of dyslipidemia include: corneal arcus, xanthomas and heptosplenomegaly) which often leads to atherosclerotic CAD (see Fig. 13.28).

vi) Conjunctiva It is examined for pallor, cyanosis, inflammation and presence of any petechial hemorrhages. ● ● ●

Pallor of anemia Suffusion of cyanosis Petechiae (lower eye lid)/subconjuctival hemorrhages in infective endocarditis (see Fig. 13.29).

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GENERAL PHYSICAL EXAMINATION

Fig. 13.27

in Kearns| Ptosis Sayre syndrome.

Fig. 13.29

in | Petechiae endocarditis. ●

Fig. 13.28

infective

| Xanthelasma (with left eye cataract).

Fig. 13.30

| Blue sclera in osteogenesis imperfecta.

Conjunctivitis with arthritis and urethritis observed in Reiters disease, which is associated with pericarditis37 and abnormal AV conduction38 in acute stage and AV block and AR in chronic stage.

vii) Sclera It is examined for: ●

●

Jaundice or icterus, which is observed in CHF, large pulmonary infarct, hemolysis due to prosthetic valves, sometimes in calcified valves. Blue sclera noted in osteogenesis imperfecta (see Fig. 13.30 and Table 13.10), Marfan synfrome, Ehlers-Danlos syndrome, and may also be familial.

viii) Cornea Examine cornea for clouding and arcus. ●

Corneal arcus (or arcus juvenalis) is one of the signs of dyslipidemia. It is a well defined yellowish white ring in the outer margin of the cornea (see Fig. 13.31).

GENERAL EXAMINATION

Fig. 13.31

arcus—a well-defined yellow white | Corneal ring, one of the signs of dyslipidemia.

Fig. 13.32

179

senilis—an ill grayish white | Arcus ring is seen in elderly individuals.

Table 13.9 Mucopolysacharidosis (MPS) and cardiovascular manifestations Cardiovascular manifestations

Syndrome

Diagnostic clinical features

1. MPS II-Hunter syndrome28

X-linked due to idurate sulfatase deficiency, grotesque (coarse) facies, clear cornea, growth and mental retardation

Similar to Hurler syndrome

2. MPS IV-Morquio’s disease39

Autosomal recessive inheritance due to N-acetyl-galactoseamine-6-sulfatase deficiency, short trunk dwarf, coxa valga, cloudy cornea, normal intelligence

Aortic regurgitation

3. MPS VI-MaroteauxLamy syndrome40

Due to arylsulfatase B deficiency, coarse facies, cloudy cornea, multiple skeletal changes and normal intelligence

Aortic regurgitation and dilated cardiomyopathy (AS, MR or MS are less common)

●

●

Arcus senilis is an ill defined grayish white crescent or rarely circle in the outer margin of the cornea due to degenerative condition of the cornea often associated with old age (see Fig. 13.32). Corneal clouding is observed in Hurler syndrome, type IV and VI mucopolysacharidosis (see Table 13.9) but clear cornea is seen in Hunter syndrome.

ix) Iris Iris is examined for spots and fissures. (i) Brushfield’s Spots It is grayish white spots at the periphery of the iris, but well appreciated in dark pigmented iris are characteristic of Down’s syndrome (see Fig. 13.33).

180

GENERAL PHYSICAL EXAMINATION

Fig. 13.33

spots in the iris | Brushfiled’s (arrows)—characteristic of

Fig. 13.34

Down syndrome.

be associated with complex | Coloboma—may congenital heart diseases such as TOF, TAPVC or VSD.

Table 13.10 Syndromes with cardiovascular manifestations Cardiovascular manifestations

Syndrome

Diagnostic clinical features

1. Ehlers-Danlos syndrome42 (type I to IV)

Hyper extensible and fragile skin with poor wound healing, ‘cigarette paper’ scarring, hyper extensible joints, hyper mobile ears (lop ears), scoliosis, umbilical and diaphragmatic hernias

Arterial dilatation and rupture, AR or mitral valve prolapse

2. CHARGE syndrome43

Coloboma, congenital heart disease, choanal atresia, retarded growth, genital hypoplasia, ear anomalies

TOF, conotruncal anomalies

3. Osteogenesis imperfecta (autosomal dominance inheritance)

‘Brittle bone disease’ (severe osteoporosis, bone fragility, repeated fractures, bowing of long bones), short stature, deafness, blue sclerae and angiod streaks in the retina. Blue sclera is due to thinness of the collagen layers of the sclera that allow the choroids layers to be seen

AR,44 aortic root dilatation,45 MR46

(ii) Congenital Coloboma It is (fissures of iris) (which change the pupillary shape from normal circular to oblong giving an appearance of cat eye) ●

●

Noted in cat eye syndrome41 (chromosomal trisomy or tetrasomy 22) in which 50% of the affected patients may be associated with complex congenital heart diseases such as TAPVC, VSD, TOF (see Fig. 13.34). Coloboma also occurs in CHARGE syndrome, which is associated with conotruncal anomalies or TOF (see Table 13.10).

GENERAL EXAMINATION

Fig. 13.35

cataract may be associated with | Premature cardiomyopathy.

Fig. 13.36

181

subluxation of lens in | Upward Marfan syndrome.

x) Pupils Pupils are examined for the presence of Argyll Robertson pupil (small irregular unequal pupils with absent light reflex but sparing accommodation and convergence) which is noted in neurosyphilis and may be associated with cardiovascular lesions such as AR. xi) Lens Lenses are examined for cataracts and for dislocation. (i) Premature Cataracts These are noted in: ●

●

● ●

Myotonic muscular dystrophy (which is associated with cardiomyopathy, see Fig. 13.35). Refsum’s disease47 (autosomal recessive inheritance due to hydroxylase deficiency and is associated with cerebellar ataxia, deafness, peripheral neuropathy, retinitis pigmentosa and dilated cardiomyopathy and/or hypertrophic cardiomyopathy), Werner’s syndrome (associated with premature coronary atherosclerosis) and Rubella (1st trimester infection and may be associated with congenital heart disease, especially PDA).

(ii) Subluxation of the Lens ● ●

Upward lens dislocation in Marfan syndrome (see Fig. 13.36) and Downward lens dislocation in homocystinuria (which may be associated with arterial and venous thrombosis, myocardial infarction or pulmonary embolism).

xii) Retina Fundus examination is helpful for diagnosis (coarctation of aorta, infective endocarditis) and prognosis of the cardiovascular conditions (hypertension) (see Table 13.11 and Fig. 13.37). The cotton wool spots are usually found around the optic disc,

182

GENERAL PHYSICAL EXAMINATION

Table 13.11 Fundus examination in patients with cardiovascular manifestations Findings

Disease

1. 2. 3. 4. 5. 6. 7.

Hypertension Atheroclerosis Takayasu’s disease Coarctation of aorta Infective endocarditis Malignant hypertension Pseudoxanthoma elasticum

Hypertensive retinopathy Arteriosclerotic retinopathy Wreathlike AV anastomosis Corkscrew tortuous retinal arteries Roth spots Papilledema Angiod streaks

Fig. 13.37

| Normal fundus.

Table 13.12 Helpful guidance for fundus examination Lesions

Most common site in the retina

1. 2. 3. 4. 5. 6.

Upper temporal quadrant Around the optic disc Between the disk and fovea Temporal to fovea Arterial bifurcation Nerve head and arcades

Arteriovenous crossings Cotton wool spots Hard exudates Microaneurysms Emboli Diabetic new vessels

microaneurysms temporal to the fovea and new vessels around the nerve head (see Table 13.12). Fundus examination is done for: (i) Hypertensive retinopathy: The duration and severity of hypertension can be judged from fundus examination. Hemorrhages and exudates are described in grade 3 fundus changes, while the presence of papilledema indicates grade 4 fundus changes (see Fig. 13.38 and Table 13.13).48 (ii) Arteriosclerotic retinopathy: Similarly the state of arteriosclerotic changes can be determined from fundus examination. The occurrence of ‘copper wire’ and ‘silver wire’ indicates grade 2 and 3 fundus chages respectively (see Table 13.14).48 (iii) Wreath-like AV anastamosis around the disc, characteristic of Takayasu’s disease.

GENERAL EXAMINATION

Fig. 13.38

183

retinopathy—characteristic flame shaped hemorrhages and | Hypertensive cotton wool exudates (arrow).

Table 13.13 Hypertensive retinopathy (Keith-Wagener-Barker classification)48

Degree/ severity

Arteriolar/venous diameter ratio (narrowing of arterioles)

Normal 3:4 Grade I 1:2 Grade II 1:3 Grade III 2:3 Grade IV Fine fibrous cords

Focal spasm (ratio of region/proximal arterioles diameter) 1:1 1:1 2:3 1:3 Obliteration of distal flow

Hemorrhages

Exudates

Papilledema

0 0 0  

0 0 0  

0 0 0 0 

Table 13.14 Fundus in arteriosclerosis (Keith-Wagener-Barker classification)48 Degree/severity

Arteriolar light reflex

Normal Grade I

Fine yellow line, red blood column Broadened yellow line, red blood column Broad yellow line, ‘copper wire’, blood column not visible Broad white line, ‘silver wire’, blood column not visible Fibrous cords, blood column not visible

Grade II Grade III Grade IV

AV crossing defects (arteriolar length and tortuosity increase with severity) 0 Mild depression of vein Depression or hump of vein Right angle deviation, tapering and disappearance of vein under arteriole Same as grade III and distal dilatation of vein

(iv) Cork-screw tortous retinal arteries with no changes of hypertensive retinopathy seen in coarctation of aorta (see Fig. 13.39). (v) Roth spots (retinal hemorrhages with pale centers near the disc, (see Fig. 13.40). ● These are seen due to perivascular collections of lymphocytes in the nerve layer of the retina, and are observed in 4–10% of infective endocarditis patients.

184

GENERAL PHYSICAL EXAMINATION

Fig. 13.39

(vii)

(viii)

(ix)

Fig. 13.40

spots—retinal hemor| Roth rhages with pale centers.

It is considered as one of the minor diagnostic criteria (immunological phenomenon), but can be found in leukemia and anemia.49 Large retinal veins ● These extend to the periphery due to the increased red cell mass and are occasionally associated with papilledema and retinal edema (in response to low systemic arterial O2 saturation). ● These are observed in cyanotic congenital heart disease. Papilledema (grade 4 changes, see Fig. 13.41) may be seen in: ● Severe hypertension (malignant hypertension) and ● Chronic severe cor-pulmonale Embolic retinal occlusions may occur in patients with: ● Rheumatic heart disease, left atrial myxoma and atherosclerosis of aorta or arch vessels. ● Calcific emboli are white, dull and near the optic disc. ● Cholesterol emboli (Hollen horst plaques) are yellowish white and are highly refractile (see Fig. 13.42). ● Fibrin platelet emboli appear as whitish plugs that are sometimes seen moving through the retinal arteries. Angiod streaks (reddish brown lines, which are wider than retinal vessels and radiate from the optic disc) are observed in: 50 ● Pseudoxanthoma elasticum: There are raised yellowish papules (pseudoxanthoma) on the skin of neck, groin, cubital and popliteal fossae and the skin is also associated with premature calcification of systemic and coronary arteries, systemic hypertension, and retinal artery involvement. ● Paget’s disease of the bone which is often associated with high output failure. ● Sickle cell anemia, which is associated with pulmonary hypertension and occlusion of small intracardiac arteries. ● Osteogenesis imperfecta. ●

(vi)

retinal arteries in | Cork-screw coarctation of aorta.

GENERAL EXAMINATION

Fig. 13.41

| Papilledema.

Fig. 13.42

185

| Retinal emboli—cholesterol emboli.

6. NOSE Broad flat nose is a part of facial dysmorphism and is observed in Cornelia de Lange syndrome, Down syndrome, William’s syndrome and Hurler’s syndrome (see Tables 13.15 and 13.16 and Fig. 13.26). ● ●

Broad nose is seen in acromegaly (see Fig. 13.25). Thin beaked nose is seen in Rubinstein Taybi syndrome.

7. EARS Examine ears for distorted shape, low set ears and for the ear lobe crease (see Table 13.16). i) Ear Lobe Crease Individuals with ear lobe crease (i.e. a crack in the pinna, Frank sign) more frequently have CAD51 (see Fig. 13.43). ii) Cauliflower (Floppy) Ear It is seen in polychondritis which is associated with arthritis, saddle shaped nose, and cardiovascular manifestations such as pericarditis (in 30%), AR and TR (in 1–2%)52 (see Fig. 13.44). iii) Low Set Ears If 1/3rd of the ear lobe present above a line drawn from the outer canther of each eye. It is a part of facial dysmorphism which is often associated with cardiovascular manifestations. Low set ears are common in: ● ●

Noonan syndrome (see Fig. 13.45), Turner syndrome,

186

GENERAL PHYSICAL EXAMINATION

Table 13.15 Syndromes and CV manifestations Syndrome

Diagnostic clinical features

Cardiovascular manifestations

1. Cornelia de Lange’s syndrome

Short stature, hirsutism, bushy eye brows, downward slanting eyes, long eye lashes, low set ears, broad flat nose, growth and mental retardation, phocomelia, and a single thumb like digit (chicken-wing extremity)

VSD Others: PDA, ASD, PS, anomalous venous return

2. Rubinstein Taybi syndrome53

Broad thumbs and toes, slanting palpebral fissures, thin beaked nose, large low set ears, short stature and microcephaly

PDA, VSD

Table 13.16 Ear, nose and teeth abnormalities and syndromes with cardiovascular manifestations Ear abnormalities

Nose abnormalities

Teeth abnormalities

1. Low set ears: 1. Broad flat nose: 1. Peg shaped teeth: i. Noonan syndrome i. Down syndrome i. Hurler’s syndrome ii. Turner syndrome ii. William’s syndrome ii. William’s syndrome iii. Klippel-Feil syndrome iii. Cornelia de Lange’s syndrome iii. Congenital syphilis iv. Down syndrome iv. Hurler’s syndrome v. Cornelia de Lange’s syndrome vi. Rubinstein-Taybi syndrome 2. Deformed ears: 2. Broad nose: 2. Widely spaced teeth: Polychondritis Acromegaly i. Morquio’s syndrome ii. Acromegaly 3. Ear lobe crease: 3. Thin beaked nose: 3. Malformed teeth: CAD Rubinstein-Taybi Non hereditary form of syndrome supravalvular AS with PS

Fig. 13.43

lobe crease (Frank sign)— | Ear more prone to coronary artery disease.

Fig. 13.44

| Cauliflower ear.

GENERAL EXAMINATION

Fig. 13.45

● ● ● ●

187

| Low set ears and hypertelorism in Noonan syndrome.

Klippel-Feil syndrome, Down’s syndrome, Cornelia de Lange’s syndrome, and Rubinstein-Taybi syndrome (see Table 13.15).

iv) Deafness It is associated with Turner’s syndrome, Klippel-Feil syndrome, Rubella and multiple lentigines syndrome. 8. ORAL CAVITY i) Lips Examine for pallor, cyanosis, thickening, fissures and capillary pulsations. ● Pallor of anemia. ● Cyanosis is detected early except in dark-skinned individual and in those using cosmetics. ● Thick lips noted in Hurler syndrome, acromegaly, myxedema and cretin. ● Absent philtrum seen in fetal alcohol syndrome (see Fig. 13.46). ● Capillary pulsations can be observed by gently pressing a slide on the mucous membrane of the lips, which is noted in AR (Quinke’s sign). Other sites of demonstration of capillary pulsations: – By rubbing the skin of the forehead and observing the alternate blushing and blanching of the hyperemic area. – Gentle pressure is applied at the tip of the nail and the nail bed is observed for a rhythmic flush. – Transilluminate the ear tip, finger or thumb tip by a torch light. ● Rhagades are ulcerative fissures at the angles of the mouth. These are observed in congenital syphilis (see Fig. 13.47) and need to be differentiated from angular stomatis of riboflavin deficiency (see Fig. 13.48).

188

GENERAL PHYSICAL EXAMINATION

Fig. 13.46

philtrum | Absent in feotal alcohol

Fig. 13.47

saddle-nose | Rhagades, and interstitial keratitis

syndrome.

in congenital syphilis.

Fig. 13.48

stomatis and | Angular glossitis in riboflavin deficiency.

ii) Mucous Membrane It is examined for petechiae and telangiectasia. (i) Petechiae occur in infective endocarditis. (ii) Clusters of small ruby patches are telangiectasia present on lips, mucous membrane, palate tongue and fingertips in Osler-Rendu-Weber syndrome,54 which may be associated with: ● Arteriovenous fistulas in lungs (which may result in hyperdynamic circulation, hemoptysis, hypoxemia, polycythemia, clubbing, paradoxical emboli through right to left shunt). ● And less commonly in liver, brain and kidneys. iii) Teeth Examine teeth for dentition, malformation and for wide spacing (see Table 13.16). (i) Delayed dentition occurs in cretins, mongolism and rickets. (ii) Malformed and premature dentition at birth with gingival hypertrophy, lip tie and multiple frenulums observed in Ellisvan Crevald sydrome.9 (iii) Peg shaped teeth occur in: ● Hurler syndrome ● William’s syndrome (see Fig. 13.49) and ● Characteristic of Hutchinson’s teeth (upper central permanent incisors are peg shaped or rounded; interstitial keratitis, deafness and Hutchinson’s teeth complete the diagnostic triad of congenital syphilis, see Fig. 13.50). (iv) Malformed teeth erupt in nonhereditary form of supravalvular AS with PS. (v) Widely spaced teeth may be seen in: ● Acromegaly ● Morquio’s syndrome and ● William’s syndrome.

GENERAL EXAMINATION

Fig. 13.49

and widely spaced teeth in | Small William’s syndrome.

Fig. 13.50

| Hutchinson’s syphilis.

189

teeth in congenital

iv) Gums Look for cyanosis and gum hypertrophy. ● ●

Cyanosis can be appreciated in the gums. Gingival hypertrophy can be seen in Ellisvan Crevald syndrome and phenytoin intake (see Fig. 13.51).

v) Tongue Examine for colour and size. (i) Color of the Tongue ● ● ● ● ● ●

Blue tongue in cyanosis Magenta (or dark red) tongue in riboflavin deficiency Bright or scarlet red tongue (angry tongue) in niacin deficiency Black tongue from fungal infection (actinomycosis) Brown tongue may be seen in uremia and Pale tongue in anemia.

(ii) Macroglossia It is seen in acromegaly (see Fig. 13.52), myxedema, large protruding tongue observed in Down’s syndrome, Hurler syndrome and in cretin. (iii) Glossoptosis (Retracted Tongue) It occurs in Pierre Robin syndrome which is associated with ‘shrew like face (hypoplastic mandible, high arch/cleft palate) and VSD. vi) Palate It is examined for cleft/perforation and for the presence of high arched palate.

190

GENERAL PHYSICAL EXAMINATION

Fig. 13.51

| Gum hypertrophy in phenytoin intake.

Fig. 13.53

| Perforated palate in tertiary syphilis. ● ●

Fig. 13.52

Fig. 13.54

| Macroglossia in acromegaly.

| Cleft palate in velo cardiofacial syndrome.

High arched palate observed in Marfan syndrome, and Pierre Robin syndrome. Cleft/perforated palate may be due to tertiary syphilis (see Fig. 13.53), velocardiofacial syndrome (see Fig. 13.54) and tuberculosis.

9. NECK Examine neck for low hair line, short and webbed neck (see Table 13.17), lymphadenopathy, thyromegaly and for any parotid gland enlargement. i) Short Neck The ratio of height to the distance between external occipital protuberance and C7 spinous process (Bird’s index): 12.8 is normal, while 13.6 indicates short neck, which is seen in: ● ●

Klippel-Feil syndrome Morquio’s syndrome (MPS IV).

GENERAL EXAMINATION

191

Table 13.17 Neck abnormalities and low hair line in syndromes with cardiovascular manifestations Short neck

Webbed neck

Low hair line

1. Klippel-Feil syndrome 2. Morquio’s syndrome

1. Noonan syndrome 2. Turner syndrome 3. Edward’s syndrome

1. 2. 3. 4.

Fig. 13.55

Noonan syndrome Turner’s syndrome Klippel-Feil syndrome Cornelia de Lange’s syndrome

| Webbed neck in Turner syndrome.

ii) Webbed Neck Noted in: ● ● ●

Noonan syndrome Turner’s syndrome (see Fig. 13.55) Trisomy 18 (Edwards) syndrome55 which is characterized by a small triangular mouth with receding chin, small mandible, clenched hand (tightly clenched fist with index finger overlapping 3rd finger and 5th over the 4th finger), low arch dermal ridge pattern on finger tips, short sternum, rocker bottom feet and mental retardation besides webbed neck. It is associated with VSD, PDA and poly-valvular dysplasia.

iii) Low Hair Line When the posterior hairline extends below the level of C5 spinous process or the ratio of the distance from the external occipital protuberance to the hair line and the distance from the hair line to C7 spinous process is 1/6 in males and 1/4 in females, it is defined as low hair line which is observed in ● ● ● ●

Noonan syndrome (see Fig. 13.17) Turner syndrome Klippel-Feil syndrome Cornelia de Lange’s syndrome.

192

GENERAL PHYSICAL EXAMINATION

Fig. 13.56

| Thyromegaly in goiter.

Fig. 13.57

| Parotid enlargement in mumps.

iv) Lymphadenopathy Cervical lymphadenopathy may be due to: ● ● ●

Tuberculosis Syphilis Sarcoidosis.

v) Thyromegaly It may be due to thyrotoxicosis (see Fig. 13.23) or goiter (see Fig. 13.56). vi) Parotid Enlargement It occurs in mumps, which may be associated with myocarditis (see Fig. 13.57).

10. SPINE Normally, there is a mild convexity (kyphosis) of thoracic spine, a mild concavity of cervical spine and a definite concavity (lordosis) of lumbar spine without any lateral curvature (scoliosis) (see Table 13.18). Examine the spine for scoliosis and loss of thoracic kyphosis and lumbar lordosis. ●

●

●

Kyphoscoliosis, pectus excavatum and pectus carnitum are observed in Marfan syndrome. Loss of thoracic kyphosis (resulting in straight back) (best observed in sitting posture) with a decrease in the anteroposterior chest dimensions results in parasternal systolic impulse and a pulmonary mid systolic murmur mimicking ASD. Ankylosing spondylitis56 is a seronegative spondyloarthropathy characterized by progressive inflammation of spine leading to chronic backache, deforming dorsal kyphosis and in advanced stage, there is a fusion of the costovertebral and sacroiliac

GENERAL EXAMINATION

193

Table 13.18 Spine abnormalities in diseases with cardiovascular manifestations 1. Marfan syndrome 2. Ankylosing spondylitis 3. Straight back syndrome

Fig. 13.58

●

● ●

●

of spine—showing | X-ray ankylosing spondylitis.

Fig. 13.59

with convexity to the | Scoliosis right.

joints with immobilization of the spine (see Fig. 13.58). It may be associated with HLA-B27 histocompatibility antigen and AR (in 10%) and the extension of inflammation results in MR and complete heart block. Functional scoliosis disappears on bending forward while structural scoliosis persists and is associated with the rotation of the vertebral bodies and with the systolic murmurs, which may lead to faulty diagnosis. Minor degrees of scoloisis can be better identified with chest X-ray. Scoliosis with convexity to the left is usually due to poliomyelitis or neuro-muscular diseases while the structural changes in the spine give rise to scoliosis with convexity to the right (see Fig. 13.59). Angle of curvature is known as Cobb angle: More the angle, the worst is the prognosis.

11. SKIN The skin lesions are the alphabets of systemic diseases (see Table 13.19) and should be examined for nature, evolution and their distribution.

194

GENERAL PHYSICAL EXAMINATION

Table 13.19 Skin lesions in systemic diseases with cardiovascular (CV) manifestations Skin lesions

Systemic disease

CV manifestations

1. Bronze pigmentation 2. Café au luit spots

Hemochromatosis, Von Recklinghausen’s disease LEOPARD syndrome Tuberous sclerosis Rheumatic fever Infective endocarditis

Cardiomyopathy Pheochromocytoma  hypertension and myocarditis Hypertrophic cardiomyopathy Rhabdomyoma and arrhythmias Carditis Valvular lesions and embolism

3. Multiple lentigines 4. Angiofibromas 5. Erythema marginatum 6. Janeway lesions

i) Pigmentation (i) Bronze pigmentation ● Bronze pigmentation on exposed areas of the skin (due to melanin and iron in dermis) with loss of axillary and pubic hair, hepatomegaly, DM, arthritis, testicular atrophy and loss of libido occur in hemochromatosis. ● It is associated with cardiomyopathy (restrictive or dilated) in about 15%. (ii) Café au luit spots (on the trunk), freckles (especially axillary: crowe’s sign) and neurofibromas (on the trunk and face) occur in von Recklinghausen’s disease that may be accompanied by pheochromocytoma (see Fig. 13.60). (iii) Multiple lentigines or large wide spread freckling characteristic of LEOPARD syndrome, which may be associated with hypertrophic cardiomyopathy especially when the lentigines are present from the first year of life. (iv) Angiofibromas (usually referred by a misnomer adenoma sebaceum): ● These are yellow to orange red nevi of a few mm to a cm on the face (symmetrically distributed on malar and nasal skin) and occur in tuberous sclerosis (see Fig. 13.61). ● Tuberous sclerosis is characterized by autosomal dominance inheritance and consists of triad of mental retardation, seizures and skin lesions. ● Other cutaneous lesions include subungual fibromas around the finger nail, café au lait spots and subcutaneous nodules. ● Seizures are due to intracranial hamartomatous lesions and calcification primarily in the basal ganglia.57 58 ● The associated cardiovascular manifestations consist of rhabdomyoma, WolffParkinson-White syndrome and supraventricular tachycardia.59 (v) Erythema marginatum ● It is an erythematous, macular non-pruritic, non-indurated rash with pale centers and rounded or serpiginous margins, which blanches completely on pressing, mainly occurring on the trunk and proximal extremities but not on the face or below elbows and knees. ● It is a rare manifestation of rheumatic fever, occurring in 3% of the patients (see Fig. 13.62). ● It is induced by heat application, is non-specific and not related to rheumatic activity.

GENERAL EXAMINATION

Fig. 13.60

in von | Neurofibromas Recklinghausen’s disease.

Fig. 13.62

Fig. 13.61

195

(orange red nevi) on the face | Angiofibromas of a patient with tuberous sclerosis.

| Erythema marginatum—in rheumatic fever.

It is considered as one of the major criteria for diagnosis of rheumatic fever,60 but it is rare or difficult to visualize in dark skinned individuals (Indian subcontinent), and could be of idiopathic etiology or could be due to drug reactions, staphylococcus infection or nephritis. (vi) Janeway lesions ● These lesions are one of the classical signs of infective endocarditis. ● They are small erythematous or hemorrhagic, non tender and non painful macular lesions on the palms of the hands or soles of the feet due to septic emboli, observed in 6–10% of the patients. ● They constitute one of the minor criteria (vascular phenomena) of Dukes criteria of diagnosis of infective endocarditis.61 (vii) Symmetric vitiligo, especially on distal extremities, is seen in Graves’s disease. ●

ii) Skin Texture ● ●

Skin is coarse, thick and dry with brittle, sparse and coarse hair in myxedema.14 Hyperextensible and rubber like skin with cigarette paper scars (due to fragility and poor wound healing) occur in Ehlers Danlos syndrome (see Fig. 13.63).

196

GENERAL PHYSICAL EXAMINATION

Fig. 13.63

skin in Ehler’s-Danlos | Hyperextensible syndrome.

Fig. 13.65

xanthoma producing | Palmar pink discoloration of the palm and digital creases.

Fig. 13.64

skin in axilla in pseudoxanthoma | Grooved elasticum.

●

●

Plucked chicken appearance/grooved skin over the neck and axillae occurs in pseudoxanthoma elasticum as the skin is reticular and telangiectatic with small tarnish yellow papules (see Fig. 13.64). Moist skin with fine silky hair and staring eyes occurs in hyperthyroidism.23

iii) Xanthomas They are small yellowish orange papules or nodules associated with hyperlipidemias in those patients whose premature atherosclerosis develops frequently. (i) Tuberous xanthomas are yellowish orange papules erupting over the elbows, knees, buttocks and heels. These are often associated with hyperlipidemia, but can occur in myxedema and liver disorders. (ii) Xanthoma striatum palmare ●

It produces yellowish, orange or pink discoloration of the palmar and digital creases (see Fig. 13.65).

GENERAL EXAMINATION

197

Table 13.20 Xanthomas and hyperlipidemia

Fig. 13.66

Xanthomas

Hyperlipoproteinemia type

1. Palmar xanthomas 2. Tendinous xanthomas 3. Eruptive xanthomas

Type III Type II Types I and V

| Achilles tendon xanthomata.

Fig. 13.67

| Tendinous xanthomas over the knees.

It occurs most commonly in type III hyperlipoproteinemia (familial dysbeta lipoproteinemia, autosomal recessive inheritance, see Table 13.20) which is due to the elevated levels of intermediate density lipoprotein, total cholesterol and triglycerides (300 mg/dl). ● They are associated with premature atherosclerosis, diabetes mellitus, and in turn with CAD, peripheral vascular disease and stroke. (iii) Xanthoma tendinosum (tendinous xanthomas) ● These are yellowish nodular swellings of the tendons, especially of the elbows, extensor surfaces of the hands and Achilles tendons (see Figs 13.66 and 13.67). ● They are commonly associated with type II hyperlipoproteinemia (familial hypercholesterolemia, due to low-density lipoprotein (LDL) receptor defect, and autosomal dominance inheritance (see Table 13.20). Heterozygous form occurs in 1:500 population and homozygous form in 1:10). ● These are characterized by elevated levels of LDL and total cholesterol but have normal levels of triglyceride. ● They are associated with corneal arcus and premature atherosclerosis. (iv) Eruptive xanthomas ● These are tiny yellowish nodules of 1–2mm in diameter on an erythematous base, which frequently occur on arms, legs, thighs and buttocks (but can occur anywhere on the body) (see Fig. 13.68). ● These are usually associated with hyperchylomicronemia and hence with Type I and V hyperlipoprotemia, DM, pancreatitis, myxedema and nephrotic syndrome (see Table 13.20). ●

198

GENERAL PHYSICAL EXAMINATION

Fig. 13.68

| Eruptive xanthomas on the elbow.

Table 13.21 Nodules associated with cardiovascular manifestations Nodules

Disease

1. Waxy flat nodules 2. SC nodules

Amyloidosis restrictive cardiomyopathy Rheumatic fever, systemic lupus erythematosis and rheumatoid arthritis Infective endocarditis

3. Osler’s node

Type I Hyperlipoproteinemia or Familial Chylomicronemia ●

●

●

It is due to lipoprotein lipase or apoprotein C II deficiency with autosomal recessive inheritance. It is characterized by increased levels of chylomicrons, triglycerides and normal to mildly elevated total cholesterol level. It is associated with recurrent abdominal pain, pancreatitis, hepatosplenomegaly but not with premature atherosclerosis.

Type V Hyperlipoproteinemia or Familial Mixed Triglyceridemia ●

●

It is characterized by elevated levels of very low-density lipoproteins (VLDL), chylomicron, total cholesterol and triglycerides. It is associated with pancreatitis and possibly premature atherosclerosis.

iv) Nodules (i) Subtle small translucent waxy flat top nodules (better visualized with hand lens). These occur in systemic amyloidosis, which may be associated with restrictive cardiomyopathy and conduction defects. They are usually clusterd in the folds of axillae, anal or inguinal regions, face and neck, ear or tongue (see Table 13.21). (ii) Subcutaneous nodules: ● These are firm painless freely movable nodules of 0.5–2 cm size seen in about 3% of rheumatic fever patients with carditis.

GENERAL EXAMINATION

Fig. 13.69

nodules over the knuckles | Rheumatic of the hand.

Fig. 13.71

nodules on the occipital protu| SC berance in a rheumatic fever.

Fig. 13.70

199

| SC nodules over the elbow.

Fig. 13.72

nodules over the spinous | Rheumatic process of thoracic vertebrae.

They are located over the extensor surfaces of the joints (on the tendons of the extensors of the fingers and toes and flexors of the wrist and ankle, see Figs 13.69 and 13.70), on the occipital protuberance (see Fig. 13.71), or over the spinous processes of thoracolumbar vertebrae (see Fig. 13.72). ● They occur in crops, and are symmetrical in distribution (when in large number). ● They heal without scar formtion and last for 1–2 weeks, rarely  one month. ● SC nodules are considered as one of the five major criteria for the diagnosis of rheumatic fever;60 however, they can also occur in rheumatoid arthritis and SLE. (iii) Osler’s nodes ● Osler’s nodes are small, tender subcutaneous nodules on the pads of fingers or toes and palms or soles, seen in 7–10% of infective endocarditis (see Fig. 13.73). ● They occur due to the deposits of immune complex in mucocutaneous vessels and infected microemboli. ● They constitute one of the minor criteria (immunological phenomena) of Duke’s criteria of the diagnosis of infective endocarditis.61 ●

200

GENERAL PHYSICAL EXAMINATION

Fig. 13.73

| Osler’s node in infective endocarditis (arrow mark).

(iv) Peripheral emboli: Emboli from prosthetic valve, LV mural thrombus or marantic endocarditis occur on the tips of fingers and toes as small tender, painful areas that suddenly become pallid or cyanotic. v) Cyanosis, Icteru, and Pallor (i) Cyanosis: See chapter 12. (ii) Icterus: Yellowish discoloration of skin, mucous membrane and sclerae is due to the deposition of bilirubin (see also sclera). (iii) Pallor of the skin and mucous membrane is often due to anemia, and sometimes due to: ● The accumulation of myxematous substance in the skin as in myxedema ● Could be racial as in Chinese or ● Occupational as in radium or lead workers.

12. EXTREMITIES Varieties of congenital and acquired cardiac malformations are associated with characteristic changes in the extremities including digits. i) Digits Examine for: (i) Arachnodactyly: (spider fingers) ● Unduly long and thin fingers and toes with positive wrist (Walker-Murdock) and thumb (Steinberg) signs are characteristics of Marfan syndrome (see Figs 13.74 and 13.75). ● In sickle cell anemia, bones of hands and feet (especially in young adults) are elongated with increased metacarpal index (MCI, a pseudo-Marfan syndrome sign).

GENERAL EXAMINATION

Fig. 13.74

and wrist (Walker| Arachnodactyly Murdock) sign in Marfan syndrome.

Fig. 13.76

syndactyly, and | Polydactyly, Ellis-van Creveld syndrome.

Fig. 13.75

201

(Steinberg) sign in Marfan | Thumb syndrome.

clindactyly in Fig. 13.77

in Laurence-Moon| Polydactyly Biedl syndrome.

Arachnodactyly is assessed by the ratio of the middle finger length to the total hand length or radiologically by the metacarpal index.62 Metacarpal index (MCI) (In L/WMi L/WRi L/WLi L/W)4 Postivie if MCI is 8.4 In index finger, Mi middle finger, Ri ring finger, Li little finger, L length of the bone, W width of the bone. (ii) Polydactyly is the presence of extra or supernumerary fingers or toes which may be familial or associated with Ellis-van Creveld syndrome, Laurence-Moon-Biedl syndrome (see Figs 13.76 and 13.77). (iii) Syndactyly (webbed fingers): Fusion between the adjacent fingers or toes may be dermal or osseous and etiology is similar to that of polydactyly. (iv) Clindactyly: (incurved fingers) th ● Clindactyly of little finger, with increased space between 4 and 5th fingers is seen in Down syndrome. ●

202

GENERAL PHYSICAL EXAMINATION

Fig. 13.78

| Fingerized thumb in Holt-Oram syndrome. Table 13.22 Abnormal thumbs and cardiovascular manifestations Abnormal thumbs

Disease

1. Fingerized thumbs 2. Single thumb like digit 3. Broad thumbs

Holt-Oram syndrome Cornelia de Lange syndrome Rubinstein-Taybi syndrome

Clindactyly of 4th and 5th fingers resulting in a claw like appearance of hands also occurs in Hurler’s syndrome. (v) Fingerized thumbs ● Thumb with an extra phalanx (triphalangeal thumb) lies in the same plane as rest of the fingers which makes it difficult to appose with the fingers, a characteristic of Holt-Oram syndrome63 (see Fig. 13.78). ● Other manifestations include radial aplasia, hypoplasia of clavicles and shoulders, phocomelia and mental retardation that is inherited by autosomal dominance. ● It is associated with ASD, VSD and conduction defects. (vi) Single thumb like digit (chicken wing extremity) occurs in Cornelia de Lange syndrome (see Table 13.22). (vii) Broad thumbs and toes are seen in Rubinstein-Taybi syndrome (see Figs 13.79, 13.80 and Table 13.23). (viii) Brachydactyly is the presence of shortened fingers, which results in short hands. ● Broad and short hands are noted in Down syndrome. ● Short and trident hands of achondroplasia: The middle finger is not longer than the others (i.e. fingers are of equal length) and fingers are divergent like the spokes of a wheel. th ● Brachydactyly due to shortened 4 metacarpal occurs in Turner syndrome. ● Shortened fingers due to the absence of one of the phalanges occur in pseudohypoparathyriodism (autosomal dominance inheritence). ●

GENERAL EXAMINATION

Fig. 13.79

| Broad thumbs in Rubinstein-Taybi syndrome.

Fig. 13.80

| Broad toes in Rubinstein-Taybi syndrome.

203

Table 13.23 Abnormal digits and diseases with cardiovascular manifestations Digits description

Disease

1. Arachnodactyly 2. Polydactyly 3. Syndactyly 4. Clindactyly 5. Brachydactyly 6. Sclerodactyly

Marfan syndrome Ellis-van Creveld and Laurence-Moon-Biedl syndromes Ellis-van Creveld and Laurence-Moon-Biedl syndromes Down, Ellis-van Creveld and Hurler’s syndromes Down and Turner syndromes, hyperparathyroidism Scleroderma

Fingers appear stubbed with bulbous ends due to the collapse of the distal phalanges in hyperparathyroidism. (ix) Clenched hand with index finger overlapping the 3rd finger and 5th overlapping the 4th finger, is seen in Edwards syndrome (Trisomy 18). (x) Phocomelia (limb without hand, like flipper) may be associated with Holt-Oram syndrome and Cornelia de Lange syndrome (see Fig. 13.81). ●

204

GENERAL PHYSICAL EXAMINATION

Fig. 13.81

in Cornelia de Lange | Phocomelia syndrome.

Fig. 13.83

Fig. 13.82

phenomenon with peripheral | Raynaud’s cyanosis and digital ulcers.

| Sclerodactyly in scleroderma.

(xi) Raynaud’s phenomenon ● It is defined as episodes of white  blue color changes of the digits (fingers more often involved than toes while thumbs are often spared) followed by reactive hyperemia (ruber) during recovery, and often induced by cold or emotional stimuli (see Fig. 13.82). ● The recovery time is usually 3–10 min but can exceed 1h in advanced cases, especially of secondary origin. ● Raynaud’s phenomenon is sometimes seen in primary pulmonary hypertension. It is also an early manifestation of progressive systemic sclerosis (scleroderma) and CREST syndrome (calcinosis, Raynaud’s phenomenon, esophageal dysmobility, sclerodactyly (see Fig. 13.83), and telangiectasia). (xii) Sclerodactyly ● Sclerodactyly is tightening of the skin of the fingers with hair loss and disappearance of subcutaneous tissue and skin creases, with the development of flexion contractures leading to claw hand deformity which is characteristic of scleroderma.64

GENERAL EXAMINATION

205

Proximal nail fold Nail plate Lateral nail fold Nail plate

Nail bed Cuticle

Lunule Cuticule

Nail matrix

Proximal nail fold

Fig. 13.85

Fig. 13.84

| Structure of the nail-lateral view.

| Normal structure of the nail-dorsal view. Table 13.24 Abnormal nails and cardiovascular manifestations

●

●

Abnormal nails

Disease

1. Nail stripes 2. Dysplastic nails 3. Plummer nails 4. Square/broad nails 5. Koilonychias 6. Clubbing

Chronic constrictive pericarditis Ellis-van Creveld syndrome Hyperthyroidism Acromegaly, cretin Iron deficiency anemia Cyanotic congenital heart disease, infective endocarditis, myxoid tumor

Tightening of the skin (scleroderma) may also extend to hands, forearms, upper chest and face. It is often associated with myocardial fibrosis (see Table 13.23).

ii) Nails Normally, nail consists of proximal nail fold, cuticle, lunule, nail plate and lateral nail fold (see Figs 13.84 and 13.85). Examine nails for (see Table 13.24): ● ●

●

● ●

● ●

Cyanosis: See symptomatology, chapter 12. ‘Tuft’ erythema of the finger tips. It is a minor variation in the theme of cyanosis, which sometimes precedes cyanosis in patients with small or intermittent right to left shunts (see Fig. 13.86). Nail stripes: Alternating dark and light lines parallel to the tips of the nails occur in chronic constritive pericarditis (due to protein losing enteropathy). Nail strips are more common in Laennec’s cirrhosis. Dysplatic nails occur in Ellis-van Creveld syndrome (see Fig. 13.87). Plummers nail is onycholysis (separation of nail from nail bed) and occurs in hyperthyroidism or trauma. Onycholysis is also a classic feature of psoriasis (see Fig. 13.88). Square or broad nails: These occur in acromegaly (see Fig. 13.89) and cretinism. Koilonychia are spoon shaped nails (see Fig. 13.90). They occur when the normal transverse convex curvature of the nail plate becomes flattened or concave, a characteristic

206

GENERAL PHYSICAL EXAMINATION

Fig. 13.87 Fig. 13.86

and dysplastic nails in Ellis-van | Brachydactyly Creveld syndrome.

erythema of the fin| Tuft gertips in a patient with a small right-to-left shunt.

Fig. 13.88

| Onycholysis in psoriasis.

●

●

●

Fig. 13.89

| Broad nails in acromegaly.

of iron deficiency anemia which in turn may cause heart failure (high output) when Hb levels are 5 gm%. Splinter (subungual) hemorrhages are one of the non-specific signs of infective endocarditis, as trauma can also produce them (see Fig. 13.91). Capillary pulsations (Quinke’s sign): It is seen in AR (see lips for methods of demonstration). Clubbing of fingers and toes (Hippocratic fingers): Clubbing is probably due to hypervascularity and opening of the anastomotic channels in the nail bed, which increases the hydrostatic pressure in the capillaries and venules promoting interstitial edema and hypertrophy of the soft tissue (see Fig. 13.92).

The stages and severity of the clubbing can be divided into 4 grades: Grades of Clubbing Grade 1 clubbing is characterized by an increased glossiness and cyanotic tinge of the skin at the root of the nails.

GENERAL EXAMINATION

Fig. 13.90

Fig. 13.91

207

| Koilonychia.

hemorrhages in infective endo| Splinter carditis.

Fig. 13.92

of a finger compared with a | Clubbing normal digit.

Grade 2 clubbing: The normal angle of the nail bed (120 160 140) is lost and may exceed 180 with hypertrophy of the subungual tissue and freely floating root i.e. increased ballotability or fluctuation of the nail on its bed. Obliteration of the angle is demonstrated by: (i) Profile sign: by viewing the side of the flexed distal index or thumb (see Fig. 13.93). (ii) Schamroth’s window test: In normals when both two fingers are placed in apposition, there is a lozenge shaped gap between the nails, while in clubbed fingers there is a reduction in this gap (see Fig. 13.94). Fluctuation of nail on its bed: Palpate the dorsum of the finger immediately proximal to the base of the nail with both index and middle fingers. A sensation of fluctuation or rocking movement can be detected. However; in the presence of marked fluctuation, palpation of the nail itself may give the impression of nail floating on its bed.

208

GENERAL PHYSICAL EXAMINATION

L

R

Normal nail

Fig. 13.93

sign in a clubbed | Profile pared with a normal digit.

Fig. 13.95

finger com-

| Parrot beak like clubbing.

Fig. 13.94

Fig. 13.96

L

R

Clubbed nail

window test—L: left, | Schamroth’s R: right hand digits.

| Drumstick clubbing with cyanosis.

Grade 3 clubbing ●

●

It is characterized by grade 2 changes and increased curvature of the nails in both planes resulting in parrot beak (see Fig. 13.95) or watch glass like clubbing or Grade 2 changes, increased curvature of the nails and excessive swelling of the finger ends resulting in drumstick clubbing (see Fig. 13.96) or serpent head deformity, which is also known as Hippocratic fingers and is often associated with cyanosis.

Grade 4 clubbing or hypertrophic osteoarthropathy: It is a severe form of clubbing, characterized by clubbing of the nails and bony changes in the terminal digits, which may rarely extend to wrists and elbows, ankles and knees (see Fig. 13.97). In early stages, it is radiologically demonstrated by thickening of the periostium of the radius, ulna, tibia and fibula or subperiostal new bone formation. Causes of Clubbing (i) Cardiovascular causes: ● Cyanotic congenital heart disease: TOF, TGA, Tricuspid atresia, TAPVC ● Infective endocarditis (within a few weeks of IE) ● Acyanotic congenital heart disease: Myxoid tumor.

GENERAL EXAMINATION

Fig. 13.97

209

IV clubbing—clubbing of the nails with bony changes extending into | Grade the wrists and ankles.

(ii) Pulmonary diseases with hypoxia: ● Bronchiectasis ● Chronic fibrosing alveolitis ● Emphysema ● Empyma ● Lung abscess ● Bronchogenic carcinoma ● Pulmonary tuberculosis. (iii) GIT causes: ● Crohn’s disease ● Ulcerative colitis ● Polyposis of the colon ● Biliary cirrhosis. (iv) Harmless familial condition. Unilateral Clubbing of Fingers It is rare and can occur in: ●

● ● ● ●

Aortic aneurysm (and aneurysm of its branches) that interferes with arterial supply to one arm It is also observed in brachial arteriovenous fistula Pan coast tumors Erythromelalgia and Lymphangitis.

210

GENERAL PHYSICAL EXAMINATION ●

Subungual fibromas of the fingers which in tuberous sclerosis may be mistaken for unilateral clubbing of the fingers.

Unidigital clubbing It may occur due to various factors: ● ● ● ● ●

Hereditary if bilateral and involves the thumbs Median nerve injury Tophaceous gout Sarcoidosis, or Trauma.

Differential Clubbing Toes may be clubbed (independent of the fingers) in PDA with reverse shunt. iii) Feet Examine feet for: (i) Pes cavus (claw foot) ● Pes cavus is the exaggeration of the longitudinal arch of the foot resulting in a marked upward convexity of the instep and drawing up of the toes (see Fig. 13.98). ● It occurs in Friedrich’s ataxia (see Fig. 13.99), muscular atrophy (peroneal) and poliomyelitis. (ii) Rocker bottom foot due to protruding heel is characteristic of Edward syndrome (see Fig. 13.100). (iii) Bow-legs (genu varum): Outward bowing of the legs with the knees wide apart (see Fig. 13.101), is seen in: ● Achondroplasia and osteogenesis imperfecta

A

B

C

Fig. 13.98

B: claw and | A:C: normal, flat foot.

Fig. 13.99

| Pes cavus in Friedrich’s ataxia.

GENERAL EXAMINATION

Fig. 13.100

| Rocker bottom foot in Edward syndrome.

Fig. 13.101

| Genu varum.

● ●

Fig. 13.102

211

| Sabre tibiae in congenital syphilis.

Rickets and osteomalacia ‘Sabre tibiae’ (bowing of the tibiae) are seen in congenital syphilis (see Fig. 13.102), and can also be seen in rickets, osteomalacia and osteitis deformans or old multiple fractures.

(iv) Genu valgum (knock-knees): It is observed in Ellis-van Creveld syndrome, Laurence-Moon-Biedl-syndrome and rickets (see Figs 13.103, 13.104 and 13.105).

212

GENERAL PHYSICAL EXAMINATION

Fig. 13.104

valgum in | Genu Laurence-MoonBiedl syndrome.

Fig. 13.103

valgum in Ellis-van | Genu Creveld syndrome.

Fig. 13.105

valgum | Genu in rickets.

iv) Joints Examine the joints for inflammation, deformity or loss of function. (i) Hypermobility of the joints (lax joints) is observed in Ehlers-Danlos syndrome (see Fig. 13.106) and in few cases of Marfan syndrome. (ii) Arthritis could be due to rheumatic polyarthritis, Jaccord’s arthritis, polychondritis, rheumatoid arthritis, gouty arthritis, Reiter’s syndrome, infective endocarditis, and polyarteritis nodosa. Migrating Polyarthritis ●

● ● ● ●

It occurs in 58% of rheumatic fever, which spontaneously abates in 2–4 weeks without leaving any residual deformity. It affects the large joints: knee, ankle, elbow and wrist. With salicylates, it produces dramatic response within 24–48 hours. It can be associated with carditis but not with rheumatic chorea. It is considered as one of major diagnostic criteria (Jones criteria), however polyarthralgia (pian in the joints, not in the muscles and other periarticular tissues with no evidence of inflammation) is more common than polyarthritis in the Indian sub-continent and should be considered as one of the major criteria than as the minor diagnostic criteria.

GENERAL EXAMINATION

Fig. 13.106

|

Fig. 13.107 Hypermobility (laxity) of the joints in Ehlers-Danlos syndrome.

213

interphalangeal arthritis in rheu| Proximal matoid arthritis.

Jaccord’s Arthritis ●

● ●

Jaccord’s arthritis is the post-streptococcal reactive arthritis, characterized by similar clinical picture as that of rheumatic polyarthritis but with no other evidence of diagnostic criteria of rheumatic fever. It does not dramatically respond to salicylates. The deformity can be voluntarily corrected as it is due to sub-luxation of the joints than due to the erosion and fusion of their articular surfaces.

Polychondritis ●

●

Polychondritis is characterized by cartilaginous inflammation, auricular chondritis in 40% (resulting in floppy ears, deafness, vertigo and ataxia due to inflammation of internal auditory artery or its cochlear branch), nasal chondritis in 50% (producing saddle nose) and eye inflammation in 50% (producing conjunctivitis, episcleritis, scleritis and cataracts). Arthritis occurs in 1/3rd, which is asymmetric oligo or poly-articular involving both large and small joints, but more likely to involve costochondral, sternomanubrial and sternoclavicular cartilages, destruction of which may result in pectus excavatum or flial anterior chest.

Rheumatoid Arthritis It is a symmetrical polyarthrtis (but it may be asymmetric in few) affecting any of the diarthrodial joints but characteristically, proximal interphalangeal and metacarpophalangeal joints are involved with morning stiffness of 1 hour (see Fig. 13.107). Persistent inflammation leads to characteristic joint deformities in hands and feet. (i) Deformities in hands: ●

‘Z’ deformity: It is the radial deviation at the wrist with ulnar deviation of the digits often associated with palmar subluxation of proximal phalanges (see Fig. 13.108).

214

GENERAL PHYSICAL EXAMINATION

Fig. 13.108

deformity of the hand-radial | Zdeviation at the wrist with

Fig. 13.109

| Swan neck deformity in rheumatoid arthritis.

ulnar deviation of the digits in rheumatoid arthritis.

Swan neck deformity: There occurs hyperextension of the proximal interphalangeal joints with compensatory flexion of the distal interphalangeal joints (see Fig. 13.109). ● Boutonniere deformity: It involves flexion contracture of the interphalangeal joints and extension of the distal interphalangeal joints. ● Hyperextension of the first interphalangeal joint and flexion of the first metacarpophalangeal joint with a consequent loss of thumb mobility and pinch. (ii) Deformities in feet: ● Eversion at the subtalar joint (hind foot) ● Plantar subluxation of metatarsal heads ● Widening of the forefoot ● Hallux valgus and ● Lateral deviation of dorsal subluxation of the toes. ●

It can also involve wrist, elbow, knee (give rise to Baker’s cyst if extends to popliteal space) and upper cervical spine. Extra articular manifestations include: ●

● ●

●

●

Rheumatoid nodules (20–30%) on extensor surfaces (but may be seen in pleura, meninges) most commonly on olecranon bursa, proximal ulna, Achilles tendon and occiput in patients with circulatory rheumatoid factor (see Fig. 13.110). Pneumonitis, pulmonary nodules and pleuritis. Felty’s syndrome with splenomegaly, neutropenia (occasionally, anemia and thrombocytopenia). Diffuse necrotizing vasculitis resulting in digital gangrene, cutaneous ulcerations, visceral infarction (lungs, bowel, liver, spleen, pancrease, MI). Cardiovascular manifestations include pericarditis (50% of autopsy) which rarely leads to cardiac tamponade and constrictive pericarditis,65 valvular infiltration of rheumatoid nodules (1–2%) which may result in AR, MR66 and conduction defects when conduction tissue is involved.67

GENERAL EXAMINATION

Fig. 13.110

nodule over the | Rheumatoid elbow.

Fig. 13.112

Fig. 13.111

215

metatarso-phalangeal joint arthritis | Classical of greater toe in gouty arthritis.

| Gouty tophi in the ear helps in the diagnosis.

Gouty Arthritis Monosodium urate arthritis: ●

●

●

Usually one joint i.e. metatarsophalangeal joint of the first toe is involved (see Fig. 13.111) but may be polyarticular (tarsal joints, ankles and knees) especially in hypertensive males with ethanol abuse and in postmenopausal woman. The tophi in the ear (small hard nodules over the helix and antihelix) containing biurate crystals are pathognomonic of gout (see Fig. 13.112). Atherosclerosis and CAD are the most common cardiovascular manifestations, but conducting system, mitral, aortic and tricuspid valve leaflets may also be involved.

13. PERIPHERAL EDEMA Edema is defined as the excess accumulation of fluid in the subcutaneous tissues due to increase in the interstitial fluid volume.

216

GENERAL PHYSICAL EXAMINATION

i) Pathogenesis Water constitutes about 50% of body weight in women and 60% in men. This total body water is distributed in two major compartments: ● ●

55–75% (approximately 3/4th) is intracellular (i.e. intracellular fluid, ICF). 25–45% (approximately 1/3rd) is extracellular (i.e. extracellular fluid, ECF).

The ECF is distributed in the ratio of 1:3 between ● ●

Intravascular i.e. plasma and Extravascular i.e. interstitial fluid

which is regulated by Starling forces i.e. Liquid Accumulation  K (Pc–Pi)(c–i)Qlymph ●

●

●

●

●

●

●

Where K is the filtration coefficient across the capillary membrane, Pc is the mean intracapillary hydrostatic pressure, Pi is the mean interstitial hydrostatic pressure, c is the oncotic (colloid osmotic) pressure of plasma, i is the interstitial oncotic (colloid osmotic) pressure and Q lymph is the lymphatic flow. The intracapillary hydrostatic pressure and interstitial oncotic pressure tend to promote the movement of fluid from the capillaries to the interstitium (i.e. extravascular spaces), while the oncotic pressure of the plasma (mainly due to plasma proteins) and interstitial hydrostatic pressure promote the movement of fluid into the vascular compartment (i.e. into the capillaries). Fluid is returned from the interstitial spaces into the vascular system at the venous end of the capillary network through the lymphatics. And in an average adult (70 kg), the lymphatic flow is about 20 ml/h.68 Hence, edema occurs when one or more Starling forces are altered, to increase the flow of fluid from the vascular system into the interstitium (or into a body cavity) which exceeds the capacity of lymphatic drainage away from the interstitial spaces (i.e. lymphatic insufficiency). When the fluid moves from the vascular system into the interstitium, secondary consequences occur, i.e. there is a fall in the plasma volume (i.e. decrease in cardiac output) which activates renin angiotensin and sympathetic systems and thereby the kidneys retain Na and water in an attempt to maintain the blood (intravascular) volume. However, this increased blood volume results in an increased venous capillary hydrostatic pressure, promoting crossing over of large amount of fluid into the interstitial tissues and thus causing edema. However, in some cases of primary renal diseases, hepatic failure and certain drugs (side effects), the primary event itself is the renal retension of Na and salt, which results Table 13.25 Pathogenesis of peripheral edema 1. 2. 3. 4.

 Capillary hydrostatic pressure  Plasma oncotic pressure  Interstitial oncotic pressure Capillary endothelial damage

GENERAL EXAMINATION

217

in an increased plasma volume, thereby increasing the venous capillary hydrostatic pressure and thus forming edema (see Table 13.25 and Fig. 13.113). ii) Causes (1) Imbalance of Starling Forces (i) Increased capillary hydrostatic pressure is due to an increased blood volume or venous obstruction. Increased blood volume due to renal Na and salt retention (secondary consequence) as in CHF. Increased blood volume due to primary renal Na and salt retention as in: ● Renal failure ● Glomerulonephritis ● Early hepatic failure Hypothyroidism

Lyphatic obstruction/ insufficiency

↑ Capillary permeability

↑ πi

Protein loss: Nephrotic syndrome Protein losing enteropathy

Venous obstruction: Hepatic cirrhosis, Local venous obst. ↑ Blood volume (secondary): CHF

Imbalance of Starling forces

↑ Pc

↓ πc

↓ Albumin synthesis: Malnutrition liver disease

↑ Blood volume (primary): 1. Renal failure, glomerulonephritis 2. Vasodilators, NSAID, steroids, cyclosporine 3. Pregnancy

EDEMA

Capillary Endothelial damage

Trauma: Mechanical, thermal

Inflammation: Viral, bacterial

Hypersensitivity

Fig. 13.113

Drugs: Interleukin-2

of peripheral edema— : interstitial oncotic pressure,  : | Pathogenesis plasma oncotic pressure, P : capillary hydrostatic pressure, NSAID: noni

c

c

steriodal anti inflammatory drugs, CHF: congestive heart failure, obst.: obstruction.

218

GENERAL PHYSICAL EXAMINATION ●

● ●

Drugs: 1. Direct arterial/arteriolar vasodilators: Minoxidil, hydralazine, clonidine, methyldopa, guanethidine 2. Ca channel blockers 3. adrenergic blockers 4. Non-steroidal anti-inflamatory drugs 5. Steroid hormones: Glucocorticoids, anabolic steroids, estrogens, progestins 6. Cyclosporine. Pregnancy and premenstrual edema Idiopathic edema (in young menstruating women).

Venous obstruction: ● ●

Hepatic cirrhosis or hepatic venous obstruction Local venous obstruction.

(ii) Decreased plasma oncotic pressure due to protein loss or reduced albumin synthesis: Protein loss: ● ●

Nephrotic syndrome Protein losing enteropathy.

Reduced albumin synthesis: Malnutrition Liver disease. (iii) Increased interstitial oncotic pressure due to: ● Lymphatic obstruction (lymphatic insufficiency) ● Hypothyroidism and ● Increased capillary permeability. ● ●

(2) Capillary Endothelial Damage Increases its permeability and permits the transfer of proteins into the interstitial compartment. This occurs in: ● ● ● ●

Inflammation due to viral or bacterial agents Trauma: Mechanical or thermal (burns) Hypersensitivity reaction: Allergic reactions, characteristic of immune injury and Drugs used for immunotherapy: Interleukin-2, OKT3 monoclonal antibody.

iii) Types and Site of Peripheral Edema (i) Localized Edema is limited to one leg or one/both arms usually due to venous and/or lymphatic obstruction (trauma, inflammation or hypersenstivity). It may be limited to a body cavity as in ascitis, pleural effusion or pericardial effusion.

GENERAL EXAMINATION

219

(ii) Anasarca It is a gross generalized edema characterized by periorbital edema (soft tissues of eyelids & face) and bilateral leg edema. Common causes include nephrotic syndrome, hypoproteinemia and severe congestive heart failure. (iii) Leg Edema It could be bilateral or unilateral (see Table 13.26); pitting or non-pitting. For pitting edema, a firm pressure is applied for 10–20 sec (30 sec) for detection. It is frequently detected in: ● ●

●

The region of ankles ( especially in ambulatory patients) The presacral region, trochanters, or the back of the thighs (especially in patients confined to bed/recumbent patients) and The region of the genital organs (particularly, the scrotum).

Bilateral pitting leg edema: occurs in ● ● ● ● ● ●

● ●

Congestive heart failure (see Fig. 13.114) Constrictive pericarditis (may be associated with ascites) Renal causes: glomerulonephritis, nephrotic syndrome (may have ascites) Cirrhosis of liver (associated with ascites) Protein-losing enteropathy Nutritional causes: hypoproteinemia, anemia (when Hb is 5 g/dl), wet beriberi, epidemic dropsy Physiological: pregnancy and premenstrual edema Idiopathic edema.

Table 13.26 Causes of leg edema Bilateral pitting

Unilateral pitting

1. CHF

1. Trauma

2. Constrictive pericarditis 3. Renal: glomerulonephritis, nephritic syndrome 4. Cirrhosis of liver (later stages) 5. Protein losing enteropathy 6. Nutritional: anemia, hypoproteinemia 7. Pregnancy, premenstrual edema 8. Idiopathic

2. Inflammation 3. Baker’s cyst 4. Varicose veins 5. Deep vein thrombophlebitis 6. Congenital venous malformations

Bilateral non-pitting

Unilateral non-pitting

1. Myxedema

1. Lymphatic obstruction: filariasis radiation trauma, malignancy 2. Milroy’s disease

220

Fig. 13.114

GENERAL PHYSICAL EXAMINATION

pitting leg edema in congestive heart | Bilateral failure.

Fig. 13.115

myxedema in Graves | Pretibial disease.

Bilateral nonpitting leg edema may occur in ●

Myxedema (see Fig. 13.115).

Unilateral pitting leg edema could be of: (i) Acute onset (72 hours): due to ● ●

Trauma: Mechanical or thermal (burns). Inflammation:69 – Bacterial cellulitis (see Fig. 13.116) – Acute deep venous thrombophlebitis – Popliteal (Baker’s) cyst – Erythema nodosum.

(ii) Late onset (72 hours): as in ● Chronic venous insufficiency: It may also cause bilateral leg edema. The most common causes are: – Varicose veins – Deep venous thrombosis – Congenital venous malformations. ● Reflex sympathetic dystrophy due to trauma, infection and vascular insufficiency, which is characterized by burning pain, hyperesthesia, hyperhydrosis, trophic changes of skin and swelling of the affected limb. ● Bone and soft tissue tumors may also cause unilateral leg edema. ● Paralysis can reduce lymphatic and venous drainage of the affected side and produce edema. Unilateral non-pitting leg edema is usually due to lymphedema. Initially, it may be pitting but later, the limb develops a woody texture and edema is no longer pitting. This occurs in: ●

Lymphatic obstruction due to infection (classical example being filariasis which often involves scrotum and penis, see Fig. 13.117 and Table 13.27), radiation, surgery, trauma, or malignancy.

GENERAL EXAMINATION

221

Elephantiasis of penis — Ram’s horn penis Lymphoedema scrotum

Lymphoedema leg

Fig. 13.116

leg in acute | Unilateral cellulites.

Fig. 13.117

non-pitting edema of the leg in filariasis | Unilateral with scrotum and penis involvement.

Table 13.27 Stages/grades of filarial lymphedema

●

Stages

Edema

Other characters

1. Stage-I

Pitting

2. Stage-II

Pitting

3. Stage-III 4. Stage-IV

Non-pitting Non-pitting

Edema completely relieved on rest and leg elevation. No skin changes Edema partially relieved on rest and leg elevation. No skin changes Thickening of the skin and subcutaneous tissue Lymphorrhea and elephantiasis present

Congenital lymphatic malformation: Milroy’s disease (chronic hereditary edema, a rare familial disorder).

iv) Characteristics of Peripheral Edema ● ●

●

●

In hypoproteinemia, edema is most pronounced in the morning, Edema associated with CHF tends to be more extensive in the legs and is accentuated in the evenings. However, edema is most prominent in the presacral region in CHF in bed-ridden patients. Edema due to renal causes (glomerulonephritis, nephritic syndrome) is initially most prominent in the periorbital area (puffiness of face) followed by leg edema. In cirrhosis of liver: Initially, the patient has ascites, and edema occurs in other parts of the body including lower extremities because of hypoalbuminemia, and impedence of venous return from the lower limbs due to increased intrabdominal pressure from ascites.

222

GENERAL PHYSICAL EXAMINATION

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■■■

CHAPTER 14

A RTERIAL P ULSE 1. DEFINITION 2. GENESIS OF THE ARTERIAL PULSE 3. PULSE WAVE PATTERN i. In Ascending Aorta ii. In Peripheral Arterial Pulse 4. EXAMINATION OF THE ARTERIAL PULSE i. Rate of the Pulse ii. Rhythm iii. Character of the Pulse

225 225 226 226 226 228 231 232 233

iv. v. vi. vii.

Volume of the Pulse Condition of the Vessel Wall Radial Pulse Synchronocity Absent or Delayed Femoral Pulsations 5. CHARACTERISTIC FEATURES OF PULSE IN COMMON CLINICAL CONDITIONS i. Aortic Stenosis ii. Aortic Regurgitation REFERENCES

244 245 245 245

246 246 246 248

1. DEFINITION Pulse is a Greek word meaning ‘move to and fro’. Arterial pulse is a wave produced by cardiac systole traversing in the peripheral direction in the arterial tree at a rate faster than the column of blood (speed of the pulse wave is 5 m/sec or 18 km/h, while the blood flows at a speed of 0.5 m/sec or 1.8 km/h).

2. GENESIS OF THE ARTERIAL PULSE ●

●

●

Despite early significance attached to the pulse, its origin in the heart was not considered till Herophilus in 344 BC. The arterial pulse wave (first described by Broadbent in 1890) begins with the aortic valve opening and onset of left ventricular (LV) ejection, when the LV pressure exceeds the aortic pressure and the LV pressure becomes the driving force for the movement of blood into the ascending aorta.1 The pulse wave consists of two positive deflections during systole (upstroke) and one deflection during diastole (descending limb). The first shoulder during systole is the ‘percussion wave’ due to the arrival of the impulse generated by LV ejection; the second is the ‘tidal wave’ due to reflection from upper part of the body. Whereas the ‘dicrotic or diastolic wave’ is due to reflection from the lower part of the body.2

226

GENERAL PHYSICAL EXAMINATION Tidal wave Dicrotic notch Dicrotic wave

Anacrotic notch

Percussion wave S1

Fig. 14.1

●

●

S2

| Normal arterial pulse.

The peripheral arterial pulse wave recorded is the summation of initial generated wave (in the ascending aorta) and reflected waves from upper and lower parts of the body (see Fig. 14.1). The driving force of the LV is dependent on: – The intrinsic contractility of the ventricular muscle – The size and shape of the LV – The heart rate. However, the forward flow of the blood (LV ejection) also depends on: – Resistance offered by the blood viscosity and geometry of the vasculature – Inertia produced by the mass of the blood column and – Compliance of the vasculature.

3. PULSE WAVE PATTERN i. In Ascending Aorta ●

●

●

●

●

Pulse wave normally rises rapidly to a rounded dome (percussion and tidal waves) which reflects the peak velocity of the blood ejected from the LV. A slight anacrotic notch (ana: up, again, krotos: to beat) is occasionally felt but frequently recorded on the ascending limb of the pulse. The descending limb is less steep than the ascending limb and is interrupted by an incisura, a sharp downward deflection due to closure of the aortic valve. The pulse wave then rises slightly (dicrotic wave) and thereafter declines gradually throughout the diastole. Ascending aorta, innominate and carotid arteries represent the central arterial pulse (see Fig. 14.2 and Table 14.1). However, clinically the carotid arterial pulse provides the most accurate representation of the central aortic pulsation.

ii. In Peripheral Arterial Pulse ●

Brachial, radial and femoral arteries represent the peripheral arterial pulse (see Fig. 14.2 and Table 14.1). However, the brachial artery is most suitable for appreciating

ARTERIAL PULSE

227

A

Ascending aorta

High descending aorta

Innominate artery

B

Subclavian artery

Fig. 14.2

Brachial artery

| Pulse wave pattern in central and peripheral arteries.

Table 14.1 Pulse wave pattern Central artery (aorta)

Peripheral artery (brachial)

1. Upstroke rises to a rounded dome 2. Ascending limb has an anacrotic notch

Upstroke is steeper Anacrotic notch in the ascending limb disappears Incisura in descending limb is replaced by dicrotic notch followed by dicrotic wave

3. Descending limb has incisura followed by dicrotic wave

●

●

●

●

●

●

the rate of rise of pulse, contour, volume and consistency of the peripheral vessels. As the normal aortic pulse wave is transmitted peripherally (reaches carotid at 30 ms, brachial 60 ms, radial 80 ms, and femoral at 75 ms), significant changes in its contour occur due to: – Distortion and damping of the pulse wave components. – Different rates of transmission of various components. – Distortion or exaggeration by reflected waves. – Conversion of kinetic energy into hydrostatic or potential energy. – Differences in distensibility and caliber of the arteries and – Changes in the vessel wall due to age and/or disease.3 As the pulse wave travels peripherally; the pulse pressure increases, upstroke (ascending limb of the pulse wave) becomes steeper, and systolic peak (percussion wave) becomes higher but the tidal wave is less significant. The anacrotic shoulder disappears, and the sharp incisura is replaced by a smoother and later dicrotic notch, followed by a dicrotic wave, which probably results from the summation of the forward pulse wave and reflected waves from the peripheral vessels. Normally, anacrotic notch, tidal wave, dicrotic notch and dicrotic wave are not palpable. Normally, percussion wave is more prominent than tidal wave. However; in older patients with increased systemic vascular resistance, arteriosclerosis and diabetes mellitus, the tidal wave may be somewhat higher than the percussion wave (i.e. late systolic peak). The height of the dicrotic wave decreases with age, hypertension and arteriosclerosis.

228

GENERAL PHYSICAL EXAMINATION

4. EXAMINATION OF THE ARTERIAL PULSE Ejection of blood with every cardiac contraction is converted into: i. Flow pulsations: i.e. longitudinal movement of blood along the arterial lumen which can be measured by electromagnetic flow meters and Doppler ultrasonic probe. ii. Pressure pulsations: The amplitude of the arterial pulse perceived by the clinician in a large accessible artery is the pressure pulse. Clinician’s perception of pulse is formed by the tactile receptors (Meissener’s corpuscles, Pacinian corpuscles and Merkel’s discs) that mediate the tactile sensation on the finger-tips. Varying degrees of pressure (which is known as trisection method ) should be applied to assess the upstroke, systolic peak and diastolic slope of the pulse.3 All major arterial pulses should be bilaterally examined for: ● ● ● ● ● ● ●

Rate of the pulse Rhythm Character Volume Condition of the arterial wall (thickness) Equal (synchronous) or inequality of the radial pulses and Presence or absence of delay of the femoral pulses compared with radials.

The radial pulse is felt with the tips of the fingers (preferably three: index, middle, and ring) compressing the vessel against the head of the radius, with the patient’s forearm slightly pronated and the wrist slightly flexed (see Fig. 14.3). The brachial artery is compressed against the humerus just above the antecubital fossa. The examiner should use either the left thumb or fingertips when examining the patient’s right brachial artery and vice versa (see Fig. 14.4). The carotid (common carotid) is gently examined one at a time best with the thumb (left thumb for patient’s right carotid and vice versa) with the sternocleidomastoid muscles relaxed and the head rotated slightly towards the examiner. It should be palpated

Fig. 14.3

| Examination of the radial pulse.

ARTERIAL PULSE

Fig. 14.4

| Examination of the brachial pulse.

Fig. 14.6

Fig. 14.5

229

| Examination of the carotid pulse.

| Examination of the femoral pulse.

in the lower half of the patient’s neck in order to avoid carotid sinus compression (see Fig. 14.5). The femoral arteries lie midway between the iliac crest and pubic ramus and are palpable against the underlying femur (see Fig. 14.6). The popliteals are best examined with the patient’s knee flexed at an angle of 120. The fingertips of both hands are placed in the popliteal fossa with the thumbs resting on the patient’s patella (see Fig. 14.7). The posterior tibial pulse is found 1 cm behind the medial malleolus of the tibia. The patient’s foot should be relaxed between plantar and dorsiflexion (see Fig. 14.8). The dorsalis pedis pulse is commonly felt between the tendons of 1st and 2nd toes, 5–7.5 cm below the joint crevice. It is compressed against the tarsal bones and the patient’s left dorsalis pedis is mostly examined with the fingers of the right hand and vice versa (see Fig. 14.9). ●

The dorsalis pedis and posterior tibial are impalpable in about 2% of normal individuals due to anomalous course.

230

GENERAL PHYSICAL EXAMINATION

Fig. 14.7

of the popliteal pulse–flex the patient’s knee at an angle of 120 | Examination and place fingers of both hands in the popliteal fossa with thumbs resting on the patient’s patella.

Fig. 14.8

of the posterior tibial pulse— | Examination patient’s foot relaxed between plantar and

Fig. 14.9

of the dorsalis pedis | Examination pulse.

dorsiflexion.

●

●

Sublingual nitroglycerine often resolves the doubt by rendering a temporarily absent dorsalis pedis or posterior tibial pulse readily palpable. In peripheral arterial occlusion, passive leg elevation intensifies the pallor in the affected limb.

The examination of the arterial pulses is tabulated using a scale as follows: ● ● ● ● ●

0 Complete absence of pulsation. 1 Small or feeble/reduced pulsation. 2 Palpable but diminished as compared to other side. 3 Normal pulsation. 4 Large or high volume/bounding pulsation.

ARTERIAL PULSE

231

Besides palpation, auscultation over the major arteries should be performed as audible bruit may give a clue to partial occlusion or transmission of a cardiac murmur (e.g. mid systolic murmur of AS may be conducted to the carotids). ● ● ●

50% obstruction of an artery may produce ⇒ a short systolic bruit. 80% obstruction of an artery may produce ⇒ a continuous bruit. 80–100% obstruction of an artery may produce ⇒ no audible bruit.

i. Rate of the Pulse ● ●

●

Examine whether the patient has tachycardia, bradycardia or pulse deficit. The range of rates of normal sinus rhythm in an adult person is between 60 and 100 beats per minute. However, the average rate of pulse in children depends upon the age and is as follows: 1 week of age 140/min, 1 yr of age 120/min, 6 yrs of age 100/min and at puberty 80/min.

(1) Tachycardia i) Sinus tachycardia: tachycardia.

A sinus rate above 100 beats per minute is defined as sinus

Causes of sinus tachycardia: ●

●

Physiological: It occurs in infancy and early childhood and in response to exercise, excitement, anxiety and other emotional stresses. Pharmacological: It results from medications or drugs. – Medications: Amyl nitrate, epinephrine, isoproterenol, ephedrine, atropine – Intoxicants: Exposure to alcohol, nicotine or caffeine.

●

Pathological: – Cardiovascular causes include congestive heart failure, acute myocardial infarction, pulmonary embolism, myocarditis or shock. – Non-cardiac causes include fever, anemia, thyrotoxicosis, hemorrhage, hypotension and hypoxemia.

ii) Tachyarrhythmias ● ●

●

Most tachycardias associated with a regular pulse are of supraventricular origin. Tachycardia with irregular pulse may be due to ventricular tachycardia and AV dissociation with variation in atrio-ventricular sequence of contraction. The resulting variation in pulse amplitude may often be detected by palpation.4 An irregularly irregular pulse with varying pulse pressure is usually due to atrial fibrillation or multifocal atrial tachycardia.

(2) Bradycardia i) Sinus bradycardia: bradycardia.

A sinus rate of 60 beats per minute is defined as sinus

232

GENERAL PHYSICAL EXAMINATION

Causes of sinus bradycardia: ●

●

●

Physiological (asymptomatic bradycardia) occurs usually in athletes (training effect) and during sleep. Pharmocological: Bradycardia resulting from medications include beta-blockers, amiodorone, propafenone, lithium, and other parasympathomimetic drugs. Pathological (symptomatic bradycardia): – Cardiovascular causes: Bradycardia occurs in inferior wall MI., SA block, during coronary angiography, following cardiac transplantation and in vasovagal syncope. – Non-cardiac causes include myxedema, increased intracranial pressure (due to meningitis, intracranial tumors), Chagas disease, hypothermia, mental depression, obstructive jaundice, enteric fever, gram negative sepsis and eye surgery.

ii) Bradyarrhythmias: They are usually due to AV conduction abnormalities especially with second degree AV block and complete heart block. (3) Pulse Deficit ●

●

The difference between the radial pulse rate and the heart rate (usually counted by auscultation) is defined as pulse deficit. It occurs in tachyarryhthmias. A pulse deficit of 6/min is diagnostic of atrial fibrillation and 6/min can occur in premature ventricular contractions (PVCs).

Mechanism of pulse deficit ●

●

In tachyarrhythmias, the diastole is shortened and subsequent systolic stroke volume is insufficient to cause opening of the aortic valve therefore, the arterial pulse will be non-existent inspite of the cardiac contraction. As diastole becomes longer in subsequent cardiac cycles, the stroke volume gradually increases and arterial pulse is felt.

ii. Rhythm The normal pulse is regular in rhythm. If the pulse is irregular, note whether it is regularly irregular or irregularly irregular. (1) Regularly Irregular Pulse It occurs in: (see Table 14.2) i) Sinus arrhythmia: Sinus arrhythmia is present when the variation between the longest and the shortest cycle (P–P interval) exceeds 0.12 s. Table 14.2 Causes and types of irregular pulse Regularly irrregular pulse

Irregularly irregular pulse

1. 2. 3. 4.

1. Atrial fibrillation 2. Multifocal atrial tachycardia 3. Frequent PVCs

Sinus arrhythmia Pulsus bigeminus (due to PVCs) Pulsus alternans Partial (1st and 2nd degrees) heart blocks

ARTERIAL PULSE ●

●

● ●

233

It is defined as ‘phasic sinus arrhythmia’ if the cycle lengths shorten with inspiration (pulse rate increases) and lengthen with expiration (pulse rate decreases). It is referred as ‘nonphasic sinus arrhythmia’ if it is unrelated to the respiration, and it may related to digitalis intoxication. Normally, it is most common in children. It decreases with age and in autonomic dysfunction and hence is considered as a risk factor for sudden cardiac death.

ii) Premature ventricular contractions (PVCs): PVCs at regular intervals (bigemini or trigemini pattern) cause regularly irregular pulse. Causes of PVCs include: ● Physiological: exercise ● Pharmacological: Either medications or intoxicants – Medications: Digoxin toxicity – Intoxicants: Intake of alcohol and coffee (caffeine) or smoking (nicotine). ● Cardiovascular causes (usually with structural heart diseases): Coronary artery disease (CAD) including acute myocardial infarction, post thrombolysis or percutaneous trans-coronary angioplasty (PTCA), myocarditis, pericarditis, cardiomyopathy, hypertensive heart disease and mitral valve prolapse. iii) Partial (1st and 2nd degree) heart blocks: Partial heart blocks usually produce regularly irregular pulse. They can occur during exercise, in CAD especially in AMI and in myocarditis. Drugs such as digitalis and propronolal may also produce partial heart blocks. (2) Irregularly Irregular Pulse Atrial fibrillation, multifocal atrial tachycardia and frequent PVCs produce irregularly irregular pulse. iii. Character of the Pulse It is best evaluated by palpation of the carotid pulse. Following are the abnormal types of pulses depending upon the character of the pulse: (1) Pulsus Tardus (Slow Rising Pulse) ●

●

Slow rising pulse with delayed systolic peak (nearer to S2) and upstroke, frequently associated with a thrill in the carotids (carotid shudder) is characteristic of AS, and often occurs with pulsus parvus (i.e. pulsus parvus et tardus) (see Fig. 14.10). It is better appreciated by simultaneous auscultation and carotid palpation, and the presence of pulsus tardus indicates atleast 70 mmHg of pressure gradient in AS.

(2) Water-Hammer (Collapsing) Pulse or Corrigan Pulse or Pulsus Celer It is characterized by rapid upstroke (percussion wave) followed by rapid descent (collapse) of the pulse wave without dicrotic notch, which reflects low systemic vascular resistance (see Fig. 14.11).5

234

GENERAL PHYSICAL EXAMINATION

EIOQ B4 B1 EC

ESM A 2

S4 S1

EC

ESM

A2

Phono

Carotid

Fig. 14.10

Pulsus parvus et tardus

| Pulsus parvus et tardus in aortic stenosis.

150 100 50 0

Fig. 14.11

● ●

| Water hammer pulse in aortic regurgitation.

Rapid upstroke is due to the rapid ejection of greatly increased stroke volume. The rapid descent or collapsing character is due to: (i) Diastolic ‘run-off ’ (back flow) into the left ventricle (ii) Reflex vasodilatation mediated by carotid baroreceptors secondary to large stroke volume (iii) The rapid run-off to the periphery due to decreased systemic vascular resistance.

Water-hammer pulse ●

●

Thomas Watson (1844), an English Physician, named this term after a Victorian toy, which refers to the rapid and forceful ascending limb of the arterial pulse. Water-hammer consisted of a sealed glass tube containing water in a vacuum.

As solids and liquids fall at the same rate in vacuum, so when this glass tube is quickly inverted, water column falls abruptly from one end of the tube to the other and finger tip holding the inverted end senses a sudden impact or jolt. Detection: It is best appreciated at the radial pulse with the palmer side of the patient’s wrist held in the examiner’s hand and with the patient’s arm suddenly elevated above the shoulder. This may be related to the artery becoming more in line with the central aorta, allowing direct systolic ejection and diastolic backward flow (see Figs 14.12A and 14.12B).

ARTERIAL PULSE A

Fig. 14.12

235

B

of water hammer pulse. (A) The palmer side of patient’s wrist is | Detection held in the examiner’s hand. (B) The patient’s arm elevated suddenly above the shoulder.

Table 14.3 Causes and types of pulse depending upon the character Pulsus tardus

Collapsing pulse

1. Aortic stenosis

1. Hyperkinetic circulatory states 2. Aortic regurgitation, patent ductus arteriosus, aortopulmonary window, RSOV into right heart, arteriovenous fistula 3. Truncus arteriosus with truncal sufficiency, PAt with bronchopulmonary collaterals, TOF with bronchoplumonary collaterals, TOF after BT shunt

RSOV: rupture of sinus of Valsalva, PAt: pulmonary atresia, TOF: tetrology of Fallot, BT: BlalockTaussig.

Causes i) Conditions with aortic run-off: AR, PDA, AP window, rupture of sinus of Valsalva into the right chambers and arteriovenous fistula. ii) Cyanotic congenital heart diseases: Truncus arteriosis with truncal run-off into PA or truncal insufficiency, pulmonary atresia with bronchopulmonary collaterals, TOF with bronchopulmonary collaterals/associated PDA/associated AR or after Blalock Taussig (BT) shunt (systemic artery to pulmonary artery). iii) Hyperkinetic circulatory states: Pregnancy, anemia, thyrotoxicosis, Beriberi, fever and Paget’s disease of the bone (see Table 14.3). (3) Twice Beating Pulse It includes anacrotic pulse, pulsus bisferiens, and dicrotic pulse (see Table 14.4).

236

GENERAL PHYSICAL EXAMINATION

Table 14.4 Causes of twice beating pulse Anacrotic pulse

Bisferiens pulse

Dicrotic pulse

1. AS

1. Hyperkinetic circulatory states 2. AR, PDA

1. Enteric fever 2. Cariomyopathy, cardiac tamponade, myocarditis 3. Hypovolemic shock 4. During intraoartic balloon pump

3. ARAS 4. Hypertrophic obstructive cardiomyopthy

A

B

S4

S1

P2 A2

Dicrotic notch

Fig. 14.13

S4

S1

P2 A2

Dicrotic notch

pulse. (A) Normal pulse, (B) anacrotic pulse in AS with distinct | Anacrotic anacrotic and percussion waves on the upstroke.

(a) Anacrotic pulse ●

●

In the slow rising pulse (pulsus tardus), a distinct notch (anacrotic) on the upstroke of the carotid pulse with two separate waves (anacrotic and percussion) can be palpated. This is characteristically found in AS (see Fig. 14.13). Lower the notch, severe is the AS, and the presence of anacrotic pulse indicates 70 mmHg pressure gradient.

(b) Bisferiens Pulse (Bisferiens is a Latin word, Bis  two, ferise  to beat): It is characterized by two systolic peaks (percussion and tidal waves) separated by a distinct midsystolic dip (see Fig. 14.14). Causes and mechanism of bisferiens pulse: i) Conditions with large stroke volume: ● It occurs in conditions in which a large stroke volume is rapidly ejected from the LV as in severe AR, PDA, hyperkinetic circulatory states. ● Normally, the percussion wave is felt but not the tidal wave (these waves are due to the elastic recoil of aorta and reflected wave from the periphery respectively). Hence in situations where the initial percussion wave is exaggerated due to large stroke volume (as in severe AR), the tidal wave also becomes prominent. ii) Combination of slow rising and collapsing pulse: ● Bisferiens pulse also occurs in patients with combined AS and AR, a combination of slow rising and collapsing pulses.

ARTERIAL PULSE A

B

S4

P2 A2

S1

S4

C

P2 A2

S1

S4

P2 A2

S1 P

P

Dicrotic notch

Fig. 14.14

237

T

T

Dicrotic notch

Dicrotic notch

Bisferiens. (A) Normal pulse, (B) pulsus bisferiens in AR with equal | Pulsus percussion (P) and tidal (T) waves, (C) pulsus bisferiens (Spike and dome pulse) in HOCM with prominent percussion (P) wave.

●

The stenosis permits a jet lateral to the increased velocity of jet which causes a fall in pressure (Bernoulli phenomenon) and results in a dip in the pulse wave with a secondary outward movement (prominent tidal wave).

iii) Hypertrophic obstructive cardiomyopathy (HOCM): Bisferiens pulse may also occur in HOCM.6 However, it is usually recordable but not palpable. ●

●

●

●

The initial percussion wave is due to rapid ejection of blood into the ascending aorta during early systole. The midsystolic dip (negative wave) coincides with marked decrease in the rate of LV ejection, as the left ventricular outflow tract obstruction becomes manifest due to the thickening of interventricular septum and the systolic anterior motion (SAM) of anterior mitral leaflet. The second systolic (tidal) wave is most likely produced by reflected waves from the periphery. Hence, pulse of HOCM behaves partly like AR (initial component) and partly as AS (second component), but percussion wave is more prominent than the tidal wave.

iv) Normals: Rarely seen in normal individuals. Other characteristic features ● ● ●

The two waves are equal or tidal wave is prominent in AR, ARAS. In HOCM, percussion is more prominent than tidal wave. Bisferiens pulse disappears when the heart failure supervenes.

Detection: It is readily detected by palpating the carotids. ●

●

However, the presence of carotid systolic thrill may mask the features of bisferiens pulse, in which case peripheral pulses like the radial or brachial are suitable for detection of this pulse. Apply graduated pressure or completely obliterate the pulse and gradually release it to appreciate the two waves.

238

GENERAL PHYSICAL EXAMINATION A

B

S4

S1

P2 A2

S4

S1

P2 A2 Dicrotic wave

Dicrotic notch

Fig. 14.15

Dicrotic notch

pulse. (A) Normal pulse, (B) dicrotic pulse in hypovolemics shock | Dicrotic with prominent dicrotic wave.

(c) Dicrotic pulse (Dicrotic is a Greek Word, di  two, krotos  beat): It is characterized by two peaks, one in systole (percussion wave) and the other in diastole (dicrotic wave) immediately after S2, which is due to accentuated and palpable reflected wave from the periphery7 (see Fig. 14.15). Commonly seen in low output states such as: ● ● ● ● ● ●

Enteric fever or any fever with vasodilatation due to the circulating vascular toxins. Cardiomyopathy Cardiac tamponade Myocarditis Hypovolemic shock and During intraoartic balloon pump (IABP).

Detection: It can be felt in carotids, but can be better appreciated in the radial artery. ●

●

It is better appreciated during inspiration and with the inhalation of amylnitrate. But it is unusual when the systolic pressure is 130 mmHg. Simultaneous auscultation is helpful as it occurs immediately after S2.

(4) Irregularly Regular Pulse It consists of pulsus bigeminus and pulsus alternans. (i) Pulsus bigeminus: It is an irregular rhythm caused by premature contractions (usually PVCs) resulting in the alteration of the strength of the pulse which may be confused with pulsus alternans (see Fig. 14.16). ●

●

●

However, in pulsus bigeminus, the weak beat always follows the short interval and the long compensatory pause following a premature beat is followed by a stronger than normal pulse in normal individuals or in states of fixed left ventricular outflow tract obstruction such as AS. Stronger pulse is due to more diastolic filling following long compensatory pause and extrasystolic potentiation of ventricular contraction. Pulsus bigeminus may also be seen in AV blocks and atrial flutter with block.

ARTERIAL PULSE

EKG

VPC

Carotid

Fig. 14.16

239

VPC

Pulse – bigeminy

| Pulsus bigeminus and ventricular premature contraction (VPC). 120

mmHg

Strong beat

Weak beat

80

Fig. 14.17

| Pulsus alternans.

Brockenbrough sign is fall or failure to increase the pulse volume in the post extra systolic beat. This sign occurs in: ●

●

●

HOCM due to post extra systolic potentiation of dynamic left ventricular outflow tract obstruction Constrictive pericarditis due to failure to fill the ventricles more even after longer diastolic periods due to constriction Severe LV dysfunction due to failure to augment contraction inspite of more preload.

(ii) Pulsus alternans: (Traube, 1872) It is a regular rhythm in which a strong beat alternates with a weak beat and is related to alternating more number of contractile elements and loss of contractile elements participating in each contraction8 (see Fig. 14.17). It is frequently precipitated by PVCs and is a sign of severe LV dysfunction. Types ●

● ●

●

Total: When the weak beat is not perceived at all or when involving both sides of the heart. Partial: When involving only RV (as in PE) or LV (as in AS). Right atrial pulsus alternans: Severe right ventricular failure rarely associated with tall ‘a’ and ‘v’ waves that alternate with short ‘a’ and ‘v’ waves of right atrial pressure. Compound pulsus alternans: Additional alteration involving the weak beats in association with a usual alteration of strong and weak beats is said to have compound pulsus alternans.

240

GENERAL PHYSICAL EXAMINATION

Causes ● ● ●

Severe AS (often with failure) Dilated cardiomyopathy, myocarditis Acute pulmonary embolism and severe pulmonary stenosis.

Detection: It is better appreciated in the peripheral pulses (radial and femoral). ●

●

●

●

●

Readily recognized and confirmed by sphygmomanometry, generally accompanied by alteration in the intensity of Korotkoff ’s sounds and occasionally by alteration in the intensity of heart sounds and murmurs. When systolic pressure alternates by 20 mmHg, it can be readily detected by palpation of a peripheral pulse (radial or femoral) than a central pulse (like carotid). Palpation should be carried out with light pressure and with patient’s breath held in mid expiration to avoid the superimposition of respiratory variation on the amplitude of the pulse. It is accurately quantified by the determination of intra-arterial pressure by catheterization. The maneuvers, which exaggerate the pulsus alternans, help in its detection. It is exaggerated: – By decreasing the venous return by adopting upright posture or by infusion of nitroglycerine – And in the presence of aortic regurgitation or systemic hypertension.

(5) Pulsus Paradoxus ●

●

It is defined as an exaggerated decrease in the strength (amplitude) of the arterial pulse during normal quiet inspiration due to the exaggeration of normal inspiratory decline in the systolic arterial pressure of 10 mmHg, reflecting an exaggerated inspiratory decline of 7% in the LV stroke volume9 (see Table 14.5). The term ‘pulsus paradoxus’ was coined by Kussmaul (1873). It is defined as the apparent paradox of disappearance of pulse during inspiration despite the presence of heart beat.

Detection: ●

●

When the inspiratory decline of systolic arterial pressure is 20 mmHg, pulsus paradoxus is easily detected by the palpation of radial or brachial artery as an inspiratory decline in the amplitude of the pulse. Milder degrees of paradoxical pulse can be readily detected by sphygmomanometry. The cuff should be inflated 20 mmHg above the systolic pressure and slowly deflated at a rate of 2 mmHg/heart beat, when the Korotkoff sounds are heard only during expiration (i.e. peak systolic pressure during expiration). The cuff is further deflated more slowly to the point at which Korotkoff sounds are heard equally well in both inspiration and expiration. The difference between these two pressures is the estimated magnitude of pulsus paradoxus. The patient should be breathing normally and should not take a deep breath as normal individuals can have pulsus paradoxus with deep breathing.

ARTERIAL PULSE

241

Table 14.5 Pulsus paradoxus

●

Cardiovascular causes

Pulmonary causes

1. 2. 3. 4. 5.

1. COPD

Cardiac tamponade Effusive constrictive pericarditis Restrictive cardiomyopathy Massive pulmonary embolism Severe hypovolemic shock

Absence of pulsus paradoxus when CT is associated with 1. 2. 3. 4.

ASD VSD AR Pericardial adhesions

The magnitude of the paradoxical pulse can be accurately quantified by means of an intra arterial catheter, but cuff sphygmomanometry is sufficient for bed side evaluation.

Causes Physiological: ● ● ●

Pregnancy Extreme obesity Student’s paradox (exaggerated inspiration voluntarily).

Cardiovascular: ● ● ● ● ●

Cardiac tamponade Effusive constrictive pericarditis (in 50%) Massive pulmonary embolism Severe hypovolemic shock (due to hemorrhage or septic shock) Restrictive cardiomyopathy

Pulmonary: ●

COPD: Severe emphysema, acute severe bronchial asthma, upper airway obstruction

Mechanism of pulsus paradoxus ●

●

●

Normally, inspiration results in fall of intrapericardial pressure (IPP, from 3 mmHg to 6 mmHg) which causes increase of right ventricular transmural pressure and venous return with slight changes in right and left ventricular sizes (see Fig. 14.18). In pulsus paradoxus inspiration causes a decline in elevated intrapericardial pressure (often from 20 mmHg to 18 mmHg) and right atrial pressure that results in the increase of RV transmural (distending) diastolic pressure which augments the venous return and the filling of the right heart. This in turn results in: (1) The increase in RV (diastolic) dimensions producing flattening and leftwards shift of the interventricular septum thereby compressing the LV (i.e. ⇓ LV dimensions and compliance) that impedes LV filling and decreases LV output and systolic arterial pressure.10 (2) The increase of intrapericardial pressure and fall of the LV transmural diastolic pressure which further impedes LA and LV filling, fall in LV output and decrease of systolic arterial pressure11 (see Figs 14.19 and 14.20). This can be substantiated by echocardiography.12

242

GENERAL PHYSICAL EXAMINATION

Pericardium

Pericardial space Normal expiration-IPP: -3 mmHg

Fig. 14.18

Normal inspiration-IPP: -6 mmHg

hemo-dynamic effects of respiration: Inspiration results in fall of | Normal IPP, which causes an increase of RV transmural pressure (RVTP

RVEDP IPP) and increase in venous return. This in turn, results in slight increase in RV size at the expense of a slight decrease in LV size due to displacement of IVS from right to left. (IPP: intrapericardial pressure, RVTP: right ventricular transmural pressure, RVEDP: right ventricular end diastolic pressure, IVS: interventricular septum).

Fig. 14.19

of pulsus paradoxus in Cardiac tamponade: Inspiration results | Mechanism in the fall of elevated intrapericardial pressure (often from 20 mmHg to 18 mmHg) which causes an increase in RV transmural pressure and augments venous return. This in turn further increase in RV size and causes septal bulging towards LV, which further decreases LV size, LV output and arterial pressure.

Additional factors for pulsus paradoxus ●

●

Inspiratory pooling of blood in the pulmonary bed (pulmonary veins and capillaries) (i.e. increase of hang out interval) produces decline in LA and LV filling and LV stroke volume and systolic arterial pressure.11 The underfilled LV (LV volume is decreased in cardiac tamponade) may be operating in the steep ascending limb of Starling curve so that any inspiratory reduction

ARTERIAL PULSE

Fig. 14.20

Pulsus paradoxus

↓ Systolic arterial pressure

Inspiration

Pulmonary vascular pooling

↓ LV filling & output

↓ Elevated IPP

↓ LVTP

↓ LV dimensions & compliance

↑ RVTP

↑ IPP

LV compression

↑ RA & RV filling

↑ RV volume & size

Left shift of IVS

243

of pulsus paradoxus—IPP: intrapericardial pressure, RVTP: right | Mechanism ventricular transmural pressure, LVTP: left ventricular transmural pressure, IVS: interventricular septum.

●

of LV filling results in marked depression of the LV stroke volume and the systolic pressure.13 Pulsus paradoxus in COPD: The decrease in lung compliance magnifies the normal inspiratory decrease in LV volume and systolic arterial pressure and expiration may be accompanied by an excessive rise in the systolic pressure above normal.

Absence of pulsus paradoxus: Pulsus paradoxus is absent, when cardiac tamponade (CT) occurs in a condition which permits equal filling of both ventricles (e.g. shunt) or more filling of LV (e.g. AR). CT without pulsus paradoxus occurs when associated with: ● ●

● ●

ASD due to equal filling of both ventricles in both phases of respiration VSD due to free communication between the ventricles preventing differential filling AR as filling of LV is maintained irrespective of respiration Pericardial adhesions especially over the right side of the heart.

Types (i) Total paradox is the complete disappearance of palpated pulse during inspiration, which occurs during very severe CT or CT combined with hypovolemia (see Table 14.6). (ii) Reversed pulsus paradoxus: There is an inspiratory increase and an expiratory decrease of systolic arterial pressure. It occurs in: ●

Positive pressure breathing with artificial ventilators: Intrathoracic pressure is higher during inspiration and lower during expiration i.e. reversal of the normal. If CT occurs in this setting, reversal of pulsus paradoxus is noted.

244

GENERAL PHYSICAL EXAMINATION ●

●

Isorhythmic AV dissociation: (atrial activity precedes QRS during inspiration and marches into QRS during expiration) The atrial activity during inspiration increases the stroke volume and its lack during expiration decreases the stroke volume and systolic pressure. HOCM: Reversed pulsus paradoxus occurs in HOCM,14 but the mechanism is not known.

iv. Volume of the Pulse It gives an idea of the pulse pressure, which depends on the stroke volume and the compliance of the arteries. The pulse volume could be normal, low or high. Pulsus parvus, pulsus magnus and hyperkinetic pulse are the types of pulse depending upon its volume (see Table 14.7). i) Pulsus Parvus It is a low volume small amplitude pulse (a small weak pulse) that occurs because of the decreased stroke volume, characteristically seen in AS with pulsus tardus. ●

● ●

Pulsus parvus et tardus refers to a small pulse with a delayed systolic peak characteristic of severe AS. Pulsus parvus is also observed in severe heart failure. It is best detected by palpating the carotids.

Table 14.6 Causes and types of pulsus paradoxus Total pulsus paradoxus

Reversed pulsus paradoxus

1. Severe cardiac tamoponade

1. Positive pressure breathing with ventilators 2. Isorhythmic AV dissociation 3. HOCM

Table 14.7 Causes and types of pulse depending upon the volume Pulsus parvus

Pulsus magnus

Hyperkinetic pulse

1. Aortic stenosis 2. Severe congestive heart failure

1. Aortic regurgitation

1. Pregnancy 2. Anemia 3. Thyrotoxicosis 4. Beriberi 5. Fever 6. Paget’s disease of the bone

ARTERIAL PULSE

245

ii) Pulsus Magnus It is a high volume large amplitude pulse because of an increased stroke volume, characteristically seen in AR. iii) Hyperkinetic or Bounding Pulse It is characterized by a large bounding pulse due to an increased stroke volume and rapid ejection from the left ventricle. ●

●

It occurs in patients with elevated stroke volume, sympathetic hyperactivity, and in patients with a rigid sclerotic aorta. It is typically seen in hyperkinetic circulatory states. In MR and VSD, the forward stroke volume (from LV into aorta) is usually normal, but the fraction ejected during early systole is greater than normal. Therefore, the pulse is of normal volume but may rise briskly (also described as abnormally rapid).

v. Condition of the Vessel Wall It is examined by flattening the artery by digital pressure and sliding it sideways. ● ●

Atherosclerotic vessel is thickened, rigid and tube like. It is hard and calcified in Monckeberg’s degeneration (medial calcification).

vi. Radial Pulse Synchronicity Examine whether the radial pulses are equal on both sides. Radial pulse on one side may be diminished or absent in patients with: ● ● ● ●

●

● ●

Takayasu arteritis Thoracic outlet syndrome (commonly a cervical rib, scalenus anticus syndrome) Subclavian steal syndrome Chronic atherosclerosis (predominantly involves innominate, more commonly the left subclavian artery) Acute microemboli to the arm from the heart or from proximal aneurysmal lesion (including aortic aneurysm) Coarctation of aorta (if proximal vessels are also involved) and Dissection of aorta.

vii. Absent or Delayed Femoral Pulsations While palpating radial pulse, place fingers of the other hand over the femoral pulse (below inguinal ligament, one third of distance from pubic tubercle) (see Fig. 14.21). A noticeable delay in the arrival of femoral pulse is suggestive of: ●

●

Coarctation of aorta (COA): In COA, the radiofemoral delay is not due to the delay in arrival time but due to the delay in its rate of rise (amplitude). Occlusive disease of the bifurcation of the aorta, common iliac or external iliac arteries.

246

GENERAL PHYSICAL EXAMINATION

Fig. 14.21

palpation of radial and femoral pulse to detect any radiofemoral | Simultaneous delay.

5. CHARACTERISTIC FEATURES OF PULSE IN COMMON CLINICAL CONDITIONS The examination of arterial pulse is specially valuable in aortic valve disease. i. Aortic Stenosis (AS) Following are the characteristic features of the pulse in aoric stenosis: ●

●

● ●

Pulsus parvus et tardus: This is a low volume and slow rising pulse with delayed systolic peak characteristic of severe AS (see Fig. 14.10). Anacrotic pulse: In slow rising pulse, a distinct notch (anacrotic) on the upstroke of the carotid pulse with two separate waves (anacrotic and percussion) can be felt (see Fig. 14.13). Pulsus alternans: It occurs in severe AS (see Fig. 14.17). Pulsus bisferiens: It occurs in patients with combined AS and AR, a combination of slow rising and collapsing pulses in which the two waves (percussion and tidal) are equal or tidal wave may be prominent.

ii. Aortic Regurgitation (AR) Following are the characteristic features of the pulse and peripheral signs in AR: These signs are mostly due to wide pulse pressure. (i) Pulse ●

●

Water hammer (collapsing) pulse: Thomas Watson first described it in 1844. It is characterized by rapid upstroke followed by rapid descent of the pulse wave and is best appreciated at the radial pulse (see Figs 14.11 and 14.12). Pulsus bisferiens: It is characterized by two systolic peaks separated by a distinct mid systolic dip. Either the percussion and tidal waves are equal or the tidal waves is

ARTERIAL PULSE

●

247

prominent. It is readily detected by palpating the carotids. Its presence indicates severe AR (see Fig. 14.14). Pulsus magnus: It is a high volume large amplitude pulse, and is best detected at the radial pulse. Its presence indicates mod-severe AR.

(ii) BP ●

●

Diastolic BP is 40 mmHg and pulse pressure is 70 mmHg or 50% of systolic BP in severe AR. BP is normalized in the presence of heart failure or LV dysfunction. In acute AR pulse pressure is narrow with high systolic and diastolic blood pressures. Hill’s sign: Hill and Rowlands in 1912 described the peak systolic pressure gradient between posterior tibial and radial arteries. It is due to greater velocity of blood in lower limb artery, which arises from the aorta in a straight course. Severity of AR from Hill’s sign may be deduced: Systolic pressure difference of 20–40 mmHg angiographic 2AR, 41–60 mmHg systolic pressure difference angiographic 3 AR, 60 mmHg systolic pressure difference angiographic 4AR.

(iii) Eyes ●

●

Landolfi’s sign (Landolfi, 1909): Due to the hyperemia of iris, there is contraction and dilatation of pupil in systole and diastole respectively, which is known as Landolfi’s sign. Becker’s sign: It presents as prominent retinal artery pulsations.

(iv) Head and Neck ●

●

● ●

●

de Musset’s sign (de Musset was a French poet suffering with AR, described by Delpinch in 1900): It is the synchronous nodding of head with heart beat. Corrigan’s sign (Sir Dominic John Corrigan, 1932): It presents as the visible (dancing) carotid pulsations. Muller’s sign (Muller, 1898): This sign presents as the pulsation of the uvula. Minervini’s sign (Minervini, 1910): Strong lingual pulsations are described as Minervini’s sign. The tongue depressor moves up and down when the tongue is lightly depressed. Logue’s sign (Logue, 1952): It is the pulsation of the sternoclavicular joint when AR is associated with aortic dissection.

(v) Upper Limb ● ●

● ● ●

Locomotor brachialis: It is worm like visible pulsations of the brachial artery. Quincke’s pulse/sign (Heinrich Quinke, 1868): It is visible capillary pulsations. Alternating blanching and reddening in the nail bed can be visualized by transmitting light on the pateint’s finger tips. The capillary pulsations can also be visualized by pressing a glass slide on the patient’s lips. Palfrey’s sign (Palfrey, 1952) is the pistol shot sounds heard over the radial artery. See above for various types of pulses. BP: See above.

248

GENERAL PHYSICAL EXAMINATION

(vi) Lower Limb ●

●

●

Traube’s sign: Booming of systolic sounds (pistol shots) heard over the femoral artery due to sudden distension of arterial wall is described as Traube’s sign. Duroziez’s sign (murmur) is more specific of all the peripheral signs of AR Paul Louis Duroziez described it in 1861. It is a brui de tambour and consists of: – Systolic murmur: A forward murmur perceived by pressing the femoral artery 2 cm above the stethoscope, which is due to powerful contraction of LV and increased stroke volume. – Diastolic murmur: A backward murmur perceived by pressing the femoral artery 2 cm below the stethoscope, which is due to the arterial recoil and back flow. Hill’s sign: See above.

(vii) Abdomen ● ● ●

Rosen bach’s sign is the pulsations in liver. Gerhardt’s sign is the pulsations in spleen. Dennison’s sign (Dennison, 1959): Presence of pulsations in the cervix in female patients is known as Dennison’s sign.

REFERENCES 1. Murgo JP, Altobelli SA, Dorethy JF. Normal ventricular ejection dynamics in man during rest and exercise. AHA Monogr 1975;46:92–101. 2. O’Rourke MF. The arterial pulse in health and disease. Am Heart J 1971;82(5):687–702. 3. Schlant RC, Felner JM. The arterial pulse- Clinical manifestations. Curr Prob Cardiol 1977;2(5): 1–50. 4. Garratt CJ, Griffith MJ, Young G, Curzen N, Brecker S, Richards AF, et al. Value of physical signs in the diagnosis of ventricular tachycardia. Circulation 1994;90(6):3103–3107. 5. Corrigan DJ. On permanent patency of the mouth of the aorta, or inadequacy of the aortic valves. Edinburg Med Surg 1832;37:225–245. 6. Talley JD. Recognition, etiology and clinical implications of pulsus bisferiens. Heart Dis Stroke 1994; 3(6):309–311. 7. Dow P. The development of the anacrotic and tardus pulse of aortic stenosis. Am J Physiol 1940; 131:432–436. 8. Cohn KE, Sandler H, Hancock EW. Mechanism of pulsus alternans. Circualtion 1967;36(3): 372–380. 9. Fowler NO. Pulsus paradoxus. Heart Dis Stroke 1994;3(2):68–69. 10. Spodick DH. Pulsus paradoxus. In: Spodick DH. The Pericardium: A Comprehensive Textbook. New York, Marcel Dekker, 1997:191–199. 11. Shabetai R, Fowler NO, Guntheroth WG. The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 1970;26(5):480–498. 12. Hoit et al. Echocardiographic correlates of pulsus paradoxus. Echocardiography 1996;11(3):265. 13. Friedman HS, Sakurai H, Choe SS, Lajam F, Celis A. Pulsus paradoxus: A manifestation of marked reduction of left ventricular end diastolic volume in cardiac tamponade. J Thorac Cardiovasc Surg 1980;79(1):74–82. 14. Massumi RA, Mason DT, Vera Z et al. Reversed pulsus paradoxus. N Eng J Med 1973;289(24): 1272–1275.

■■■

CHAPTER 15

M EASUREMENT OF THE B LOOD P RESSURE 1.

DEFINITION AND COMPONENTS OF ARTERIAL BLOOD PRESSURE 2. DETERMINANTS OF ARTERIAL BLOOD PRESSURE 3. MEASUREMENT OF ARTERIAL BLOOD PRESSURE Direct Methods

249 250 250 250

Indirect Methods 4. HYPERTENSION Causes of Hypertension Mechanisms of Primary Hypertension Complications of Hypertension REFERENCES

251 262 262 265 267 267

1. DEFINITION AND COMPONENTS OF ARTERIAL BLOOD PRESSURE The arterial blood pressure is a measure of its potential energy or lateral force per unit area of vascular wall, which is expressed in units of dynes per cm2 (in the metric system). However physiologically and clinically, measurements of arterial pressure are usually obtained by mercury manometer, which is expressed in mmHg. i.e. 1 mmHg 1.332 dynes/cm2, 120/80 mmHg 160/106.5 dynes/cm2. The systemic arterial blood pressure consists of (see Table 15.1): (i) Systolic blood pressure (SBP) is the maximum pressure exerted during systole. Table 15.1 Definitions of the components of blood pressure Pressure

Definition

1. Systolic blood pressure

Maximum pressure exerted during systole and indicates the extent of work done by the heart Minimum pressure exerted during diastole and indicates the load against which heart has to work Difference of systolic and diastolic blood pressure, which determines the pulse volume Average blood pressure throughout the cardiac cycle, which determines the pressure head. Sum of diastolic blood pressure and 1/3rd of pulse pressure gives the mean blood pressure Pulse pressure/systolic blood pressure

2. Diastolic blood pressure 3. Pulse pressure 4. Mean blood pressure

5. Proportional pulse pressure

250

GENERAL PHYSICAL EXAMINATION ●

●

It indicates the extent of work done by the heart or the force with which the heart is working and the degree of pressure that the arterial walls have to withstand. Normal SBP is 120 mmHg.1

(ii) Diastolic blood pressure (DBP) is the minimum pressure exerted during diastole. ●

●

It is the measure of the total peripheral resistance and indicates the constant load against which the heart has to work. Normal DBP is 80 mmHg.1

(iii) Pulse pressure (PP) is the difference of systolic and diastolic blood pressure (PP SBP DBP). It determines the pulse volume and normal average PP is 40 mmHg. (iv) Mean blood pressure (MBP) is the average blood pressure throughout the cardiac cycle. ● ●

●

It is the sum of DBP and 1/3rd of PP (MBP DBP  1/3 PP). It is same for each organ and determines the pressure head i.e. regional blood flow through an organ depends on it. Normal MBP ranges between 95–100 mmHg with an average of 96 mmHg.

(v) Proportional pulse pressure (PPP) is the pulse pressure/systolic blood pressure (PPP PP/SBP) PPP of 25% identifies 90% of patients with left ventricular failure (LVF) and cardiac index of 2.21/min/m2.

2. DETERMINANTS OF ARTERIAL BLOOD PRESSURE ●

●

●

●

●

Arterial BP is the product of cardiac output (CO) and peripheral resistance (PR) i.e. BP CO  PR. Hence, any condition, which alters the CO or the PR or both, will cause a change in arterial BP. CO is the functional product of heart rate (HR) and stroke volume (SV) i.e. CO HR  SV. SBP increases if the increase in CO is due to increase in SV and DBP increases if the increase is due to increased HR. If increase of CO is due to increase of both SV and HR, both SBP and DBP increase. Arterioles are the chief seat of PR, which depends on the elasticity of the vessel wall, velocity, viscosity and total blood volume in the arterial system.

3. MEASUREMENT OF ARTERIAL BLOOD PRESSURE Direct Methods Stephen Hales (1783) first recorded the arterial pressures in mares and other animals by cannulation and by the use of blood-filled glass column.2 ●

Current techniques for the direct and continuous measurement of arterial pressure utilize electromanometer, a transducer that converts mechanical energy into an electrical signal suitable for amplification, display and recording.

MEASUREMENT OF THE BLOOD PRESSURE ●

●

●

●

251

The artery is cannulated with a saline filled catheter or needle that machanically couples the circulation to the arterial manometer. The use of side-hole catheter (instead of end-hole catheter) positioned in a large, patent artery allows the measurement of true arterial pressure with less measurement errors. Miniature, self-flushing strain gauge manometers that are directly attached to an intravascular catheter or needle eliminate many of the problems related to transducer mounting and flushing and overdamping by connecting tubes. However, the use of intravascular electromanometers mounted on cardiac catheters or the ones that are surgically implanted in vessel walls are the best method of direct measurement of the arterial pressures.

Indirect Methods History ●

●

●

Karl Vierdot (1818–1884) introduced the first sphygmographic method for indirect measurement of BP, and Samuel Siegfried von Basch (in 1881) developed the first non-invasive sphygmomanometer.3 This led to further work by Scipione Riva-Rocci in 1896, who developed the prototype of the present day instrument.4 The invention of inflatable manometer permitted the clinical, non-invasive and indirect measurement of the arterial pressure. The original method of measuring SBP was the palpation of radial pulse. With the discovery of arterial sounds (Nikolai Korotkoff, a Russian surgeon in 1905)5 and exhaustive description of these sounds (as Ki and Kc by McCutcheon and Rushmer in 1967), the auscultatory method became the most common and popular non-invasive method of measurement of arterial pressure.6 The various indirect methods are: – Sphygmomanometric measurement: palpatory, ausculatatory and flush methods – Ultrasound Doppler method – Oscillometric method – Self measurement (home BP recordings) – Ambulatory BP monitoring.

(i) Palpatory Method With sphygmomanometer ●

●

After the standard cuff inflation (30 mmHg above the anticipated SBP) which obliterates the brachial pulse, the cuff is slowly deflated and the approximate peak systolic pressure is the point at which the brachial pulse first reappears consistently. The diastolic pressure is estimated by a distinct snapping quality of the palpable pulse as the cuff is further deflated.

Without sphygmomanometer ●

Approximation of the systolic pressure without sphygmomanometer may be done by the amount of brachial artery compression required to obliterate the ipsilateral radial pulse.

252

GENERAL PHYSICAL EXAMINATION ●

When relatively mild brachial artery compression obliterates the radial pulse, the SBP is 120 mmHg, and it usually may be 160 mmHg when considerable compression is required.

(ii) Auscultatory Method This method of blood pressure measurement requires proper understanding of Korotkoff sounds and phases, proper technique and adequate cuff size. Korotkoff sounds: ●

●

●

●

Korotkoff sounds consist of two major components:6

The initial transient sound (Ki): The initial clear tapping sound occurs at the instant the cuff pressure reaches the arterial systolic pressure and is probably caused by the oscillation of the arterial wall as the occluded segment is suddenly opened by systolic pressure. The compression murmur (Kc) is caused by a turbulent jet of flow distal to the partially compressed segment. The audibility of the Korotkoff sounds is improved by opening and closing of the fist vigorously, a dozen times. Vasodilatation increases the intensity of Ki, while vasoconstriction or circulatory collapse decreases its intensity.

Korotkoff phases: The Korotkoff sounds (sound and murmur) have been divided into five phases occurring in sequence as the occluding pressure declines (see Fig. 15.1). ● PHASE-I consists of clear tapping sounds (K ) which occur when the cuff pressure i has reached the arterial peak systolic pressure.

Phase of silence Systolic pressure

Phase I Tapping sounds (Ki) Phase II Soft murmurs (Kc)

Phase III Loud slapping sounds

Phase IV Muffled sounds Diastolic pressure

Fig. 15.1

| Korotkoff phases.

Phase V Phase of silence

MEASUREMENT OF THE BLOOD PRESSURE ●

●

●

●

●

●

●

253

PHASE-II consists of Ki sounds followed by soft murmurs (Kc), 5–10 mmHg lower than the peak systolic pressure. Auscultatory silent gap occurs when phase II sounds and murmurs are faint or not heard. This phenomenon tends to occur when there is a venous distension or reduced velocity of arterial flow into the arm. PHASE-III is an augmentation of phase II sounds and murmurs, 5–10 mmHg below phase II, as increased volume of blood passes through the partially compressed artery. PHASE-IV is sudden muffling of sounds due to loss of Ki and diminution of Kc components, resulting in a blowing quality as the cuff pressure approaches arterial diastolic levels, 5–10 mmHg higher than the phase V. In severe AR and hyperkinetic circulatory states, this phase represents the diastolic pressure. PHASE-V is complete disappearance of Korotkoff sounds (Kc) when the artery is no longer compressed to produce turbulent flow, occurring 5–10 mmHg lower than phase IV and represents the diastolic pressure. Correlation of Korotkoff phases and blood pressure: – SBP is the point at which phase I occurs and onset of phase V is used to define as DBP. – Correlation of phases I and V with direct measurement of systolic and diastolic pressures respectively was good,7 even though the indirect methods have the tendency to underestimate the systolic pressure and overestimate the diastolic pressure (when phase IV is used as an end point). – However, diastolic pressure should be recorded both at phase IV and V in severe AR and hyperkinetic circulatory states. Failure to detect auscultatory gap when the second appearance of sounds is taken as systolic pressure, may result in an erroneously low systolic pressure, and the gap will be over estimated if the first muffling of sounds (silent gap) is considered as diastolic pressure. Sounds transmitted from the prosthetic valves may be responsible for falsely high readings.

Adequate equipment and cuff size ●

● ●

●

●

●

The width of the cuff should be 20% more than the limb diameter or 40% of the limb circumference, and length of the cuff should be adequate to encircle atleast 80% of the limb,1 with a ratio of 1:2 between the width and the length (see Fig. 15.2). The standard cuff size is 5 with a length of 10 (see Fig. 15.3). When this cuff is applied to a large arm in an obese or to a normal adult thigh, arterial systolic pressure is overestimated, and when it is applied to a small arm, the systolic pressure is underestimated. In patients with arteriosclerosis (with rigid sclerotic arteries), the systolic pressure may also be overestimated by as much as 30 mmHg. If the thigh cuff is too small, a higher diastolic pressure is recorded in the legs than in the arms. This cuff mismatch may be corrected to some extent by the following formula: If cuff is relatively smaller: 32 – (1.05  arm circumference in cm), if () add to the BP recording and if (–) subtract from the BP recording.

254

Fig. 15.2

GENERAL PHYSICAL EXAMINATION

| Pediatric and adult cuffs.

Fig. 15.4

●

●

●

Fig. 15.3

cuff size for an adult (width 5 | Standard and length 10).

| Usual cuff size for children (width 3).

The cuff width should be approximately 1.5 in infants and small children, 3 in young children (2–5 years of age) and 8 in obese adults (see Fig. 15.4). Mercury manometers (see Fig. 15.5) in general are more accurate and reliable than the aneroid type (see Fig. 15.6) and other electronic equipments. BP recordings using manual or automatic inflation and deflation of the cuff and detection of Korotkoff sounds by a stethoscope, microphone or ultrasonic transducer are being increasingly used for home blood pressure recordings (see Fig. 15.7) and ambulatory assessment. As mercury manometers are being replaced by new equipment due to environmental contamination (by mercury spillage), the new equipment should be appropriately validated and regularly checked for accuracy.8

Proper technique ● Patient should avoid caffeine, exercise and smoking atleast 30 min prior to BP measurement. If patient had caffeine, exercise and smoking, BP will be elevated which may return to the baseline in about 15–30 min.

MEASUREMENT OF THE BLOOD PRESSURE

Fig. 15.5

Fig. 15.7

●

●

●

| Mercury manometer.

Fig. 15.6

255

| Aneroid manometer.

digital manometer in which systolic, diastolic and pulse readings | Automatic are displayed once the cuff is inflated.

Patient should be seated for atleast 5 min quietly and comfortably in a chair with feet on the floor and arm supported at the heart level. Anxiety may give rise to ‘white coat hypertension.’ Ambulatory or self-monitoring of BP may be recommended in such cases. The cuff should be snuggly applied over the artery, at the level of the heart, with its lower edge atleast 1 above the antecubital fossa (see Fig. 15.8). Inflate the cuff to a pressure of 20 mmHg above the anticipated systolic pressure, as indicated by the obliteration of radial pulse. Stethoscope is then applied lightly but firmly over the artery, and auscultatory pressures are determined as the cuff is deflated at a rate of 2 mmHg/sec. A rapid deflation of the cuff may cause the sounds to be

256

GENERAL PHYSICAL EXAMINATION

Fig. 15.8

●

●

●

●

| BP recording in upper limb.

missed especially in the presence of bradycardia or irregular rhythm and arterial pressure may be underestimated. When the cuff is deflated too slowly or is immediately re-inflated for repeat pressure recordings, the resultant venous congestion may artificially elevate the diastolic pressure and falsely decrease the systolic pressure by decreasing the intensity of phase I or II sounds to inaudible levels. The cuff should be deflated rapidly and completely after the diastolic pressure is noted and a full minute is allowed to elapse before the pressure is re-measured in the same limb. Excessive pressure on the stethoscope head may not affect the systolic pressure recording but it may give erroneously low diastolic readings. Determination of BP in both arms and atleast one lower limb is recommended.

BP measurement in the lower limbs ●

●

●

The patient lies on the abdomen and preferably, 8 wide cuff is applied with compression over the posterior aspect of the mid thigh. Auscultation is carried out in the popliteal fossa (see Fig. 15.9). To measure pressure in the lower leg (when 8 wide cuff is not available), an arm cuff is placed over the calf and auscultation is done over the posterior tibial artery (or over the dorsalis pedis). Exercising the limb improves the audibility of the Korotkoff sounds.

BP recording in special circumstances ●

●

In severe aortic regurgitation and hyperkinetic circulatory states, diastolic pressure should be recorded both at phase IV and V. Patients with atrial fibrillation have a significant beat-to-beat variation in their arterial pressure, which may result in underestimation of their BP. Hence, several recordings should be taken (atleast 3 recordings) and the average is noted in each limb.

MEASUREMENT OF THE BLOOD PRESSURE

Fig. 15.9

257

| BP recording in lower limb.

Table 15.2 Variations in arm and leg systolic pressures Pressure difference of 10 mmHg between the two arms

Pressure difference of 20 mmHg between arm and leg

1. Aortic arch syndrome, coarctation of aorta 2. Thrombosis/aneurysm of innominate or subclavian arteries 3. Subclavian steal syndrome 4. Supravalvular aortic stenosis 5. Scalenus anticus syndrome, cervical rib

1. Coarctation of aorta, aortic dissection, aortic arch syndrome 2. Subclavian steal syndrome 3. Severe aortic regurgitation

Varible BP recordings ●

Differences in systolic pressures between the two arms that exceed 10 mmHg (see Table 15.2): When measurements are made simultaneously or in rapid sequence9 (switch the limbs and re-measure the pressures for confirmation) and the difference in systolic pressures between the two arms exceeds 10 mmHg, it suggest the presence of: – Obstructive lesions in the aorta, origin of the innominate and subclavian arteries (due to arotic arch syndrome, coarctation, aneurysm and thrombosis) – Supravalvular AS10 (right arm pressure exceeds that in the left arm, see Fig. 15.10) – Subclavian steal syndrome in adults (lower or absent ipsilateral brachial artery pressure accompanied by cerebrovascular symptoms in patients with vertebrobasilar artery insufficiency) – Scalenus anticus syndrome and cervical rib.

●

Difference in arm and leg pressures: Normally, a progressive increase in systolic pressure occurs as the point of BP measurement is moved from the central aorta to the

258

GENERAL PHYSICAL EXAMINATION

Coarctation High pressure Low pressure Supravalvular aortic stenosis Possible bicuspid aortic valve Left ventricular hypertrophy

Fig. 15.10

AS, right arm pres| Insuresupravalvular exceeds that in left arm.

Fig. 15.11

of aorta—A high brac| Coarctation hial arterial pressure is detected.

periphery and increment is equal in large arteries of both arm and thigh. However, the direct measurement of brachial and femoral arterial pressures11 and indirect measurement of brachial and popliteal pressures by using appropriate cuffs,12 have shown that the mean BP is equal in all the sites. A difference in arm and leg pressures (a difference of 20 mmHg usually of the systolic pressure) may occur in the following conditions (see Table 15.2): – A relative high brachial systolic pressure occurs in coarctation of aorta or aortic dissection (see Fig. 15.11). – A relative high crural systolic pressure occurs in aortic arch syndrome, subclavian steal syndrome and severe AR (Hill’s sign13, see Fig. 15.12). – A higher diastolic pressure in the legs than in the arms, suggests that the thigh cuff is too small. ●

An increase in arterial pulse pressure usually results from an increase in stroke volume and ejection velocity, often with a decreased PR. A wide PP is commonly observed in: – Hyperkinetic circulatory states such as pregnancy, hot weather, exercise, anemia, hyperthyroidism, arteriovenous fistulas – AR, PDA, truncus arteriosus – Complete heart block and marked sinus bradycardia.

●

A narrow pulse pressure may result from (see Table 15.3): – An increased PR, e.g. in heart failure due to increased circulating catecholamines – Decreased stroke volume, e.g. severe AS – Markedly decreased intravascular volume, e.g. diabetic ketoacidosis.

●

Variation with respiration (also see pulsus paradoxus): With normal respiration, the peak SBP is greater during expiration by as much as 10 mmHg and falls during

MEASUREMENT OF THE BLOOD PRESSURE

259

Dilated aorta

Aortic valve

Dilated left ventricle

Fig. 15.12

| Aortic regurgitation—A high crural systolic pressure is found (i.e. Hill’s sign). Table 15.3 Conditions with wide and narrow pulse pressures Wide pulse pressure

Narrow pulse pressure

1. 2. 3. 4.

1. Heart failure 2. Severe aortic stenosis 3. Diabetic ketoacidosis

Hyperkinetic circulatory states Aortic regurgitation PDA, truncus arteriosus Complete heart block

inspiration by 10 mmHg. A fall in systolic pressure by 10 mmHg during inspiration (pulsus paradoxus) occurs: – During hyperventilation – In patients with pericardial tamponade, restrictive cardiomyopathy and COPD which may be detected by the examination of pulse, but is best detected by sphygmomanometry. ●

Variation with exercise – Isotonic exercise (both supine or upright) produces moderate increase in BP (systolic  mean  diastolic pressure). – While sustained isometric exercise produces an abrupt increase in all pressures (systolic, mean and diastolic).14

●

BP in pulsus alternans – Pulsus alternans can be detected by palpating a peripheral artery (femoral or radial). – However, sphygmomanometer can be used to accurately measure the beat-tobeat variation in the pressure that characterizes pulsus alternans.

260

GENERAL PHYSICAL EXAMINATION ●

Orthostatic hypotension (OH) is present when there is a supine to standing BP decrease by 20 mmHg systolic or 10 mmHg diastolic pressure. – Severe volume depletion, baroreflex dysfunction, autonomic insufficiency and venodilators ( blockers,  blockers, nitrates and diuretics) may cause OH. – OH is more common in DM and in elderly individuals (70 years of age). – There is a strong correlation between the severity of OH, premature death and increased morbidity from falls and fractures.15,16

●

In children, average SBP at 1 year of age is 90 mmHg and increases by 5 mmHg every 3 years and reaches 120 mmHg (adult level) by 12–13 years of age, while the DBP is usually 60  10 mmHg. Following simple formula gives the expectant systolic pressure in children: SBP 90  (age  5)/3.

(iii) Flush Method of BP Recording ●

●

●

●

●

Snuggly apply the BP cuff to the limb (arm or thigh), elevate the limb and an elastic bandage is applied from fingertips or toes proximally to eliminate the blood from the skin capillaries and veins and to blanch the distal forearm and hand or leg and foot. With the bandage still in position, the cuff is inflated 20 mmHg above the anticipated systolic pressure, and then the bandage is removed. The distal limb should now be pale and white, and cuff should be deflated at a rate of 2 mmHg/sec. The pressure at which first blush appears in the limb is recorded which is closer to the mean pressure than to peak systolic pressure. The reading is 10–30 mmHg lower than the systolic pressure obtained by the auscultatory method. This method is helpful in suspected coarctation of aorta where auscultatory and palpated pressures in the lower limb are not obtainable.

(iv) Ultrasound Doppler Method ● ●

●

The transducer is placed over the artery, which requires the recording of pressures. The arterial wall oscillations are transformed into an audible signal (sounds) at the peak intravascular systolic pressure and the sounds terminate when the intravascular pressure dips below the end diastolic pressure. With this method, systolic pressure is accurately recorded, while diastolic pressure recording is not very reliable.

(v) Continuous Non-invasive BP Monitoring by Oscillometric Method or Arterial Tonometry ●

● ●

In the arterial tonometry method, a probe with a micromanometer in its tip which operates on the principle of a piezo-resistive transducer of cantilever construction, is used.17,18 In oscillometric technique, a special cuff that senses the arterial waves is used. Systolic, diastolic and mean arterial pressures as well as HR are digitally displayed (see Fig. 15.13). The mean pressure is the most accurate.

MEASUREMENT OF THE BLOOD PRESSURE

Fig. 15.13

261

BP monitoring by oscillometric method in ICU by which | Continuous systolic, diastolic and mean pressures as well as HR are digitally displayed.

(vi) Self-monitoring of BP Self-monitoring of BP at home or work using manual or automatic inflation and deflation of the cuff, and detection of Korotkoff sounds by stethoscope, microphone or ultrasound transducer is a practical approach: ● ●

To assess the difference between office (clinic/hospital) and out of office BP and to assess BP in smokers prior to consideration of ambulatory monitoring or drug therapy.

(vii) Ambulatory BP Monitoring (ABPM) This provides the information about BP during daily activities and sleep,19 and either arterial tonometry or oscillometric technique is used. ●

BP has a reproducible circadian profile with higher values: – While awake – When mentally and physically active – And during early morning for  3 hrs during the transition of sleep to wakefulness.20

● ●

BP has much lower values during rest and sleep (drops by 10–20% during sleep). Hence, ABPM may be indicated and could be helpful in the following (see Table 15.4): – Suspected ‘white coat hypertension’ with no target organ damage which may be noted in 20–35% of patients diagnosed with hypertension.21 – Apparent drug resistance in hypertensive patients – Hypotensive symptoms with antihypertensive drugs – Episodic hypertension – Autonomic dysfunction – Assessing BP in smokers: Smoking causes an acute rise in the BP and it returns to the baseline in about 15 min of stopping the smoking.

262

GENERAL PHYSICAL EXAMINATION

Table 15.4 Indications of ambulatory BP monitoring 1. 2. 3. 4. 5.

●

●

●

Drug resistance hypertension Episodic hypertension “White coat” hypertension Drug induced hypotension Autonomic dysfunction

The level of BP measurement using ABPM correlates better in a given clinical condition than the clinic/hospital BP measurement.22 Individuals in whom BP does not fall (by 10–20%) during night, are at increased risk of the cardiovascular events. In ABPM patients with 24 hr BP exceeding 135/85 mmHg, are likely to have a cardiovascular event twice as those with 24 hr BP 135/85 mmHg, irrespective of the level of the clinic/hospital BP.23

4. HYPERTENSION The term ‘hyperpiesia’ was introduced by Albutt (in 1896) to distinguish patients with elevated BP alone from those with Bright’s disease, which was later renamed as ‘essential hypertension’.24 Causes of Hypertension An adult individual has normal BP when SBP is 120 mmHg and DBP 80 mmHg. Hypertension is defined as SBP of 140 mmHg or DBP of 90 mmHg1 (see Table 15.5). (i) Primary or essential hypertension: about 89.50%25 (ii) Secondary hypertension: 5–10% (see Table 15.6). (a) Renovascular hypertension (about 1–3.3%): 25 ● ●

Two major types are (causes):

Atherosclertic renal artery disease (2/3rd, males) Non-atherosclerotic: Fibro-muscular dysplasia (1/3rd, young females). Other uncommon causes of Renovascular hypertension are:

● ● ●

Aneurysm of renal artery Embolism of renal artery Extravascular compression of renal artery by tumor or fibrosis.

(b) Renal parenchymal disease (2–5%) ● ● ● ●

Acute glomerulonephritis Chronic glomerulonephritis (1.8%)25 Diabetic nephropathy Polycystic renal disease

MEASUREMENT OF THE BLOOD PRESSURE

263

Table 15.5 Classification of BP for adults (JNC 7)1 BP classification

Systolic BP (mmHg)

Diastolic BP (mmHg)

1. 2. 3. 4.

120 120–139 140–159 160

and 80 or 80–89 or 90–99 or 100

Normal Pre-hypertension Stage 1 hypertension Stage 2 hypertension

Table 15.6 Secondary hypertension

● ●

●

Cause

Incidence

1. Renovascular disease 2. Renal parenchymal diseases 3. Coarctation of aorta 4. Endocrinal diseases 5. Neurological diseases 6. Drugs and other substances induced hypertension 7. Pregnancy induced hypertension

1–3.3% 2–5% 0.2% 1% 1% 1% 10% of primi

Hydronephrosis Hypertension during dialysis (blood pressure increases during the 2nd day as a result of excessive fluid retention)26 After renal transplantation (within one year due to renal artery stenosis or drugs).27 Other causes:

● ●

Renin producing tumors Primary sodium retention (Liddle syndrome, Gordon syndrome).

(c) Coarctation of aorta (0.2%)28 (d) Endocrinal diseases Adrenal causes of hypertension (1%) ●

Adrenal cortical disease – Cushing’s syndrome (0.6%)25 – Primary aldosteronism (1.5%)25 due to adenoma or bilateral adrenal hyperplasia.

●

Adrenal medullary disease – Pheochromocytoma (0.3%)25 (predominantly epinephrine) – Extra-adrenal chromoffin tumors (predominantly nor-epinephrine).

Thyroid gland related hypertension ● ● ●

Hyperthyroidism Hypothyroidism Hashimoto’s thyroiditis.

264

GENERAL PHYSICAL EXAMINATION

Hyperparathyroidism ●

Hypercalcemia.

Pituitary disease: Growth hormone excess ●

Acromegaly.

(e) Neurological disorders: ● ● ● ● ●

Causing hypertension (uncommon causes)

Increased intracranial tension: Brain tumors, encephalitis Sleep apnea Acute porphyria Familial dysautonomia Guillian-Barre syndrome.

(f) Acute stress including surgery ● ● ● ● ● ●

Post-operative Hypoglycemia Burns Pancreatitis Sickle cell crisis Alcohol withdrawal.

(g) Hypertension in pregnancy: 29 Hypertension may occur in 10% of the previously normotensive women after 20 weeks of gestation of the first pregnancy. Following types of hypertension have been described during pregnancy: ●

●

● ●

●

Chronic hypertension: 140 mmHg SBP or 90 mmHg DBP prior to pregnancy or before 20 weeks of gestation and persists for 12 weeks postpartum. Pregnancy induced hypertension: preeclampsia, eclampsia (140 mmHg SBP or 90 mmHg DBP with proteinuria after 20 weeks of gestation). Chronic hypertension with superimposed preeclampsia. Gestational hypertension without proteinuria occurring after 20 weeks of gestation: It may be a temporary phenomenon or a pre-proteinuric phase. Transient hypertension: BP is normalized by 12 weeks of postpartum. But it may recur in subsequent pregnancies and may predict future primary hypertension.

(h) Common substances associated with hypertension1 ●

Drugs: – Exogenous hormones: Estrogen (oral contraceptives: 1%),30 glucocorticoids (cortisone), mineralocorticoids, ACTH – Nonsteroidal anti-inflammatory drugs – Drugs used for cold: Phenylpropanolamines and analogues (used as nasal decongestants) – Immunosupressives: Cyclosporine and tacrolimus – Antidepressants: Tricyclics, MAO inhibitors (especially with venlafaxine) – Erythropoietin – Sibutramine

MEASUREMENT OF THE BLOOD PRESSURE

●

●

●

265

– Others: Metclopramide, ketamine, carbamazepine, bromocriptine, clozapine, ergotamine and other ergot containing herbal preparations. Addictions (street drugs): – Cocaine and its withdrawal – Nicotine and its withdrawal – Narcotic withdrawal – Excess ethanol intake – Anabolic steroids. Food substances: – Sodium chloride – Licorice – Tyramine-containing foods (with MAO inhibitors). Chemicals: – Lead poisoning – Mercury – Thallium and other heavy metals – Lithium chloride.

Mechanisms of Primary Hypertension Hypertension is due to increased CO and/or increased PR.31 (see Table 15.7 and Fig. 15.14). Hence, increased CO could be due to increased preload or increased contractility, while increased PR could be due to functional vascular constriction or structural (vascular) hypertrophy. Increased preload: It is due to excess Na intake or due to reduced number of nephrons. ● ●

●

Excess Na intake (10 g) causes  fluid volume ⇒  preload and CO. Reduced nephron number (congenital or acquired)  leads to decreased filtration surface ⇒ which causes renal retention of excess dietary Na  which in turn leads to  preload and CO. Low birth weight due to fetal undernutrition, results in increased incidence of high BP later in life32, and this intra-uterine growth retardation is responsible for decreased number of nephrons.33 Table 15.7 Pathogenesis of hypertension  cardiac output (CO) and/or  peripheral resistance (PR) by the following mechanisms Mechanism

CO or PR

1. Increased preload 2. Increased contractility 3. Functional vasoconstriction  4. Vascular hypertrophy

CO CO PR and vascular hypertrophy PR and vasoconstriction

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GENERAL PHYSICAL EXAMINATION

↑ Cardiac output

↑ Contractility

↑ Sympathetic activity

↑ Peripheral

HTN

↑ Preload

resistance

Vasoconstriction

Vascular hypertrophy

Cell membrane alteration

↑ Fluid volume Renal sodium retention

Hyper insulinemia

↓ Filtration surface

Stress and sleep apnea

Fig. 15.14

Excess sodium intake

IUGR

Genetic predisposition

Obesity

of primary hypertension (HTN)—IUGR: intra-uterine growth | Mechanisms retardation.

Increased contractility: It is due to increased sympathetic activity and endothelin release. ●

● ●

Stress and sleep apnea lead to increased sympathetic activity  which increases myocardial contractility and CO. Sleep apnea also causes endothelin release in response to hypoxemia during apnea. Stress also increases renin-angiotensin through increased sympathetic activity, which decreases filtration surface and thereby results in renal Na retention, increased fluid volume and preload.

Functional vasoconstriction: It directly increases PR. It also causes vascular hypertrophy, which in turn again elevates PR. ●

●

Excess renin-angiotensin due to sympathetic stimulation (stress induced) causes vasoconstriction that elevates the peripheral resistance. Genetic alteration causes cell membrane alteration which leads to both ⇒ vasoconstriction and vascular hypertrophy that elevate peripheral resistance.

Genetic contributions have been estimated to range between 30–60%.34 Structural (vascular) hypertrophy: It directly increases PR and causes functional vasoconstriction, which again elevates PR. ●

Hyperinsulinemia due to obesity causes: (i) Structural hypertrophy (ii)  Sympathetic activity ⇒  contractility and preload (iii) Na retention and thereby increase preload.

MEASUREMENT OF THE BLOOD PRESSURE ●

267

Endothelial dysfunction due to (a) Lack of endothelial derived relaxing factors (EDRF), mainly the nitric oxide (NO) synthesis (as in insulin resistance) or due to impaired NO mediated vasodilation and (b) Increased endothelial derived constricting factors (EDCF), mainly endothelin-1 ⇒ leads to vasoconstriction and vascular hypertrophy

Hence, excess Na intake, stress, obesity, sleep apnea, intrauterine growth retardation and genetic predisposition alter neurohumoral system, which causes increase in preload, contractility, vasoconstiction or vascular hypertrophy alone or in combination resulting in hypertension. Complications of Hypertension These are broadly classified into two categories. Hypertensive complications ● ● ● ● ●

Accelerated-malignant hypertension LVF and CHF Hemorrhagic stroke Nephrosclerosis leading to renal failure Aortic dissection

Atherosclerotic complications ● ● ● ●

Coronary artery disease Sudden death and other arrhythmias Athero-thrombotic stroke Peripheral vascular disease

REFERENCES 1. Chobanian AV, Bakris GL, Black HR et al. The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report. JAMA 2003;289:2560–2572. PR. 2. Hales S. Statistical Essays: Containing Haema-staticks; or, an Account of some Hydraulick and Hydrostatical Experiments Made on the Blood and Blood Vessels of Animals. London: Innys W, Manby R; 1733. 3. Booth J. A short history of blood pressure measurement. Proc R Soc Med 1977;70(11):793–799. 4. Riva-Rocci S. Un sfigmomanometro nuovo. Gaz Med Torino 1896;47:981–996, 1001–1007. 5. Korotkoff NS. On methods of studying blood pressure: second presentation [in Russian]. Izv Imper Voen-Med Acad. 1906;12:254–257. 6. McCutcheon EP, Rushmer RF. Korotkov sounds: An experimental critique. Cir Res 1967;20: 149–161. 7. Neilsen PE, Janniche H. The accuracy of auscultatory measurement of arm blood pressure in very obese subjects. Acta Med Scand 1974;195(5):403–409. 8. Canznello VJ, Jensen PL, Schwartz GL. Are aneroid sphygmomanometers accurate in hospital and clinic settings? Arch Intern Med 2001;161:729–731. 9. Gould BA, Hornung RS, Kieso HA et al. Is the blood pressure the same in both arms? Clin Cardiol 1985;8(8):423–426.

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10. Wooley CF, Hosier DM, Booth RW, et al. Supravalvular aortic stenosis. Am J Med 1961;31:717–725. 11. Park MK, Guntheroth WG. Direct blood pressure measurements in brachial and femoral arteries in children. Circulation 1970;41(2):231–237. 12. Felix WR, Hochbert HM, George MED, et al. Ultrasound measurement of arm and leg blood pressure. JAMA 1973;226(9):1096–1099. 13. Sapira JD, Quincke, de Musset, et al. Some aortic regurgitations. South Med J 1981;74:459–467. 14. Donald KW, Lind AR, McNicol GW et al. Cardiovascular response to sustained contractions. Circ Res 1967;20(suppl 1):15–30. 15. Masaki KH, Schatz IJ, Burchfiel CM, et al. Orthostatic hypotension predicts mortality in elderly men: Honolulu Heart Program. Circulation 1998;98(21):2290–2295. 16. Mukai S, Lipsitz LA. Orthostatic hypotension. Clin Geriatr Med 2002;18(2):253–268. 17. Sato T, Nishnaga M, Kawamoto A, et al. Accuracy of a continuous blood pressure monitor based on arterial tonometry. Hypertension 1993;21(6 pt 1):866–874. 18. Asmar R, Benetos A, Topouchian J, et al. Assessment of arterial distensibility by automatic pulse wave velocity measurement: Validation and clinical application studies. Hypertension 1995;26:485–490. 19. Pickering T. Recommendations for the use of home (self) and ambulatory blood pressure monitoring. American Society of Hypertension Ad Hoc Panel. Am J Hypertens 1996;9(1):1–11. 20. Kario K, Pickering TG, Umeda Y, et al. Morning surge in blood pressure as a predictor of silent and clinical cerebrovascular disease in elderly hypertensives: a prospective study. Circulation 2003;107: 1401–1406. 21. Pickering TG, Coats A, Mallion JM, et al. Blood Pressure Monitoring. Task force V: White-coat hypertension. Blood Press Monit 1999;4:333–341. 22. Franklin SS, Gustin W, Wong ND, et al. Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study. Circulation 1997;96(1):308–315. 23. Clement DL, De Buyzere ML, De Bacquer DA, et al. Prognostic value of ambulatory blood pressure recordings in patients with treated hypertension. N Eng J Med 2003;348(24):2407–2415. 24. Wain H. The story behind the word. Springfield, Illinois: Charles C Thomas 1958:159. 25. Anderson GH Jr., Blakemann N, Streeten DHP. The effect of age on prevalence of secondary forms of hypertension in 4429 consecutively referred patients. J Hypertens 1994;12(5):609–615. 26. Rahman M, Dixit A, Donley V, et al. Factors associated with inadequate blood pressure control in hypertensive hemodialysis patients. Am J Kidney Dis 1999;33(3):498–506. 27. Martinez–Caselao A, Hueso M, Sanz V, et al. Treatment of hypertension after renal transplantation: Long term efficacy of verapamil, enalapril and doxazosin. Kidney Int 1998;68(suppl):130–134. 28. Rudnick JV, Sackett DL, Hirst S, et al. Hypertension in family practice. Can Med Assoc J 1977; 3; 492. 29. National High Blood Pressure Education Program. Report of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol 2000;183(1):S1–S22. 30. Sinclair AM, Isles CG, Brown I, et al. Secondary hypertension in a blood pressure clinic. Arch Intern Med 1987;147(7):1289–1293. 31. Kaplan NM: Clinical Hypertension. 7th ed. Baltimore, Williams & Wilkins, 1998:45. 32. Law CM, Shiell AW. Is blood pressure inversely related to birth weight? The strength of evidence from a systematic review of the literature. J Hypertens 1996;14(8):935–941. 33. Brenner BM, Chertow GM. Congenital oligonephropathy: An inborn cause of adult hypertension and progressive renal injury? Curr Opin Nephrol Hypertens 1993;2(5):691–695. 34. Harrap SB. Hypertension: Genes versus environment. Lancet 1994;344:169–171.

JUGULAR VENOUS PULSE 16. Introduction and jugular venous pulse waves

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17. Estimation of venous pressure and JVP in diseased conditions

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■■■

CHAPTER 16

I NTRODUCTION AND J UGULAR V ENOUS P ULSE WAVES INTRODUCTION History EXAMINATION OF JUGULAR VENOUS PULSE (JVP) 1) Which JVP? 2) Position of the Patient ANALYSIS OF THE JUGULAR VENOUS PULSATIONS 1) a Wave 2) x Descent (Systolic Collapse)

271 271 272 272 274 275 275 276

3) c Wave 4) v Wave 5) y Descent or Diastolic Collapse 6) h Wave ABNORMALITIES OF THE WAVES 1) Abnormalities of a Wave 2) Abnormalities of x Descent 3) Abnormalities of v Wave 4) Abnormalities of y Descent REFERENCES

276 276 277 277 277 277 279 279 281 282

INTRODUCTION ●

●

●

The venous system contains about 70–80% of the circulating blood volume which is non-pulsatile. However, changes in flow and pressure caused by the right atrial and right ventricular filling produce pulsations in the central veins that are transmitted to the peripheral veins (e.g. jugular veins) and are opposite to the direction of the blood flow. The arterial pulse and blood pressure reflects the dynamics of the left side of the heart, while the jugular veins provide the information about the hemodynamic events from the right side of the heart-right atrial pressure during systole and right ventricular filling pressure during diastole. Hence, an accurate assessment of the venous pulse, the jugular venous pulse (JVP) reflects the dynamics of the right side of the heart.1

History ●

●

●

Lancis (1728) first described the cervical venous pulse of the external jugular vein in a patient with tricuspid regurgitation (see Table 16.1). However, the classic graphic recordings of the JVP were done by Chauvea and Marey (1863). But it was Potain (1869) who accurately described the wave pattern in the internal jugular vein.

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Table 16.1 History of jugular venous pulse Author

Year

Description

1. 2. 3. 4. 5.

1728 1863 1869 1902 1950s

Venous pulse of external jugular vein Graphic recordings of JVP Wave pattern in internal jugular vein Nomenclature of JVP Rekindle the interest in assessment of JVP

Lancis Chauvea and Marey Potain James Mackenzie Paul Wood

●

●

Subsequently, James Mackenzie (1902) provided the nomenclature of JVP and applied this principle of examination at the bedside. The Mackenzie’s nomenclature is being used today with little or no significant modifications. In 1950’s Paul Wood rekindled this interest of assessment of JVP.

EXAMINATION OF JUGULAR VENOUS PULSE (JVP) The bedside examination of the JVP is done: ● ●

To estimate the central venous pressure (CVP) and Assess the waveform.

1) Which JVP? ●

●

As the venous pulse is not palpable, the right internal jugular vein is usually assessed both for waveform and for the estimation of the CVP. The internal jugular vein is located deep within the neck, covered by sternocleidomastoid muscle and hence usually not visible as a discrete structure (except in the presence of venous hypertension). However, the venous pulsations of the jugular bulb (a slight dilatation of the internal jugular vein at its junction with the subclavian vein and located between the two heads of the sternocleidomastoid muscle) are transmitted to the overlying skin and soft tissues.

The Internal Jugular Vein is Preferred to the External Jugular Vein ●

●

●

Anatomically, the internal jugular veins (IJVs) are closer to the right atrium (see Fig. 16.1) as they take a direct course (‘straight line’) through innominate veins to the superior vena cava (SVC) and right atrium (RA), while the external jugular veins (EJVs) follow a more circuitous route, and hence IJVs more accurately reflect the dynamics of the right heart (see Table 16.2). The prominent valves at the proximal portion of the EJVs may prevent the transmission of the pulsations from the RA, while there are no or less significant numbers of valves in the internal jugular veins. EJV passes through more fascial planes than the IJV so is more likely to be affected by an extrinsic compression from other structures in the neck and upper thorax.

INTRODUCTION AND JUGULAR VENOUS PULSE WAVES

273

Sternocleidomastoid muscle

Internal jugular vein

External jugular vein

Fig. 16.1

Clavicle

| Jugular veins—internal jugular vein is in direct continuity with the right atrium.

Table 16.2 Reasons for preference of internal jugular vein (IJV) over external jugular vein (EJV) 1. 2. 3. 4.

Direct continuation of right atrium (RA) Transmission of RA pulsations prevented by Other structures of neck and upper thorax  Sympathetic activity (as in CHF)

●

With IJV Prominent valves at the proximal EJV Causes extrinsic compression of EJV Causes vasoconstriction of EJV  Pulsations become barely visible

Due to increased sympathetic activity as in CHF, the EJVs may become small and pulsations are barely visible as a result of vasoconstriction.

The Right IJV is Preferred to Left IJV ●

●

The right IJV and innominate vein extend in an almost straight line from the SVC and RA, while the left innominate vein into which left IJV drains, does not extend in a straight line from the SVC and RA. The left innominate vein may be kinked or compressed by a variety of normal structures, by a dilated aorta or by an aneurysm.

However, if there is any difficulty in visualization of the JVP on the right side, both sides of the neck should be carefully examined. Sometimes, it is difficult to differentiate between carotid and jugular venous pulses especially when the latter exhibits prominent waves (e.g. prominent v waves in a patient with TR). Following are the helpful clues (see Table 16.3): ●

●

●

The carotid pulse is deep and medial in the neck, well localized, while jugular pulse is more superficial and lateral in the neck. The carotid pulse is felt better than seen, while pulsating jugular vein is readily visible than felt. The carotid pulse usually exhibits a single upstroke (single peaked) in patients with sinus rhythm, while the JVP usually has two peaks (double peaked) and two troughs per cardiac cycle.

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Table 16.3 Differences between jugular venous and carotid pulses Jugular venous pulsation

Carotid pulsation

1. Superficial and lateral in the neck 2. Better seen than felt 3. Has two peaks and two troughs/cardiac cycle 4. Descents  obvious than crests 5. x and y  prominent during inspiration 6. a  and v  transiently during expiration 7. Jugular venous pressure falls during inspiration 8. Digital compression at the root of neck abolishes jugular venous pulse

Deeper and medial in the neck Better felt than seen Has single upstroke Upstroke brisker and visible than descent No effect No effect No effect No effect

●

●

●

●

●

The carotid upstroke is brisker ( visible) than its descent, whereas the descents are more obvious than their crests in JVP. The carotid pulsations do not change when the patient assumes upright posture, whereas the mean venous pressure falls, unless the venous pressure is greatly elevated. The carotid pulsations do not change during respiration, whereas x and y descents become more prominent with increased venous return to the right heart during inspiration and thereby there is increased RA and RV contraction. During expiration, a wave diminishes in size and v wave may become transiently dominant. Abdominal compression elevates the jugular venous pressure transiently, while it has no effect on the carotid pulsations. Gentle digital compression at the root of the neck, just above the clavicle does not affect the carotid pulse but usually abolishes the JVP, except in the presence of extreme venous hypertension.

2) Position of the Patient The patient should lie comfortably and in most normal subjects, it is examined when the trunk is inclined by less than 30. It is often helpful to elevate the chin and slightly rotate the head to the left, gently stretching the skin of the right lower neck and supraclavicular area (see Fig. 16.2). ●

●

●

●

However, most patients with heart disease are examined most effectively in the 45 position. But in patients with high venous pressure, a greater (60–90) inclination is required to obtain visible venous pulsations. Whereas in patients with low jugular venous pressure, a lesser ( 30) inclination is desirable. The inclination angle should be subtended between the trunk and the bed and at the neck, while the neck and trunk should be in the same line.

When the neck muscles are relaxed, shining a beam of light tangentially across the skin overlying the IJV often exposes its pulsations. Simultaneous palpation of the left carotid artery and/or cardiac auscultation aids in the timing of the jugular venous pulsations in the cardiac cycle (see Fig. 16.3).

INTRODUCTION AND JUGULAR VENOUS PULSE WAVES

Fig. 16.2

of the patient for examining jugular | Position venous pulse.

Fig. 16.3

275

palpation of left | Simultaneous common carotid artery for timing of jugular venous pulsations.

a x

a

c

h x

v wave y

x trough

S1

Fig. 16.4

Ascending limb S2

| Normal jugular venous wave pattern.

ANALYSIS OF THE JUGULAR VENOUS PULSATIONS The normal JVP reflects the phasic pressure changes in the RA and consists of two visible positive waves (a and v) and two negative troughs (x and y) (see Fig. 16.4). However, two additional positives can be recorded: c wave which interrupts the x descent and h wave which precedes the next a wave (see Table 16.4). 1) a Wave The first positive presystolic a wave is: ●

●

Due to the right atrial contraction which results in retrograde blood flow into the SVC and jugular veins during RA systole. Normally, it is the dominant wave in the JVP especially during inspiration. It is larger than v wave.

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Table 16.4 Normal Jugular venous pulse Features

Crest/trough

Causes

1. a wave 2. x descent 3. x descent

Crest Trough Trough

4. c wave 5. v wave 6. y descent

Crest Crest Trough

Right atrial (RA) contraction Atrial relaxation RA floor descent and downward pulling of tricuspid valve (TV) by contracting right ventricle (RV) Impact of the carotid artery and upward bulging of the closed TV RA filling during RV systole when TV is closed RA emptying during early RV diastole when TV opens

●

It precedes the upstroke of the carotid pulse, almost synchronous with S1, but follows the P wave of the ECG.

2) x Descent (Systolic Collapse) The a wave is followed by the systolic x descent which is due to atrial relaxation during atrial diastole. ●

●

Often, the x descent is the most prominent motion of the normal JVP which begins during systole and ends just before S2. It is larger than y descent.

x Descent More often x descent is interrupted (when recorded) by a second positive venous wave, the c wave. The x descent below the c wave is the x descent which is due to ● ● ●

Fall in the right atrial pressure during early RV systole Descent of the floor of the RA and Downward pulling of the tricuspid valve (TV) by the contracting right ventricle.

3) c Wave This second positive venous wave interrupts the x descent and is produced by: ● ●

The impact of the carotid artery which is adjacent to the IJV and Upward bulging of the closed TV into the RA during RV isovolumic contraction.2

4) v Wave It is the third positive wave (but the second major positive wave) which begins in late systole and ends in early diastole. ●

●

It results from the rise in right atrial pressure due to continued right atrial filling during ventricular systole when the TV is closed. It is roughly synchronous with carotid upstroke and peaks after S2.

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277

5) y Descent or Diastolic Collapse It is the down slope of v wave. ●

●

It results from the decline in the right atrial pressure due to right atrial emptying and right ventricular filling when the TV opens in early diastole. The initial y descent which occurs in early diastole corresponds to the RV rapid filling phase, while the ascending limb of the y wave is produced by the continued diastolic inflow of blood into the right side of the heart, i.e. it begins and ends during diastole well after S2.

6) h Wave When the diastole is long (as in slow heart rates), ascending limb of the y wave is often followed by a small, brief, positive wave known as h wave, which occurs prior to the next a wave during the period of diastasis. It was described by Hirschfelder in 1907 (h from Hirschfelder). ● ● ●

At times, there is a plateau phase rather than a distinct h wave. With increasing heart rate, the y descent is immediately followed by the next a wave. h plateau without a prominent a wave and a prominent y descent is common in constrictive pericarditis.

With faster heart rates, some of the venous pulse waves may merge together, which makes the accurate analysis difficult at the bedside.

ABNORMALITIES OF THE WAVES 1) Abnormalities of a Wave The a wave may be prominent or absent or may occur regularly or irregularly (see Table 16.5). Prominent or Large a Waves These may be due to: ●

●

●

Increased resistance to RA emptying and thereby increased RA contraction as in TS, RA myxomas, or tricuspid atresia (see Fig. 16.5). Decreased RV compliance which is usually associated with increased right ventricular end diastolic pressure leading to right ventricular hypertrophy and is seen in: – PS – PH due to any cause e.g. mitral stenosis – RV cardiomyopathy – Acute pulmonary embolism – RV infarction in association with inferior wall MI. Bernheim’s effect: Severe LVH with thickened ventricular septum (symmetrical or asymmetrical) interferes with RV filling as in severe AS, HCM (with asymmetrical septal hypertrophy).

278

JUGULAR VENOUS PULSE

Table 16.5 Abnormal a waves Large a waves

Cannon waves

Absent a waves

1. TS, RA myxomas, tricuspid atresia 2. PH, PS, acute PE

1. Junctional rhythm VT 1:1 retrograde conduction, isorhythmic AV dissociation 2. CHB, VT, VPC, classic AV dissociation, ventricular pacing

1. Atrial fibrillation 2. Sinus tachycardia

3. RV cardiomyopthy, RV infarction 4. Severe AS, HCM TS: tricuspid stenosis, RA: right atrial, PH: pulmonary hypertension, PS: pulmonary stenosis, PE: pulmonary embolism, CHB: complete heart block, VT: ventricular tachycardia, VPC: ventricular premature contraction, AS: aortic stenosis, HCM: hypertrophic cardiomyopathy, AV: atrioventricular, RV: right ventriclar.

a

a a v a

Fig. 16.5

c

a waves in tri| Prominent cuspid stenosis. Fig. 16.6

v

| Irregular cannon waves in complete AV block.

Giant a Waves or Cannon Waves These occur whenever the RA contracts against the closed TV during RV systole. Paul Wood described the giant a wave as ‘venous Corrigan’. Cannon waves may occur either regularly or irregularly and are most common in the presence of arrhythmias. ●

●

Regular cannon waves occur in – Junctional rhythm – Ventricular tachycardia (VT) 1:1 retrograde conduction – Isorhythmic AV dissociation Irregular cannon waves occur in – Complete heart block (see Fig. 16.6) – Classic AV dissociation – VT – Ventricular pacing – Ventricular ectopics

Absent a Waves ●

The a wave is absent when there is no effective atrial contraction as in atrial fibrillation (see Fig. 16.7).

INTRODUCTION AND JUGULAR VENOUS PULSE WAVES c

v

x

Fig. 16.7

y

| Absent a waves in atrial fibrillation. v

a

|

Table 16.6 Abnormal x descent y

x

Fig. 16.8

279

Prominent x and y descents in constrictive pericarditis.

●

Prominent x descent

Absent x descent

1. Constrictive pericarditis 2. Cardiac tamponade 3. Atrial septal defect

1. Tricuspid regurgitation (TR)

In sinus tachycardia, when a wave may fuse with preceding v wave, especially when the PR interval is prolonged or a wave may occur during the v or y descent and may be small or absent.

2) Abnormalities of x Descent Absent x Descent ● ● ●

The x descent is usually absent due to tricuspid regurgitation.3 Blunting of x descent is the early sign of tricuspid regurgitation. In patients with moderate tricuspid regurgitation, x descent is replaced by a fairly large positive s (systolic) or r (regurgitant) wave.

The development of atrial fibrillation does not obliterate the x descent except in the presence of TR, but its size may be reduced. Prominent x Descent The x descent becomes prominent: ●

●

when RV contracts vigorously as in cardiac tamponade and constrictive pericarditis (x descent may be more prominent than y descent, see Fig. 16.8) and in RV overload as in ASD (see Table 16.6).

3) Abnormalities of v Wave Prominent v Wave It results from an increased right atrial blood volume during ventricular systole when normally TV is closed as in tricuspid regurgitation (see Fig. 16.9). In significant tricuspid regurgitation, obliteration of x descent and prominent v wave result in a large positive

280

JUGULAR VENOUS PULSE v

a y

Fig. 16.9

Prominent v waves with absent x descent but | rapid y descent in severe tricuspid regurgitation.

c

Table 16.7 Abnormal v waves Prominent v waves

Diminished v waves

1. Tricuspid regurgitation (TR) 2. Large atrial septal defect 3. Gerbode’s defect 4. Severe congestive heart failure 5. Atrial fibrillation 6. Corpulmonale

1. Hypovolemia 2. Use of nitrates

v x

Fig. 16.10

y

v waves become | The prominent in atrial fibrillation due to absence of a waves.

systolic (s) or regurgitant (r) wave (Lanci’s sign) which simulate the RV pressure (tracing) and is known as ventricularization of the atrial pressure/jugular venous pressure (see Table 16.7). This giant v wave sometimes causes; ● ● ● ●

A systolic movement of the earlobe,4 A right to left head bobbing (movement) with each ventricular systole Pistol shots heard over the IJV and Pulsatile exophthalmos.

Prominent v Wave in Absence of Tricuspid Regurgitation ● ● ● ● ●

Large ASD VSD of LV to RA shunt (Gerbode’s defect) Severe CHF Atrial fibrillation (see Fig. 16.10) Cor pulmonale

Prominent a and v Waves Prominent and equal a and v waves in RA and JVP occur in ● ● ●

Non restricted ASD with normal venous pressure5 (see Fig. 16.11) Constrictive pericarditis with increased venous pressure (see Fig. 16.12) RVF with sinus rhythm and increased venous pressure. Sometimes, the tall a and v waves may alternate with each other, that results in ‘right atrial pulsus alternans.’

INTRODUCTION AND JUGULAR VENOUS PULSE WAVES a

v

a

v y

x

Fig. 16.11

|

Fig. 16.12 Prominent a and v waves in nonrestricted ASD.

281

a and v waves with rapid x and | Prominent y descents in constrictive pericarditis.

Table 16.8 Abnormal y descent Rapid y descent

Slow y descent

1. 2. 3. 4.

1. Tricuspid stenosis 2. Right atrial myxoma 3. Pericardial tamponade

Severe tricuspid regurgitation Constrictive pericarditis Severe right ventricular failure ASD with mitral regurgitation

a

v

v y

Fig. 16.14 Fig. 16.13

y descent with prominent | Slow a in tricuspid stenosis.

y descent with prominent v in | Rapid tricuspid regurgitation.

Diminished v waves may be seen in conditions of hypovolemia and treatment with venodilators such as nitrates. 4) Abnormalities of y Descent Rapid (Diastolic Collapse) y Descent It occurs in conditions with elevated venous pressure, myocardial dysfunction or severe ventricular dilatation as in (see Table 16.8): ● ●

● ●

Severe tricuspid regurgitation (see Fig. 16.13). Constrictive pericarditis. This diastolic collapse is known as Friedreich’s sign which is usually accompanied by pericardial knock (Friedreich, 1864). Severe RVF. ASD with mitral regurgitation.

Slow y Descent When right atrial emptying and RV filling are impeded, y descent is slow and gradual as in ●

Tricuspid stenosis6 (see Fig. 16.14)

282

JUGULAR VENOUS PULSE ● ●

Right atrial myxoma6 and Pericardial tamponade (y descent may even be absent).

REFERENCES 1. 2. 3. 4.

5. 6.

Swartz MH. Jugular venous pressure pulse: its value in cardiac diagnosis. Prim Cardiol 1982;8:197. Wood P. Diseases pf the Heart and Circulation, 2nd ed. Philadelphia: Lippincott; 1957. Messer AL, Hurst JW, Rappaport MB, Sprague HB. A study of the venous pulse in tricuspid valve disease. Circulation 1950;1(3):388–393. Butman SM, Ewy GA, Standen JR, et al. Bed side cardiovascular examination in patients with severe chronic heart failure: importance of rest or inducible jugular venous distension. J Am Coll Cardiol 1993;22(4):968–974. Dexter L. Atrial septal defect. Br Heart J 1956;18(2):209–225. Perloff JK, Harvey WP. Clinical recognition of tricuspid stenosis. Circulation 1960;22:346–364.

■ ■ ■ CHAPTER 17

ESTIMATION OF V ENOUS P RESSURE AND JVP IN D ISEASED CONDITIONS 1.

ESTIMATION OF VENOUS PRESSURE a) Measurement of Jugular Venous Pressure b) Abdominal–Jugular Reflux c) Measurement of Venous Pressure by Examining the Veins of the Hand (Gaertner’s Method) d) Assessment of Venous Pressure by Examining the Visible Engorged Veins

283 283 286

287

on the Undersurface of the Tongue (May’s Sign) 2. JVP IN DISEASED CONDITIONS a) JVP in Arrhythmias b) JVP in Conduction Defects c) JVP in Valvular Lesions d) JVP in Acyanotic CHD e) JVP in Cyanotic CHD f) JVP in Cardiomyopathy g) JVP in Pericardial Diseases REFERENCES

287 288 288 288 289 291 292 294 295 295

1. ESTIMATION OF VENOUS PRESSURE The estimation of venous pressure can be done at bed side by: ● ● ● ●

Measuring jugular venous pressure1 (usually internal jugular venous pressure) Hepatojugular reflux Examining the veins on the dorsum of the hand Examining the veins of the undersurface of the tongue.

a) Measurement of Jugular Venous Pressure ●

●

Jugular veins could be markedly distended with minimal increase in pressure (especially EJV) or not visibly distended despite a highly elevated pressure. In adults with normal chest, the sternal angle or angle of Louis (Pierre Charles Alexander Louis, 1787–1872) is found to be approximately 5 cm above the center of the right atrium. As the distance between the sternal angle and center of right atrium remains relatively constant regardless of the position of the thorax and as the sternal angle is approachable in all positions of the body, Paul Wood recommended sternal

284

JUGULAR VENOUS PULSE

Normal

Sternal angle = venous pressure Right atrium 45°

Upright

Fig. 17.1

distance between the sternal angle and center of the RA remains relatively | The constant regardless of the position of the thorax.

Fig. 17.2

of JV pressure by two scale method—A horizontal scale at the | Measurement top of the oscillating venous column in IJV cuts the vertical scale at the sternal angle. The vertical distance from the sternal angle gives the RA pressure in cm.

●

●

●

●

angle to be taken as reference point for measurement of jugular venous pressure at bed side2 (see Fig. 17.1). Use of sternal angle as the zero reference is simple and practical, besides it provides a reproducible and readily identified standard for bed side appraisal of venous pressure. With the patient in an optimum position (30–90 recline) and relaxed neck muscles, shining a beam of light tangentially across the skin overlying the internal jugular vein exposes the top of the oscillating venous column (the height of the venous column at the peak of a and v waves usually taken). One horizontal is drawn (in relation to the ground by using a scale) at the top level of the venous column and another at the sternal angle. The vertical distance in cms (use another scale) between the two horizontals, i.e. from the top of the oscillating venous column in the IJV to the sternal angle will give the JV pressure which reflects the mean right atrial pressure (see Fig. 17.2). In normal, JV pressure does not exceed 4 cm above the sternal angle which corresponds to a central venous pressure (RA mean pressure) of 9 cm, since the right

ESTIMATION OF VENOUS PRESSURE AND JVP IN DISEASED CONDITIONS

●

285

atrium is approximately 5 cm below the sternal angle (4  5 9 cm). By way of conversion, 1.3 cm column of water is equal to 1 mmHg. Hence, normal right atrial mean pressure does not exceed 7 mmHg (9 cm of JVP/1.3 6.92). Elevated venous pressure can also be identified if EJV is distended and prominent. Empty the EJV digitally and selective release at the inferior site results in prompt filling of EJV from below in case of high central venous pressure.

Elevated JV pressure: i.e. JV pressure of  4 cm above the sternal angle reflects an increase in RA pressure (see Fig. 17.3 and Table 17.1) which could be due to: ●

●

Increased RV pressure and thereby reduced compliance occurs in patients with: – Pulmonary stenosis – Pulmonary hypertension – RVF secondary to LVF or any cause – RV infarction. Obstruction/impedance to RV inflow as in: – Tricuspid stenosis – Right atrial myxoma – Constrictive pericarditis.

Raised right atrial pressure

Venous pressure Sternal angle

Right atrium 45°

Fig. 17.3

Upright

| Measurement of JV pressure—raised JVP indicating raised RA pressure.

Table 17.1 Elevated jugular venous pressure  RV compliance

RV inflow impedance

Circulatory overload

Others

1. Pulmonary stenosis 2. Pulmonary hypertension

1. Tricuspid stenosis 2. Right atrial myxoma

1. Renal failure 2. Excessive fluid administration

1. SVC obstruction 2. COPD

3. RVF (any cause including LVF) 4. RV infarct

3. Constrictive pericarditis

SVC: superior vena cava, COPD: chronic obstructive pulmonary disorders, RVF: right ventricular failure, LVF: left ventricular failure.

286

JUGULAR VENOUS PULSE ●

●

● ●

Hypervolemia/circulatory over load as in: – Renal failure – Excessive fluid administration. Superior vena caval obstruction: Bilateral jugular veins are distended with little or no pulsations, and are associated with cyanosis, edema of face and eyes. COPD: JV pressure may be elevated only during expiration. Kussmaul’s sign:3 Normally, JV pulsations (especially a wave) become prominent during inspiration, while the mean JV pressure decreases as a result of increased filling of the right side associated with decreased intrathoracic pressure. But if the venous pressure increases during inspiration, it is known as Kussmaul’s sign, which occurs in patients with: – Constrictive pericarditis (first described in constrictive pericarditis) – Sever right heart failure – Right ventricular infarction4 – Restrictive cardiomyopathy.

b) Abdominal–Jugular Reflux (AJR) Rondot (1898) coined the term ‘hepatojugular reflux’. ●

●

It is a useful diagnostic maneuver when the JVP is borderline elevated or when the latent RVF or silent TR is suspected. Gently apply firm pressure to the periumbilical region for 10–30 sec with patient lying comfortably and breathing quietly (should avoid Valsalva maneuver) while JVP is observed (see Fig. 17.4). Pressure should not be applied over the liver in right hypochondrium region, as it be may be painful in presence of hepatic congestion.

Fig. 17.4

for abdominal jugular reflex-by applying gentle pressure in | Examination periumbilical area.

ESTIMATION OF VENOUS PRESSURE AND JVP IN DISEASED CONDITIONS ●

●

287

In normal subjects, JV pressure rises transiently (15 sec.) to 3 cm while abdominal pressure is continued, whereas in positive AJR, JV pressure remains elevated, as failing RV may not be able to receive the augmented venous return to the right heart without a rise in mean venous pressure.5 Positive AJR suggests elevated central venous pressure or pulmonary artery wedge pressure6 and occurs in (see Table 17.2): 1. 2. 3. 4.

Incipient or actual right ventricular failure LVF with hypervolemia or fluid overload Tricuspid regurgitation7 COPD: In COPD, a sudden disproportionate increase in intrathoracic pressure impedes venous return, which elevates the venous pressure and results in false positive AJR. 5. In conditions with increased generalized sympathetic tone, systemic vasoconstriction (resulting in decreased distensibility of the venous bed) may also show positive AJR.

c) Measurement of Venous Pressure by Examining the Veins of the Hand (Gaertner’s Method) Prominent antecubital veins or superficial veins on the dorsum of the hand are utilized for estimation of venous pressure. ●

●

●

With the patient sitting or lying at a 30 elevation, the arm is slowly and passively raised from a dependent position until the vein collapses. The height of the limb above the level of sternal angle at which the vein collapses represents the venous pressure. When the venous pressure is normal, the veins of the hand collapse at the level of the sternal angle. However, the local venous obstruction or augmented peripheral venous constriction diminishes the accuracy of this method.

d) Assessment of Venous Pressure by Examining the Visible Engorged Veins on the Undersurface of the Tongue (May’s Sign) In sitting posture, visible engorged veins on the undersurface of the tongue also indicate elevated venous pressure (see Fig. 17.5). Table 17.2 Conditions with positive abdominal–jugular reflux (AJR) Positive AJR

False positive AJR

1. Incipient right ventricular failure (RVF)

1. Chronic obstructive pulmonary disorders 2.  Generalized sympathetic tone 3. Systemic vasoconstriction

2. RVF (compensated) 3. Left ventricular failure with volume overload 4. Tricuspid regurgitation

288

JUGULAR VENOUS PULSE

Fig. 17.5

veins on the undersurface of the tongue—May’s sign indicating | Engorged elevated venous pressure.

2. JVP IN DISEASED CONDITIONS a) JVP in Arrhythmias Occasionally, a wave is better seen in JVP than P wave in ECG in some arrhythmias. ● In sinus bradycardia, slow normal regular sequence of a and v waves is maintained. ● In atrial fibrillation, JVP simulates TR as v wave is prominent due to the absence of a wave and diminution of x descent. So, the absence of a wave in a patient of irregular pulse is diagnostic of fibrillation; while in other irregular rhythms such as VPC, irregular cannon waves are present. ● In atrial premature contractions, normal sequence of a wave carotid pulse and v wave is maintained. ● In SVT with heart rates of  160/min, a and v waves merge into a single venous crest which resembles cannon waves of junctional tachycardia. ● In VT and junctional tachycardia, cannon waves are characteristic. b) JVP in Conduction Defects PR interval can be estimated from the interval between a wave and carotid pulse (C) so, increase a-C duration indicates prolonged PR interval. ● Hence, 1 AV block can be made out from a-C interval. However, complete LBBB also prolongs the a-C interval slightly. ● In Wenkebach (Mobitz type I), gradual lengthening of sequential a-C intervals, ending with an a wave that is not followed by a carotid pulse (nonconducted beat), can be made out. ● In Mobitz type II AV block, a-C interval does not vary but is suddenly interrupted by isolated a waves that are not followed by a carotid pulse (nonconducted beat). ● In 2:1 AV block, two a waves for every one carotid pulse are present.

ESTIMATION OF VENOUS PRESSURE AND JVP IN DISEASED CONDITIONS

289

With RVF JV pressure

With ASD

With TS a waves: with PH & TS

Absent a waves: with Af

Mitral stenosis

JV pulse

↓ or absent x descent: with Af & TR Rapid y descent: with TR & RVF

v waves: with TR & RVF

Fig. 17.6

Slow y descent: with TS

in Mitral stenosis—RVF: right ventricular failure, PH: pulmonary hyperten| JVP sion, TS: tricuspid stenosis, TR: tricuspid regurgitation, Af: atrial fibrillation, ASD: atrial septal defect.

●

Complete AV block is characterized by intermittent cannon waves in a patient with bradycardia.

c) JVP in Valvular Lesions (1) JVP in Mitral Stenosis (MS) ● ● ● ● ● ● ●

JV pressure is elevated with RVF or when associated with TS or ASD Prominent a waves with PH or when associated with TR Absent a waves with atrial fibrillation Diminished or absent x descent with atrial fibrillation or when associated with TR Prominent v waves with RVF and when associated with TR Rapid y descent: with TR or RVF Slow y descent when associated with TS (see Fig. 17.6).

(2) JVP in Mitral Regurgitation (MR) ●

● ● ●

Elevated JV pressure: (i) With RVF (ii) When associated with ASD or TS (iii) In secondary MR due to cardiomyopathy or CAD Prominent a waves with PH or MR due to HOCM Prominent v waves with RVF or associated with TR or ASD Rapid y descent: with RVF and TR (see Fig. 17.7).

(3) JVP in Tricuspid Stenosis (TS) ● ● ●

Elevated JV pressure, but may be normal in mild or moderate TS on diuretics Prominent a waves associated with presystolic hepatic pulsations Slow y descent.

290

JUGULAR VENOUS PULSE

With ASD

With RVF ↑ JV pressure

Secondary MR: CM or CAD

With TS Mitral regurgitation ↑ a waves: with PH due to HOCM JV pulse ↑ v waves: with TR, RVF or ASD

Fig. 17.7

Rapid y descent: with TR and RVF

in Mitral regurgitation—RVF: right ventricular failure, PH: pulmonary | JVP hypertension, TR: tricuspid regurgitation, TS: tricuspid stenosis, Af: atrial fibrillation, CM: cardiomyopathy, CAD: coronary artery disease, ASD: atrial septal defect, HOCM: hypertrophic obstructive cardiomyopathy. With RVF ↑ JV pressure

With MS and PH

With TS Aortic stenosis

↑ a waves: with MS, PH and TS

Fig. 17.8

JV pulse

↑ a waves: in HOCM

in Aortic stenosis—RVF: right ventricular failure, MS: mitral stenosis, | JVP PH: pulmonary hypertension, TS: tricuspid stenosis, HOCM: hypertrophic obstructive cardiomyopathy.

(4) JVP in Tricuspid Regurgitation (TR) ● ●

●

Elevated JV pressure with RVF or PH Prominent v waves: with obliteration of x descent, forms a prominent s wave, i.e. Lanci’s sign and ventricularization of the RA pressure Rapid y descent, but slow descent when associated with TS.

(5) JVP in Aortic Stenosis (AS) ● ●

Elevated JV pressure with RVF or when associated with MS and PH, or TS Prominent a waves in severe AS, HOCM or when associated with MS and PH or TS (see Fig. 17.8).

(6) JVP in Aortic Regurgitation (AR) ● ● ●

Elevated JV pressure with RVF; with CRF and fluid overload Prominent a waves with TS, MS and PH Prominent v waves and rapid y descent with RVF (see Fig. 17.9).

ESTIMATION OF VENOUS PRESSURE AND JVP IN DISEASED CONDITIONS

↑ JV pressure

With RVF

291

With MS and PH

Aortic regurgitation ↑ a waves: with MS, PH and TS JV pulse ↑ v waves: with RVF

Fig. 17.9

Rapid y descent: with RVF

in aortic regurgitation—RVF: right ventricular failure, MS: mitral steno| JVP sis, PH: pulmonary hypertension, TS: tricuspid stenosis.

With RVF ↑ JV pressure

With severe PH

With MS or MR Atrial septal defect

↑ a waves: with MS, PH and PS

JV pulse

↑ v waves: with TR

Fig. 17.10

Equal a and v waves: usual

Rapid y descent: with TR and RVF

in Atrial septal defect—RVF: right ventricular failure, MS: mitral steno| JVP sis, MR: mitral regurgitation, PH: pulmonary hypertension, TR: tricuspid regurgitation, PS: pulmonary stenosis.

(7) JVP in Pulmonary Stenosis (PS) ● ● ●

Elevated JV pressure with RVF Prominent a waves in severe PS Prominent v waves and rapid y descent: with RVF or TR.

d) JVP in Acyanotic CHD (1) JVP in Atrial Septal Defect (ASD) ● ● ● ●

Elevated JV pressure with RVF; when associated with MS/MR or severe PH Prominent a waves with PS or MS and PH Equal a and v waves, but more prominent v waves with TR Rapid y descent with TR or RVF (see Fig. 17.10).

292

JUGULAR VENOUS PULSE

With CHF In Gerbode’s defect

JV pressure In AV canal defect Ventricular septal defect

a waves: with severe PS

JV pulse

v waves: with CHF, TR and in Gerbode’s defect

Fig. 17.11

Absent x descent: with TR and in Gerbode’s defect

Rapid y descent: with CHF, TR and in Gerbode’s defect

in Ventricular septal defect—CHF: congestive heart failure, PS: pulmonary | JVP stenosis, TR: tricuspid regurgitation.

Table 17.3 JVP in Eisenmenger complex and syndrome ASD with R 䉴 L shunt

VSD with R 䉴 L shunt

PDA with R 䉴 L shunt

1. JV pressure may be elevated 2. Normal a waves, but absent with atrial fibrillation 3. Prominent v waves with CHF or TR

Usually normal Normal a waves

May be elevated a waves may be prominent

Normal v waves · CHF and TR are rare

Prominent v waves with CHF or TR

R 䉴 L: right to left, CHF: congestive heart failure, TR: tricuspid regurgitation.

(2) JVP in Ventricular Septal Defect (VSD) ●

● ● ●

Elevated JV pressure with CHF; in AV canal defect (VSD with MR/TR), VSD with LV to RA shunt (Gerbode’s defect) Prominent a waves with severe PS Prominent v waves and rapid y descent with CHF, TR, and in Gerbode’s defect Absent x descent with TR and in Gerbode’s defect (see Fig. 17.11).

e) JVP in Cyanotic CHD (1) JVP in Eisenmenger Complex and Syndrome In Eisenmenger complex (VSD with right to left shunt), the jugular venous pressure is usually normal with normal a and v waves. In Eisenmenger syndrome with ASD and PDA, jugular venous pressure may be elevated with prominent v waves (see Table 17.3). (2) JVP in Tetralogy of Fallot (TOF) or TOF Like Physiology ●

●

JV pressure: normal, but may be elevated in TOF when associated with PDA, AR, after shunt operation, or in adult TOF Normal a and v waves (see Fig. 17.12).

ESTIMATION OF VENOUS PRESSURE AND JVP IN DISEASED CONDITIONS

Usually normal

JV pressure

293

↑ in Adult TOF, after shunt surgery

Tetralogy of Fallot

a waves: normal

Fig. 17.12

JV pulse

v waves: normal

| JVP in Tetralogy of Fallot (TOF). ↑ JV pressure

TGA with ↑ PBF

↑ a waves

JV pulse

v waves: normal

↑ v waves: with CHF and TR

Fig. 17.13

in Transposition of great arteries (TGA)—PBF: pulmonary blood flow, | JVP CHF: congestive heart failure, TR: tricuspid regurgitation.

(3) JVP in PS with Intact Interventricular Septum and Right to Left Shunt ● ● ●

Elevated JV pressure Prominent a waves Normal v waves, but prominent with TR.

(4) JVP in Tricuspid Atresia ● ● ●

Elevated JV pressure with restrictive ASD Prominent a waves Normal v waves, but prominent with MR.

(5) JVP in Transposition of Great Arteries (TGA) or Total Anomalous Pulmonary Venous Connection (TAPVC) with Increased Pulmonary Blood Flow ● ● ●

Usually elevated JV pressure May be prominent a waves Normal v waves, but prominent with CHF or TR (see Fig. 17.13).

294

JUGULAR VENOUS PULSE

Table 17.4 JVP in cardiomyopathy JVP

Dilated CM

Restrictive CM

EMF

1. JV pressure 2. a waves 3. v waves 4. x descent 5. y descent

May be elevated Normal May be prominent Normal May be rapid descent Negative

May be elevated Prominent Normal Normal Normal

Usually elevated Prominent Prominent due to TR Obliterated with TR Rapid descent due to TR Negative

6. Kussmaul’s sign

May be positive

EMF: endomyocardial fibrosis, CM: cardiomyopathy, TR: tricuspid regurgitation.

Table 17.5 JVP in pericardial diseases JVP

Cardiac tamponade

Constrictive pericarditis

1. JV pressure 2. a waves 3. v waves 4. x descent 5. y descent 6. Kussmaul’s sign

Elevated Never prominent Normal Normal ⇓ or absent Negative, may be positive

Elevated Normal, may be prominent Usually equal to a waves Prominent Rapid Usually positive

↑ JV pressure

Constrictive pericarditis

Equal a and v waves

Kussmaul’s sign: usually positive

Fig. 17.14

JV pulse

x descent: prominent

y descent: rapid

| JVP in constrictive pericarditis.

Elevated JV pressure in cyanotic CHD (other than Eisenmenger’s syndrome) indicates intact IVS or increased pulmonary blood flow or both. f) JVP in Cardiomyopathy Examination of jugular venous pulse helps in the differentiation of various causes of cardiomyopathy (see Table 17.4).

ESTIMATION OF VENOUS PRESSURE AND JVP IN DISEASED CONDITIONS

295

↑ JV pressure

Cardiac tamponade

a waves: normal

v waves: normal

Fig. 17.15

JV pulse

x descent: normal

Kussmaul’s sign: usually ve, may be ve

y descent: slow or absent

| JVP in cardiac tamponade.

g) JVP in Pericardial Diseases Examination of jugular venous pulse is essential in the diagnosis of the pericardial diseases (see Table 17.5). The prominent and rapid x and y descents with positive Kussmaul’s sign are diagnostic of constrictive pericarditis (see Figs 17.14 and 17.15).

REFERENCES 1. 2. 3. 4. 5. 6. 7.

Ewy GA, Marcus FI. Bedside estimation of the venous pressure. Heart Bull 1968;17:41–44. Wood P. Diseases of the Heart and Circulation, 2nd ed. Philadelphia: Lippincott; 1957. Kussmaul A. Uber schwielige Mediastino-Pericarditis und den paradoxen Puls. (3 parts) Berl Klin Wochenschr 1873;10:433, 445, 461. Dell’Italia L, Starling MR, O’Rourke RA. Physical examination for exclusion of hemodynamically important right ventricular infarction. Ann Intern Med 1983;99(5):608–611. Ewy GA. The abdominojugular test: Technique and hemodynamic correlates. Ann Inter Med 1988; 109(6):456–460. Ducas J, Magder S, McGregor M. Validity of the hepatojugular reflux as a clinical test for congestive heart failure. Am J Cardiol 1983;52(10):1299–1303. Maisel AS, Atwood JE, Goldberger AL. Hepatojugular reflux: Useful in the bedside diagnosis of tricuspid regurgitation. Ann Intern Med 1984;101(6):781–782.

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CARDIOVASCULAR SYSTEM EXAMINATION 18. Inspection of the precordium

299

19. Palpation of the precordium

315

20. Percussion of the precordium and precordial findings in common heart diseases

333

21. Cardiac auscultation

354

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■ ■ ■ CHAPTER 18

I NSPECTION 1.

EXAMINATION OF THE CHEST a) Shape of the Chest b) Cutaneous Lesions c) Breast Abnormalities d) Distended Vessels Over the Chest and Back 2. EXAMINATION OF THE PRECORDIUM a) Ossification of the Sternum b) Ossification of the Ribs 3. CARDIOVASCULAR PULSATIONS

OF THE

299 300 303 303 304 305 305 306 306

P RECORDIUM

a) Apical Impulse 306 b) Pulsations in the (Aortic Area) Right and Left (Pulmonary Area) 2nd Intercostal Spaces 310 c) Pulsations in the Sternoclavicular Area 310 d) Left Parasternal Pulsations 311 e) Pulsations in the Epigastrium 312 f) Pulsations in the Ectopic Areas 313 REFERENCES 314

Since ancient times, ‘inspection and palpation’ of the anterior chest and precordium have been practiced as a part of the cardiovascular examination by the Physicians, the results of which have been correlated with noninvasive studies, hemodynamic data, surgical and autopsy studies.1,2 Hence, they are an important part in the evaluation of the cardiovascular disorders. Inspection of the anterior chest and precordium includes the following: ●

● ●

Examination of the chest: for its shape, cutaneous lesions, breast abnormalities and distended vessels over the chest and back Examination of the precordium for any precordial bulging Examination of the cardiovascular pulsations, which include: – Apical impulse – Pulsations in the right and left 2nd intercostal spaces (aortic and pulmonary areas) – Pulsations in the right and left sternoclavicular area – Left parasternal pulsations – Pulsations in the epigastrium – Pulsations in ectopic areas.

1. EXAMINATION OF THE CHEST The patient should lie comfortably in supine position with thorax elevated to 30. Examine the thorax tangentially, first from the foot end of the bed and then from the patient’s right side directing a beam of light across the precordium (see Fig. 18.1).

300

CARDIOVASCULAR SYSTEM EXAMINATION

A

Fig. 18.1

B

| Examination of the chest (A) from foot end of the bed, and (B) from patient’s right side. a) Shape of the Chest The normal chest in an adult is bilaterally symmetrical and elliptical in cross section with the transverse diameter greater than the anteroposterior diameter and has a subcostal angle of about 90. However; in a normal infant the cross section of the chest is almost circular with its anteroposterior and transverse diameters being equal (see Fig. 18.2). The chest may be distorted by various disorders (see Table 18.1). An abnormal chest may cause precordial bulging and displace the apex with functional murmurs mimicking an organic lesion (see Fig. 18.3). ●

●

●

●

●

In barrel shaped chest (The chest’s anteroposterior diameter is more than its transverse diameter and is usually suggestive of emphysema, chronic bronchitis), the normal cardiovascular pulsations may not be visible/palpable over the chest (see Fig. 18.4). A muscular thorax in contrast to less developed lower limbs occurs in coarctation of aorta. A broad chest with a prominent angle between the manubrium and body of the sternum is known as ‘shield chest’, which is associated with widely separated nipples and is frequently observed in: – Turner syndrome and – Noonan syndrome. Pectus carnitum (pigeon chest): marked forward protrusion of the sternum and adjacent costal cartilages, (see Figs 18.5 and 18.6) is associated with: – Marfan syndrome – Noonan syndrome – Or may be secondary to the chronic nasal or nasopharyngeal obstruction or rickets in childhood. Pectus excavatum (funnel chest: exaggerated normal hollow over the lower end of the sternum, i.e. the sternum is displaced posteriorly, see Figs 18.7 and 18.8) is observed in: – Marfan syndrome – Homocystinuria

INSPECTION OF THE PRECORDIUM

A

Fig. 18.2

301

B

| Cross section of a normal chest in A: adult, B: infant.

Table 18.1 Cardiovascular significance of chest abnormalities Shape of the chest

Causes

1. Barrel shape

Chronic obstructive pulmonary disorders Coarctation of aorta Turner and Noonan syndromes Marfan and Noonan syndromes Marfan, Ehler-Danlos, Hunter-Hurler syndromes and Homocystinuria

2. 3. 4. 5.

Muscular thorax with thin lower limbs Shield chest (broad chest) Pigeon chest (pectus carinatum) Funnel chest (pectus excavatum)

Kyphoscoliosis

Straight back Abnormal chest

Barrel shaped

Apex displacement

Funnel chest

Precordial bulging

Murmurs and abnormal S2 split

Mimics organic lesion

Fig. 18.3

| Effects of abnormal chest on cardiovascular examination.

– Ehlers-Danlos syndrome – Hunter-Hurler syndrome – Cobblers as an occupational hazard. The cobblers present with the caving-in of the lower part of the sternum due to the constant pressure of the shoe against it. However, presently this type of acquired chest deformity is rarely seen with the mechanized and improved techniques. – Secondary to rickets in childhood.

302

CARDIOVASCULAR SYSTEM EXAMINATION

A

Fig. 18.4

| Cross sections of normal chest (A) and barrel shaped chest (E).

A

Fig. 18.5

E

D

sections of normal chest (A) and pigeon | Cross chest (D). Fig. 18.6

A

Fig. 18.7

| Pigeon chest.

F

| Cross sections of normal chest (A) and funnel chest (F).

Depending upon the degree of deformity (hollowness), pectus excavatum is catagorized as saucer, cup or funnel type. This deformity may compress/displace the heart to the left, elevate the systemic or pulmonary venous pressures, with prominent pulmonary artery pulsations. The parasternal mid systolic murmur may falsely suggest the presence of organic heart disease.

INSPECTION OF THE PRECORDIUM

Fig. 18.8

| Pectus excavatum.

Fig. 18.9

303

| Aneurysm of aorta eroding the sternum.

Table 18.2 Cardiovascular significance of breast abnormalities

●

●

●

Abnormality

Causes

1. Male gynecomastia 2. Female hypomastia 3. Widely spaced nipples

Adverse effect of digitalis, Klinefelters syndrome Mitral-valve prolapse Turner and Noonan syndromes

Straight back syndrome (i.e. loss of normal thoracic kypohsis) is associated with expiratory splitting of S2, parasternal systolic impulse, mid systolic murmur and prominence of pulmonary artery on radiography, mimicking the atrial septal defect. Aortic aneurysm may present as a bulging to the right of the upper sternum (see Fig. 18.9). Harrison’s sulci extend transversely as grooves from the sides of the xiphisternum on either side, giving the thorax an appearance of transverse constriction. These grooves correspond to the costal attachments of the diaphragm and are due to the pulling of the softened ribs, which are observed in children with rickets or chronic nasal or nasopharyngeal obstruction.

b) Cutaneous Lesions Lesions such as spider nevi are seen in: ● ●

Hepatic cirrhosis and Osler-Weber-Rendu syndrome.

c) Breast Abnormalities These abnormalities should also be noted carefully (see Table 18.2). ●

Male gynecomastia either unilateral or bilateral is observed in patients on digitalis (as one of its adverse effects). It also occurs in Klinefelter syndrome (see Fig. 18.10).

304

CARDIOVASCULAR SYSTEM EXAMINATION

Fig. 18.10

| Gynecomastia in Klinefelters syndrome. ●

●

Fig. 18.11

chest and widely spaced nipples | Shield in Turner’s syndrome.

Female hypomastia is a part of the asthenic habitus in the patients with mitral valve prolapse. Widely spaced nipples associated with broad shield chest are typical of Turner’s and Noonan syndromes (see Fig. 18.11).

d) Distended Vessels Over the Chest and Back Veins Distended veins on the anterior chest wall (with caudal flow) suggest obstruction of superior vena cava, while the distended veins with cranial flow indicate inferior vena caval obstruction. Arteries Collateral vessels may be seen in the interscapular and infrascapular regions or in the posterior intercostal spaces and are palpable in patients with coarctation of aorta, when the patient stands and bends forward with arms hanging down by the sides (Suzman’s sign, see Figs 18.12 and 18.13).

INSPECTION OF THE PRECORDIUM

Fig. 18.12

305

of collateral vessels in | Examination the inter-scapular and infra-scapular regions.

Fig. 18.13

collaterals in a patient of coarc| Visible tation of aorta (Suzman’s sign).

2. EXAMINATION OF THE PRECORDIUM The precordium is examined for any bulging: ● Precordial prominence with bulging of the intercostal spaces without the involvement of the ribs is suggestive of pericardial effusion. ● Precordial prominence involving both intercostal spaces and ribs suggests cardiac enlargement (usually due to RV dilatation) of long standing duration, which usually develops before puberty. However, precordial prominence may also be present to a lesser extent in patients in whom cardiomegaly has developed in adult life, after the period of thoracic growth3 (i.e. after ossification of sternum and ribs). ● Precordial bulging of non-cardiovascular origin can occur in: —

— —

Skeletal deformities such as scoliosis, kyphoscoliosis or rickety deformity of the chest (see Fig. 18.14) Diseases of the lungs such as bronchogenic carcinoma Mediastinal new growths (see Table 18.3).

a) Ossification of the Sternum The sternum is developed from the fusion of the two cartilaginous plates along the mid-vertical line. The primary centers of ossification for manubrium and body of the sternum appear in 5–6th months of foetus. ●

●

Manubrium: secondary centers of ossification (1–3) appear at about puberty and are completed by about 25th year. Body of the sternum has four sternal segments, known as sternebrea. The fusion of the sternebrea starts at about puberty and is completed by about 25th year.

306

CARDIOVASCULAR SYSTEM EXAMINATION

Table 18.3 Causes of precordial bulging

Fig. 18.14

Precordial bulging

Causes

1. Cardiac 2. Non-cardiac

Pericardial effusion, cardiomegaly Skeletal abnormality: scoliosis, kyphoscoliosis, rickety chest, bronchogenic carcinoma, mediastinal new growth

bulging due to | Precordial severe khyphoscliosis.

●

●

The xiphoid process begins to ossify in the 3rd year and fuses with the body of the sternum at about 40th year. The bony fusion of the manubriosternal joint (sternal angle) may take place at about 60th year or after.

b) Ossification of the Ribs A rib is ossified from primary and secondary centers of ossification. The primary ossification appears at about 2nd month of intra-uterine life, while secondary centers appear at about puberty and fuse with the rest of the bone after 20 years.

3. CARDIOVASCULAR PULSATIONS Besides examining the main areas of precordium (apex, pulmonary, aortic, tricuspid and left parasternal areas), the cardiovascular pulsations should also be sought over sternoclavicular, epigastric and other ectopic areas (see Fig. 18.15). a) Apical Impulse It is examined for its site, extent and any lateral retraction. The normal apical impulse is due to (see Table 18.4). ●

●

An anterior and counter clock-wise rotation of the LV on its long axis as the isovolumic intraventricular pressure rises, which lifts the cardiac apex (lower part of the IVS and anteroseptal portion of LV) and makes a contact with the left anterior chest wall during early systole. Followed by medial retraction during late systole due to recoil of the heart as it rotates clock-wise with the completion of the LV ejection.

INSPECTION OF THE PRECORDIUM

307

1 2

3

4 6

Fig. 18.15

E 5

pulsations are examined in the following areas— | Cardiovascular 1: Sternoclavicular area, 2: Right parasternal area, 3: Pulmonary area, 4: Left parasternal area, 5: Apical area, 6: Epigastric area, E: Ectopic areas.

Table 18.4 Cause for normal apical impulse Cause

Chamber

Timing

1. Anterior and counter clock-wise rotation 2. Medial retraction due to clock-wise rotation

LV

Early systole

LV

Late systole

Table 18.5 Characteristics of normal apical impulse 1. Early systole 2. Late systole 3. Location 4. Extent 5. Duration

Outermost and lowermost point of maximum impulse Medial retraction Fifth left ICS at or medial to mid-clavicular line and 10 cm from the mid sternal line 3 cm in diameter, one intercostal space 50% of systole

Normal apical impulse is defined as: ●

●

●

The outermost and lowermost point of maximum impulse (PMI) in early systole, which imparts a perpendicular gentle thrust to a palpating finger, followed by a slight medial retraction in the late systole. The medial retraction is better seen than felt (see Table 18.5). It is located in the 4th or 5th left intercostal space at or inside the mid-clavicular line,

10 cm from the mid sternal line. It is confined to one intercostal space, which is 3 cm in diameter, and lasts for 50% of systole.

However, the point of maximum impulse or maximum precordial pulsation may be produced by a hypertrophied RV, a dilated aorta or pulmonary artery or due to the LV wall motion abnormality instead of a normal cardiac apex.

308

CARDIOVASCULAR SYSTEM EXAMINATION

(i) Absent Apical Impulse It could be due to (see Table 18.6): Cardiovascular causes: ● ● ●

CAD with decreased apical motion and reduced ejection fraction (EF) Dilated cardiomyopathy Pericardial effusion.

Non-cardiovascular causes: ● ● ● ● ●

When it is behind the rib Muscular chest wall Obesity COPD including emphysema with barrel chest Left pleural effusion.

(ii) Double Apical Impulse It may be seen in: ● ●

HOCM (could be double or triple apical impulse) LV dyssynergy or LV aneurysm.

(iii) Lateral Retraction of the Apical Impulse (Skoda’s Sign) It is due to: ●

●

Right ventricular hypertrophy (RVH), when RV occupies the apex, extending from left sternal edge to cardiac apex with exaggerated lateral apical retraction. It may be due to adhesive pericarditis.

Broadbent’s sign: It is a systolic in-drawing or retraction of 10th and 11th left intercostal spaces, in the scapular or posterior axillary line. It is typically described in adhesive pericarditis. The apical retraction is equivalent of paradoxical septal motion in echocardiogram. (iv) Displacement of Apical Impulse Lateral displacement is often due to: ●

Skeletal abnormalities: scoliosis, straight back syndrome, marked pectus excavatum. Table 18.6 Causes of absent apical impulse CV causes

Non-CV causes

1. Dilated cardiomyopathy 2. Pericardial effusion 3. CAD with decreased apical motion and ejection fraction

1. 2. 3. 4. 5.

Behind the rib Muscular chest wall Obesity COPD Left pleural effusion

INSPECTION OF THE PRECORDIUM ●

●

●

309

Intrathoracic pathology: marked right-sided pleural effusion, right-sided pneumothorax, or left lung collapse. Eccentric LVH due to mitral regurgitation or aortic regurgitation: apical impulse is displaced outwards and downwards. RVH, e.g. due to mitral stenosis apical impulse is displaced laterally.

Downward displacement only: Aortic aneurysm and mediastinal new growth may push the apical impulse downwards. Upward displacement ●

● ●

In children apical impulse is usually seen and felt in 4th left intercostal space at or inside the mid-clavicular line. Intra-abdominal causes: ascites, massive abdominal tumor, or advanced pregnancy. Pericardial effusion: it may displace apical impulse usually upwards and to the left, since fluid, as a rule, first collects in the lower portion of the pericardial sac.

Right-sided apical impulse ● ●

●

Often due to dextrocardia and congenital heart disease. Sometimes due to intra-thoracic pathology such as left-sided massive pleural effusion or pnuemothorax and right lung collapse. Skeletal abnormalities such as scoliosis (see Table 18.7).

(v) Extent of Apical Impulse Diffuse apical impulse of 3 cm in diameter or apical impulse present in more than one intercostal space may be due to: Cardiovascular causes: ● ●

Eccentric LVH as in aortic regurgitation LV aneurysm.

Table 18.7 Displacement of apical impulse Lateral displacement

Upward displacement

Downward displacement

1. Skeletal abnormalities: scoliosis, straight back syndrome, pectus excavatum 2. Intrathoracic abnormality: right pleural effusion, pneumothorax, left lung collapse 3. Eccentric LVH (mitral regurgitation, aortic regurgitation—also downwards) 4. RVH (mitral stenosis)

1. Normal children

1. Aortic aneurysm

2. Pregnancy

2. Mediastinal new growth

3. Ascitis

4. Abdominal tumor 5. Pericardial effusion (displaced upward and left)

310

CARDIOVASCULAR SYSTEM EXAMINATION

Table 18.8 Pulsations in aortic and pulmonary areas Aortic area

Pulmonary area

1. Aneurysm of ascending aorta 1. PH of any cause: mitral stenosis, primary pulmonary hypertension 2. Chronic aortic regurgitation 2. Pulmonary artery dilatation: idiopathic or aneurysmal 3.  pulmonary blood flow: PDA, ASD 4. Hyperdynamic circulation: fever, pregnancy PH: pulmonary hypertension, PDA: patent ductus arteriosis, ASD: atrial septal defect.

Non-cardiovascular causes: ● ● ●

Subjects with thin chest wall Hyperdynamic circulation: fever, thyrotoxicosis Retraction of the lung due to fibrosis or collapse.

b) Pulsations in the (Aortic Area) Right and Left (Pulmonary Area) 2nd Intercostal Spaces Ascending aorta lies to the right of the sternum at the level of 2nd right intercostal space and the pulmonary trunk lies beneath the 2nd left intercostal space, while RV outflow (infundibulum) lies beneath the 3rd left intercostal space (see Table 18.8). ●

Presence of abnormal pulsations in the aortic area may be due to the dilatation of ascending aorta because of: – Aneurysm of ascending aorta or – Chronic aortic regurgitation.

●

Pulsations in the 2nd or 3rd left intercostal space may be due to dilated pulmonary artery as a result of: – Pulmonary hypertension of any cause e.g. mitral stenosis, primary pulmonary hypertension – Idiopathic pulmonary artery dilatation2 – Increased pulmonary blood flow as in PDA, ASD – Aneurysmal dilatation of pulmonary artery – Hyperdynamic circulation as in fever, pregnancy and – Rarely due to retraction of the left lung from fibrosis or collapse.

c) Pulsations in the Sternoclavicular Area The sternoclavicular area includes the right and left sterno-clavicular joints, manubrium sterni and supra-sternal notch (Table 18.9). No pulsations are normally visible or palpable in this area. Abnormal pulsations in this area are usually due to: ●

Aortic dissection: sternoclavicular joint pulsation in a patient with chest pain may be an early clue to the diagnosis of aortic dissection.4

INSPECTION OF THE PRECORDIUM

311

Table 18.9 Pulsations in the sternoclavicular area

Fig. 18.16

● ●

●

●

●

●

Sternoclavicular pulsations

Suprasternal pulsations

1. 2. 3. 4. 5.

1. Aneurysm of arch of aorta 2. Thyroidea ima artery

Aortic dissection Aneurysm of aorta Aortic regurgitation Right aortic arch Blalock-Taussig shunt

parasternal pulsations better appreciated by placing a light object | Left (paper, pencil) in the parasternal area.

Aneurysm of aorta: atherosclerotic or syphilitic.2 Systolic pulsation of the right sternoclavicular joint or manubrium may be due to aortic regurgitation. Pulsation in the right sternoclavicular area may suggest right aortic arch as in patients with cyanotic congenital heart disease e.g. TOF.5 Blalock-Taussig shunt (classical on the opposite side of aortic arch while the modified shunt is performed on the same side of aortic arch). Suprasternal pulsations may be due to: – Aneurysm of aorta (arch of aorta) – Thyroidea ima artery. Pulsations in the suprasternal notch or supraclavicular area may be due to: – Kinked tortuous right carotid artery2 – Dilated and tortuous of brachiocephalic artery2 – Anomalous right subclavian artery.

d) Left Parasternal Pulsations RV inflow portion underlies the mid to lower left sternal edge (4th and 5th intercostal space) while its outflow portion (infundibulum) lies behind the 3rd left intercostal space. In normal adults of average build, RV activity is neither visible nor palpable as it retracts away from the anterior chest wall during systole (see Fig. 18.16).

312

CARDIOVASCULAR SYSTEM EXAMINATION

Table 18.10 Left parasternal pulsations Due to right ventricular hypertrophy

Normal right ventricle

1. Pressure over-load: Pulmonary hypertension Primary pulmonary hypertension Pulmonary stenosis 2. Volume over-load: Tricupid regurgitation (moderate) ASD, VSD

1. Mod-severe mitral regurgitation (squid effect)

2. Regional wall motion Abnormality (RWMA) of left ventricle

ASD: atrial septal defect, VSD: ventricular septal defect, RWMA: regional wall motion abnormality.

Left parasternal pulsations may be seen in: ●

●

●

●

Children and thin adults with a small antero-posterior diameter or in patients with pectus excavatum. RVH with pressure over-load conditions (see Table 18.10): – Pulmonary stenosis – PH due to mitral valve disease, LVF, left to right shunt (PDA, VSD and ASD) – Pulmonary embolism – Corpulmonale – Primary pulmonary hypertension. RVH with volume over-load conditions (see Table 18.10): Mild-moderate tricuspid regurgitation, ASD, VSD.6 Left parasternal pulsations due to anterior systolic movement of normal RV: (i) Moderate to severe mitral regurgitation in the absence of PH produces apparent RV impulse at the left parasternal area. This apparent late anterior systolic movement of RV is due to: – Jet or squid effect as a result of regurgitation of blood into the LA which lies behind the RV7 and – Subsequent systolic expansion of the enlarged LA causing anterior displacement of RV. With a coexisting PH, the left parasternal impulse will be sustained throughout the systole, and the squid effect and subsequent expansion of LA may not be detectable. (ii) Regional wall motion abnormalities (RWMA) of LV: Dyskinetic motion of the ventricular septum during angina pectoris displaces the RV forward and results in a transient left parasternal impulse that promptly disappears on relief of the angina.

e) Pulsations in the Epigastrium The pulsations in the epigastrium may be: ●

Cardiac, aortic or hepatic in origin (see Table 18.11 and Fig. 18.17).

INSPECTION OF THE PRECORDIUM

313

Table 18.11 Epigastric pulsations Cardiac

Aortic

Hepatic

1. Right ventricular hypertrophy

1. Thin built/hyperkinetic individuals 2. Aneurysm of descending aorta 3. Aortic regurgitation

1. Tricuspid regurgitation 2. Tricuspid stenosis

Cardiac

Epigastric pulsations

Hepatic

Right ventricular hypertrophy

Aortic

Tricuspid regurgitation, tricuspid stenosis

Aortic aneurysm, aortic regurgitation, thin individuals

Fig. 18.17

| Causes and importance of epigastric pulsations.

Cardiac Pulsations in the Epigastrium ●

●

These pulsations are due to marked RV dilatation or RVH of any cause. The inferior portion of the RV transmits its impulse to the sub-xiphoid or epigastric region, which is accessible to palpation during held inspiration. In COPD with RVH, RV impulse is accessible only in this region.

Aortic Pulsations in the Epigastrium ●

●

In thin built or hyperkinetic individuals, aortic pulsations may be visible or palpable in the epigastrium. However, abnormally large pulsations in the epigastrium may be due to aneurysm of descending aorta or due to aortic regurgitation.

Hepatic Pulsations in the Epigastrium These may be due to: ● ●

Tricuspid regurgitation (systolic pulsations) Tricuspid stenosis (presystolic pulsations).

f) Pulsations in the Ectopic Areas Occasionally, cardiac pulsations are encountered in areas other than in the usual areas of the precordium.

314

CARDIOVASCULAR SYSTEM EXAMINATION ●

●

●

●

Ectopic LV impulse is located usually above and medial to the normally expected cardiac impulse: – Due to dyskinesia of the LV either during the episodes of angina pectoris or after acute myocardial infarction. – Persistent paradoxical ectopic pulsations due to ventricular aneurysm because of myocardial infarction or trauma. Ectopic LA impulse: In a patient of severe MR with giant LA that extends to the right, an ectopic systolic pulsation may be encountered in the right anterior or lateral chest or in the left axilla.2 RA impulse: Normally, RA forms the right lower cardiac border, which lies behind the right lateral border of the sternum in the 4th intercostal space, and RA impulse is not visible or palpable. However; in enlarged RA as in tricuspid regurgitation, systolic expansion of the enlarged RA causes late systolic movement of the entire right lower chest especially in the 4th right intercostal space. Ectopic impulse beneath the left clavicle is seen in patients with PDA.

REFERENCES 1. 2. 3. 4. 5. 6. 7.

Corvisart JN. An Essay on the Organic Diseases and Lesions of the Heart and Great vessels. Translated from the French, with notes by Jacob Gates. New York: Hafner, 1962. Schlant RC, Hurst JW. Examination of the precordium: Inspection and Palpation. New York: Am Heart Assoc 1990:1–28. Davies H. Chest deformities in congenital heart diseases. Br J Dis Chest 1959;53:151–157. Logue RB, Sikes C. A new sign in dissecting aneurysm of aorta: Pulsation of a sternoclavicular joint. JAMA 1952;148(14):1209–1212. Perloff JK. The movements of the heart—observation, palpation and percussion. In: Physical Examination of the Heart and Circulation. Philadelphia, Saunders, 1982:130–170. Nagle RE, Tamara FA. Left parasternal impulse in pulmonary stenosis and atrial septal defect. Br Heart J 1967;29:735–741. Basta LL, Wolfston P, Eckberg DL, et al. The value of left parasternal impulse recordings in the assessment of mitral regurgitation. Circulation 1973;48(5):1055–1065.

PALPATION 1.

EXAMINATION OF THE CHEST FOR THE SHAPE AND DISTENDED VESSELS 2. PALPATION OF THE PRECORDIUM FOR ANY TENDERNESS 3. PALPATION OF THE CARDIOVASCULAR PULSATIONS, PALPABLE SOUNDS, THRILLS AND RUBS a) Palpation of the Cardiac Apex b) Palpation of Left Parasternal Area c) Palpation of Lower Left Sternal Area (Tricuspid Area) d) Palpation of Aortic and Pulmonary Areas e) Palpation of Sternoclavicular Areas

316 316

316 318 322 326 326 328

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CHAPTER 19

OF THE

PRECORDIUM

f) Palpation of Epigastrium g) Palpation in the Ectopic Areas 4. TRACHEAL TUG (OLIVER’S SIGN) 5. KINETIC CARDIOGRAM a) The Apical Impulse in Normal Adults b) Hyperdynamic/Hyperkinetic Apex c) Sustained/Heaving Apex d) Hyperkinetic RV Impulse e) Sustained RV Impulse f) Systolic Movements are Inconspicuous in Cardiomyopathy g) In Constrictive Pericarditis REFERENCES

328 328 329 330 330 331 331 331 331

331 332 332

Egyptian physicians and priests employed the technique of palpation, and it was one of the techniques of examination in the ancient Greece. Practice of precordial palpation was recorded in the Ebers papurus (1500 BC). William Harvey (1628) was familiar with the movements of the chest wall and described, “Motion of the heart”. In 1857, Chauvea confirmed Harvey’s contention that precordial movement seen when the heart strikes against the breast resulted from the ventricular contraction. Jean Nicolas Corvisart, French physician pioneered the art of bedside inspection and palpation of the precordium.1 Method of examination: Palpation of the precordium includes systematic examination of the following: ● ● ● ●

Examination of the chest for the shape and distended vessels Palpation of the precordium for tenderness Palpation of the cardiovascular pulsations, palpable sounds, thrills and rubs Examination for tracheal tug.

316

CARDIOVASCULAR SYSTEM EXAMINATION

1. EXAMINATION OF THE CHEST FOR THE SHAPE AND DISTENDED VESSELS i) Confirm the barrel shape chest by measuring the antero-posterior (AP) and transverse diameters, in which AP diameter is  transverse diameter. ii) For associated abnormalities, see inspection of the precordium. iii) Distended veins over the anterior chest with caudal flow suggest SVC obstruction; while with the cranial flow indicate IVC obstruction. iv) Collateral arteries may be seen in the infrascapular and interscapular regions or in the posterior intercostal spaces in a patient with coarctation of aorta and are palpable when the patient stands and leans forward with arms hanging down by the sides (Suzman’s sign).

2. PALPATION OF THE PRECORDIUM FOR ANY TENDERNESS ●

●

Tenderness of the costochondral junction occurs in Tietze syndrome, which is important to rule out myocardial ischemia in a patient with chest pain. Precordial tenderness may be associated with acute pericarditis and acute myocarditis (see Table 19.1).

3. PALPATION OF THE CARDIOVASCULAR PULSATIONS, PALPABLE SOUNDS, THRILLS AND RUBS ●

●

●

Palpation of the precordium is performed from the right side of the supine patient with the upper trunk elevated to 30 and the chest completely exposed. Palpation of the apex should also be done in the left lateral position, rotated 45–90,2 which causes the heart to move laterally and increases the palpability of apex (see Fig. 19.1). Palm of the hand and ventral surface of the proximal metacarpals are used for the initial localization of palpable cardiac motion such as the cardiac apex and for the detection of the precordial thrills, while the pads of the fingers are used for precise localization and assessment of left and right ventricular activity (see Fig. 19.2). Once the precordial impulse is identified, varying pressure should be applied with the hand. While high frequency movements such as ejection sounds, valve closure sounds and mitral opening sounds are more easily detected with the palm and proximal metacarpals held firmly against the chest, the low frequency movements such as ventricular diastolic filling events (S3, S4) are best felt by applying light pressure with the fingertips. Table 19.1 Precordial tenderness 1. Tietze syndrome 2. Acute pericarditis 3. Acute myocarditis

PALPATION OF THE PRECORDIUM ●

317

Thrills are most easily palpated with fingertips or by applying firm pressure with palm and proximal metacarpals. Occasionally, thrills are readily detected with the right palm firmly placed over the anterior chest and the left hand supporting the posterior thorax with equal force.3

All precordial movements should be timed with the simultaneous palpation of carotid pulse with the left hand or auscultation of the heart sounds (see Fig. 19.3).4 Palpation of the cardiovascular pulsations includes: ● ●

Cardiac apex Left parasternal area Localized pulsations

Thrills

Heaves or lifts

Fig. 19.2 Fig. 19.1

areas on the examiner’s hand | Optimal for precordial palpation.

palpation of the apex in left lateral | Initial position.

Fig. 19.3

and determining the character of the apex beat while timing | Localization with the carotid.

318

CARDIOVASCULAR SYSTEM EXAMINATION ● ● ● ● ●

Lower left sternal area (tricuspid area) Aortic and pulmonary areas Sternoclavicular areas Epigastrium Ectopic areas.

a) Palpation of the Cardiac Apex (i) Size and Extent of the Cardiac Apex Confirm site and extent of the cardiac apex by palpation in supine position with trunk elevated to 30. If the apical impulse was not visible, palpate for the cardiac apex and determine its location and extent. ● ● ●

Normal cardiac apex: See apical impulse Displaced cardiac apex: See displaced apical impulse Double or triple cardiac apex: See double apical impulse.

In HOCM, a mid or late systolic secondary bulge may be present that results in a double or bifid apical impulse. When S4 is palpable, the apex beat may actually be triple or trifid in nature (triple ripple). Extent of cardiac apex: See extent of apical impulse. (ii) Character of the Apex Beat The apex should be palpated first in supine position with trunk elevated to 30 and then the character of the cardiac apex is determined in left lateral position rotated to 45–90. The outward movement of the apical impulse is normally felt during the first third of systole, but the systolic inward movement is only visible as medial retraction. The cardiac apex may be (see Table 19.2 and Fig. 19.4): ● ● ● ●

Absent or feeble Tapping Hyperdynamic Heaving.

Absent or feeble apex beat: See absent apical impulse.

Table 19.2 Types of apex beat Tapping

Hyperdynamic

Heaving

1. Mitral stenosis

1. Aortic regurgitation, mitral regurgitation 2. PDA, VSD 3. AV fistula 4. Blalock and Waterston shunts 5. Hyperkinetic states: anemia, pregnancy, thyrotoxicosis 6. Thin chest, pectus excavatum

1. Pressure overload: aortic stenosis, HCM, systemic hypertension 2. Severe LV dysfunction 3. LV aneurysm 4. Severe aortic regurgitation 5. Severe mitral regurgitation of ischemic origin

PALPATION OF THE PRECORDIUM

CAD, DCM, pericardial effusion

Mitral stenosis

Tapping

Apex beat

Hyperdynamic

AR, MR, VSD, PDA, AV fistula

Fig. 19.4

Heaving

319

MCW, obesity, COPD, behind the rib

Absent or feeble

AS, HCM, LV aneurysm, severe LVD

Hyperdynamic circulation, thin chest, pectus excavatum

beat and its importance—CAD: coronary artery disease, DCM: dilated | Apex cardiomyopathy, MCW: muscular chest wall, COPD: chronic obstructive pulmonary disorders, AR: aortic regurgitation, AS: aortic stenosis, MR: mitral regurgitation, MS: mitral stenosis, VSD: ventricular septal defect, PDA: patent ductus arteriosus, HCM: hypertrophic cardiomyopathy, LVD: left ventricular dysfunction, AV: arteriovenous.

Tapping apex beat ●

●

Tapping apex beat is characteristic of mitral stenosis in which the apex beat is often impalpable and is replaced by a short systolic tap, a palpable equivalent of a loud S1. A shortened outward movement of the apex during early systole due to the reduced ventricular filling during diastole gives the apex beat its sharp, short and tapping nature in mitral stenosis.

Hyperdynamic/hyperkinetic/forceful apex beat ●

●

There is an increase in amplitude and duration of excursion of the apical impulse, but is ill sustained i.e. duration of excursion is 50% of systole with partial lifting of the examining fingers. This type of cardiac apex is characteristic of volume overload conditions and eccentric LVH. It is best appreciated by simultaneous auscultation and palpation.

Cardiovascular causes ● ●

Valvular regurgitations: Aortic regurgitation, mitral regurgitation Left to right shunts: – Congenital: VSD, PDA, systemic arteriovenous fistula – Acquired: Systemic to pulmonary artery shunt: Blalock and Waterston shunts, systemic arteriovenous fistula.

Non-cardiovascular causes ● ●

Hyperkinetic circulatory states: Pregnancy, anemia, thyrotoxicosis, Beri-beri Thin chest wall, pectus excavatum.

320

CARDIOVASCULAR SYSTEM EXAMINATION

Heaving/sustained apex beat ●

●

There is a sustained increase in the duration of excursion of apical impulse besides its amplitude, due to increased duration of the LV ejection i.e. duration of excursion is 50% of systole with sustained lift of the examining fingers. This type of cardiac apex is characteristic of pressure overload conditions and concentric LVH. It is also better appreciated by simultaneous auscultation and palpation.

Cardiovascular causes ● ● ●

Pressure overload: Aortic stenosis, systemic hypertension, hypertrophic cardiomyopathy CAD: LV aneurysm, severe LV dysfunction Severe volume overload conditions such as severe aortic regurgitation and severe mitral regurgitation secondary to CAD may also present with sustained apex beat.

(iii) Palpable Low Frequency Sounds at the Apex Normally, the diastolic events such as the ventricular filling during rapid filling phase and presystole are neither visible nor palpable. Low frequency sounds such as S3, S4 and pericardial knock are best felt by light palpation with fingertips in held expiration, but firm pressure would dampen them. Palpable LV S3 (rapid filling wave, see Table 19.3) Cardiovascular causes ● ●

Left ventricular failure Chronic mitral regurgitation

Non-cardiovascular causes ● ●

Physiological: Children and pregnancy Hyperkinetic circulatory states: Anemia, thyrotoxicosis

Palpable pericardial knock: It occurs in constrictive pericarditis with systolic retraction of whole of the pericardium especially in the left 10th and 11th intercostal spaces in the posterior axillary/scapular line (Broadbent’s sign). Palpable LV S4 (“a” wave/presystolic impulse, see Table 19.3): Presystolic atrial contraction, which distends the LV is normally not palpable, but is felt in the non-compliant LV when the left ventricular end diastolic pressure (LVEDP) is 15–18 mmHg (normal LVEDP is 12 mmHg). Table 19.3 Palpable S3 and S4 Palpable S3

Palpable S4

1. Children 2. Pregnancy 3. Left ventricular failure

1. Aortic stenosis 2. Hypertrophic cardiomyopathy 3. Acute mitral regurgitation and acute aortic regurgitation 4. Acute or CAD 5. Normal women of 40 years of age

4. Chronic significant mitral regurgitation

PALPATION OF THE PRECORDIUM

321

Cardiovascular causes ● ● ● ●

Aortic stenosis Hypertrophic cardiomyopathy Acute mitral regurgitation, acute aortic regurgitation CAD—acute or chronic

It is sometimes palpable in normal women of 40 years of age. (iv) Palpable High Frequency Sounds at the Apex Opening snaps, tumor plops and ejection sounds (clicks) are best felt by applying firm pressure to the chest with palm and proximal metacarpals (see Table 19.4). Palpable loud S1: apex beat.

It occurs due to mitral stenosis, which imparts a tapping type of

Palpable opening snap: It occurs in early diastole due to mitral stenosis with pliable mitral valve. It may radiate to the lower left sternal edge when loud. Palpable tumor plop: It is a rarely palpable early diastolic sound due to abrupt deceleration of a mobile pedunculated LA or RA myxoma as the tumor sits in the mitral or tricuspid orifice. Palpable ejection sounds ●

●

●

Ejection sound (click) of congenital aortic stenosis sometimes more readily palpable over the apex than in the 2nd right intercostal space (ICS). However, the ejection sounds due to dilated aortic root are better felt at the right base (2nd right ICS) and Pulmonary ejection sound is felt in 2nd left ICS during normal expiration.

(v) Palpable Murmurs—Thrills at the Apex Diastolic or presystolic thrill ●

●

Diastolic thrill of mitral stenosis is highly localized to the apex, which generally indicates mobile and non-calcified mitral valve. If thrill is equivocal even in the left lateral position, a brisk cough will make it more pronounced as it transiently increases the heart rate and mitral flow.

Table 19.4 Palpable high frequency sounds at the apex Sounds

Cause

1. 2. 3. 4.

Mitral stenosis Mitral stenosis (pliable mitral valve) LA myxoma (mobile) Congenital aortic stenosis (bicuspid aortic valve)

Loud S1 Opening snap Tumor plop Systolic ejection sound

322

CARDIOVASCULAR SYSTEM EXAMINATION

Systolic thrills: ●

●

●

These are not common at the apex. They may occur due to:

Severe mitral regurgitation especially due to chordal rupture. However, systolic thrills due to mitral regurgitation are not common. Aortic stenosis: Thrill may be traced from 2nd right ICS to the apex and may get conducted to the carotids. However, it may only be felt at the apex in calcified aortic atenosis in the elderly patients. VSD: It is better felt in the 3rd–4th ICS at the left sternal edge.

Palpable pericardial rub: It occurs in acute pericarditis and is best felt at the left sternal border in sitting and leaning forward positions. b) Palpation of Left Parasternal Area A French Physician, Jean Nicolas Corvisart (in the late 18th and early 19th century) pioneered the art of inspection and palpation of precordium (especially the left parasternal area) and correlated the clinical findings with the autopsy findings.1 i) Left Parasternal Lift ●

●

●

For parasternal lift due to RV hypertrophy; heel of the hand with the wrist cocked upwards, is placed over the lower half of the sternum during the held end expiration (see Fig. 19.5). The movements of the examining hand and fingers should be carefully observed as the low amplitude RV activity is better seen than felt. Alternatively, tips of three fingers (index, middle, ring) are placed in the 3rd, 4th, and 5th intercostal spaces near the left sternal edge during the full held expiration which not only permits the detection of gentle RV systolic impulses but also localizes the movements to the inflow portion (4th and 5th ICS) or to the infundibulum/outflow portion (3rd ICS) (see Fig. 19.6). The left parasternal area can also be palpated with the ulnar border of the hand and the pulmonary artery pressure can be judged clinically by applying varying pressure (see Fig. 19.7).

Fig. 19.5

of left parasternal area (LPA) with heel of the hand and wrist | Palpation cocked upwards.

PALPATION OF THE PRECORDIUM

323

Grading of parasternal lift: There is no standard method of grading parasternal lift (PSL). However, in general, there are two accepted methods: subjective and objective. The subjective method assesses the amplitude of excursion of PSL while for the objective assessment; the duration of the PSL (sustained/ill sustained) is noted by simultaneous auscultation. More clinical information is obtained with the combination of these two methods (see Table 19.5). GRADE-1/3 (mild): Mild lift can be made out after careful inspection of the parasternal area (see Fig. 19.8). ●

●

Light objects such as pencil or scale kept along the parasternal region, may make it more obvious. It disappears with the application of mild counter pressure. It is short of systole i.e. ill sustained, 1/3rd of systole.

Fig. 19.6

| Palpation of left parasternal area (LPA) with tips of the three fingers.

Fig. 19.7

method of palpation of left parasternal area (LPA) with ulnar border | Alternative of the hand.

324

CARDIOVASCULAR SYSTEM EXAMINATION

Table 19.5 Left parasternal lift Grade-1/3

Grade-2/3

Grade-3/3

1. Normal children and young adults 2. Thin chest wall

1. Mild-moderate pulmonary hypertension 2. RV volume overload: tricuspid regurgitation, ASD, VSD 3. Moderate-severe mitral regurgitation

1. Moderate-severe pulmonary stenosis 2. Severe pulmonary hypertension

3. Pectus excavatum

Fig. 19.8

●

| Grade I left parasternal left.

It may be seen – normally in children and young adults – in thin adults with a small AP thoracic diameter or – in subjects with pectus excavatum.

GRADE-2/3 (moderate): An obvious lift that can be easily made out. ● ● ●

It disappears/diminishes with the application of moderate counter pressure. It is not well sustained i.e. 50% of systole but not throughout the systole. It is usually seen in: – RV volume overload conditions such as tricuspid regurgitation, ASD, VSD – Mild-moderate pulmonary hypertension of any cause e.g. moderate mitral stenosis, left ventricular failure, left to right shunts (VSD, PDA) – Moderate-severe mitral regurgitation due to jet/squid effect.5

Characteristics of PSL in mitral regurgitation ●

Simultaneous palpation of the apex and the parasternal area is mandatory to identify this type of PSL due to the anterior movement of normal right ventricle.

PALPATION OF THE PRECORDIUM

Fig. 19.9

325

palpation of apex (with index finger) and left parasternal area | Simultaneous (with ulnar border of the hand) for parasternal lift in mitral regurgitation— ICS: intercostal space.

Fig. 19.10

palpation of apex (with index finger) and left parasternal area | Simultaneous (with index finger of other hand) for parasternal lift in mitral regurgitation— ICS: intercostal space.

● ●

●

PSL occurs in the second half of systole following S1 and after the cardiac apex is felt. It is short in duration (ill sustained) and more diffused and indicates a non compliant enlarged left atrium. It can be recognized by placing the index finger of one hand at the cardiac apex and the index finger or ulnar border of the other hand at the left parasternal region in the 3rd–4th ICS (see Figs 19.9 and 19.10). The movement of the latter begins and ends slightly later than that of the former.

GRADE-3/3(severe): It is a very prominent parasternal lift. ● ●

Application of moderate counter pressure does not diminish the PSL. It is well sustained i.e. PSL is present throughout the systole and beyond A2.

326

CARDIOVASCULAR SYSTEM EXAMINATION ●

Characteristic of RV pressure overload conditions such as: – Pulmonary stenosis (moderate-severe) – And severe pulmonary hypertension due to severe mitral stenosis, left to right shunts (PDA, VSD) and left ventricular failure.

No PSL in TOF: There is no PSL in RVH due to TOF2 ● ●

As it can decompress easily into the overriding of aorta and through VSD and RV is not excessively dilated.

(ii) Palpable Low Frequency Sounds RV S3 and S4 may be palpable in this area or occasionally in the epigastrium in held inspiration which is attenuated or even disappears during expiration. ●

●

RV S3 usually indicates RV dysfunction or failure, chronic severe tricuspid regurgitation and ASD RV S4 is associated with pulmonary stenosis, decreased RV compliance secondary to pulmonary hypertension.

c) Palpation of Lower Left Sternal Area (Tricuspid Area) Patient should be in supine position with right lateral rotation. Palpable Low Frequency Sounds RV S3 and RV S4 may only be palpable in this area in supine and right lateral rotation. Palpable High Frequency Sounds Opening snap of organic tricuspid stenosis is sometimes palpable with the fingers firmly applied in this area or in the epigastrium. Palpable Murmurs—Thrills Occasionally, diastolic thrill of organic tricuspid stenosis and rarely, systolic thrill of severe tricuspid regurgitation may be palpable. d) Palpation of Aortic and Pulmonary Areas The basal areas of the heart (2nd right ICS and 2nd–3rd left ICS) should be palpated in the sitting and leaning forward positions in held expiration, which increases the palpability of these areas (see Figs 19.11 and 19.12). (i) Palpable High Frequency Sounds In aortic area: Palpable A2 in the aortic area occurs in: ● ●

Systemic hypertension, dilated aortic root and moderate aortic stenosis Cyanotic congenital heart disease: When pulmonary trunk is small as in TOF or when the aortic root is anterior to the pulmonary trunk as in transposition of great arteries (TGA).

PALPATION OF THE PRECORDIUM

Fig. 19.11

| Palpation of aortic area. Fig. 19.12

327

| Palpation of pulmonary area.

Palpable ejection sound originating in the dilated aortic root. Ejection sound of congenital aortic stenosis is sometimes more readily palpable over the apex than in the right 2nd ICS and should be differentiated from a loud S1. In pulmonary area ●

●

Palpable P2 in the pulmonary area occurs in pulmonary hypertension of any cause, which may be widely transmitted to mid and lower left sternal edge and apex especially when the RV occupies the apex. Palpable ejection sound in the pulmonary area occurs in pulmonary stenosis during normal expiration.

(ii) Palpable Murmurs—Thrills In aortic area ●

●

Systolic thrill in the aortic area (palpable in held expiration with firm application of fingertips) occurs in aortic stenosis, which may be conducted to the carotids. It may be occasionally detected at the apex in the older patients with calcified aortic stenosis. Rarely, a diastolic thrill may be palpable due to dilated aortic root as in Marfan syndrome.

In pulmonary area ●

●

Palpable systolic thrill in the pulmonary area may be felt in pulmonary stenosis in sitting and leaning forward positions in held expiration, while thrill of infundibular pulmonary stenosis is best felt in the left 3rd ICS. Continuous thrill of PDA is felt maximal beneath the left clavicle, which begins in systole, is reinforced before and after S2 and proceeds into the diastole without interruption.

328

CARDIOVASCULAR SYSTEM EXAMINATION

Table 19.6 Precordial thrills Apex

Tricuspid area

1. Diastolic: mitral stenosis

1. Diastolic: tricuspid stenosis 2. Systolic: acute severe mitral 2. Systolic: rarely regurgitation (chordal rupture), severe tricuspid calcified aortic stenosis regurgitation

●

●

Pulmonary area

Aortic area

1. Systolic: pulmonary 1. Systolic: aortic stenosis stenosis 2. Continous: patent ductus arteriosus

Rarely, Graham Steel murmur (early diastolic) of high pressure pulmonary regurgitation may be palpable. It is rare to detect a palpable diastolic thrill of aortic regurgitation along the left sternal edge in the 3rd ICS (neo aortic area), unless there is perforation or eversion of an aortic cusp resulting in an extremely loud diastolic murmur.

Presence of thrills in main areas of the precordium (i.e. at the apex, tricuspid, pulmonary and aortic areas) is helpful in the diagnosis of underlying disorders (see Table 19.6). e) Palpation of Sternoclavicular Areas Continuous/systolic thrill is palpable on the left side due to Blalock-Taussig shunt operation, while it is felt on the same side in the modified shunt operation. f) Palpation of Epigastrium ●

●

●

●

The subxiphoid region, which allows the palpation of RV, should be examined with the tip of the index finger. It should be done during held inspiration and in supine position (see Figs 19.13 and 19.14). This technique is particularly useful in patients with an increased AP diameter, COPD, obesity or muscular chest when the RV enlargement is suspected, but precordial impulse is not felt for evaluation. However, pulsations in the epigastrium could also due to the aortic pulsations or hepatic pulsations. While palpating the epigastrium, the pulsations due to RV hypertrophy are felt by the fingertip, aortic pulsations by the palmar surface and hepatic pulsations by the lateral surface of the examining index finger.

g) Palpation in the Ectopic Areas Occasionally, cardiac pulsations may be palpable in the areas other than in the usual areas of the precordium. (i) Ectopic LV Impulse It is usually palpable above and medial to the normally expected cardiac apex ●

Due to dyskinesia of CAD, during the episodes of angina pectoris or after acute myocardial infarction

PALPATION OF THE PRECORDIUM

Fig. 19.14

Fig. 19.13

329

of the epigastrium with the tip of | Palpation the index finger.

| Initial palpation. ●

Ventricular aneurysm: Persistent paradoxical palpable ectopic pulsations due to ventricular aneurysm because of myocardial infarction or trauma.

(ii) Ectopic LA Impulse In patients with severe mitral regurgitation with giant LA that extends to the right, ectopic systolic pulsations of the enlarged LA may be felt in the right anterior or lateral chest or in the left axilla.3 (iii) Ectopic RA Impulse Normally RA impulse is not visible or palpable. However if RA is enlarged as in tricuspid regurgitation, systolic expansion of the enlarged RA may be palpable in the entire right lower chest especially in the 4th right ICS. (iv) Due to PDA Palpable ectopic impulse beneath the left clavicle in patients with PDA.

4. TRACHEAL TUG (OLIVER’S SIGN) ●

Raise the chin of the patient and apply firm upward pressure with fingers on the two sides of the circoid cartilage (see Fig. 19.15).

330

CARDIOVASCULAR SYSTEM EXAMINATION

S4

E S1

A2

P2

S3

a

o

Fig. 19.16

Fig. 19.15

RFW

| Normal apex cardiogram (ACG).

| Examination for tracheal tug. ●

●

●

A downward ‘tug’ felt by the fingers with each beat of the heart suggests the possibility of the presence of an aortic aneurysm. It is due to the downward pull exerted by the aneurysmal aortic arch on the left bronchus, later transmitted to the trachea and cricoid. However, the movement of the cricoid is forward and backward due to transmitted pulsations from the vessels of the neck to the cricoid, but not a distinct forward pull as in tracheal tug.

5. KINETIC CARDIOGRAM It is the graphic representation of the precordial movements. Kinetic apex cardiogram is the graphic representation of the apical movements, which consists of systolic and diastolic events (see Fig. 19.16). a) The Apical Impulse in Normal Adults ●

●

●

The normal apex cardiogram (ACG) is characterized by palpable outward apical movements in early systole (E point) lasting for a brief period (up to 0.08 sec.), and later systolic inward movement partly due to recoil of the heart as it rotates clockwise on its long axis, which is only visible as medial retraction. Diastolic events which occur with the opening of the mitral valve (O point), consist of an early diastolic outward movement due to the rapid ventricular filling (Rapid filling wave, RFW) corresponding to S3 and a late diastolic outward movement due to the late ventricular filling {because of left atrial contraction (a wave)} corresponding to S4, are normally not palpable. Occasionally, RFW may be palpable in normal children and young adults.

PALPATION OF THE PRECORDIUM A

331

B S4 S4

E S1

A2

E S1

A2

P2

S3

P2 S3

a a RFW o

Fig. 19.17

o

RFW

| ACG—Normal apex (B) and Hyperdynamic LV apex (A).

b) Hyperdynamic/Hyperkinetic Apex ●

●

It is associated with eccentric LVH and is characterized by the exaggeration of the normal apex (E point) with rapid upstroke both in amplitude and duration (50% of systole) followed by marked mid or late systolic retraction (see Fig. 19.17). RFW may be palpable coinciding with the S3 as in mitral regurgitation.

c) Sustained/Heaving Apex ●

● ●

It is associated with concentric LVH and is characterized by slow LV upstroke but increase in duration (50% of systole) (see Fig. 19.18). ‘a’ wave may be palpable coinciding with S4. A double outward systolic thrust (which is often palpable) may be recorded in hypertrophic cardiomyopathy. (see Fig. 19.19).

d) Hyperkinetic RV Impulse ● ●

It is associated with RV volume overload conditions. It is characterized by outward movement in both amplitude and duration (50% of systole) of the left sternal edge in 3rd and 4th ICS followed by retraction, which is augmented during inspiration.

e) Sustained RV Impulse ● ●

It is associated with RV pressure overload conditions. It is characterized by sustained (50% of systole) outward movement of the left sternal edge in 3rd and 4th ICS, which is augmented during inspiration.

f) Systolic Movements are Inconspicuous in Cardiomyopathy While diastolic movements of RFW and ‘a’ wave (corresponding to S3 and S4) may be prominent and may merge to form a summation gallop in tachycardia.

332

CARDIOVASCULAR SYSTEM EXAMINATION A

B S4

E S1

A2

E

P2 S3 S4

a

P2

S3

a o

Fig. 19.18

A2

S1

RFW

o

RFW

| ACG—Normal apex (A) and Sustained LV apex (B).

A

B S4

E S1

P S A2 2 3 S1 S4

SM

S2

a

a o

Fig. 19.19

RFW

apex (A) and Double outward systolic thrust in hypertrophic | ACG—Normal cardiomyopathy (B).

g) In Constrictive Pericarditis There is a conspicuous inward apical movement (retraction) during systole with an exaggerated RFW (corresponding to the pericardial knock) which is often palpable.

REFERENCES 1. 2. 3. 4. 5.

Corvisat JN. An Essay on the Organic Diseases and Lesions of the Heart and Great vessels. Translated from the French, with notes by Jacob Gates. New York: Hafner, 1962. Stapleton JF, Groves BM. Precordial palpation. Am Heart J 1971;82:409–427. Schlant RC, Hurst JW. Examination of the precordium: Inspection and Palpation, New York: Am heart Assoc 1990:1–28. O’Neill TW, Smith M, Barry M, et al. Diagnostic value of the apex beat. Lancet 1989;1(8635): 410–411. Basta LL, Wolfson P, Eckberg DL, et al. The value of left parasternal impulse recordings in the assessment of mitral regurgitation. Circulation 1973;48:1055–1065.

■ ■ ■ CHAPTER 20

P ERCUSSION OF THE P RECORDIUM AND P RECORDIAL F INDINGS IN COMMON H EART D ISEASES METHODS OF PERCUSSION Direct Percussion Indirect Percussion Auscultatory Percussion THE SCHEME OF PERCUSSION Determination of the Cardiac Borders Percussion of the Pulmonary and Aortic Areas Direct Percussion of the Sternum Special Percussions

334 334 334 334 334 335 336 337 337

PRECORDIAL FINDINGS IN COMMON HEART DISEASES Acquired Heart Diseases Acyanotic Congenital Heart Diseases Cyanotic Congenital Heart Diseases (CCHD) Precordial Findings in Cardiomyopathy REFERENCES

338 338 343 349 351 353

Joseph Leopold Auenbrugger introduced percussion of the thorax, as a new method of clinical examination in 1761, after witnessing the practice of tapping of the wine barrels in his father’s cellar to determine their contents.1 However, his invention remained dormant until Corvisart, personal Physician to Napoleon, published Auenbrugger’s text in 1821. Percussion was once employed routinely and was regarded as a valuable and indispensable method of clinical examination of cardiovascular system, but some clinicians have lately abandoned it. However, it is still a useful and informative method of clinical examination provided its limitations are understood. ● ●

● ●

●

It furnishes information about the size and shape of the heart. It is particularly useful in patients in whom apical thrust is neither visible nor palpable as in pericardial effusion or dilated cardiomyopathy or marked displacement of the hypokinetic apex. It is of undoubted value in the diagnosis of aortic aneurysm. It is useful in the detection of enlarged right atrium, right ventricle and pulmonary conus. It is a useful tool in determining the visceral status i.e. situs solitus or situs inversus.

334

CARDIOVASCULAR SYSTEM EXAMINATION

Percussing finger: Perpendicular stroke

Movement at the wrist

Vertical position of terminal phalanx

Percussed finger in close contact with body surface

Fig. 20.1

| Indirect method of percussion.

METHODS OF PERCUSSION Generally, there are three methods of percussion: Direct Percussion In direct percussion, strokes are aimed directly at the chest wall especially over the bony structures such as clavicle and sternum. Indirect Percussion In indirect percussion, strokes are aimed at some intermediate object, e.g. finger (pleximeter) applied to the surface of the chest wall. Percussing finger is the plexor and percussed finger is the pleximeter (see Fig. 20.1). Auscultatory Percussion It is a special technique of percussion to determine the cardiac borders, in which chest piece of the stethoscope is placed over the sternum just above the xiphisternum, and the skin is lightly scratched inwards from the axillae towards the sternum. The point at which the soft scratching sound becomes suddenly intense corresponds to the cardiac border on that side2 (see Fig. 20.2).

THE SCHEME OF PERCUSSION Percussion of the precordium includes the systematic examination of the following: ● ● ●

Determination of the cardiac borders Percussion of the pulmonary and aortic areas Direct percussion of the sternum.

PRECORDIAL FINDINGS IN COMMON HEART DISEASES

Fig. 20.2

percussion for determination | Auscultatory of right heart border.

Fig. 20.4a

Fig. 20.3

335

of right | Determination heart border.

for right border of the heart—upper border of the liver dullness | Percussion is dilenated (5 ICS in mid-clavicular line). th

Determination of the Cardiac Borders Besides the conventional indirect method of percussion, auscultatory percussion may be used to determine the cardiac borders. It is customary to percuss from resonant to dull areas or centripetally from surrounding areas towards the heart when indirect percussion method is used. (See above for auscultatory percussion.) Right Border of the Heart (see Figs 20.3, 20.4a and 20.4b) ●

●

The upper margin of liver dullness on the right side is defined first by percussing from above downwards in each intercostal space in the mid-clavicular line. Usually, the upper border of liver dullness is in the 5th intercostal space (ICS). Percussion is then carried out in the intercostal space above this level (usually 4th ICS) moving inwards towards the sternum, either parallel or at right angles to the right cardiac border.

336

CARDIOVASCULAR SYSTEM EXAMINATION

4th ICS parallel to sternum

Fig. 20.4b

Then, Percussion is carried out in 4 inter| costal space (ICS) parallel to sternum. th

● ●

Fig. 20.5

| Percussion of the aortic area.

Normally, right cardiac border corresponds to the right sternal margin. If the percussed border is 1 cm outside the right sternal margin, following should be entertained: – Cardiac enlargement (often RA/sometimes LA enlargement, rarely both) – Displacement of the heart to the right (often due to intrathoracic pathology) or – Pericardial effusion.

Left Border of the Heart The cardiac apex is palpated and percussion is done in the same ICS from the axilla towards the left cardiac border. Usually, the left cardiac dullness corresponds to the cardiac apex. However, it does not correspond to the apex beat in the following conditions: ●

●

In a patient with large pericardial effusion, the apex beat may actually be detected medial to the lateral border of the percussible cardiac silhoutte. LV aneurysm: Ectopic LV impulse is often above and medial to the left border of the apex.

Percussion of the Pulmonary and Aortic Areas Percuss the 2nd ICS to the right of the sternum (aortic area, see Fig. 20.5). Normally, it is resonant and dullness in this area, if present may be due to: ● ● ●

Aortic aneurysm, dilated ascending aorta Superior mediastinal tumor or Pericardial effusion.

Percuss the 2nd ICS to the left of the sternum (pulmonary area, see Fig. 20.6). It is normally resonant. Dullness in this area indicates the presence of: ● ● ●

Dilated pulmonary artery PDA or Sometimes, enlarged LA appendage.

PRECORDIAL FINDINGS IN COMMON HEART DISEASES

Fig. 20.6

| Percussion of the pulmonary area.

Fig. 20.7

337

| Direct percussion of the sternum.

Direct Percussion of the Sternum Direct percussion of the sternum is done with the patient in supine position,3 and normally whole of the sternum except for a small area at the xiphisternum is resonant (see Fig. 20.7). Flat note or dullness of the manubrium sternum (which extends to the 1st or 2nd ICS) is due to: ● ●

Aortic aneurysm Mediastinal pathology (especially tumor). Flat note or dullness of the lower part of sternum indicates:

● ●

RV hypertrophy or Pericardial effusion.

Special Percussions Auscultatory Percussion It is used to determine the cardiac borders. Rotch’s Sign The upper border of liver dullness and the right border of cardiac dullness along the right sternal edge form the cardio-hepatic angle. In moderate to large pericardial effusion, the cardio-hepatic angle becomes obtuse (Rotch’s sign) which is frequently associated with dullness in the 2nd right ICS. Enlarged LA Appendage The cardiac dullness (left cardiac border) in the 3rd ICS if extends 3.5 cm from the mid sternal line, may suggest enlarged LA appendage as in severe MS or MR. Determination of the Situs Percuss over the fundus of the stomach (normally resonant) and determine liver dullness (see Fig. 20.8). In the situs solitus (see Fig. 20.9), fundus of the stomach is on

338

CARDIOVASCULAR SYSTEM EXAMINATION

Absolute dullness (cardiac) Tympany (traube’s semilunar space)

Relative dullness (liver)

Fig. 20.8

of percussion over the fun| Method dus of the stomach for determina-

Fig. 20.9

tion of the situs.

solitus with liver dullness on the | Situs right side and tympany of the fundus on the left side.

AK AAo PT DAo

Apex S

Fig. 20.10

L

with situs inversus—S: spleen, L: liver, PT: pulmonary trunk, | Dextrocardia DAo: descending aorta, AAo: ascending aorta, AK: aoric knuckle.

the left side and liver dullness is on the right while it is reversed in situs inversus (see Fig. 20.10). PRECORDIAL FINDINGS IN COMMON HEART DISEASES Acquired Heart Diseases 1. Mitral Stenosis (MS) Apex ●

●

Apex is formed by hypertrophied RV, which is localized, laterally displaced, and tapping in character (due to palpable S1) in moderate to severe MS (see Table 20.1 and Fig. 20.11). Palpable S1 and Opening snap medial to apex indicate a relatively mobile mitral valve.

PRECORDIAL FINDINGS IN COMMON HEART DISEASES

339

Table 20.1 Precordium in mitral stenosis (MS) Features

Significance

1. Apex

Formed by hypertrophied right ventricle, and tapping in character, palpable opening snap, and diastolic thrill Sustained heave Palpable P2: with pulmonary hypertension Right ventricular hypertrophy Associated tricuspid regurgitation/stenosis Enlarged right ventricle; /flat note in left 2nd ICS;  note over lower sternum

2. Left parasternal lift 3. Pulmonary area 4. Epigastric pulsations 5. Pulsatile liver 6. Precordial percussion

Palpable P2 with PH

Diastolic thrill Pulmonary area (PA)

Systolic thrill with ASD

Palpable S1, OS

Tapping

Apex

Due to RVH

Epigastric pulsations

Mitral stenosis

Left parasternal

Due to PH and TR

PSH with PH

RV S3 in RVF Tricuspid area

Precordial percussion

RAE with TS or TR

Diastolic thrill with TS ↓ Note over LS due to RVH

Fig. 20.11

↓ Note in PA with RH

in mitral stenosis—OS: opening snap, RVH: right ventricular hypertrophy, PH: | Precordium pulmonary hypertension, RVF: right ventricular failure, TS: tricuspid stenosis, TR: tricuspid regurgitation, ASD: atrial septal defect, PSH: parasternal heave, RAE: right atrial enlargement, LS: lower sternum, PA: pulmonary area. ●

Diastolic thrill in moderate-severe MS indicates a relatively mobile valve. It may be absent in mild MS, severe calcified MS and in severe RVF.

Left parasternal area ● ● ●

●

Sustained parasternal heave (Gr 2-3/3) in moderate to severe MS with PH Hyperkinetic parasternal lift when MS is associated with ASD (Lutembacher syndrome) Both sustained and hyperkinetic parasternal lift: moderate-severe MSPH with TR/PR or both Normal or Gr 1/3 LPS impulse: mild MS, thick chest wall, or associated TS.

340

CARDIOVASCULAR SYSTEM EXAMINATION

Table 20.2 Precordium in mitral regurgitation (MR) Features

Significance

1. Apex

Formed by hypertrophied left ventricle, and hyperkinetic in character; systolic thrill less common (only in chordal rupture), LV S3: in chronic MR, LV S4: in acute MR Late, lower and ill sustained (skid effect). Sustained with pulmonary hypertension

2. Left parasternal lift

Tricuspid area ●

●

●

Palpable RV S3 occurs in RVF that correlates with rapid Y descent in JVP, and rules out associated TS. Palpable RV S4 occurs in severe PH with noncompliant RV and associated PS but rules out TS. It correlates with prominent a wave in JVP. Palpable diastolic thrill is present in associated moderate-severe TS.

Epigastric pulsations ● ●

These indicate RV enlargement. May occur in MSPH with TR

Pulmonary area ● ●

Visible pulsations and palpable P2 indicate PH. Systolic thrill is felt when associated with ASD.

Precordial percussion ● ● ●

Enlarged RA when associated with TR/TS Flat note or dullness in pulmonary area in the dilated pulmonary artery due to PH Dullness over the lower part of the sternum in hypertrophied RV.

2. Mitral Regurgitation (MR) Apex ●

●

●

●

●

Apex is formed by the hypertrophied (eccentric) LV, which is displaced laterally and downwards, and is hyperdynamic in character in moderate-severe MR (see Table 20.2 and Fig. 20.12). Sustained/heaving apex is felt in MR when it is associated with hypertrophied obstructed cardiomyopathy (HOCM). Palpable systolic thrill is less common. Thrill is felt in severe MR, usually due to the chordal rupture. Palpable S3 in chronic moderate MR, and when complicated with congestive heart failure Palpable S4 in acute MR, and when associated with CAD or HOCM.

Left parasternal area ●

Late ill sustained parasternal lift in severe MR without PH (due to skid effect), and parasternal heave with significant PH.

PRECORDIAL FINDINGS IN COMMON HEART DISEASES

341

Palpable P2 with PH Pulmonary area (PA)

Systolic thrill: in severe MR

Systolic thrill with ASD Palpable S3; S4 with CAD or HOCM Mitral regurgitation

PSH with PH

Hyperdynamic Apex

Left parasternal

Sustained with HOCM Precordial percussion ↓ Note in PA with PH

Fig. 20.12

PSL in severe MR LAE (appendage)

in mitral regurgitation (MR)—PH: pulmonary hypertension, | Precordium ASD: atrial septal defect, PSH: parasternal heave, LAE: left atrial enlargement, PSL: parasternal lift, CAD: coronary artery disease, HOCM: hypertrophic obstructive cardiomyopathy.

Table 20.3 Precordium in aortic stenosis (AS) Features

Significance

1. Apex

Formed by hypertrophied left ventricle, and heaving in character; systolic thrill in calcified AS, S4 may be palpable Systolic thrill, and conducted to the carotids /falt note in 2nd right Intercostal space

2. Aortic area 3. Percussion

Pulmonary area ● ●

Visble pulsations and palpable P2 with PH Systolic thrill is felt when associated with ASD.

Precordial percussion ●

●

Left cardiac dullness may be 3.5 cm from the mid-sternal line in the 3rd ICS due to the enlarged LA appendage. Flat note or dullness is noted in the pulmonary area with PH.

3. Aortic Stenosis (AS) Apex ●

●

Apex is formed by hypertrophied (concentric) LV, which is normal in position or there is a little lateral displacement with sustained/heaving apex in moderate-severe AS (see Table 20.3 and Fig. 20.13). It is displaced downwards and outwards when associated with dominant AR, PDA, or is complicated by CHF.

342

CARDIOVASCULAR SYSTEM EXAMINATION

Systolic thrill in sclerotic AS

Palpable S4

Systolic thrill

Aortic area (AA)

Apex

Heaving

Fig. 20.13

Aortic stenosis (AS)

Precordial percussion

↓ Note in AA

| Precordium in aortic stenosis.

Table 20.4 Precordium in aortic regurgitation (AR) Features

Significance

1. Apex

Formed hypertrophied left ventricle and hyperdynamic in character; palpable S4: in acute AR Diastolic thrill: rare (in root causes due to cusps retroversion) Systolic thrill due to functional aortic stenosis in severe AR /flat note in 2nd right ICS: AR of root causes

2. Aortic area 3. Carotids 4. Percussion

●

●

●

Sustained/heaving apex is noted in mild AS when it is associated with systemic hypertension, severe AR, large PDA or myocardial infarction. Palpable S4: Moderate-severe AS, rules out associated significant MS; HOCM unlikely in the absence of palpable S4 Palpable S3: AS complicated by LVF; AS associated with MR or PDA.

Aortic area ●

●

●

Systolic thrill at the aortic area and conducting to the carotids: It may also occur in the functional AS with severe AR. Systolic thrill only at the carotids favors supravalvular AS. Other conditions associated with thrill at the carotids are carotid stenosis and Takayasu aortitis. Systolic thrill at the apex in calcified AS in elderly patients.

Precordial percussion ●

Flat note or dullness in the 2nd right ICS may be present.

4. Aortic Regurgitation (AR) Apex ●

●

Apex is formed by the hypertrophied (eccentric) LV, which is displaced outwards and downwards, and is hyperdynamic in character in moderate-severe AR with medial systolic retraction (see Table 20.4 and Fig. 20.14). It is normal in location in mild AR, but also gets displaced laterally and downwards when associated with MR, PDA, VSD or coarctation of aorta.

PRECORDIAL FINDINGS IN COMMON HEART DISEASES

Palpable S3 with LVF or MR

Sustained in severe chr AR

Systolic thrill

Carotids

Apex

Hyperdynamic

Fig. 20.14

Aortic regurgitation

343

Precordial percussion

↓ Note in AA in root causes

in aortic regurgitation—LVF: left ventricular failure, MR: mitral | Precordium regurgitation, chr: chronic, AA: aortic area.

Table 20.5 Precordium in atrial septal defect Features

Significance

1. Apex

Formed by enlarged right ventricle which is diffused systolic retraction: when left to right shunt is 1.5:1 Hyperkinetic, but sustained with pulmonary hypertension (PH) RV S3: with right ventricular failure (RVF) Pulsations; palpable P2: with PH/large shunt Due to right ventricular enlargement RA enlarged, /flat note over lower sternum due to right ventricular hypertrophy (RVH)

2. Left parasternal lift 3. Tricuspid area 4. Pulmonary area 5. Epigastric pulsations 6. Percussion

● ● ●

●

It is also hyperdynamic in character when mild AR is associated with MR, VSD or PDA. It may be sustained/ heaving, especially in chronic AR. Palpable S4 (‘a’ wave) is noted in acute AR, and may be associated with systemic hypertension or acute aortic dissection. Palpable S3 is noted when complicated with LVF or it is associated with significant MR.

Aortic area ●

●

Diastolic thrill is rarely palpable due to the retroversion of the aortic cusps as in aortic root diseases. Systolic thrill is palpable only at the carotids in functional AS with severe AR.

Precordial percussion ●

Due to the aortic root causes, flat note or dullness is noted in the 2nd right ICS in AR.

Acyanotic Congenital Heart Diseases 1) Atrial Septal Defect (ASD) Apex ● ●

Apex is formed by the enlarged RV (see Table 20.5 and Fig. 20.15). Apical impulse is diffused and hyperdynamic with systolic lateral retraction. The systolic retraction often suggests a moderate-large left to right shunt (1.5:1).

344

CARDIOVASCULAR SYSTEM EXAMINATION Sustained with PH, MS or PS Visible pulsations Palpable S3 with RVF

LP impulse

Hyperkinetic

Pulmonary area (PA) Tricuspid area Palpable P2 with LS or PH

Hyperkinetic Atrial septal defect

Diffused Apex

Systolic retraction

Systolic thrill may with LS Epigastric pulsations

Precordial percussion Sustained with LS or PH

Due to RVH RAE

↓ Note in PA with PH

Fig. 20.15

↓ Note over lower sternum due to RVH

in atrial septal defect—MS: mitral stenosis, PH: pulmonary | Precordium hypertension, PS: pulmonary stenosis, RVH: right ventricular hypertrophy, RAE: right atrial enlargement, LS: large shunt, LP: left parasternal.

● ●

Apical impulse is localized when associated with MR or ostium primum defect. It may be sustained with PH or in the presence of a large shunt without elevated pulmonary artery pressure.

Left parasternal area ● ●

Usually, hyperkinetic left parasternal lift is noted. Sustained/heaving is noted when complicated with PH, or is associated with PS or MS.

Lower left sternal area ● ●

Palpable S3 is noted with RVF. Palpable diastolic thrill is more likely due to Ebstein’s anomaly than with simple ASD.

Pulmonary area ● ● ●

Visible pulsations are more likely with ASD than with PS. Palpable P2 is noted in a large shunt or with PH. Systolic thrill is noted in a large left to right shunt in 25% of the cases, however PS is more likely than ASD.

Epigastric pulsations ●

These pulsations occur due to RV enlargement.

Precordial percussion ●

Flat note or dullness is noted in the pulmonary area with moderate-large shunt or with PH.

PRECORDIAL FINDINGS IN COMMON HEART DISEASES

345

Table 20.6 Precordium in ventricular septal defect (VSD) Features

Significance

1. Apex

Formed by hypertrophied left ventricle and hyperdynamic in character; palpable S3: with left ventricular failure/associated significance mitral regurgitation In 3rd–4th intercostal space (ICS): systolic thrill Hyperkinetic but sustained with pulmonary hypertension (PH) Pulsations and palpable P2: with PH systolic thrill: in supracristal/ subpulmonary VSD /flat note in 2nd left ICS: in large shunt or with PH

2. Left sternal border 3. Left parasternal lift 4. Pulmonary area 5. Percussion

Visible pulsations with LS or PH

Sustained with PH Systolic thrill in SA VSD

Pulmonary area (PA)

LP impulse LSB Hyperkinetic Hyperdynamic

Apex

Localized

Palpable P2 with PH Ventricular septal defect

Precordial percussion Sustained with HF or MR

↓ Note in PA with PH

Fig. 20.16

Systolic thrill in SP VSD RSB

Systolic thrill in Gerbode’s defect RAE in Gerbode’s defect

in ventricular septal defect (VSD)—PH: pulmonary hypertension, | Precordium LS: large shunt, LP: left parasternal, SA: subaortic, SP: sub pulmonary, MR: mitral regurgitation, HF: heart failure, LSB: left sternal border, RSB: right sternal border.

●

●

Flat note or dullness of lower part of the sternum (direct percussion) occurs due to the RV enlargement. Right heart border (RA) may be enlarged.

2) Ventricular Septal Defect (VSD) Apex ●

● ● ●

Apex is usually formed by the hypertrophied left ventricle (see Table 20.6 and Fig. 20.16). It is localized and hyperdynamic in moderate-large VSD. It is sustained when associated with coarctation of aorta or AS. Palpable S3 is noted with heart failure or when associated with significant MR.

346

CARDIOVASCULAR SYSTEM EXAMINATION

Table 20.7 Precordium in patent ductus arteriosus (PDA) Features

Significance

1. Apex

Formed by hypertrophied left ventricle and hyperdynamic in character; palpable S3: with left ventricular failure Hyperkinetic; but sustained: with pulmonary hypertension (PH) Pulsations and palpable P2: with PH or large PDA; continuous thrill, but only systolic with PH /flat note in 2nd left intercostal space, left infraclavicular region: moderate-large shunt/PH

2. Left parasternal lift 3. Pulmonary area and left infraclavicular region 4. Percussion

Left parasternal area ● ● ●

Hyperkinetic left parasternal lift is noted in moderate VSD without PH. It becomes sustained with PH. Isolated sustained parasternal lift with the loss of characteristic apical impulse occurs in VSD associated with PH with little or no left to right shunt.

Pulmonary area ● ● ●

Visible and palpable pulsations occur in moderate-large left to right shunt or with PH. Palpable P2 suggests PH and rules out PS. Systolic thrill suggests supracristal/subpulmonary VSD.

Left sternal border ●

Systolic thrill is consistent with VSD (subaortic) in the 3rd–4th ICS.

Right sternal border ●

Systolic thrill suggests LV to RA communication (Gerbode’s defect) in the 4th ICS.

Precordial percussion ● ●

Flat note or dullness in the pulmonary area occurs in moderate-large shunt or with PH. Enlarged RA may be noted in Gerbode’s defect.

3) Patent Ductus Arteriosus (PDA) Apex ● ●

● ●

Apex is formed by the hypertrophied left ventricle (see Table 20.7 and Fig. 20.17). It is localized, hyperdynamic and is displaced downwards & outwards in moderatelarge PDA with left to right shunt. It becomes sustained when associated with coarctation of aorta or with AS. Palpable S3 is noted in heart failure.

Left parasternal area ● ●

Hyperkinetic parasternal lift is noted in moderate-large PDA without PH. It becomes sustained with PH.

Pulmonary area ● ●

Visible and palpable pulsations are noted in moderate-large PDA or with PH. Palpable P2 is noted in moderate-large ductus or with PH.

PRECORDIAL FINDINGS IN COMMON HEART DISEASES

Sustained with PH Systolic thrill in SA VSD

Visible pulsations with MLD or PH

LSB

Palpable P2 with MLD or PH

Patent ductus arteriosus

Pulmonary area (PA)

347

LP impulse

Hyperkinetic Hyperdynamic

Apex

Localized

Precordial percussion Sustained with COA

Palpable S3 with HF

Fig. 20.17

Continuous thrill extending to LIC Systolic thrill with PH

↓ Note in PA and LIC with PH or MLD

in patent ductus arteriosus—PH: pulmonary hypertension, | Precordium MLD: moderate-large ductus, LP: left parasternal, SA VSD: subaortic ventricular septal defect, HF: heart failure, LSB: left sternal border, LIC: left infraclavicular region, COA: coarctation of aorta.

●

●

Continuous thrill extending to the left infra-clavicular region or the supra-sternal notch is consistent with ductus. (Differtial diagnosis: peripheral pulmonary artery stenosis in which isolated right ventricular enlargement is present) Only systolic thrill is noted in PDA with PH.

Left sternal border ●

Systolic thrill is noted when associated with VSD.

Precordial percussion ●

Flat note or dullness in the pulmonary area and the left infraclavicular region is noted in moderate-large PDA or with PH.

4) Pulmonary Stenosis (PS) Apex ●

Apex is formed by the diffuse hypertrophied RV (see Table 20.8 and Fig. 20.18).

Left parasternal area ● ●

●

Sustained parasternal lift is noted in moderate-severe PS. Palpable RV S4 is present in the left parasternal/tricuspid area in severe PS and it favors intact ventricular septum. Palpable RV S3 is present in the left parasternal/tricuspid area in RV failure.

Pulmonary area ● ●

Systolic thrill is noted in valvular PS. Diastolic thrill occurs in dysplastic pulmonary valve (PSPR) of Noonan syndrome or it is noted when complicated by infective endocarditis.

348

CARDIOVASCULAR SYSTEM EXAMINATION

Table 20.8 Precordium in pulmonary stenosis (PS) Features

Significance

1. Apex 2. Left parasternal lift 3. Left parasternal area/ tricuspid area 4. Pulmonary area 5. Third/fourth left ICS 6. Percussion

Hypertrophied right ventricle (RV) and diffused Sustained Palpable RV S4 in severe PS; palpable RV S3: with right ventriclar failure Systolic thrill; diastolic thrill: in dysplastic pulmonary valve Systolic thrill: in infundibular PS /flat note in 2nd left intercostal space (ICS): valvular PS; in 3rd–4th left ICS: infundibular PS, in left infraclavicular region: supravalvular PS

Sustained lift Systolic thrill in IPS LP Palpable RV S4

3rd–4th LICS

Systolic thrill in SPS

Palpable RV S3 with RVF

Pulmonary stenosis

LIC Systolic thrill

Apex

Precordial percussion

Pulmonary area (PA)

Diffused ↓ Note in PA

↓ Note in LIC in SPS

Diastolic thrill with dysplastic PV

By HRV ↓ Note in third to fourth LICS in IPS

Fig. 20.18

RAE with TR

in pulmonary stenosis—LP: left parasternal, LIC: left infraclavicular region, LICS: | Precordium left intercostal spaces, IPS: infundibular pulmonary stenosis, SPS: supravalvular pulmonary stenosis, PV: pulmonary valve, RV: right ventricle, HRV: hypertrophied right ventricle, RAE: right atrial enlargement, TR: tricuspid regurgitation.

Systolic thrill in other regions ● ●

It is noted in the 3rd/4th left ICS in the infundibular PS. It is present in the infraclavicular region/lateral to pulmonary area in the supravalvular PS.

Epigastric pulsations ●

These occur when associated with TR.

Precordial percussion ●

●

Flat note or dullness is felt in the pulmonary area (valvular PS), 3rd/4th left ICS (infundibular PS) or in the left infraclavicular region (supravalvular PS). There is enlarged RA when associated with TR.

PRECORDIAL FINDINGS IN COMMON HEART DISEASES

349

Table 20.9 Precordium in cyanotic congenital heart diseases (CCHD) with decreased pulmonary blood flow Features

Significance

1. Apex

Formed by the hypertrophied right ventricle (left ventricle in tricuspid atresia), unimpressive; no S3 Unimpressive Unimpressive; systolic thrill if pulmonary stenosis is present

2. Left parasternal lift 3. Pulmonary area

Cyanotic Congenital Heart Diseases (CCHD) It is broadly classified depending upon the pulmonary blood flow: CCHD with decreased pulmonary blood flow: a) With right ventricular hypertrophy (RVH) ● Tetralogy of Fallot (TOF) ● VSD PS (TOF like) physiology: – Double outlet right ventricle (DORV) with PS – Transposition of great arteries (TGA) with VSD and PS – Single ventricle with PS. b) With left ventricular hypertrophy (LVH) ● Tricuspid atresia (increased pulmonary blood flow with d TGA) ● Pulmonary atresia with intact ventricular septum, ASD and hypoplastic right ventricle. CCHD with increased pulmonary blood flow a) With right ventricular hypertrophy ● Total anomalous pulmonary venous connection (TAPVC). b) With biventricular hypertrophy (BVH) ● TGA, VSD without PS ● DORV without PS ● Truncus arteriosus ● Pulmonary atresia with bronchial collaterals or PDA ● TOF with PDA. c) With left ventricular hypertrophy ● Single ventricle (double inlet left ventricle). Precordial Findings in CCHD with Decreased Pulmonary Blood Flow Apex ● It is mostly formed by the hypertrophied RV (with no gross cardiac enlargement) except in the tricuspid atresia in which it is formed by the hypertrophied LV (see Table 20.9 and Fig. 20.19). ● Normal or unimpressive/impalpable apex is present. Left parasternal area ● Unimpressive or Gr 1/3 left parasternal lift is noted.

350

CARDIOVASCULAR SYSTEM EXAMINATION

Unimpressive

Left parasternal

No pulsations No palpable P2

Unimpressive

Apex

Palpable S3

Systolic thrill with PS

CE

Cyanotic CHD

Apex

↑ PBF

Pulmonary area

LSB-3rd–4th ICS

Palpable P2

Systolic thrill due to VSD

Fig. 20.19

↓ PBF

Pulmonary area

Visible pulsation

in cyanotic congenital heart diseases (CCHD)—PBF: pulmonary blood flow, CE: | Precordium cardiac enlargement, mostly biventricular, PS: pulmonary stenosis, VSD: ventricular septal defect, LSB: left sternal border, ICS: intercostal space.

Table 20.10 Precordium in cyanotic congenital heart diseases (CCHD) with increased pulmonary blood flow Features

Significance

1. Apex

Mostly due to biventricular hypertrophy; but right ventricular hypertrophy in total anomalous pulmonary venous connection and left ventricular hypertrophy in single ventricle; palpable S3 Systolic thrill due to presence of ventricular sepal defect

2. 3rd–4th left intercostal space at sternal edge 3. Pulmonary area

Pulsations; palpable P2

Pulmonary area ● ●

There are no palpable pulmonary pulsations or palpable P2. Systolic thrill is noted if PS is present.

Other accompanying diagnostic features ● ● ● ●

There is absence of heart failure. There is absence of S3. Jugular venous pressure is normal. There is absence of flow murmurs (diastolic) across the AV valves.

Precordial Findings in CCHD with Increased Pulmonary Blood Flow Apex ●

●

There occurs cardiac enlargement mostly due to BVH. There is RVH in TAPVC while LVH is present in single ventricle (double inlet left ventricle, DILV) (see Table 20.10 and Fig. 20.19). Palpable S3 is often present.

PRECORDIAL FINDINGS IN COMMON HEART DISEASES

351

Table 20.11 Precordium in tetralogy of Fallot (TOF) Features

Significance

1. Apex

Formed by hypertrophied right ventricle and unimpressive; no S3/S4 are palpable Unimpressive No pulsations/palpable P2/thrills

2. Left parasternal lift 3. Pulmonary area

Left sternal edge (3rd–4th ICS) ● Systolic thrill (due to VSD) is palpable. Pulmonary area ● Visible/palpable pulmonary pulsations are present. ● Palpable P is noted. 2 Other accompanying diagnostic features ● Heart failure is noted with S . 3 ● Jugular venous pressure is elevated. ● Flow murmurs (diastolic) are present across the AV valves. Precordial Findings in TOF Apex ●

● ●

Apex is formed by the hypertrophied RV, but there is no gross cardiac enlargement (see Table 20.11). Normal or unimpressive/impalpable apex beat is present. It is hyperdynamic when associated with AR, PDA or sometimes in pink TOF with left to right shunt.

Left parasternal area ● Insignificant or Gr 1/3 parasternal pulsations are present. Pulmonary area ● There are no pulmonary pulsations. P is not palpable and no systolic thrill is felt. 2 ● Continuous thrill is present at the pulmonary area/infraclavicular region when associated with PDA. Other features ● No S or S are palpable. 3 4 ● Signs of heart failure are present when associated with AR, systemic hypertension and in adult type of TOF. Precordial Findings in Cardiomyopathy It is broadly classified into the following three categories (see Table 20.12): ● Dilated congestive cardiomyopathy

352

CARDIOVASCULAR SYSTEM EXAMINATION

Table 20.12 Precordium in cardiomyopathy Features 1. Apex

2. Palpable S3 3. Palpable S4 4. Thrills

● ●

Dilated congestive cardiomyopathy

Hypertrophic cardiomyopathy

Restrictive cardiomyopathy

Diffused and displaced; never hyperdynamic/ sustained Common Not palpable No thrills

Formed by left ventricle and sustained, may be triple-ripple May in failure Common Systolic thrill with left ventricular outflow tract obstruction

Normal; hyperdynamic with significant mitral regurgitation May palpable Common Absent, may be with signigicant tricuspid regurgitation/mitral regurgitation

Hypertrophic cardiomyopathy Restrictive cardiomyopathy.

The diagnosis of cardiomyopathy is unlikely in the presence of the following features: ●

● ●

Systolic retraction of the apical impulse (more likely constrictive pericarditis which simulates restrictive cardiomyopathy) Impalpable S3 or S4 Signs of significant pulmonary hypertension: – Visible or palpable pulmonary artery pulsations in the pulmonary area – Palpable P2 in the pulmonary area – Left parasternal impulse of Gr 2/3

●

Prominent systolic or diastolic thrill.

1) Dilated Congestive Coardiomyopathy ● ● ●

Apex is diffused and displaced but is never hyperdynamic or sustained. Palpable S3 is common. No systolic/diastolic thrills are present.

2) Hypertrophic Cardiomyopathy ●

● ● ● ●

Apex is formed by hypertrophied (concentric) LV, which is localized and often sustained. Palpable S4 (‘a’ wave) is common. Occasionally, mid or late systolic lift (giving a ‘triple ripple’) is present. Palpable S3 may occur in heart failure. Systolic thrill is superior and medial to the apical impulse (usually with the LV outflow tract obstruction).

3) Restrictive Cardiomyopathy ●

Apical impulse is often normal unless it is associated with significant AV regurgitation (when it may be hyperdynamic).

PRECORDIAL FINDINGS IN COMMON HEART DISEASES ● ● ●

353

Palpable S4 is common. S3 may be palpable. Thrills are usually absent, but may be palpable with significant TR/MR as in endomyocardial fibrosis.

REFERENCES 1. Vakil RJ, Golwalla AF. The Cardiovascular system-Historical note on percussion. In: Clinical Diagnosis. 2nd ed, Bombay, Asia Publshing House, 1967:200. 2. Vakil RJ, Golwalla AF. The Cardiovascular system-Special techniques of percussion. In: Clinical Diagnosis. 2nd ed, Bombay, Asia Publshing House, 1967:214. 3. Vakil RJ, Golwalla AF. The Cardiovascular system-Percussion of the sternum. In: Clinical Diagnosis. 2nd ed, Bombay, Asia Publshing House, 1967:213–214.

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CHAPTER 21

CARDIAC AUSCULTATION PRINCIPLES AND TECHNIQUES The Human Acoustic Acuity Factors Affecting Cardiac Sound Transmission Characteristics of the Cardiac Sounds The Stethoscope Examination of the Patient Phonocardiography THE HEART SOUNDS The First Heart Sound The Second Heart Sound Diastolic Sounds The Systolic Sounds

354 354 355 355 356 358 361 361 362 369 383 396

Prosthetic Valve Sounds Extra-Cardiac Sounds THE HEART MURMURS Definition Mechanism of Production of the Murmurs Factors for the Production of Murmurs Characteristics of Murmurs Systolic Murmurs Diastolic Murmurs Continuous Murmurs REFERENCES

400 402 404 404 404 406 406 422 431 441 451

PRINCIPLES AND TECHNIQUES Direct or immediate auscultation was practiced by Hippocrates (400 B.C) and was an established diagnostic technique in the ancient medicine. It is performed by applying the ear to the chest,1 However, there is no recorded account of precordial auscultation until William Harvey (1616) referred the heart beat as ‘two clicks of a water bellow.’2 The modern era of cardiac auscultation began in 1826 with the invention of the stethoscope by RTH Laennec, which initiated “the Golden Century of Stethoscopy.”3 The Human Acoustic Acuity ●

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The human ear is capable of detecting sound vibrations from 20 to 20000 Hz (cycles per s, CPS). However, it is most sensitive to the auditory vibrations between 1000 and 5000 Hz, while the optimal range of auditory acuity is 1000 to 2000 Hz (see Table 21.1). In humans, higher frequency events are better heard at any level of sound intensity than low frequency sounds, and most of the cardiovascular sounds and murmurs are in the range of 30 to 1000 Hz. As the normal ear’s acoustic sensitivity decreases at frequencies below 1000 Hz, and as the low frequency sounds and murmurs are more commonly missed by the examiner, the clinician has to use an instrument such as the

CARDIAC AUSCULTATION

355

Table 21.1 Human acoustic acuity

●

Features

Significance

1. 2. 3. 4. 5.

Human ear capability Human ear sensitivity Optimal human auditory acuity Most cardiovascular sounds and murmurs Human ear capable of detecting two sounds

20–20000 Hz 1000–5000 Hz 1000–2000 Hz 30–1000 Hz 0.02 s interval between two sounds

stethoscope for auscultation of the heart which has a bell (for lower frequency events) and a diaphragm (for higher frequency events). Human ear is capable of detecting two sounds separated by an interval of as little as 0.02 s when the sounds are relatively high pitched.

Factors Affecting Cardiac Sound Transmission ●

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●

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The sound transmission from the heart is affected by the factors such as chest wall thickness, obesity, breast size and emphysema that attenuate the cardiac sounds, while the lean individuals with little excess body tissue tend to have louder heart sounds and murmurs. The level of noise in the hospital rooms, clinics, or typical examination rooms is 60–70 decibels, which is well above the optimal setting of an ideal soundproof auscultation room (i.e. 35 decibels). This environmental noise in the routine hospital surroundings can prevent the detection of the cardiac murmurs, particularly those of high frequency. Excessive noise levels due to auto or air traffic, construction work or human conversation near the examination area, higher frequency cardiac sounds and murmurs may be inaudible even to the most experienced clinicians. However, coryza does not interfere with the ability of the physician to hear the cardiac sounds and murmurs through a stethoscope, but with aging, a selective high frequency ( 3000 Hz) hearing loss is common.

Characteristics of the Cardiac Sounds Loudness of sound is a subjective judgement and is closely related to the amplitude or intensity of sound waves, while the pitch of a heart sound or murmur is related to the underlying frequency. The heart sounds and murmurs are classified depending upon their frequency as follows (see Table 21.2): ●

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Low frequency: (25–125 CPS) Low-pitched sounds e.g. S3, S4 and pericardial knock; low-pitched murmurs are rough and rumbling in character e.g. mid diastolic murmur (MDM) of mitral and tricuspid stenosis. Medium frequency: (125–300 CPS) Rough flow murmurs e.g. innocent systolic murmurs, physiological flow murmurs.

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CARDIOVASCULAR SYSTEM EXAMINATION

Table 21.2 Frequencies of heart sounds and murmurs Low frequency

High frequency

Medium frequency

Mixed frequency

1. 25–125 cycles per second (CPS) 2. Low pitched

300 CPS

125–300 CPS

High pitched

Rough

Combination of medium and high frequencies Harsh

●

●

High frequency: (300 CPS) High-pitched sounds e.g. A2, P2, opening snap (OS) and ejection sound; high pitched murmurs could be soft and blowing in character e.g. systolic murmur (SM) of mitral regurgitation, early diastolic murmur (EDM) of aortic regurgitation or musical in nature e.g. cooing murmur of papillary muscle rupture. Mixed frequency: Sounds and murmurs result from a combination of medium and high frequencies. Mixed frequency sound e.g. S1; while the murmurs are harsh in character e.g. SM of aortic and pulmonary stenosis and pansystolic murmur (PSM) of VSD.

The Stethoscope ●

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●

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Remembering a well-known acoustic fact that “if the ear be applied to one end of a plank, it is easy to hear a pin scratching at the other end”, French physician Rene Theophile Hyacinthe Laennec (1826) constructed his primitive monoaural stethoscope. It had a perforated wooden cylinder with a chest piece at one end and an earpiece at the other end. Presently available stethoscope does not represent a major advance over the wooden cylinder of Laennec. However, electronic and magnetic stethoscopes are available but clinicians are not using them on a routine basis. Although considered as out-dated or primitive by some in the present high tech era with easy availability of sophisticated equipment for the diagnosis of cardiac ailment, the stethoscope continues to remain ‘a bed side source of vital information about the heart’. A stethoscope consists of a dual chest piece with a valve that allows switching from bell to diaphragm, tubing, binaural connectors and earpieces (see Fig. 21.1). It should be durable without air leaks and should be easy to use. A good stethoscope should not distort the cardiac sounds and it is useful to examine the acoustic and practical characteristics, such as sound transmission, frequency filtration, masking and interference of this indispensable instrument.

The Bell of the Stethoscope It should be trumpet shaped with a diameter of atleast an inch and should have a rubber lining which allows light skin contact pressure, minimizes air leakage, does not get cold in winters, and amplifies the sound by increasing the diameter of the bell (see Fig. 21.2). ●

The bell is used for the detection of low frequency heart sounds and murmurs.

CARDIAC AUSCULTATION

Dual chest piece

Tubing

357

Binaural connectors

Earpiece

Fig. 21.1

| Stethoscope earpieces.

with a dual chest piece, tubing, binaural connectors and

Bell Diaphragm

Fig. 21.2

of the stethoscope with 1" in | Bell diameter. ●

Fig. 21.3

of the stethoscope with 1½" in | Diaphragm diameter.

It should be used with the lightest possible contact pressure. If increased pressure is applied to the bell, the firm pressure stretches the skin of the chest wall, due to which the bell acts like the diaphragm of the stethoscope attenuating the low frequencies but accentuating the higher frequency sounds.

The Diaphragm of the Stethoscope It should be 1½" in diameter (see Fig. 21.3). To prevent air leakages due to incomplete contact of the stethoscope with the chest wall, an ideal diaphragm should be slightly bowed outward or may have a small central elevated ridge for firmer stethoscope-chest wall compression without causing the diaphragm to bulge inwards and interfer with the sound transmission. ● ●

The diaphragm is used for the detection of high frequency heart sounds and murmurs. It should be used with firm pressure, which filters out the low frequencies and amplifies the high frequency sounds.

Tubing of the Stethoscope The optimum tubing length is 10–12". ●

Double tubing or double lumen within a single external tube is ideal, while single tube or Y tubing attenuates high frequencies.

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CARDIOVASCULAR SYSTEM EXAMINATION ●

The tubing should be thick, durable and made of plastic (than rubber) with an ideal internal diameter of 1/8" (3 mm) to minimize buckling of the tube and external noise contamination.

Binaurals and Earpiece These should be comfortable and properly fit, as improper fit of the binaurals and earpieces can result in decreased acuity in cardiac auscultation. ●

●

The binaurals should be adjustable, oriented slightly forwards and upwards without creating undue pressure on the ear canal and without producing any air leakage. The earpieces should comfortably fit into the external ear canal. Large rather than small earpieces are best, since small earpieces can penetrate too far into the external ear canal and may become occluded.

Examination of the Patient The examination should be done in a quite, well lighted comfortable room with the patient properly gowned and adequately exposed to the waist. Usually, examination is initiated from the right side. Adequate clinical history, general physical examination, inspection, palpation and percussion of the precordium should precede auscultation, as auscultatory counterparts will definitely aid for confident clinical diagnosis e.g. ●

●

●

●

●

●

A history of repeated abortions may be a clue to seek for syphilitic aortic regurgitation. A wide pulse pressure, collapsing pulse may be a clue for the diagnosis of aortic regurgitation. A tall stature with increased arm-span length should alert the clinician to aortic regurgitation murmur. Prominent a waves in jugular venous pulse, should alert the examiner to a lowpitched right-sided S4. Large v waves in jugular venous pulse, which augments with inspiration should seek for tricuspid regurgitation murmur. A rapid jerky rise of the carotid pulse may be a clue to seek for the diagnosis of hypertrophic cardiomyopathy.

The topographical areas of cardiac auscultation are (see Fig. 21.4): ●

● ●

●

The aortic area: Primary in the 2nd right ICS, secondary (Erb’s neo aortic area) in the 3rd left ICS adjacent to the sternum The pulmonary area in the 2nd left ICS The tricuspid area in the 4th and 5th intercostal spaces adjacent to the left sternal border The mitral area at the cardiac apex.

In addition, auscultation should regularly be carried out at: ●

The axillae (for radiation of PSM of MR)

CARDIAC AUSCULTATION Ao

RV

Fig. 21.4

●

● ● ● ●

●

359

PA

LV

precordial sites of auscultation—Ao: aortic area, PA: pulmonary area, | Classic LV: left ventricular (mitral) area, RV: right ventricular (tricuspid) area.

The back: Interscapula (murmurs of coarctation of aorta, aneurysm of descending thoracic aorta often better heard), infrascapula (brui of collateral circulation) and over the spine (murmurs of aneurysm of descending thoracic aorta, coarctation of aorta) Anterior chest on the opposite side (right side in case of dextrocardia) Over the carotids (for conduction of systolic murmurs of aortic valve disease) Above and below the clavicles (for characteristic continuous murmur of PDA) Epigastrium (for tricuspid regurgitation murmur in emphysematous patient with PH) and Over the peripheral arterial sites, especially over the femorals may disclose the murmurs of great diagnostic significance (e.g. Duroziez’s murmur of aortic regurgitation).

Method of Auscultation Levine and Harvey’s inching:4 One should adopt a systematic way of ausculatation, starting at the apex (mitral area) and left axilla, moving to the lower left sternal area (tricuspid area) and epigastrium, and progressing along the sternal border (neo-aortic area) to the base of the heart (aortic and pulmonary areas, below and above the clavicles) and over the carotids. Identification of systole and diastole: Identify systole and diastole in each area. ●

●

S1 identifies the onset of ventricular systole and S2 identifies the onset of ventricular diastole. The carotid upstroke and beginning outward thrust of the apex beat immediately follow S1, while S2 occurs shortly after the carotid pulse and apex beat.

Selective listening: Use both the bell and the diaphragm at each area and divide systole and diastole into three parts- early, mid, and late, selectively focusing on only one segment of the cardiac cycle (e.g. assessing S1 in early systole).

360

Fig. 21.5

CARDIOVASCULAR SYSTEM EXAMINATION

at the apex in supine and | Auscultation left lateral position.

Fig. 21.6

at the apex in supine | Auscultation position and timing with the carotids.

Aortic area

Fig. 21.7

at the bases—aortic area | Ausculatation in sitting and leaning forward position.

Pulmonary area

Fig. 21.8

at the bases—pulmonary | Ausculatation area in sitting and leaning forward position.

●

●

First, the heart sounds (S1, S2, S3, S4 and OS) are assessed, followed by attention to the murmurs (systolic, diastolic) in each segment of systole and diastole selectively at each area. Heart sounds and murmurs are heard and discovered only when they are searched out carefully with intent listening and concentration, which is a key to competent cardiac auscultation.

Position of the patient ●

●

In general, three positions are routinely employed-left lateral decubitus (for mitral area), supine (for tricuspid area), and sitting and leaning forward (for basal areas) (see Figs 21.5–21.8). In addition, patient should also be examined in right lateral decubitus (for making the tricuspid valve murmurs more prominent, see Figs 21.9 and 21.10) standing, and squatting positions, which alter the circulatory dynamics and may yield the diagnostic information.

CARDIAC AUSCULTATION

Fig. 21.9

at the tricuspid area in | Auscultation supine and right lateral position.

Fig. 21.10

361

for tricuspid events in | Auscultation supine position with passive legs raising.

Dynamic auscultation ●

●

The impact of respiration on the heart sounds and murmurs should be assessed routinely (besides the postural changes), as it gives clue to their site of origin (right-sided/left-sided). In selected cases, isometric exercises, the Valsalva maneuver, the Muller maneuver and pharmacological maneuvers (amyl nitrate inhalation) should be employed, which cause changes in the pre- and afterloads of the heart affecting the heart sounds and murmurs.

Phonocardiography It is the graphic recording of the auscultatory events of the precordium, carotid, jugular venous and apical precordial pulsations simultaneously with the ECG. ●

●

In essence, it is the graphic representation of the cardiovascular examination enhancing its accuracy. It is an excellent teaching aid even though the high frequency events (such as EDM of aortic regurgitation) are difficult to record.

THE HEART SOUNDS ●

●

●

The heart sounds are relatively brief discrete auditory vibrations that are characterized by intensity (loudness), frequency (pitch), and quality (timber). Sudden deceleration of the blood within the cardiovascular system produces the heart sounds. The rapid deceleration of blood initiates vibrations of the cardiac structures immediately after the coaptation of the valves that produces S1 and S2, while the rapid deceleration of blood in the ventricular inflow producing the vibrations of the cardiovascular structures appear to be responsible for the production of S3 and S4 (see Fig. 21.11). Basically, the heart sounds are of two types: – High frequency transients due to closing and opening of the valves – Low frequency sounds that are related to early and late diastolic filling events of the ventricles.

362

CARDIOVASCULAR SYSTEM EXAMINATION

S1

Fig. 21.11

S2

S3

S4

| Basic heart sounds.

i) High frequency sounds due to opening of the atrioventricular valves are: ● Sounds due to opening of the atrioventricular valves: Opening snaps (mitral and tricuspid), non-ejection sounds ● Sounds related to closure of the atrioventricular valves: S (mitral and tricuspid 1 closing sounds—M1 and T1) are mixed frequency sounds. ii) High frequency sounds due to closing and opening of semilunar valves are: ● Sounds related to closure of the semilunar valves: S (aortic and pulmonary clo2 sure sounds—A2 and P2) ● Sounds related to opening of the semilunar valves: Early valvular ejection sounds or clicks. iii) Low frequency sounds related to diastolic filling of the ventricles are: ● Physiological and pathological third heart sound (S ) which is associated with 3 early ventricular filling events ● Presystolic atrial gallop (S ) associated with late diastolic filling events 4 ● Summation gallop due to merging of S and S (synchronous occurrence of S 3 4 3 and S4) as occurs in tachycrdia. iv) Other heart sounds include ● Pericardial knock and rubs ● Tumor plops (atrial myxoma) ● Prosthetic valvular sounds. Depending upon the cardiac cycle, the heart sounds are also classified into: ●

●

Diastolic sounds – Early diastolic sounds: Opening snaps, (OS), tumor plops, pericardial knock, opening sounds of prosthetic valves – Mid diastolic sounds: S3 – Late diastolic sounds: S4. Systolic sounds – Early systolic sounds: Aortic and pulmonary ejection sounds, closing sounds of prosthetic valves – Mid to late systolic sounds: Non-ejection sounds or clicks.

The First Heart Sound (S1) The first heart sound signals the onset of left ventricular contraction and consists of two major audible components (M1 and T1) and two inaudible components.

CARDIAC AUSCULTATION

363

Table 21.3 Characteristics of S1 Characters

Value

1. Frequency 2. Duration 3. M1–T1 interval 4. C point of MV echocardiogram 5. Down stroke of c wave of LA pressure 6. Down stroke of c wave of RA pressure

Medium to high 0.14 s 20–30 ms Coincides with M1 Coincides with M1 Coincides with T1

M1

Apex phono

A2

Aorta LV a c

LA

v 30 ms

EKG

Fig. 21.12

●

●

●

of S —phonocardiogram and LV-LA pressures—M coincides | Characteristics with down stroke c wave of the LA pressure. 1

1

The first inaudible low frequency vibrations coincide with the beginning of the LV contraction and are muscular in origin. It is followed by high frequency audible M1 and T1 components, which are produced due to the closure of mitral and tricuspid valves (Dock’s hypothesis5 and Leatham6). The last inaudible low frequency vibrations coincide with opening of the semilunar valves with ejection of blood into the aorta and the pulmonary trunk.

Characteristics of S1 S1 is typically medium to high frequency with an average duration of 0.14 s (see Table 21.3). ●

●

●

●

M1 is followed by T1 which are separated by 20–30 m. Hence, in normal subjects S1 is appreciated as a single sound, but split S1 can be recorded with a phonocardiogram. It is auscultated with diaphragm of the stethoscope timed simultaneously with the palpation of the carotid or cardiac apex. M1 coinicides with C point of the mitral valve echocardiogram7 and down stroke of the left atrial c wave of LA pressure tracing, which is delayed from the LV-LA pressure crossover by 30 ms8 (see Fig. 21.12). Similar echocardiographic correlates are more difficult to demonstrate for T1 in the normal subjects, but T1 has shown to coincide with the down stroke of the RA c wave pressure tracing9 with greater delay between T1 and RV-RA pressure cross-over.

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CARDIOVASCULAR SYSTEM EXAMINATION

Table 21.4 Determinants of intensity of S1 1. Structural integrity of AV valve 2. Velocity of the MV closure 3. Status of ventricular contraction 4. Physical characteristics 5. Transmission characteristics

Thickness and mobility of the leaflets Position of AV valve at the time of ventricular systole Isovolumic systole, myocardial contractility, heart rate Vibrating structutres Thoracic cavity and chest wall

Determinants of the Intensity of S1 The intensity of S1 often gives clues to the diagnosis and degree of abnormality of the involved structures. The primary factors determining the intensity of S1 are (see Table 21.4): (1) Structural integrity of the AV valve: Thickness and mobility of the leaflets. (2) Velocity of the valve closure: Position of the mitral valve at the onset of ventricular systole. (3) Status of ventricular contraction: The rate of rise of LV pressure (dP/dt, isovolumic systole), myocardial contractility and heart rate. (4) Physical characteristics of the vibrating structures. (5) Transmission characteristics of the thoracic cavity and chest wall. 1) Structural integrity of the mitral valve: The normal mitral valve has thin pliable leaflets, which are capable of producing a normal S1. ●

● ●

However, there is an inadequate coaptation of the mitral leaflets causing attenuation of S1 in the setting of severe MR. Also, the loss of leaflet tissue as in infective endocarditis attenuates the intensity of S1. A calcified mitral valve as in long standing MS immobilizes the valve leaflets, which results in diminished or absent M1.

2) Velocity of the valve closure: It is one of the most important factors affecting the intensity of S1, which is determined by the position of the mitral valve at the onset of ventricular systole. The position of the mitral valve at the onset of ventricular systole is altered by (i) relative timing of the atrial and ventricular systole (PR interval) and (ii) the rate of LV filling during atrial systole. (i) PR intervals from 140–200 ms usually result in a normal S1 (see Fig. 21.13). ● At short PR interval (80–140 ms) as in Wolff-Parkinson-White and LownGanong-Levine syndromes, the mitral leaflets are maximally separated by the LA contraction at end diastole, due to which the MV closes at a high speed with a large excursion, which results in a loud and late M1.10,11 ● At longer PR intervals (200–500 ms), there is less separation of the mitral valve leaflets which have already begun to close with atrial relaxation (premature MV closure due to LV diastolic pressure exceeding LA pressure), and there is less excursion of the mitral valve with LV contraction (which occurs at lower LV pressure) which results in softer and early M1. ● However; when PR interval is 500 ms, the mitral valve reopens and closes with rapid velocity producing a loud S1.

CARDIAC AUSCULTATION S1

365

S2

Short PR Increased S1

Normal PR Normal S1

Long PR Soft S1

Fig. 21.13

| Relationship of intensity of S and PR interval. 1

(ii) The rate of LV filling during atrial systole:11 ●

●

When venous return is decreased in noncompliant hypertensive LV, there is more effective transportation of atrial volume into the relatively underfilled LV resulting in widely separated mitral leaflets that produce a loud S1 but soft and late S4. Increased venous return causes more vigorous atrial contraction, which results in less wide separation of the mitral leaflets (at the onset of ventricular systole) producing a loud and early S4 but a softer S1. This is the most likely explanation of a soft S1 in hypertensive patients with normal PR intervals.

3) Status of ventricular contraction: It is also an independent factor affecting the intensity of S1.11 Ventricular contraction is affected by i) the rate of rise of LV pressure (dP/dt, isovolumic contraction) and ii) heart rate. (i) Increased myocardial contractility: Following causes increase myocardial contractility, this increases the rate of rise of LV pressure (dP/dt) and thereby increases the velocity of the closing mitral leaflets. This further produces a loud S1.12 ● ● ● ● ● ●

Exercise Hypoglycemia Thyrotoxicosis Pheochromocytoma Catecholamine infusion High output states: Anemia, pregnancy, AV fistula, fever and anxiety

In addition, high output states are associated with tachycardia that causes (i) shortened PR interval, and (ii) widely open valve due to the high flow through a shortened diastole resulting in a loud S1.

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CARDIOVASCULAR SYSTEM EXAMINATION

Similarly, a loud T1 in ASD is due to the high flow through the tricuspid valve secondary to the left-to-right shunt at the atrial level. (ii) Decreased myocardial contractility results in decreased rate of rise of LV pressure producing a soft S1, which may be found in: ● Acute myocardial infarction ● Cardiomyopathy ● Myocarditis ● Myxedema ● Ventricular aneurysm ● Drug induced myocardial depression: beta-blockers, Ca blockers, disopyramide. (iii) Loss of isovolumic contraction (dP/dt) results in decreased velocity of MV closure producing muffling of S1, as in: ● ● ● ●

Severe mitral regurgitation Severe aortic regurgitation Large ventricular septal defect Ventricular aneurysm.

(iv) Heart rate: Tachycardia accentuates S1 due to: ● ● ●

The Shortening of PR interval Wide open valve as diastole is shortened and Increase in myocardial contractility as a result of Stair-case phenomenon (while bradycardia has the opposite effect).

4) Physical characteristics of the vibrating structures ●

●

Alterations in the physical characteristics of the vibrating structures may also vary the intensity of S1. Pacing-induced myocardial infarction and ischemia have been shown to decrease the intensity of S1 secondary to these alterations.13

5) Transmission characteristics of the thoracic cavity and chest wall ●

●

●

Higher frequency heart sounds are attenuated to a greater extent than the lower frequency sounds.14 Conditions such as obesity, emphysema, large pleural or pericardial effusions will decrease the intensity of all the auscultatory events. Whereas a thin body habitus tends to increase the intensity of heart sounds and murmurs.

Evaluation of S1 (1) Increased intensity of S1:

It occurs in (see Fig. 21.14):

(i) Mitral stenosis: Loud S1 is due to: ● The thickened but mobile leaflets ● The presystolic gradient between LA and LV prevents preclosure of the mitral leaflets but kept wide open at end diastole. Delayed MV closure at a higher LV

CARDIAC AUSCULTATION

1. Severe MR 2. Severe AR 3. Calcified MS

1. MS 2. LA myxoma 3. MVP Loud 1. Hyperkinetic states 2. Exercise 1. Af 2. Afl with varying block 3. AT with varying block 4. VT with AV dissociation

Fig. 21.14

367

Diminished 1. LV aneurysm 2. AMI 3. CM 4. LBBB

S1

Split

Variable 1. CHB with AV dissociation 2. Mobitz I with AV dissociation

Wide splitting 1. RBBB 2. LV pacing/ectopics 3. Ebstein’s anomaly 4. RA myxoma

Reverse splitting 1. RV pacing/ectopics 2. LA myxoma 3. Significant MS

of first heart sound (S )—MS: mitral stenosis, MR: mitral regurgi| Evaluation tation, MVP: mitral valve prolapse, AR: aortic regurgitation, AMI: acute 1

myocardial infarction, CM: cardiomyopathy, LBBB: left bundle branch block, RBBB: right bundle branch block, LV: left ventricular, RV: right ventricular, LA: left atrial, RA: right atrial, Af: atrial fibrillation, Afl: atrial flutter, AT: atrial tachycardia, VT: ventricular tachycardia.

(ii) (iii)

(iv)

(v)

(vi)

pressure at a time when there is a more rapid rise of LV pressure (dP/dt) increases the velocity of valve closure. Left atrial myxoma: Similar mechanism for booming S1 as that of MS. Exercise: Loud S1 is due to: ● Tachycardia induced shortened PR interval, increased myocardial contractility (due to Treppe phenomenon) and due to the wide open valve (as diastole is shortened) and ● Increased flow across the AV valve. Hyperkinetic circulatory states: These accentuate S1 due to: ● Increased flow across the AV valve and ● Tachycardia. Holosystolic mitral valve prolapse (non rheumatic MR)15: Loud M1 is due to: ● Increased amplitude of leaflet excursion ● May be due to the summation of normal M and an early non-ejection click of 1 valvular prolapse. Loud T1 occurs in: ● TS: similar mechanism as in MS ● ASD: due to increased tricuspid flow secondary to the left to right shunt at the atrial level ● Anomalous pulmonary venous connection: due to increased tricuspid flow.

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CARDIOVASCULAR SYSTEM EXAMINATION

(2) Decreased intensity of S1:

It occurs in:

(i) Severe mitral regurgitation: Diminished S1 is due to: ● Diminished mobility of the leaflets as a result of fibrosis and shortening ● Failure of the leaflets to close and ● Loss of isovolumic contraction ● Myocardial depression that contributes in secondary MR (due to ischemia). (ii) Flail mitral leaflet: MVP with middle or late systolic prolapse usually has normal S1 while MVP patients with flail leaflet have a soft S1. (iii) Severe aortic regurgitation: Attenuated S1 is due to: ● Premature closure of normal mitral valve due to marked increase in the enddiastolic pressure as a result of volume overload as seen in acute severe AR. ● Loss of isovolumic contraction as in chronic severe AR. (iv) Ventricular aneurysm results in soft S1 due to: ● Loss of isovolumic contraction and ● Decreased myocardial contractility. (v) Acute myocardial infarction: S1 is muffled because of: ● Diminished ventricular contractility ● Mitral regurgitation ● Ventricular aneurysm and ● Left bundle branch block (LBBB). (vi) Cardiomyopathy: Soft S1 is due to: ● Decreased myocardial contractility ● MR/TR and ● LBBB. (vii) Myocarditis attenuates S1 because of the diminished myocardial contractility. (viii) Calcified MS: Attenuated S1 is due to immobility of the mitral valve. (ix) LBBB:16 M1 is delayed and decreased in intensity due to: ● ● ●

●

Delay in the onset of LV contraction Decreased LV contractility Presence of noncompliant LV facilitates atriogenic preclosure of the mitral valve Presence of concomitant first degree heart block.

It is likely that more than one mechanism is operative in most of the patients with LBBB. At times there could be a reversal of the sequence of S1 (i.e. T1 followed by M1). (3) Variable intensity of S1: Variation in the intensity of S1 occurs because of variation in the PR intervals and varying force of ventricular contraction. Loud S1 occurs at short PR intervals, while a softer S1 occurs at longer intervals when the valve leaflets have partially closed.17 Variable S1 occurs in (see Table 21.5): ● ●

Atrial fibrillation Complete heart block with AV dissociation

CARDIAC AUSCULTATION

369

Table 21.5 Intensity of S1 Increased (loud S1)

Decreased (diminished S1)

Variable S1

1. Mitral stenosis 2. LA myxoma 3. Holosystolic mitral valve prolapse (non rheumatic) 4. Exercise 5. Hyperkinetic circulatory states 6. Loud T1: tricuspid stenosis, atrial septal defect, anomalous pulmonary venous connection

1. Severe mitral regurgitation 2. Flail mitral leaflet (middle/late systolic prolapse) 3. Severe aortic regurgitation 4. Ventricular aneurysm 5. Acute myocardial infarction 6. Cardiomyopathy 7. Myocarditis 8. Calcified mitral stenosis 9. Left bundle branch block

1. Atrial fibrillation 2. Complete heart block with AV dissociation 3. Mobitz type I heart block with AV dissociation 4. Ventricular tachycardia with AV dissociation 5. Atrial tachycardia with varying block

● ● ● ●

Mobitz type I heart block with AV dissociation Ventricular tachycardia with AV dissociation Atrial flutter with varying block Atrial tachycardia with varying block.

(4) Abnormal wide split of S1: Split of S1 into M1 and T1 is normally not audible as two components are synchronous or narrowly split (0.02–0.03 s) but may be audible in 40% of the normal individuals when the split is more wide (0.03 s). However, it is readily recordable with a phonocardiogram. The split of S1 is best detected at the lower left sternal border with firm pressure on the diaphragm of the stethoscope. (i) Abnormal wide split with normal sequence (M1, T1) occurs because of delayed tricuspid component, which is due to: ●

●

Electrical delays (delayed contraction of RV): as in complete RBBB (proximal type), LV ectopics, LV pacing and idioventricular rhythms originating from LV.18 Mechanical delays as in Ebstein’s anomaly19 (sail sound due to delayed activation and  RA pressure), and sometimes in TS and right atrial myxoma (due to  RA pressure).

(ii) Reverse splitting of S1 (T1, M1) because of delayed mitral component, which is due to: ●

●

Electrical delays (delayed contraction of LV): as in RV pacing, RV ectopics and idiovenricular rhythm originating from the RV. Mechanical delays (due to increased LA pressure): Reverse splitting may also be present in significant MS,20 and left atrial myxoma.

The Second Heart Sound (S2) ●

The second heart sound signals the onset of ventricular diastole and has two components: A2 (first component) and P2 (second component).

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CARDIOVASCULAR SYSTEM EXAMINATION

Table 21.6 Characteristics of S2

●

Characters

Findings

1. Frequency 2. Duration 3. Incisura of aortic pressure coincides 4. Incisura of pulmonary pressure coincides 5. A2–P2 interval: during expiration : during inspiration 6. A2 is earlier than 7. A2 is louder than 8. Well heard at aortic, pulmonary areas and apex 9. Well heard only at pulmonary area

High 0.11 s With A2 With P2 30 ms 40–50 ms P2 P2 even at pulmonary area A2 P2

It is produced by the sudden deceleration of retrograde flow of blood column in the aorta and the pulmonary artery, which initiates the vibrations of the haemocardiac structures coinciding with the closure of aortic and pulmonary leaflets.

Characteristics of S2 The second sound is the “key to auscultation of the heart”21 (see Table 21.6). (i) S2 is a high frequency sound with an average duration of 0.11 s. (ii) A2 and P2 are coincident with the incisura of aorta and pulmonary artery pressure tracing, which signals the end of LV and RV ejection periods. (iii) Compared to S1, S2 is higher in pitch and frequency due to: ● Low elasticity of semilunar valves and arterial trunks than that of AV valves and ventricles. ● Less blood volume in arteries than ventricles and so low inertia of the vibrating mass producing higher frequency of vibrations. ● S is shorter and snappier than S as the higher frequency vibrations damp out 2 1 earlier and more rapidly. (iv) A2 is earlier and louder than P2 ● A is louder due to higher pressure in the aorta than in the pulmonary artery. 2 ● A occurs earlier than P as: 2 2 – RV ejection begins earlier, lasts longer than LV ejection, and ends after LV ejection resulting in P2 occurring after A2. – Hang out interval on the aortic side (approximately 30 ms) is less than on the pulmonary side (approximately 80 ms). (v) Normally, A2 is well heard in aortic and pulmonary areas as well as at the apex, while P2 is well audible only at the pulmonary area and rarely at the apex.22 (vi) Even at the pulmonary area, P2 is softer than A2. (vii) Normal physiological split of S2 was first recognized by Potain in 1866. ● During expiration, A and P are separated by an interval of 30 ms so, these are 2 2 heard as a single sound (S2); while during inspiration, splitting or separation of the two components (A2, P2) is distinctly audible23 as the interval widens to 40–50 ms.

CARDIAC AUSCULTATION

EKG

EKG A2 P 2

P1

P1

371

A2 P

2

PHONO

PHONO Aortic pressure Inspiration Expiration

Aortic pressure

MPA pressure Hang out interval (60 ms)

(80 ms)

Right ventricular pressure

Fig. 21.15

Hang out interval 30 ms

Left ventricular pressure

out interval on the right side— | Hang MPA: main pulmonary artery.

●

●

Fig. 21.16

| Hang out interval on the left side.

However, in recumbent position in some normal subjects expiratory separation of A2 and P2 may be 30 ms and expiratory split is audible but becomes single on assuming upright position24 and hence basal areas should always be examined in upright position. Splitting of S2 is usually best heart at the second or the third left intercostal space.

Hang out interval ●

●

●

●

●

●

The semilunar valves are expected to close at the point of cross-over of the pressures, i.e. the point where the ventricular pressures fall lower than the arterial pressures (LV pressure falls lower than aortic pressure, RV pressure falls lower than PAP), however in reality these valves close slightly later (at the incisura of aorta and pulmonary artery pressure tracing). This time interval from the crossover of the pressures to the actual closer (occurrence of A2 and P2) is called “hang out interval”. In general, the duration of hang out interval depends upon the pressures in the arteries, vascular resistance, distensibility and recoil of the arterial system. Due to higher pressure and less distensibility (complaint), the hang out interval on the aortic side is less than that of on the pulmonary side. The hang out interval is measured between the incisura of aorta and LV pressure at the same level on the left side and between the incisura of pulmonary artery and RV pressure at the same level on the right side (see Figs 21.15 and 21.16). The ventricular mechanical systole is the sum of the isovolumic contraction time and ejection period minus the hang out interval.

Mechanism of normal split of S2:25 Fig. 21.17): ● ●

Normal inspiratory split of S2 is due to (see

Delayed P2 accounting for 73% Early occurrence of A2 contributing about 27%.

372

CARDIOVASCULAR SYSTEM EXAMINATION A2 P 2

A2 P 2

S1

S2

S1

Expiration

Fig. 21.17

S2 Inspiration

| Normal physiological splitting of S . 2

Table 21.7 Abnormal splitting of S2 Wide splitting

Reversed splitting

1. 2. 3. 4. 5. 6. 7.

Atrial septal defect 1. Significant mitral regurgitation Ventricular septal defect 2. Complete right bundle branch block 3. Premature ventricular contractions 4. Left ventricular pacing 5. Mod-severe pulmonary stenosis with 6. intact ventricular septum 8. Acute pulmonary embolism 7. 9. Pulmonary hypertension with right heart failure 8. 10. Idiopathic dilatation of pulmonary artery 9.

Left ventricular outflow tract obstruction: aortic stenosis Complete left bundle branch block Right ventricular ectopic beats Right ventricular pacing Patent ductus arteriosus Post stenotic dilatation of aorta secondary to aortic stenosis and aortic regurgitation Wolff-Parkinson-White syndrome type B Chronic ischemic heart disease Hypertensive cardiovascular disease

The inspiration results in changes in the systemic and pulmonary venous return. (i) The inspiratory increase in the systemic venous return due to fall in the intrathoracic pressure increases the RV stroke volume. This causes a delay in P2 by: – Decreasing the pulmonary vascular impedance (i.e.  capacitance of the pulmonary vascular bed) and thereby increasing pulmonary artery hang out interval (contributing about 45% for delayed P2) and – Prolonging the RV ejection (contributing about 28%). (ii) The inspiratory decrease in the pulmonary venous return (due to pooling of blood in the pulmonary vasculature) decreases LV stroke volume which causes an early occurrence of A2 by – Decreasing the LV ejection, and – Decreasing the hang out interval on the aortic side. The net result is the wide inspiratory splitting of S2. Abnormal splitting of S2 is defined as the presence of audible expiratory split (of 30 ms) both in supine and upright positions26 (see Table 21.7). Abnormal splitting of S2 could be ● ● ● ●

Persistent physiological splitting of S2 Wide fixed splitting of S2 Reversed or paradoxical splitting of S2 Single S2.

CARDIAC AUSCULTATION A2

A2 P 2

S1

S2 Expiration

Fig. 21.18

A2

P2

P2

373

A2

P2

S2

S1 Inspiration

S1

| Wide physiological splitting of S .

S2 Expiration

2

Fig. 21.19

(i) Persistent physiological splitting of S2:

S2

S1 Inspiration

| Narrow physiological splitting of S . 2

It could be wide or narrow.

(a) Wide physiological splitting of S2 (see Fig. 21.18): (i) Due to delayed pulmonic closure (P2): 27 ● Delayed electrical activation of the right ventricle : – Complete RBBB (proximal type) – LV ectopic beats (premature ventricular contrations) – LV pacing ● Prolonged RV mechanical systole: – Moderate to severe PS with intact ventricular septum18 – PH with right heart failure28 – Acute pulmonary embolism29 ● Increased hang out interval (80 ms) (decreased impedence of pulmonary vascular bed) – Mild PS30 – Idiopathic dilatation of pulmonary artery30 – Normotensive ASD30 – Postoperative ASD (in 70%)8 (ii) Early aortic closure (A2): ● Shortened LV mechanical systole (LV ejection time due to the loss of isovolumic contraction) – Significant MR30 – VSD31 (iii) Other benign causes which mimic wide splitting of S2 ● Pectus excavatum ● Straight back syndrome ● Occasionally, in normal children (b) Narrow physiological splitting of S2: The splitting of S2 into A2 and P2 during expiration with narrow splitting interval (30 ms) and loud P2, is a common finding in severe PH (see Fig. 21.19). However, in PH, the split could be wide with loud P232 or could be a wide fixed split32, which indicates a more severely compromised RV. ● ●

The wide split in PH could be due to the prolongation of RV systole. While the wide fixed split in PH could be due to

374

CARDIOVASCULAR SYSTEM EXAMINATION

– Inability of the compromised RV to accept the augmented venous return associated with inspiration and – Altered pulmonary vasculature.23 (ii) Wide fixed splitting of S2: It is defined when the interval between A2 and P2 is not only wide and persistent but also remains unchanged during the respiratory cycle (i.e. inspiration and expiration)33 i.e. A2 and P2 are widely separated during expiration and exhibit little or no change in the degree of splitting with inspiration or Valsalva maneuver. ●

●

Wide split is caused by a delay in P2 due to the increased pulmonary vascular capacitance prolonging the hang out interval While fixed split is due to little or no inspiratory delay in P2 because of little or no change in RV filling and stroke volume during inspiration.

Clinical recognition of wide fixed splitting of S2: Apparent fixed split is occasionally audible in young normal subjects in supine position but it disappears in upright position. Hence for wide fixed split, the patient should always be auscultated both in supine and upright positions. In doubtful cases auscultation should be done during the straining phase of Valsalva maneuver. Wide fixed splitting of S2 occurs: ●

● ●

Due to failure to increase RV stroke volume with inspiration as in RV failure, acute and chronic pulmonary embolism Due to simultaneous increase in RV and LV filling as in secundum ASD Due to obligatory ASD as in total anomalous venous connection (TAPVC).

Wide splitting of S2 in ASD: It is caused by the delay in P2, which is due to increased systemic venous return and  RV filling during inspiration, which in turn results in ● ● ●

Prolong RV systole Prolong hang out interval (i.e. PV impedence) and Delayed electrical activation of RV if associated with RBBB.

Fixed splitting of S2 in ASD: Fixed splitting of S2 is an ausculatatory hallmark of ostium secundum ASD. ●

●

The phasic changes in systemic venous return during respiration are associated with reciprocal changes in the volume of the left-to-right shunt minimizing respiratory variations in the RV filling34 i.e –  Venous return during inspiration is associated with no left-to-right shunt through interatrial communication and –  Venous return during expiration is associated with left-to-right shunt through interatrial communication minimizing the respiratory variations in RV filling, resulting in simultaneous increase in RV and LV filling. Since the impedance of pulmonary vascular (PV) bed is appreciably decreased (i.e. PV capacitance), there is little or no additional  of PV impedance (i.e. PV capaciance) during inspiration and no or little inspiratory delay in P2.

The net effect is the characteristic wide and fixed splitting of S2 (see Fig. 21.20).

CARDIAC AUSCULTATION A2 P

A2 P

2

Normal

S1

S2

375

2

S1

S2 A2

A2 P 2

P2

ASD S1

S2 Expiration

Fig. 21.20

S1

S2 Inspiration

| Wide and fixed split of S

2

in ASD.

Importance of Valsalva maneuver in ASD patients: In patients suspected of having an ASD, the Valsalva maneuver may be used to assess the splitting of S2. ●

●

In normal subjects, S2 fuses during the strain phase as both RV and LV filling decreases, and on release of the strain, immediate surge in RV filling and stroke volume produces delay in P2 resulting in a prominent S2 splitting for 6–8 beats. When augmented blood volume reaches the left heart (i.e.  LV filling and stroke volume), it prolongs the LV systole resulting in the narrowing of S2 splitting (i.e. narrow split  wide split  narrow split). However, in patients with ASD, S2 splitting widens during the strain phase due to  leftto-right shunt (and thereby  RV filling and stroke volume and delay in P2). On release of the strain, the expected S2 split does not occur due to the altered interatrial shunting.

In patients of ASD with atrial fibrillation: S2 splitting is prominent after the long cycle due to greater left-to-right shunting with long diastoles in contrast to patients with Af without ASD. (iii) Reversed or paradoxical splitting of S2: It is an inaudible split during inspiration and an audible split during expiration due to the reverse sequence of semilunar valve closure i.e. P2 preceding A2.33 Types of reversed splitting of S2 ●

●

●

Type I or classic reversed splitting of S2: There is no split or single S2 during inspiration and split during expiration with reverse sequence due to delay in A2 (see Fig. 21.21). It occurs in delayed LV electromechanical systole i.e.  Q-A2 interval. During expiration, prolonged LV systole causes A2 to follow P2 (i.e. audible expiratory split); while during inspiration, Q-P2 normally increases, but Q-A2 shortens or remains unchanged (i.e. no split/single S2). Type II or partial reversed splitting of S2: Normal inspiratory S2 splitting and expiratory splitting of S2 with reverse sequence (see Fig. 21.22). Type III reversed splitting of S2: It is similar to type II but A2 P2 separation is

20 ms with reverse sequence during expiration and S2 is heard as a single sound in both the phases of respiration.

376

CARDIOVASCULAR SYSTEM EXAMINATION A2 P2

P2 A2

S1

S2

S1

Expiration

Fig. 21.21

S2 Inspiration

| Reversed splitting of S

2

(type I).

A2

P2 A2

S1

S2

S1

Expiration

Fig. 21.22

| Partial reversed splitting of S

P2

S2 Inspiration

2

(type II).

Clinical recognition of reversed splitting of S2 ●

●

●

Only type I is recognizable clinically while type II and III are detectable only by a phonocardiogram. The reversed splitting of S2 may be confused with wide physiological (variable) or wide fixed splitting of S2. Trace the two components of S2 (i.e. A2 and P2) away from the pulmonary area, since normally, only first of the two components (A2) is traced to the apex while the second component (P2) is usually not (or faintly) audible away from the pulmonary area. When the later (A2) of the two components is traceable to the apex, a reversed splitting of S2 is likely. Valsalva maneuver in patients with reversed S2 split, results in widening of S2 split during the strain phase, narrowing of S2 split upon release of the strain and subsequent widening of the S2 split again (wide split  narrow split  wide split). In contrast, a normal S2 narrows during the strain phase, widens upon release and then narrows again (i.e. narrow split  wide split  narrow split). Causes of reversed splitting of S2

a) Due to delayed aortic closure (A2) ●

●

Due to delayed electrical activation of the LV – Complete LBBB (proximal type)35 – RV pacing18 – RV ectopic beats.18 Due to prolonged LV mechanical systole – Complete LBBB (peripheral type)35 – Left ventricular outflow tract obstruction (AS)35 – Hypertensive cardiovascular disease36 – Arteriosclerotic heart disease37: chronic ischemic heart disease, angina pectoris.

CARDIAC AUSCULTATION

1. Significant MR 2. PH with RVF 3. Acute PE

1. CRBBB 2. LV ectopy/ LV pacing

Fig. 21.23

1. Funnel chest 2. Straight back syndrome

1. ASD 2. TAPVC 3. RVF 4. PE

Wide split

S2 splitting

1. PS with intact IVS 2. ASD 3. VSD

377

Wide fixed split

Narrow split

Reverse split

Severe PH

Type II: WPW syndrome type B

Type I: 1. CLBBB 2. RV ectopics/ RV pacing 3. PDA 4. Chronic IHD

| Splitting of second heart sound (S )—CRBBB: complete right bundle branch block, CLBBB: 2

complete left bundle branch block, MR: mitral regurgitation, PH: pulmonary hypertension, PE: pulmonary embolism, PS: pulmonary stenosis, RVF: right ventricular failure, ASD: atrial septal defect, VSD: ventricular septal defect, IVS: inter ventricular septum, PDA: patent ductus arteriosus, TAPVC: total anomalous pulmonary venous connection, IHD: ischemic heart diease, WPW: Wolff-Parkinson-White.

Due to decreased impedance of systemic vascular bed ( hangout interval) – Post-stenotic dilatation of the aorta secondary to AS or AR35 – PDA35 LBBB is the most common cause of reversed splitting of S2. ●

b) Due to early pulmonic closure (P2) ●

Due to early electrical activation of RV as in Wolff-Parkinson-White syndrome (Type B)38, it commonly results in type II reversed splitting of S2.

c) Rarely to shortened RV systole because of decreased RV filling as in right atrial myxoma and TR (see Fig. 21.23). (iv) Single S2: Absence of an audible S2 split in either phases of respiration results in single S2 (see Table 21.8). A single S2 is heard when the separation of A2 and P2 is narrow (30 ms) often due to delayed A2 (i.e. type III reverse splitting of S2) or when either of two components (A2 or P2) is absent or inaudible. The common causes of single S2 are: a) When P2 is absent or undetectable: ●

Aging: upto 50% in subjects of 60 yrs of age due to: – Age related lengthening of LV isovolumic contraction resulting in  Q–A2 interval and delay of A239

378

CARDIOVASCULAR SYSTEM EXAMINATION

Table 21.8 Single S2

● ●

●

P2 absent/undetectable

A2 absent/undetectable

1. 60 yrs of age 2. Obesity, thick chest wall, emphysema 3. Severe pulmonary stenosis (PS) 4. Severe aortic stenosis 5. Tetralogy of Fallot 6. Pulmonary atresia 7. Tricuspid atresia 8. Double outlet right ventricle with PS 9. Transposition of great arteries 10. Eisenmenger’s ventricular septal defect 11. Single ventricle

1. Severe aortic stenosis 2. Severe pulmonary stenosis 3. Severe pulmonary hypertension 4. Aortic atresia 5. Eisenmenger’s ventricular septal defect 6.Single ventricle 7. All causes of reversed splitting of S2 due to delayed A2

– Age related physiological decrease in pulmonary vascular compliance and a shortening of hangout interval resulting in  Q–P2 interval and early P2.40 – Age related increase in thoracic A-P diameter resulting in muffling or masking of P2. Obesity, thick chest wall or emphysema results in muffling of P2. Acyanotic CHD: – Deformed pulmonary valve: severe PS in which P2 is late and soft – Concealed or masked by the systolic murmur: severe AS – Masked by a sound: loud A2 in AS or AR and loud opening snap in significant MS. Cyanotic CHD: – Deformed pulmonary valve: TOF, pulmonary atresia, tricuspid atresia (due to associated PS in most cases), DORV with PS – Posterior location of pulmonary valve: TGA – Only one semilunar valve is present, and could be due to synchronous closure of quadricuspid valve: Truncus arteriosus – P2 is synchronous with A2 due to the equalization of hangout intervals because of equal RV and LV systoles: Eisenmenger’s VSD, single ventricle. b) When A2 is absent or undetected

● ●

●

Deformed aortic valve: severe AS, aortic atresia A2 is synchronous with P2 due to the equalization of hangout intervals because of equal RV and LV systoles: Eisenmenger’s VSD, single ventricle Concealed or masked by a murmur or sound: – Severe PH: loud P2 may mask A2 by the phenomenon of retrograde masking. However, both the components are detected at the apex and the lower sternal area. – Severe PS: prolonged SM may mask A2, but both components are audible at the apex or at the lower sternal area.

CARDIAC AUSCULTATION

379

Table 21.9 Intensity of A2  A2

 A2

1. Hyperkinetic circulatory states 2. Systemic hypertension 3. Dilatation of ascending aorta: aneurysm, syphilis, ankylosing spondylitis 4. Congenital biscuspid aortic valve with no significant AS 5. Transposition of greart arteries 6. Pulmonary atresia

1. Aortic sclerosis 2. Valvular aortic stenosis (AS) 3. Valvular aortic regurgitation

Table 21.10 Intensity of P2 Loud P2

Diminished P2

1. 2. 3. 4.

1. 2. 3. 4.

Thin chest wall, straight back syndrome Hyperkinetic circulatory states Pulmonary hypertension of any cause Atrial septal defect

Thick chest wall, obesity, COPD Pulmonary stenosis Dysplastic pulmonary valve Mild tetralogy of Fallot

c) All conditions that delay A2 and cause reverse splitting of S2: When the splitting interval is 30 ms, single S2 is produced. d) The continuous murmur may mask the split of S2: As in PDA and sometimes in severe MR. Intensity of S2 The intensity of the two components should also be assessed. It could be loud A2 or P2, or diminished or soft A2 or P2 (see Table 21.9 and Table 21.10). Determinants of the intensity of S2 are: 1. Pressure in the vessel 2. Flow across the valve 3. Size of the vessel beyond the valve: The dilated vessel becomes closer to the anterior chest wall resulting in loud S2 (A2 or P2) 4. Status of the valve (stenosis or regurgitation) 5. Site of origin of the vessel: The vessel becomes closer to the anterior chest wall if it arises anteriorly. Increased size of the vessel, increased pressure in the vessel beyond the valve and increased flow across the valve results in accentuated S2, while a stenotic or regurgitant valve usually causes diminished S2. a) Loud or accentuated A2: ● ●

It occurs in:

Hyperkinetic states: Due to increased flow across the normal valve Systemic hypertension: Due to elevated pressure in the vessel beyond the valve, and dilatation of the ascending aorta

380

CARDIOVASCULAR SYSTEM EXAMINATION ● ●

●

Aneurysm of ascending aorta: Due to dilatation of the ascending aorta Aortic root related causes of AR e.g. syphilis, ankylosing spondylitis. Loud S2 is due to the dilatation of the ascending aorta and the increased flow across the valve with a well preserved leaflet mobility. Congenital heart disease: – Congenital bicuspid aortic valve when stenosis is not significant: Due to thickened but mobile leaflets – TGA as aorta arises anteriorly34 – Pulmonary atresia in which anterior pulmonary trunk is small or absent, which causes aorta to be more closer to the anterior chest wall.34

b) Diminished or muffled A2: It occurs in: ●

● ●

Elderly individuals with aortic sclerosis: Due to thickened leaflets and diminished mobility Valvular AS: Due to distorted valve anatomy and diminished valve mobility Valvular AR: Due to restricted valve mobility.

A2 is normal in hypertrophic cardiomyopathy and subaortic stenosis, but may be diminished in supravalvular AS. c) Loud or accentuated P2: ●

● ●

●

It occurs in:

Thin chest wall ( anteroposterior diameter) or loss of thoracic kyphosis (as in straight back syndrome) due to more nearness to the anterior chest wall.41 Hyperkinetic states: increased flow across the normal valve. Pulmonary hypertension (PH) of any cause: increase pressure in pulmonary artery results in higher closing pressure of the valve and dilated pulmonary trunk. Loud P2 is the sine qua non of PH. ASD (secundum): due to dilatation of pulmonary trunk and increased flow across the valve in the absence of PH.

Grading of accentuated or loud P2 1. Mild or grade 1 (): when intensity of P2 is equal to A2: occurs in mild PH (systolic pressure: 30–49 mmHg, mean pressure: 21–34 mmHg) 2. Moderate or grade 2 (): when intensity of P2 exceeds A2, i.e. P2 is louder than A2: occurs in moderate PH (systolic pressure: 50–75 mmHg, mean pressure: 35–50 mmHg) 3. Severe or grade 3 (): when P2 is loud and banging and is audible beyond the pulmonary area: occurs in severe PH (systolic pressure: 75 mmHg, mean pressure 50 mmHg) d) Diminished or decreased P2: ● ● ●

●

It occurs in:

Thick chest wall, obesity and COPD: due to the masking effect PS: due to thickened leaflet and diminished valve mobility Dysplastic PV as in Noonan’s syndrome: due to distorted valve anatomy and diminished mobility Mild TOF (Pink TOF): soft and delayed P2 may be heard due to mild PS.

CARDIAC AUSCULTATION

381

Evaluation of S2 in Common Clinical Conditions (a) Valvular heart diseases (i) Mitral stenosis ● Mild to moderate MS without PH: normal S and normal intensity of P 2 2 ● Severe MS with severe PH: S is closely (narrow) split with loud P 2 2 ● Intensity of P correlates with the severity of PH 2 ● S –OS is often mistaken for a wide split of S in MS. However, it is initial of the two 2 2 components i.e. S2 is loudest in S2–OS; while in split S2 it is the last of the two components i.e. P2 is loudest. (ii) Mitral regurgitation ●

● ●

●

Mild to moderate MR: S2 split is normal and P2 is accentuated when complicated with PH Severe MR: S2 split is wide and variable S2 split becomes wide and fixed when complicated with heart failure, when associated with ASD, or when MR is a part of the AV canal defect Reverse splitting of S2: it occurs in MR due to HOCM or CAD (see Fig. 21.24). 1. Age >60 yrs 2. Obese 3. TC wall 4. Emphysema 1. TOF 2. P At 3. T At 4. TGA 5. DORV with PS 6. SV 7. Eis VSD

1. Severe PS 2. Severe AS

Single – P2 absent or undectable

Fig. 21.24

↑A2

Single – A2 absent or undectable

↑P2 ↓P2 1. PH 2. ASD

1. TC wall 2. Obese 3. COPD

1. Bicuspid AoV 2. TGA 3. P At

1. AA aneurysm 2. Syphilis 3. Anky spond

↓A2

S2

1. Severe AS 2. Severe PS 3. Severe PH 4. Aortic At

1. Eis VSD 2. SV

1. Hyperkinetic states 2. Systemic HTN

1. Valvular AS 2. Valvular AR 3. Aortic sclerosis 1. Th C wall 2. SB syndrome 3. Hyperkinetic states

1. PS 2. Dysplastic PV 3. TOF

of second heart sound (S )—PH: pulmonary hypertension, PS: pul| Evaluation monary stenosis, ASD: atrial septal defect, VSD: ventricular septal defect, Eis: 2

Eisenmenger, SV: single ventricle, P At: pulmonary atresia, T At: tricuspid atresia, At: atresia, TC: thick chest, ThC: thin chest, SB: straight back, Bicuspid AoV: congenital bicuspid aortic valve with insignificant AS, AS: aortic stenosis, AR: aortic regurgitation, AA: ascending aorta, TOF: tetralogy of Fallot, TGA: transposition of great arteries, DORV: double outlet right ventricle, HTN: hypertension, COPD: chronic obstructive pulmonary diseases, Anky spond: ankylosing spondylitis.

382

CARDIOVASCULAR SYSTEM EXAMINATION

(iii) Aortic stenosis ● ●

Reverse splitting of S2: due to delayed A2 Single S2 due to masking effect of P2 or absence of A2 (deformed valve).

(iv) Aortic regurgitation ● ● ● ●

Usually, S2 split is normal A2 is loud in aortic root causes of AR A2 is soft in valvular causes of AR A2 may be loud when associated with VSD or TOF.

(b) Congenital heart disease—Acyanotic (i) ASD ● ●

S2 split is wide and fixed with loud P2 even in the absence of PH Eisenmenger’s syndrome: S2 split remains wide and fixed with loud banging P2.

(ii) VSD ● ● ● ● ●

Small VSD: normal S2 split with normal intensity of P2 Moderated VSD: normal S2 split with moderate accentuation of P2 Large VSD: narrow S2 split with loud P2 Eisenmenger VSD: single loud P2 VSD with PS physiology (as TOF, TGA, DORV): single loud A2.

(iii) PDA ●

● ●

Small PDA: normal S2 split and normal intensity of P2 however S2 is masked by the continuous machinery murmur Large PDA: normal S2 split with accentuated P2 Eisenmenger PDA: closely S2 split with loud P2.

(iv) Pulmonary stenosis ● ●

●

Mild PS: normal S2 split with normal intensity of P2 Moderate-severe PS (with post-stenotic dilatation): wide variable split of S2 with diminished P2. P2 may be absent in severe cases Dysplastic pulmonary valve or when associated with TOF: P2 is absent.

(v) Bicuspid aortic valve ●

In the absence of significant AS or AR: S2 is normal split with accentuated A2.

(vi) Coarctation of aorta ●

Usually, normal splitting of S2 with accentuated A2 due to hypertension. There may be reverse splitting of S2.

(c) Congenital heart disease—Cyanotic: Normal S2 is uncommon (i) Single S2 ●

Single loud A2 in TOF: due to the absence of P2 and anterior and dextroposed aorta

CARDIAC AUSCULTATION ●

● ●

383

Single loud A2 in TGA, DORV, Single ventricle: inaudible P2 due to the posteriorly placed pulmonary trunk Single loud A2 in Tricuspid atresia: due to PS resulting in the absence of P2 Single loud S2 in Truncus arteriosus: due to the presence of single semilunar valve with a dilated truncal root.

(ii) Wide splitting of S2: It occurs in: ● ● ● ● ●

Total anomalous pulmonary venous connection Eisenmenger ASD Ebstein’s anomaly Single atrium PS with intact ventricular septum and right-to-left shunt (through PFO).

Diastolic Sounds a) The Third Heart Sound (S3) It is a low frequency mid-diastolic sound, which occurs during the rapid ventricular filling phase (see Fig. 21.25). When heard in disease states, S3 is called as S3 gallop, protodiastolic gallop, or ventricular diastolic gallop. i) Characteristics of S3: S3 is of two types: physiological and pathological (see Table 21.11). S1

A2

A2

Base Phono Apex Phono

S3 S1

S3

ACG

RFW

Fig. 21.25

heart sound occurring during rapid filling wave (RFW) of apex cardio| Third gram (ACG).

Table 21.11 Characteristics of S3 1. 2. 3. 4. 5.

Low frequency sound Physiological S3 occurs: 120–200 ms after A2 Pathological S3 occurs: 140–160 ms after A2 Coincides with RFW of apex cardiogram Coincides with y descent of atrial pressure

384

CARDIOVASCULAR SYSTEM EXAMINATION

(i) Physiological S3 ● ● ●

●

●

●

●

It occurs 120–200 ms after A2. It is normally heard in children, adolescents and young adults.42 It is rare in adults after 40 yrs of age (40 yrs in men and 50 yrs in women), but may be present in thin asthenic individuals.43 It coincides with the rapid filling wave of the apex cardiogram,44 and y descent of the atrial pressure tracing. It is best heard with lightly placed bell of the stethoscope at the apex in left lateral position. It is differentiated from the pathological S3 primarily by the company it keeps,45 (i.e. cardiac enlargement in pathological S3, besides it is early and loud). The genesis of physiological and pathological S3 is same. However, whether the RV contributes to the physiological S3 is unknown.

(ii) Pathological S3 ● ●

● ● ● ●

●

It occurs in mid-diastole 140–160 ms after A2. When S3 is heard in disease states, it is called as a gallop sound (protodiastolic, ventricular diastolic gallop). Pathological S3 is generally regarded as an exaggeration of the physiological S3. Often, it is quite faint and easily overlooked. Often, S3 is heard only intermittently rather than with each beat. Presence of S3 or S4 results in triple rhythm (gallop), while presence of both S3 and S4 produces quadruple rhythm, which may simulate a mid diastolic murmur of MS. Quadruple rhythm is commonly heard in patients with LV aneurysm, cardiomyopathy, or severe LV failure and dilatation of any cause. S3 may summate (fuse) with S4 producing a single loud summation sound or gallop during sinus tachycardia (when ventricular diastole is shortened) or long PR intervals,46 while an incomplete summation may simulate a mid diastolic rumble of MS.

ii) Mechanism of production of S3 (i) Prerequisites for genesis of S3 ●

Non-obstructed AV valve: A non-stenotic AV valve is a prerequisite for the generation of S3 as the presence of a stenotic AV valve impedes ventricular inflow.

(ii) Theories for production of S3: Three major theories have been proposed for the genesis of S3: valvular theory, ventricular theory and impact theory. ●

●

●

The valvular theory: Diastolic tensing of the AV valves at the termination of rapid ventricular filling results in S3. However, recent phonocardiographic studies disproved this explanation.45 The ventricular theory: Sudden deceleration of the onrushing column of blood in the ventricular inflow during rapid ventricular filling phase sets the entire cardiovascular system into vibration, producing S3.47–49 The impact theory (of Reddy et al)50: The ventricular mechanism could explain for S3 recorded within the ventricular cavity and epicardial surface, but the external S3 recorded from the chest wall was not due to passive transmission of the sound originating

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from the LV through the intervening structures to the chest wall. Hence, S3 heard with the stethoscope is due to the dynamic impact of the heart with the chest wall. The force of impact and resultant intensity of S3 are primarily dependent on: – The size of the heart ( space between the enlarged heart and chest wall, thereby facilitating a more forceful impact) – The motion of the heart within the thorax ( motion more impact) – The chest wall configuration (thick chest wall, COPD, and obesity dampens the S3) – Phase of respiration (inspiration for RV S3) – Position of the patient (e.g. left lateral for LV S3, supine for RV S3). This theory explains the presence of S3 in hyperdynamic states as well as in conditions with increased end-systolic volume secondary to LV dysfunction. ●

However, the ventricular mechanism together with dynamic impact of the heart on the chest wall explains the presence of S3 in most disease states.

iii) Causes of S3 (see Table 21.12 and Fig. 21.26) (i) Physiological S3 ● ●

Children and young adults (men 40 yrs, women of 50 yrs)51 High output states (diastolic overload): 3rd trimester pregnancy, after exertion and anxiety related tachycardia.

(ii) Pathological S3 ●

Excessive rapid ventricular filling (diastolic overload states with  atrial pressures): As RV is more compliant than LV; presence of a RV S3 is relatively uncommon. 1. Hyperkinetic states (high output states): – Anemia – Thyrotoxicosis – Arteriovenous fistula. Table 21.12 Causes of S3 Physiological 1. Children 2. Young adults (men 40 yrs, women 50 yrs of age) 3. Pregnancy

Pathological 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

Heart failure Hyperkinetic circulatory states Mitral regurgitation Tricuspid regurgitation Ventricular septal defect (VSD) Patent ductus arteriosus Total anomalous pulmonary venous connection Double outlet right ventricle without pulmonary stenosis Truncus arteriosus Transposition of great arteries with VSD Ischemic heart disease Dilated congested cardiomyopathy

386

CARDIOVASCULAR SYSTEM EXAMINATION

●

2. Atrioventricular valve incompetence: – MR (chronic moderate to severe) – TR (RV S3) 3. Left-to-right shunts: – VSD – PDA – ASD (RV S3) (rare) 4. Cyanotic CHD with increased pulmonary blood flow: TAPVC, DORV without PS, truncus arteriosus, TGA with VSD Increased end-systolic and end-diastolic volumes and high filling pressures secondary to ventricular dysfunction (i.e.  ejection fraction and ventricular failure): – Ischemic heart disease – Dilated cardiomyopathy – Systemic hypertension – Pulmonary hypertension – Valvular heart disease – Congenital heart diseases.

Children and young adults

Physiological

High output states: 1. 3rd TM 2. After exertion 3. Anxiety related tachycardia

1. Heart failure 2. IHD 3. DCM 4. Sytemic HTN 5. PH

Hyperkinetic states: 1. Anemia 2. Thryotoxicosis 3. AV fistula

Pathological

S3

VHD: 1. MR 2. TR

ACHD: 1. VSD 2. PDA CCHD with ↑ PBF: 1. TAPVC 2. DORV without PS 3. TGA with VSD 4. Truncus arteriosus

Fig. 21.26

of third heart sound (S )—TM: trimester of pregnancy, AV: arterio | Evaluation venous, MR: mitral regurgitation, TR: tricuspid regurgitation, VSD: ventricular 3

septal defect, PS: pulmonary stenosis, TGA: transposition of great arteries, DORV: double outlet right ventricle, PDA: patent ductus arteriosus, TAPVC: total anomalous pulmonary venous connection, IHD: ischemic heart disease, DCM: dilated cardiomyopathy, HTN: hypertension, PH: pulmonary hypertension, VHD: valvular heart disease, ACHD: acyanotic congenital heart disease, CCHD: cyanotic congenital heart disease,  PBF: increased pulmonary blood flow.

CARDIAC AUSCULTATION ●

●

●

387

Conditions in which S3 is expected but rarely heard at the bed side: – ASD and AR inspite of volume overload – A loud S3 in ASD should suggest (i) the possibility of Ebstein’s anomaly mistaken for ASD, (ii) ASD with mitral valve disease, (iii) ostium primum ASD with MR or TR – In chronic AR, S3 is audible when end-systolic volume increases with the development of LV dysfunction. S3 is sometimes audible in restrictive and hypertrophic cardiomyopathy when congestive heart failure occurs. Pericardial knock of constrictive pericarditis is a high-pitched early diastolic sound occurring 100–120 ms after A2 exaggerated with inspiration (see Table 21.13).

iv) Clinical Recognition of S3: Pathological S3 may be palpable and often sounds like a distant thud. It is often heard only with the bell of the stethoscope, as it is a low frequency sound with the lightest possible pressure. ●

●

●

LV S3 is best heard at the (LV impulse) apex in left lateral position during expiration, and increases its intensity with isometric handgrip exercise. RV S3 is best heard at the (RV impulse) lower left sternal edge (or occasionally subxiphoid region) in supine position, and is exaggerated during inspiration but no change occurs with isometric handgrip exercise. Maneuvers, which increase the venous return increase the intensity of the sound and thereby improve the audibility of S3. These maneuvers are as follows: – – – – –

●

●

Passive elevation of the legs Coughing Isotonic exercises (few sit-ups) Abdominal exercise Release phase of Valsalva maneuver.

The maneuvers that decrease the venous return, also decrease the intensity of S3, and include upright posture, tourniquets around the extremities, and the strain phase of Valsalva maneuver. In the presence of sinus tachycardia, it is often difficult to recognize S3 from the gallop rhythms or from the summation gallop. Carotid sinus massage transiently slows the heart and helps in timing the gallop rhythm.

Table 21.13 Early diastolic intervals Interval 1. 2. 3. 4. 5. 6.

A2–P2 during expiration A2–P2 during inspiration A2–S3 (physiological S3 in children) A2–S3 (pathological S3) A2–OS A2–pericardial knock

Duration (s) 0.03 0.04–0.05 0.12–0.20 0.14–0.16 0.03–0.15 0.10–0.12

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CARDIOVASCULAR SYSTEM EXAMINATION

b) Pericardial Knock (PK) It is an early diastolic rapid filling sound. The term ‘pericardial knock’ was coined by Dominic J Corrigan in 1842.52 The diastolic pericardial knock is characteristic of constrictive pericarditis occurring 0.10–0.12 s after A2 [while S3 occurs 0.14–0.16 s (pathological) and 0.12–0.20 s (physiologoical) after A2] (see Fig. 21.27). ● ●

●

●

It is due to the sudden cessation of ventricular filling.53 It is best heard with the bell of the stethoscope in supine position along the left sternal border in rigid constrictive pericarditis and infrequently in the subacute cases of fibroelastic variety. PK is earlier and higher frequency than typical S3 and so may be confused with an opening snap of MS. However, other clinical features such as elevated JV pressure with rapid y descent and Kussmaul’s sign, systolic retraction of the apex (Broadbent’s sign) and congestive hepatomegaly with ascites help in its detection.

c) The Fourth Heart Sound (S4) The fourth heart sound is a low frequency late diastolic or presystolic sound heard during atrial contraction (last rapid ventricular filling phase, see Fig. 21.28). It is also called as a presystolic or an atrial diastolic gallop (even though it is ventricular in origin). i) Characteristics of S4 ● ●

● ●

●

S4 follows the onset of P wave of ECG by approximately 70 ms and precedes S1. Presence of S4 indicates a hard working ventricle (while presence of S3 usually means ventricular failure). It may occur in elderly subjects (60 yrs) due to the loss of LV compliance with aging. Presence of S4 or S3 results in triple rhythm (gallop), while occurrence of both S4 and S3 produces quadruple rhythm. During tachycardia (induced by mild exercise or forced coughing) or long PR intervals, S3 may summate (fuse) with S4, producing a loud single summation gallop and an incomplete summation simulates a diastolic rumble of MS. A

V X

Y

S4 S1

A2 P

2

Fig. 21.28 PK

Fig. 21.27

PK

knock | Pericardial pericarditis.

S3 S1

S2

and fourth heart sounds (S | Third and S ) with atrial pressure tracing—

3

4

(PK) in constrictive

S3 coincides with Y descent and S4 with last rapid filling phase following atrial contraction (A).

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ii) Mechanism of production of S4 (i) Prerequisites for genesis of S4 ● ● ●

A healthy contracting atrium Non-obstructive AV valve Non-complaint ventricle

As the ventricular compliance decreases, atrial systole becomes responsible for more than 25% of ventricular filling (which normally accounts for 15%) (rapid ventricular filling phase: 85%, diastasis: 5%) and this vigorous atrial contraction is necessary to produce S4. Therefore, it is not present in atrial fibrillation. (ii) Theories for production of S4: These are similar to genesis of S3, ventricular and impact theories have been proposed for the production of S4. ●

●

●

The ventricular theory: Rapid deceleration of in-coming blood in the ventricular inflow during late diastolic filling sets the entire cardiovascular system into vibration producing S4.49 This theory explains the S4 recorded in the ventricles or on the epicardial surfaces. The impact theory:50 S4 auscultated at the chest wall is due to dynamic impact of the heart with the chest wall. Similarly, the ventricular mechanism together with a dynamic impact of the heart on the chest wall explains the presence of S4 in most diseases states.

iii) Causes of S4 a) Physiological S4 occurs in elderly subjects (60 yrs)54: recordable (in 50%) and rarely audible b) Pathological S4 occurs in: (i) Excessive rapid late diastolic filling secondary to: ● Hyperkinetic states (often associated with S 3 producing quadruple rhythm): Anemia, thyrotoxicosis ● Arteriovenous fistula ● Acute valvular regurgitation: MR, TR, AR. S4 is characteristic of acute MR,55 while S3 is characteristic of chronic significant MR ● ●

The acute LA volume overload results in a forceful atrial contraction resulting in S4. S4 is usually absent in MR of rheumatic etiology due to: – The chronicity of MR in which LV is dilated and complaint – Dilated unhealthy LA: LA is incapable of generating enough force – Often complicated by atrial fibrillation which results in the absence of atrial contraction and – Often associated with MS due to which enough atrial contraction cannot be transmitted to LV.

In acute AR, S4 may be audible due to LA volume overload and decreased LV compliance and its presence rules out associated MS.

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CARDIOVASCULAR SYSTEM EXAMINATION

(ii) Decreased ventricular compliance due to: VENTRICULAR HYPERTROPHY: An echocardiographic finding of an increase in wall thickness to cavity ratio is common in: Concentric LVH due to: – Left ventricular outflow tract obstruction (moderate–severe AS) – Hypertrophic cardiomyopathy – Systemic hypertension (moderate-severe). S4 in chronic hypertension: Audible S4 is a common feature in chronic hypertension suggesting LVH and decreased compliance. S4 in valvular AS ● It indicates a significant LV-aortic gradient (peak systolic gradient of 70 mmHg and left ventricular end diastolic pressure of 13 mmHg56) and significant AS. ● Hence; when associated with MS or complicated with atrial fibrillation, S is masked 4 due to obliteration of the pressure gradient across the aortic valve. S4 in hypertrophic cardiomyopathy: S4 is characteristic of hypertrophic cardiomyopathy producing a typical triple apical impulse, and an absence of S4 makes its diagnosis unlikely. Concentric RVH due to: – Right ventricular outflow tract obstruction (moderate–severe PS) – Pulmonary hypertension (moderate–severe) S4 in pulmonary stenosis: ● RV S correlates with a prominent ‘a’ wave in the JV pulse and right ventricular end 4 diastolic pressure of 12 mmHg. ● Occasionally, S in severe valvular PS may be long enough to be mistaken for presys4 tolic murmur of TS and inspiratory prominence of S4 is often accompanied by decrease or disappearance of ejection click. S4 in pulmonary embolism: Presence of S4 in a suspected case of pulmonary embolism suggests a significant RV pressure overload. ISCHEMIC HEART DISEASES: ● ● ●

Myocardial infarction: both acute and old Angina pectoris Ventricular aneurysm often associated with S3 (producing quadruple rhythm). S4 in ischemic heart disease: S4 is a hallmark of ischemic heart disease.

●

●

●

S4, which is audible during anginal pain, may disappear after the administration of nitroglycerine or after rest. Persistence of S4 into the post-infarction period may indicate a higher risk for the subsequent cardiac events. Presence of S4 in an apparently healthy adult may be a harbinger of a future coronary event.

A palpable S4 is common in LV asynergy or aneurysm. (iii) Arrhythmias: S1 is loud with short PR interval while S4 is easily audible with long PR interval i.e. in heart blocks.

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Table 21.14 Causes of S4

●

●

●

Physiological

Pathological

1. Elderly 60 yrs of age

1. Hyperkinetic circulatory states 2. Arteriovenous fistula 3. Acute mitral regurgitation, tricuspid regurgitation, aortic regurgitation 4. Left ventricular outflow tract obstruction: mod–severe aortic stenosis 5. Mod–severe systemic hypertension 6. Right ventricular outflow tract obstruction: mod–severe pulmonary stenosis 7. Mod–severe pulmonary hypertension 8. Ischemic heart disease 9. Heart blocks

First-degree AV block as it further separates S4 from S1. S4 may be audible even in the absence of significant cardiovascular disease. Second-degree 2:1 AV block: Due to increased diastolic volume, S4 is audible (when mitral valve is open). Complete heart block: S4 is randomly heard throughout diastole when mitral valve is open, and summation gallop may occur when S4 occurs simultaneously with rapid early ventricular filling (see Table 21.14).

iv) Clinical recognition of S4 (i) LV S4: ● LV S is best heard at the apex with bell of the stethoscope gently applied in left 4 lateral position during expiration. ● Since its intensity is closely related to the left ventricular end diastolic volume, any maneuver that increases venous return further separates it from S1 and increases its intensity. Maneuver that decreases venous return does the opposite. ● A loud S masks the audibility of a preceding S . So also, the presence of emphy1 4 sema and obesity mask S4. (ii) S4–S1 complex: S4 may be difficult to differentiate from S1. ● However, S becomes attenuated or disappears with firm pressure on the stetho4 scope and in upright position. ● S accentuates with handgrip, following sit-ups or coughing. 4 ● So also, maneuvers that increase venous return further separate it from S , 1 enhancing its audibility (besides it is often palpable). (iii) RV S4: ● RV S is best heard with bell of the stethoscope at the lower left sternal border 4 during inspiration. ● It is often accompanied by prominent ‘a’ waves in the JV pulse and is occasionally audible over the right jugular vein57 (see Fig. 21.29).

392

CARDIOVASCULAR SYSTEM EXAMINATION

Elderly 60 yrs

Physiological Hyperkinetic states: 1. Anemia 2. Thyrotoxicosis 3. AV fistula

S4

1. Acute MR 2. Acute AR 3. Acute TR

Pathological 1. Moderate–severe aortic stenosis 2. HCM 3. Chronic systemic hypertension

Fig. 21.29

1. Moderate–severe PS 2. Moderate–severe PH 3. Pulmonary embolism

1. IHD: MI, angina 2. Ventricular aneurysm 3. Heart blocks

of fourth heart sound (S )—AV: arteriovenous, MR: mitral regur| Evaluation gitation, TR: tricuspid regurgitation, AR: aortic regurgitation, AS: aortic 4

stenosis, PS: pulmonary stenosis, PH: pulmonary hypertension, HCM: hypertropic cardiomyopathy.

Table 21.15 Characteristics of OS Features

Findings

1. Frequency 2. Mobile leaflets and high atrial pressure 3. A2–OS interval (0.03–0.15 s) 4. Common causes

High Pre-requisite Predicts left atrial pressure and severity of MS MS, TS MR, TR VSD, PDA, ASD Ebstein’s anomaly, tricuspid atresia with ASD

d) Opening Snaps (OS) The opening of the normal AV valves is noiseless, but with thickening and deformity of the leaflets, a high frequency clicky sound is generated in early diastole, which is called as ‘opening snap’. This term ‘opening snap’ was coined by Thayer WS in 1908.58 i) Characteristics of OS: ●

●

●

OS is an early diastolic crisp, sharp sound, which correlates with the mobility of the AV valve i.e. anterior mitral leaflet (AML) in MS and septal leaflet in TS. The intensity of OS parallels the intensity of mitral component (M1) of S1. The mobile valves in MS have a loud OS and an accentuated M1, while immobile valves have an attenuated M1 and a decreased or absent OS, though OS may be found in 50–60% of the calcified MS patients, since mere presence of valvular calcium does not preclude the mobility of valve leaflets. OS follows A2 by an interval of 0.03 to 0.15 s and A2–OS interval has been used to predict the level of left atrial pressure (LAP) and the severity of MS59,60 (see Table 21.15).

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ii) Mechanism of production of OS (i) Prerequisites for genesis of OS ●

●

●

Thickened but mobile AV leaflets: immobile valve precludes OS as in severely calcified MS High atrial pressure ( LAP or  RAP): OS may occur early or late depending upon the atrial pressure High velocity flow across AV valves causes rapid excursion of leaflets producing OS in the absence of MS or TS.

(ii) Margolies and Wolferth theory: It is due to sudden stopping of the opening movement of the valve.61 This has been confirmed by hemodynamic and angiographic studies.62,63 (iii) It is precisely phonocardiographically correlated with the maximum opening motion of anterior mitral leaflet in MS,64 and near the ‘O’ point of apex cardiogram. Hemodynamically, OS occurs at the maximal MV opening shortly (20–40 ms) after LV-LA pressure crossover. iii) Causes of OS ● ●

Stenotic OS in stenosed but mobile AV valves: MS, TS65 Non-stenotic OS66: Due to high velocity and increased flow across the AV valves causing rapid excursion of the leaflets producing OS, which is often recordable than audible (see Fig. 21.30). (i) Mitral OS Thyrotoxicosis66 MR67 VSD (large)66 PDA Tricuspid atresia with a large ASD66 Hypertrophic cardiomyopathy

(ii) Tricuspid OS TR ASD (large)68 Ebstein anomaly TOF after shunt operation

iv) A2–OS interval can clinically predict LAP and thereby the severity of MS. A2–OS is 1/ to LAP i.e. higher the LAP (severe MS), earlier the OS (i.e. shorter A2–OS interval) whereas with lower LAP as in patients with mild MS, OS tends to occur late (i.e. longer A2–OS interval) (see Fig. 21.31). However, there is an imperfect correlation between A2–OS and mitral valve area (MVA).69 ● In mild MS: A –OS interval is 120 ms with LAP of 15 mmHg (mean LAP 2 5 mmHg) ● In moderate MS: A –OS interval is 60–80 ms with LAP of 20 mmHg (mean LAP 2 5–10 mmHg) ● In severe MS: A –OS interval is 40–60 ms with LAP of 25 mmHg (mean LAP  2 10 mmHg) Factors affecting A2–OS interval: A2–OS interval is unreliable in predicting the severity of MS as many factors affect this relationship and hence the occurrence of a wide A2–OS interval cannot rule out tight MS. These factors include: 1. Heart rate 2. Peak systolic pressure

394

CARDIOVASCULAR SYSTEM EXAMINATION

Opening snap (OS)

Stenotic

1. MS 2. TS

Mitral OS

Tricuspid OS

Thyrotoxicosis

1. MR 2. HCM

Fig. 21.30

Aortic diastolic pressure

Non-stenotic

1. Large VSD 2. PDA 3. T At with a large ASD

TR

1. ASD 2. Ebstein’s anomaly 3. TOF after shunt surgery

Aortic pressure LAP in severe MS LAP in mod MS

20 mmHg 15 mmHg

LAP in mild MS Left ventricular pressure

and causes of opening snap (OS)— | Types MR: mitral regurgitation, TR: tricuspid regurgitation, HCM: hypertropic cardiomyopathy, MS: mitral stenosis, TS: tricuspid stenosis, VSD: ventricular septal defect, PDA: patent ductus arteriosus, T At: tricuspid atresia, ASD: atrial septal defect, TOF: tetralogy of Fallot.

25 mmHg

Normal LAP A2

Fig. 21.31

In mild, moderate, severe MS OS

S1 (M1)

A –OS interval in mild, mod, and | severe mitral stenosis (MS) has an 2

inverse correlation with left atrial pressures.

3. Rate of decline of LV pressure during isovolumic relaxation (i.e. left ventricular end diastolic pressure, LVEDP) 4. Factors affecting the velocity of MV opening such as AR, calcified MV, decreased LV complaince (i.e. left ventricular dysfunction) increases A2–OS interval. ●

●

●

●

Heart rate (i) Tachycardia:  A2–OS interval due to the shortening of diastole and (ii) Bradycardia:  A2–OS interval due to the prolonged diastole (iii) In atrial fibrillation, A2–OS interval varies with the cycle length. With a short preceding PR interval, the LAP remains high and OS occurs early (i.e. short A2–OS interval); while with a longer preceding PR interval, the LAP declines and OS occurs late (i.e. longer A2–OS interval). Hypertension: There is  A2–OS interval as LV systolic pressure takes longer time to descend below the LAP and there is an early occurrence of A2. Increased LVEDP as in LV failure, LV dysfunction (diastolic), CAD, and some cases of cardiomyopathy:  A2–OS due to obliteration of the trans-mitral gradient. Conditions affecting MV opening velocity:  A2–OS interval occurs in – calcified MV: due to late occurrence of OS – AR: due to the early occurrence of A2 –  LV compliance (LV diastolic dysfunction) due to obliteration of the trans-mitral gradient.

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Table 21.16 Characteristics of tumor plop 1. 2. 3. 4. 5.

● ●

High pitched Due to mobile atrial myxoma Occurs earlier than S3 Occurs later than OS Often occurs with diastolic rumble

AS:  A2–OS interval in AS is due to the delayed occurrence of A2 Low CO states as in severe RVF:  A2–OS interval due to the late occurrence of OS as a result of lower LAP.

v) Absent OS in MS is noted in: ● ● ● ● ●

Severly calcified (immobile) mitral valve Associated with significant MR Associated with severe AR Associated with severe AS Associated with CAD and LV dysfunction.

vi) Clinical recognition of OS (i) Mitral OS ●

●

● ● ●

As OS is a high frequency sound, it is best heard with diaphragm of the stethoscope in the midprecordium between the left sternal border and just inside the apex without any significant change with respiration. It is often well heard at the base of the heart (pulmonary area) and may be confused with S2 split. The MDM follows the OS after a short interval. It becomes more prominent with exercise. A2–OS interval: It sounds like a split S2 with the shortest interval (about 40 ms), simulates wide fixed split of ASD with moderate A2–OS interval and it may be mistaken for S3 of MR or severe heart failure with widest A2–OS interval (120 ms).

(ii) Tricuspid OS ● ●

●

It is frequently not detected due to prominence of the findings of coexisting MS. It is best heard with diaphragm of the stethoscope with the maximum intensity closer to the left sternal border during inspiration. When audible, it generally follows the mitral OS.

e) Tumor Plop (TP) It is a high frequency early diastolic sound heard in left or right atrial myxomas70 (see Table 21.16). ●

●

The generation of tumor plop requires a mobile myxoma attached to the atrial septum by a long stalk. It results from an abrupt diastolic seating of the tumor within the right or left AV orifice70 i.e. it occurs at the maximal diastolic descent of the myxoma.

396

CARDIOVASCULAR SYSTEM EXAMINATION

Table 21.17 Characteristics of systolic ejection sound (ES) Aortic valvular ES

Pulmonary valvular ES

1. High frequency sound with S1–ES interval of 0.05 s 2. Coincides with anacrotic notch of upstroke of aortic pressure 3. Indicates mobile aortic leaflets 4. Defines left ventricular outflow tract obstruction at valvular level 5. Heard best at apex and aortic area 6. Does not vary with respiration (constant ES) 7. Associated with wide/reverse S2 splitting 8. Common causes: congenital bicuspid aortic valve, valvular aortic stenosis, truncus arteriosus

1. High frequency sound

●

●

●

●

2. Similar coincidence with pulmonary artery pressure 3. Indicates mobile pulmoanry leaflets 4. Defines right ventricular outflow tract at valvular level 5. Heard best at pulmonary area 6. Accentuation with expiration 7. Associated with wide S2 split and soft P2 8. Common causes: valvular pulmonary stenosis (PS), tetralogy of Fallot (with valvular PS)

It may be confused with OS or S3 as it occurs later than OS and earlier than S3, but intensity of TP and diastolic rumble may vary with patient’s body position. The clinical features of atrial myxomas mimic those of mitral value disease especially MS. However, often symptoms are sudden, intermittent and related to the patient’s body position.71 The right atrial myxoma may also have a diastolic rumble, holosystolic murmur (of TR), elevated jugular venous pressure with a prominent a wave and rapid y descent besides TP. Familial myxomas which constitute 10% of all myxomas occurs more in young females with an autosomal dominant transmission72 and are often associated with other tumors, pigmentation, NAME (nevi, atrial myxoma, myxoid neurofibroma, ephilides)72 or LAMB (lentigines, atrial myxoma, blue nevi)73 which are clubbed together into a syndrome called Carney’s syndrome or syndrome of myxoma.74

The Systolic Sounds a) Systolic Ejection Sounds The systolic ejection sounds are high frequency early systolic sounds originating from the right or left side of the heart75 (see Table 21.17). ●

●

The ejection sounds originating from the valves (aortic or pulmonic) are called valvular ejection sounds (see Fig. 21.32) and Those originating from the roots of the great vessels are called vascular ejection sounds (see Fig. 21.33).

i) Mechanism of production of systolic ejection sound (i) Valvular ejection sounds: The ejection sound (ES) is caused by the abrupt cephalad doming and halting movements of the SL valve at the onset of ejection, coinciding with fully opened position of the valve.76 Prerequisites: Thickened mobile semilunar valves. In severe calcified valve (as in severe AS), no excursion or piston-like ascent of the deformed valve is possible and

CARDIAC AUSCULTATION

Fig. 21.32

| Valvular systolic ejection sounds.

Fig. 21.33

397

| Vascular systolic ejection sounds.

therefore no sudden tensing of the valve leaflets or abrupt deceleration of the column of blood occurs. (ii) Vascular or root ejection sounds: The origin of this non-valvular ejection sounds is less certain. It could be due to opening movement of the leaflets that resonate in the arterial trunk or due to reverberations of the proximal arterial wall of the dilated great artery. ii) Causes of ES (i) Valvular ES ●

●

Aortic valve: Valvular AS, congenital bicuspid aortic valve, truncus arteriosus with quadricuspid valves Pulmonary valve: Valvular PS, TOF (with valvular PS)

(ii) Vascular ES ●

●

●

Due to an increased pressure beyond the valve: – Systemic hypertension – Pulmonary hypertension Due to an increased flow across the valve: – Hyperkinetic circulatory states e.g. anemia, thyrotoxicosis – Left to right shunt: ASD (pulmonary ES) Due to dilatation of the vessel beyond the valve: – Dilatation or aneurysm of ascending aorta – Dilatation of pulmonary artery: due to increased flow, pulmonary hypertension, idiopathic dilatation.

iii) Characteristics and clinical recognition of ES (i) Aortic valvular ES ●

●

●

●

ES is a high frequency, sharp, discrete sound, similar to S1 in intensity and follows S1 by 0.05 s. ES is coincident with the sharp anacrotic notch on the upstroke of the aortic pressure tracing. It defines the left ventricular outflow tract obstruction (LVOTO) at the valvular level with mobile leaflets. The intensity of ES correlates directly with the mobility of the valve, and not with the severity of the obstruction.

398

CARDIOVASCULAR SYSTEM EXAMINATION ●

●

●

●

●

It is best heard at the base (aortic area) and apex with the diaphragm of the stethoscope in sitting and leaning forward position. It does not vary with respiration, i.e. it is a constant ES (previously known as constant click). It may be loudest at the apex and at times may be heard only at the apex especially in elderly patients or with COPD, and may be mistaken for loud S1 or split S1. The left ventricular end diastolic pressure (LVEDP) in AS does not vary with respiration and is never higher than the aortic diastolic pressure (unlike valvular PS). However, variable ES may be heard in large biventricular aorta of Truncus arteriosus and TOF with PS. The mechanism of this variation is not known. S2 is often normal or diminished in intensity but splitting is always abnormal i.e. wide or reverse split. In general, the presence of ES excludes supra- or subvalvular AS or HCM as a cause of LVOTO and most often it indicates the diagnosis of bicuspid aortic valve. Audible ES in a patient of coarctation of aorta implies a coexisting congenital bicuspid aortic valve, a common associated anomaly.

(ii) Aortic vascular ES ●

● ●

ES is similarly coincident with the complete opening of the aortic valve and upstroke of the aortic pressure curve.76 It is poorly transmitted from the aortic area and is not well heard at the apex. S2 is often loud and may be normal split.

(iii) Pulmonary valvular ES ●

●

●

●

ES also occurs at the maximal excursion of the stenotic pulmonary valve76 and similar correlation with the pressure curve.77 It is best heard during expiration at 2nd and 3rd left intercostal spaces (but poorly audible or inaudible at the apex) in sitting and leaning forward position with the diaphragm of the stethoscope, unlike most right-sided auscultatory events. This variability of the pulmonary valvular ES is related to the elevated right ventricular end diastolic pressure (RVEDP) in moderate-severe PS. During inspiration, the increased venous return to the RV leads to the elevation of RVEDP beyond the pulmonary diastolic pressure (PADP) resulting in premature opening of the PV in diastole itself, and this premature opening of the PV decreases the intensity of the ES during inspiration. In very mild PS, there may not be respiratory variation in the intensity of ES while in some severe PS, RVEDP may exceed the PADP throughout the respiratory cycle and ES not audible. S2 is usually wide split with P2 often soft or inaudible and usually delayed due to very low pulmonary artery pressure.

(iv) Pulmonary vascular ES ●

●

●

ES is similarly coincident with the complete opening of the pulmonary valve and occurs at the upstroke of the pulmonary artery pressure curve.76 ES is best heard at the pulmonary area and may also be heard lower down the sternum in sitting and leaning forward position during inspiration. It is often palpable over the pulmonary artery. P2 is often loud and S2 is usually narrow split.

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b) Non-ejection Sounds or Systolic Clicks Cuffer B in 1887 first described these sounds as a systolic gallop (bruit gallop).78 However, it was Carl Potain in 1894 who described these sounds as well localized, and small short clicking sounds.79 i) Characteristics of non-ejection sounds (NES) or systolic clicks (SC) ●

●

These mid-to-late systolic sounds have sharp, high frequency and clicking quality and the term “click” is appropriate. The systolic click could be single or multiple and often occurs with late systolic murmur in AV valve prolapse.

ii) Mechanism of NES: Initially in 1932, it was thought to be extracardiac in origin.80 ●

●

●

However, it occurs due to tensing of the redundant leaflets and elongated chordea tendinea of the AV valves during systole81 which is confirmed by angiographic,82 intra-cardiac phonocardiographic,83 and echocardiographic studies.84 This systolic click coincides with the maximum systolic excursion of the prolapsed leaflet into the atrium. The multiple clicks occur because of asynchronous tensing of the different portions of the redundant mitral leaflets, especially the triscalloped posterior leaflet.

iii) Causes of NES ●

●

SC is characteristic of the prolapse of the AV valves more commonly mitral valve prolapse (MVP), but also tricuspid valve prolapse (TVP). It has also been described in: – LV aneurysm – Aneurysm of the membraneous ventricular septum associated with VSD85 – Incompetent heterograft valves86 – Atrial myxomas87 – Adhesive pericarditis and – Left-sided pneumothorax.88

iv) Clinical recognition of SC: ● ●

●

●

Presence of SC is the diagnostic of MVP.

It is often associated with loud S1 and systolic murmur. The clicks of MVP are better heard at the apex with diaphragm of the stethoscope but if loud, it may be widely transmitted over the precordium, while the SC of TVP is usually heard best at the lower sternal border. The physical and pharmacological maneuvers that decrease the left ventricular end diastolic (LVED) volume and LV size cause earlier and greater degree of prolapse that result in earlier (closer to S1) and loud click.89 These maneuvers include standing, Valsalva maneuver (phase II), nitroglycerine and amylnitrate inhalation (see Fig. 21.34). The maneuvers such as squatting, supine position, vasopressor (phenyl epinephrine), Valsalva maneuver (phase IV) and sustained handgrip which increase LVED volume and LV size, reduce the degree of prolapse and the click is delayed or absent.

400

CARDIOVASCULAR SYSTEM EXAMINATION S1 S2 SC

Supine S1 S2 SC

Standing

S1 S2 SC

Squatting

Fig. 21.34

of postural changes on systolic click (SC) in MVP—standing results | Impact in an early occurrence of click, while click is delayed on sqatting.

Prosthetic Valve Sounds The prosthetic valves normally produce murmurs and both opening and closing sounds which may be systolic or diastolic depending upon the type of valve and its position of implantation. The prosthetic valve sounds are of high frequency and clicky in quality, hence are better heard with diaphragm of the stethoscope (see Table 21.18). i) Both opening and closing sounds or clicks (OC, CC) are audible in: ● ● ●

Ball-in-cage valves: Starr-Edwards valves in both mitral and aortic position Bileaflet valve: St Judes valves at aortic position Porcine valves: However, OC is audible in 50% at mitral position and it is uncommon at aortic position.

ii) Only closing sound (CC) is present in tilting disc valves. Only a soft OC may be phonocardiographically demonstrable at the mitral position: Bjork Shiley, Lillehikaster, Sri Chitra are the tilting disc valves. Ball-in-Cage Valves (Starr-Edwards) (i) In aortic position (see Fig. 21.35) ●

OC occurs 0.06–0.07 s after S1 and is coincident with maximal ball excursion.90

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Table 21.18 Prosthetic valve sounds Type

Mitral position

Aortic position

1. 2. 3. 4.

OC and CC with SEM CC, may OC, with SEM, and DM OC and CC, with SEM, may DM CC, OC in 50% with SEM and DM

OC  CC, with SEM CC, with SEM, occasional DM OC and CC, with SEM CC with SEM

Ball-in-cage Tilting disc Bileaflet Bioprosthetic

CC: closing click, OC: opening click, SEM: systolic ejection murmur, DM: diastolic murmur.

Fig. 21.35

| Starr-Edwards ball in cage valve. ●

● ●

Fig. 21.36

| Meditronic Hall tilting disc valve.

Multiple CCs are produced when the freely moving ball bounces against the cage during an early systolic ejection.91 These clicks are accompanied by 2/6 harsh systolic ejection murmur, but no diastolic murmur is audible. OC is more prominent than CC in the ratio of 0.5. Decrease in the intensity of the clicks or absence of OC indicates malfunctioning of the valve.90

(ii) In mitral position ●

●

●

●

OC occurs 0.05–0.15 s after A2.92 Narrowing of this interval indicates an elevation of LAP, which may be due to valvular obstruction or regurgitation. A closing click accompanies the normal S1, which varies with changing RR intervals of atrial fibrillation. CC is loudest with short RR intervals and soft with long RR intervals. These clicks are accompanied by 2–3/6 systolic ejection murmur, but no diastolic murmur is audible. Similarly, decrease in the intensity of the clicks occurs with the malfunctioning valve or with severe LV dysfunction.93

Tilting Disc Valves (Meditronic Hall) The malfunctioning valve, LV dysfunction, 1 AV block or other arrhythmias soften the clicks (see Fig. 21.36).

402

CARDIOVASCULAR SYSTEM EXAMINATION

Fig. 21.37

| St. Judes bileaflet valve.

Fig. 21.38

| Porcine bioprosthetic valve.

i) In the aortic position ●

Only CC is distinct with 2/6 systolic ejection murmur and occasionally diastolic murmur.

(ii) In mitral position ● ●

Similarly, CC is prominent with 2/6 systolic and diastolic murmurs. OC may be demonstrable and occurs 0.05–0.09 s after A2. Shortening of this interval (A2–OC) is due to the elevation of LAP resulting from valvular obstruction or regurgitation.

Bileaflet Valves (St. Judes) ● ●

Both OC and CC are common with a soft systolic ejection murmur.94 Similarly, malfunctioning of the valve or LV dysfunction result in muffling of the clicks (see Fig. 21.37).

Bioprosthetic Valves (Porcine Valves) (i) In aortic position ● ●

It is characterized by CC and 2/6 systolic ejection murmur. OC and diastolic murmur are usually not audible (see Fig. 21.38).

(ii) In mitral position ●

●

CC is constant with 2/6 apical systolic murmur in 50% and diastolic murmur in 50–70%. OC is audible in 50% of the patients at an interval of 0.07–0.11 s after A2.

Extra-Cardiac Sounds These include pacemaker sounds, pericardial rub and mediastinal crunch.

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i) Pacemaker Sounds These sounds are brief and high frequency sounds occasionally produced by transvenous pacemakers implanted in RV apex, due to stimulation of the intercostal muscles (through intercostal nerves) by the endocardial electrodes.95 ● ●

●

Pectoral muscles and diaphragmatic stimulation can also occur. They occur synchronously with pacemaker spike and often associated with twitching of the muscles. The audible high frequency pacemaker sounds always suggest myocardial perforation by the endocardial lead, although it is not always present.

ii) Pericardial Rub Pericardial rub is the hallmark of pericardial inflammation. a) Mechanism of production of pericardial rub (PR): It is due to the movement of the parietal and visceral surfaces of the pericardium moving against each other. b) Components of PR: The classic rub is triple phased: systolic, mid-diastolic and late diastolic (or presystolic/atrial systole). ●

●

● ●

However, it is often biphasic, i.e. to and fro rubs due to ventricular systolic and atrial systolic components. The diagnosis is the simplest when all the three phases are present, which occurs only in 50% of the cases. It is commonly audible in uremic pericarditis especially when associated with hypertension. The systolic phase is most consistent followed by the presystolic phase. In the setting of atrial fibrillation presystolic component disappears. c) Causes:

● ● ● ● ●

●

Acute pericarditis of any etiology: especially tubercular in origin Following open heart surgery: post cardiotomy pericarditis Uremic pericarditis Rheumatic pancarditis Acute phase of transmural MI giving rise to post MI pericarditis, which dramatically responds to steroids Infective endocarditis due to ring abscess. d) Clinical recognition:

● ●

●

●

●

These friction rubs are high-pitched, leathery and scratchy in nature. They are best heard over the 2nd and 3rd left intercostal spaces over the ‘bare area’ of the heart. They seem close to the ear and are auscultated best with diaphragm of the stethoscope with the patient leaning forward or in knee-chest position and holding the breath after forced expiration (see Fig. 21.39). Unlike pleural rub, pericardial rub can be present even with large pericardial effusion and cardiac tamponade.96 Occasionally, the short scratchy pulmonic ejection systolic murmur heard in hyperthyroidism (Means-Lerman sign) is misinterpreted as pericardial rub.97

404

CARDIOVASCULAR SYSTEM EXAMINATION

Fig. 21.39

| Eliciting pericardial rub in knee-chest position.

iii) Mediastinal Crunch It is a series of high-pitched scratchy sounds heard in mediastinal emphysema, which is designated as Hamman’s sign.98 ● ● ● ●

These sounds are common following cardiac surgery. They occur most frequently during ventricular systole in a random fashion. They may be prominent during different phases of respiration or different postures. The mediastinal emphysema is clinically confirmed by noting the crepitations in the neck secondary to subcutaneous air.

THE HEART MURMURS Definition Murmur is a Latin word. A heart murmur is defined as a prolonged series of audible signals/vibrations of varying intensity (loudness), frequency (pitch), configuration, and duration detectable with the aid of a sthetoscope.99 Mechanism of Production of the Murmurs The sudden deceleration of blood results in ‘heart sounds’, while most of the murmurs are produced by turbulent blood flow100 (see Fig. 21.40). Turbulence arises when the Reynolds number reaches 2000, i.e. ● ● ●

When the blood flow velocity is high Orifice (vessel/chamber) diameter is small or Kinetic viscosity is low (as in anemia).

Therefore, turbulence (Reynolds number 2000) Flow/2 (diameter) (kinetic velocity)

CARDIAC AUSCULTATION

High flow velocity

Small orifice diameter

405

Low kinetic viscosity

Turbulence

Jet impact

Cavitation

Eddies formation

Vortex shedding

Flitter

Periodic wake

Murmur

Fig. 21.40

| Mechanism for production of murmurs. Table 21.19 Turbulent blood flow Causes of turbulence

Consequences of turbulence

1. High blood flow velocity 2. Small orifice diameter 3. Low kinetic viscosity

1. 2. 3. 4. 5. 6.

Vortex shedding Jet impact Cavitations Eddies Periodic wake phenomenon Flitter

Turbulence occurs when there is disproportion between the velocity of blood flow and the dimensions of the orifice through which it flows. It is the consequence of turbulence rather than turbulence itself that explains the genesis of most of the cardiac murmurs. Rushmer RF described six theoretical consequences of turbulence that may produce a heart murmur100 (see Table 21.19). 1. 2. 3. 4. 5. 6.

Vortex shedding of the orifices Jet impact Cavitations (micro-bubbles) Eddies around the jet Periodic wake phenomenon and Flitter.

1. Vortex shedding: As the blood flow passes a narrow orifice, vortices produced at the tip of the orifice are shed laterally to hit the vessel wall producing vibrations and thereby a high-pitched (musical) murmur. 2. Jet impact: A jet of turbulent blood flow may directly hit the wall of the heart or blood vessel producing vibrations and thereby a murmur. 3. Cavitations: A high turbulent blood flow can theoretically produce cavitations (micro-bubbles) that generate a sound of different frequencies, which is often described as a harsh murmur.

406

CARDIOVASCULAR SYSTEM EXAMINATION

4. Eddies around a jet: A high velocity jet of blood produces eddy currents in the adjacent slow moving blood. These eddies cause vibrations in the surrounding soft tissues that are transmitted to the skin surface, where they are appreciated as a murmur. 5. Periodic wake phenomenon: As blood passes to either side of a structure placed in its path, a periodic wake phenomenon arises, producing relatively pure musical tones, i.e. high pitched (musical) murmurs. This mechanism is akin to the Aeolian tones, which are made by passing the wind through, along and across the cylinders. 6. Flitter: A high-speed jet of blood in a blood vessel may pull the walls of blood vessel inward by ‘Bernoulli effect’. Variations in the speed of the jet, passing a particular point in the vessel produces a continually varying strength of the ‘Bernoulli effect’, which in turn causes the vessel wall to vibrate and generate a murmur. This is known as flitter. Factors for the Production of Murmurs According to Leatham, three main factors are responsible.101 However, most often a combination of these factors is responsible for the production of murmurs. ● ●

●

High flow rate through normal or abnormal orifices Forward flow through a constricted or an irregular orifice or into a dilated vessel or chamber and Backward or regurgitant flow through an incompetent valve, septal defect or PDA.

Characteristics of Murmurs Following characteristics of the murmurs should be noted during auscultation: ● ● ● ● ● ● ● ●

Timing of the murmur in relation to the heart sounds (i.e. systolic/diastolic/continuous) Location i.e. site of maximum intensity Duration or length of the murmur Intensity or loudness of the murmur i.e. its grade Frequency or pitch of the murmur Configuration or shape of the murmur Transmission of the murmur (i.e. radiation or conduction) (site and direction) Dynamic auscultation.

Timing of the Murmur Cardiac murmurs should be timed and are classified into: ● ● ●

Systolic murmurs: Murmur begins with or after S1 and ends at or before S2. Diastolic murmurs: Murmur begins with or after S2 and ends before the subsequent S1. Continuous murmurs: Murmur begins in systole and continues without interruption through S2 into all or a part of diastole. They usually have their peak intensity around S2.

Systolic and diastolic murmurs are sub-classified as early, mid, late or pan (holo). (i) At normal heart rate, systole is shorter than diastole and identification of the murmur is seldom difficult. (ii) But timing of the murmurs may sometimes be difficult in the presence of rapid heart rates.

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407

– In such conditions, the murmur can be timed by simultaneous palpation of the lower right carotid artery or by identifying the loud S2 at the base. – However, if the murmur in question is at the apex, move the stethoscope from the base to the apex while fixing the cardiac cycle in mind, using S2 as a reference point. This method of auscultation is known as “inching technique of Harvey and Levine”.4 – With sinus tachycardia, carotid sinus pressure may temporarily slow the rate and make it possible to differentiate systole from diastole. – In the presence of extra systoles, identify the beat that follows a compensatory pause and the first subsequent sound will be S1. Location of the Murmur It must be determined by careful auscultation as it may suggest its site of genesis. The location of the murmur depends upon its site of origin and intensity and physical characteristics of the chest.102 Murmurs at the apex: (i) Murmurs heard only at the apex: ● Mid diastolic murmur (MDM) of MS, functional MDM of MR ● Systolic murmur (SM) of mild MR ● Ejection systolic murmur (ESM) of calcified AS in elderly patients with emphysema as: – Calcified valve results in the loss of jet effect and prevents conduction of the murmur to the carotids – LV is exposed to the emphysematous chest wall only at the apex. (ii) Murmurs best heard somewhere else but are also heard at the apex: ● Early diastolic murmur (EDM) of AR ● ESM of AS ● MDM of TS ● Pansystolic murmur (PSM) of TR ● PSM of VSD. (iii) Murmurs usually not heard at the apex: ● Murmurs of right-sided origin, but can be audible when RV forms the apex e.g. TS and TR murmurs ● ESM of PS ● EDM of PR. Murmurs at the lower sternal area (tricuspid area, TA): (i) Murmurs heard only at TA: SM of mild TR, MDM of TS (exceptions see above). (ii) Murmurs best heard somewhere else but also heard at TA: ● PSM of MR and VSD ● ESM of AS and PS. (iii) Murmurs usually not heard at TA: MDM of MS.

408

CARDIOVASCULAR SYSTEM EXAMINATION

Murmurs at the left sternal border of 3rd intercostal space: (i) Murmurs best heard in this area are: ● PSM of VSD (commonest) ● EDM of AR ● ESM of infundibular PS. (ii) Murmurs best heard somewhere else but also heard in this area are the murmurs of valvular PS and TR. (iii) Murmurs usually not heard in this area: MDM of MS. Murmurs at the pulmonary area (PA) (2nd left intercostal space): (i) Murmurs best heard at PA: ● ESM of PS ● Flow murmur of pulmonary origin in ASD ● Continuous murmur of PDA ● EDM of PR ● Murmur of sub-pulmonary VSD. (ii) Murmurs usually not heard at PA: MDM of MS and TS (see Table 21.20). Murmurs at the aortic area (AA) (2nd right intercostal space): (i) Murmurs best heard at the AA: ● ESM of AS (valvular, subvalvular), aortic sclerosis ● EDM of AR (aortic root origin). (ii) Murmurs rarely heard at the AA: ESM of PS. (iii) Murmurs never heard at the AA: MDM of MS. Duration or Length of the Murmur It may be short, long or holo (pansystolic/pandiastolic). ●

●

It depends on the duration of the event, such as the pressure gradient between the two sites or cardiac chambers, and reflects the severity of the lesion. This is true in all stenotic lesions: MS, AS, PS. Even though the regurgitant murmurs are longer than the stenotic murmurs, the length of a regurgitant murmur is not related to the severity of the lesion. e.g. MR, VSD or TR. Long or short murmur may be associated with any degree of severity and accompanying features are of diagnostic importance.

Table 21.20 Non-audible murmurs At apex

At pulmonary area

1. Systolic murmur of pulmonary stenosis 2. Diastolic murmur of pulmonary regurgitation 3. Murmurs of tricuspid stenosis and tricuspid regurgitation (may be heard when RV forms the apex)

1. Mid diastolic murmur of mitral stenosis 2. Mid diastolic murmur of tricuspid stenosis

CARDIAC AUSCULTATION ●

409

In AR: To some extent, length of the murmur correlates with the severity of the lesion except in a few conditions such as acute AR, when complicated with LVF, and when associated with systemic hypertension.

Intensity or Loudness of the Murmur At bed side, the intensity of the murmur is graded from 1 to 6 as described by Freeman and Levine (1933).103 1. Grade 1/6 murmur: the faintest murmur that can be heard only with special effort (close concentration) and under optimal conditions (quiet room, relaxed patient and clinician). 2. Grade 2/6 murmur: a soft or faint murmur that can be readily detected. 3. Grade 3/6 murmur: a moderately loud murmur without associated thrill. 4. Grade 4/6 murmur: a very loud murmur that is palpable (i.e. associated with thrill). 5. Grade 5/6 murmur: an extremely loud murmur that can be heard only if edge of the stethoscope is in contact with the chest, but cannot be heard if the stethoscope is removed from the skin. It is accompanied by a thrill. 6. Grade 6/6 murmur: exceptionally loud murmur that can be heard with a stethoscope, which has just removed contact from the chest wall. It is accompanied by a thrill. In general, systolic murmurs of grade 3/6 or more in intensity are usually hemodynamically significant i.e. with few exceptions the intensity of the murmur is directly related to the severity of the underlying condition, while a diastolic murmur of any degree of intensity is organic in nature. Factors affecting the intensity of the murmurs: The intensity or loudness of the murmurs is directly related to: ●

●

●

Quantity and velocity of blood flow across the sound producing area i.e. degree of turbulence e.g. – High velocity of blood flow through a small VSD produces a loud murmur, while a large flow at low velocity through an ASD produces no murmur. – So in high output (hyperdynamic) states, murmurs are accentuated while in hypodynamic states (due to decreased cardiac output as in CHF) the intensity of the murmurs is decreased. Its distance from the stethoscope e.g. murmurs are accentuated in an individual with thin chest wall. Transmission qualities of the tissue between the origin of a murmur and a stethoscope e.g. obesity, emphysema, significant pericardial or pleural fluid will decrease the intensity of a murmur.

Functional murmurs with thrill: Grade 4/6 murmurs are usually organic in nature and are palpable (i.e. associated with thrill). However, there are some functional murmurs, which are accompanied by a thrill (see Table 21.21): ● ● ●

Thrill over the neck veins in venous hum Diastolic thrill (functional MS) in severe MR Systolic thrill over the carotids (functional AS) in severe AR

410

CARDIOVASCULAR SYSTEM EXAMINATION

Table 21.21 Functional murmurs that are accompanied by thrills Site

Thrill

Functional lesion

Cause

1. 2. 3. 4. 5.

Diastolic Systolic Diastolic Systolic Continuous

Mitral stenosis Aortic stenosis Pulmonary regurgitation Pulmonary stenosis Mimicking patent ductus arteriosus/AV fistula

Severe mitral regurgitation Severe aortic regurgitation Severe pulmonary hypertension Mod-large atrial septal defect Cervical venous hum

Apex Carotids Pulmonary area Pulmonary area Neck veins

●

●

Diastolic thrill (functional PR) in severe PH (especially in primary pulmonary hypertension) Systolic thrill in pulmonary area (mimicking PS) in moderate to large ASD.

Character and Frequency (Pitch) of the Murmur These give a clue to the nature of their origin. The frequency of a murmur like its intensity has a direct relationship to the velocity of blood flow.104 (i) High pressure gradient between two sites/chambers results in high velocity flow producing: ● A high-pitched murmur (300 CPS) which could be soft (as in AR), blowing (as in MR) or musical (as in papillary muscle rupture) in character. ● A mixed frequency murmur [combination of high and medium (125–300 CPS) frequencies], which is harsh in character as in AS, PS, VSD. (ii) Low pressure gradient between two sites/chambers results in low velocity flow producing a low-pitched murmur (25–125 CPS), which could be rough/rumbling in character as in MS, TS. In general, all regurgitant murmurs are high pitched and more widely audible, stenotic murmurs of AV valves are low pitched and confined to the valve area of its origin. But stenotic murmurs of SL valves are of mixed frequency, with its medium frequency component best heard at the site of its origin, while high frequency component is more widely audible and transmitted to other sites, e.g. ESM of AS soft at the apex while it is harsh at the aortic area. Configuration or Shape of the Murmurs (Murmur “Envelope”) It is also related to the pattern of blood flow velocity and may help in identification of nature of the lesion. It is described as: ● ● ●

●

Crescendo (increasing) e.g. ESM of AS Decrescendo (decreasing) e.g. EDM of AR Crescendo-decrescendo (increasing-decreasing or diamond shaped) e.g. SM of AS and PS Plateau (even or unchanged) e.g. PSM of MR and

CARDIAC AUSCULTATION

411

Table 21.22 Dynamic auscultation Bedside maneuvers

Heart sounds

Heart murmurs

1. Inspiration

Right-sided murmurs

3. Valsalva

RV S3 S4, tricusp OS; S2 split widens LV S3 S4, mitral OS, pulmonary ES; S2 split narrows S3 S4; S2 split narrows

4. Supine from standing or sitting 5. Squatting

RV S3 S4; later LV S3 S4; S2 split widens S3 S4 of both sides

6. Isometric hand grip

LV S3 S4

7. Amylnitrate inhalation

S3 OS of both sides, S1; A2, S3 of MR origin; A2-OS shortened

2. Expiration

●

Left-sided murmurs except SM of MR SM of HOCM SM of AS, PS, MR, TR DM of AR, PR, MS, TS SM of PS, AS, MR, TR, VSD; SM of HOCM SM of PS, AS, MR, VSD SM of HOCM SM of MR, VSD; DM of MS, AR SM of AS, HOCM SM of PS, AS, TR; DM of MS, TS, PR SM of MR, small VSD, TOF; DM of AR, Austin Flint M, diastolic component of PDA

Variable (uneven) e.g. classical PSM of MR may have late systolic accentuation or may taper off in late systole.

However, the true shape of a murmur is usually more difficult to determine clinically, especially the diastolic murmurs than recording on a phonocardiogram. Transmission of the Murmurs A murmur may radiate or conduct to other sites. This is determined by its site of origin, intensity and direction of blood flow as well as by the physical characteristics of the chest.102 ●

● ●

●

Conduction of the murmur occurs when direct anatomical continuity is present e.g. SM of AS is conducted to the carotids while PSM of MR is radiated to the left axilla or back. Loud murmurs transmit widely while soft murmurs are confined to their area of origin. High frequency sound/murmur transmits best proximal (“upstream”) to its origin while low frequency sound/murmur transmits best distal (“downstream”) to its origin e.g. harsh component of AS murmur is conducted to base and carotids, while higher frequency vibrations of the murmur are best heard at the apex. Low frequency sound/murmur transmits better through the thoracic tissue and is readily felt as a thrill while a high frequency sound/murmur poorly transmits through the thoracic tissue and is not accompanied by a thrill.

Dynamic Auscultation Dynamic auscultation is the technique of altering circulatory dynamics by a variety of physical and pharmacological maneuvers and determining the effects of these maneuvers on heart sounds and murmurs105 (see Table 21.22).

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CARDIOVASCULAR SYSTEM EXAMINATION

Types of bedside maneuvers 1. Physical: Respiration, postural changes, isometric hand grip, Valsalva and Muller maneuvers. 2. Non deliberate: Changes in cardiac cycle length non deliberately due to PVC, atrial fibrillation or heart blocks. 3. Pharmacological: By the use of vasoactive agents such as amyl nitrate, methoxamine and phenylephrine. 1) Normal respiration Normal physiological changes during respiration: Inspiration results in changes in the systemic and pulmonary venous return. (i) The inspiratory increase in systemic venous return due to fall in intra-thoracic pressure. ● ●

Increases RV stroke volume and duration of RV ejection. Decreases pulmonary vascular impedance thereby increasing the pulmonary hangout interval (80 ms).

(ii) The inspiratory decrease in pulmonary venous return due to pooling of blood in the pulmonary vasculature. ● ●

Decreases LV stroke volume and LV ejection. Decreases hangout interval on the aortic side.

During expiration, the events are opposite to that of inspiration. Effects on heart sound (i) S2: Potaine in 1866 first noticed normal respiratory variation in the splitting of S2. During inspiration, normal split of S2 into A2 and P2 occurs, while during expiration S2 is heard as a single sound. Mechanism of normal S2 split: See second heart sound. (ii) S3, S4 and OS: RV S3 and S4 and right-sided OS increase in intensity with inspiration due to increase in the RV stroke volume. So also, LV S3 and S4 and mitral OS are accentuated with expiration due to an increase in LV stroke volume. (iii) Aortic ejection sound: ●

●

●

Aortic valvular ejection sound does not vary with respiration i.e. it is a constant ES (previously known as constant click) as LVEDP does not vary with respiration and it is never higher than the aortic diastolic pressure. However, ES is variable in a large biventricular Truncus arteriosus and TOF with pulmonary atesia, but the mechanism of variable ES is not known. Aortic vascular ES may increase with expiration.

(iv) Pulmonary ejection sound: ●

●

Pulmonary valvular ejection sound is best heard during expiration, and its intensity decreases with inspiration. Inspiratory increase of venous return and RV stroke volume leads to the elevation of RVEDP beyond the pulmonary artery diastolic pressure (PADP) causing

CARDIAC AUSCULTATION

●

413

premature opening of the pulmonary valve in diastole itself and less upward motion of the valve leaflets resulting in the decreased intensity of ejection sound. Pulmonary vascular ES may increase with inspiration.

Effect on heart murmurs (i) All right-sided murmurs are accentuated during inspiration including the TR murmur (Carvallo sign) due to the increased RV stroke volume. Conversely, leftsided murmurs except MR murmur are best heard during expiration when the LV stroke volume is maximum. (ii) The inspiratory decrease in LV stroke volume and LV size in patients with MVP increases the redundancy of mitral valve and thereby increases the degree of valvular prolapse which results in louder and early occurrence of midsystolic click and murmur during systole.106 No Change (i) However, patients complicated with RVF may not demonstrate inspiratory augmentation of right-sided heart sounds and murmurs, as there is a little or no increase in the systemic venous return due to high RVEDP. But when these patients are auscultated on standing posture (thus reducing the resting right heart filling), expected respiratory changes may be appreciated. (ii) Aortic valvular ES: It does not vary with respiration. (iii) MR murmur does not vary with respiration. 2) The Valsalva maneuver107: It was initially described in 1704 as a method for expelling pus from the middle ear by straining with mouth and nose closed.34 ●

●

It consists of a relatively deep inspiration followed by forced expiration against a closed glottis for 10–20 s or Blowing into a BP manometer to maintain a level of 40 mmHg for 30 s.

It is helpful to demonstrate to the technique of performing this maneuver beforehand. The normal response to the Valsalva maneuver consists of four phases: (i) Phase I: As straining commences, intra-thoracic pressure increases which is associated with: ● A transient rise of LV output and systemic arterial pressure (see Fig. 21.41) ● But there occurs a fall in heart rate. (ii) Phase II (straining phase) is associated with perceptible decrease in systemic venous return and stroke volume (initially right side followed by left side) which results in: ● Decrease of systolic, diastolic and pulse pressures (small pulse) and ● Reflex tachycardia. (iii) Phase III (cessation of straining phase or release of Valsalva maneuver): Cessation of straining results in: ● Sudden increase in systemic venous return ● But there is an abrupt, transient decrease in arterial pressure equivalent to the fall in intra-thoracic pressure.

CARDIOVASCULAR SYSTEM EXAMINATION Arterial pressure (mmHg)

414

Fig. 21.41

300

4

250 200 150

1

2

3

100 50 0

systemic arterial pressure response to Valsalva maneuver in a | Normal normal individual— 1, 2, 3 and 4 are phases of Valsalva maneuver.

(iv) Phase IV (overshoot phase) consists of return of the events to pre-Valsalva levels after 6–8 beats with: ● A transient overshoot of systemic arterial pressure, wide pulse pressure and ● Reflex bradycardia. This occurs due to a transient rise in cardiac output as a result of: – Return of pooled blood in the venous system and – Reflex vasoconstriction and tachycardia secondary to low perfusion pressure of the carotid and baro-receptors during phase III. Hence; in normal individuals, arterial pressure tracing shows four distinct phases and the ratio between the longest and shortest RR intervals is 1.6, which is described as the Valsalva ratio. Phase I and III are not usually perceptible at bedside. Since coronary blood flow transiently falls during this maneuver, it should not be performed in patients with ischemic heart disease. Effects on heart sounds (i) During phase II: S3 and S4 are attenuated and S2 split narrows (i.e. A2–P2 interval is narrowed or abolished). (ii) During phase III: Due to a sudden increase in systemic venous return, right-sided S3 and S4 augment and S2 split widens. (iii) During phase IV: Left-sided S3 and S4 return to controlled levels and may transiently be accentuated. Effects on murmurs (i) During phase II: As stroke volume and systemic arterial pressure fall, there is an attenuation of the following murmurs: ● Systolic murmurs of AS, PS, MR and TR ● Diastolic murmurs of AR, PR, MS and TS. (ii) During phase II: Reduction in LV volume and size leads to: ● Increase in LVOTO with increased pressure gradient resulting in the amplification of SM in patients with HOCM. ● Increase in the degree of valve prolapse in patients with MVP resulting in loud and early occurrence of mid systolic click and systolic murmur.

Arterial pressure (mmHg)

CARDIAC AUSCULTATION

Fig. 21.42

200 150

1

415

2 3

4

100 50 0

wave” arterial pressure response to Valsalva maneuver in a patient | “Square with heart failure with severe LV dysfunction.

(iii) During phase III: Sudden increase in systemic venous return results in the augmentation of right-sided murmurs. (iv) During phase IV: Left-sided murmurs return to controlled levels and may transiently be accentuated. (v) Arterial pressure tracing in ASD, MS and heart failure:108 Phases I and III responses are normal, but as baroreceptor reflexes are not activated, it results in: ● The absence of a normal decrease in the arterial pressure during phase II and ● No overshoot of arterial pressure during phase IV 1) This gives the arterial pressure tracing a “square wave” response (instead of distinct four phases, see Fig. 21.42) 2) Valsalva ratio of 1.0 (instead of normal 1.6) and 3) “Pseudo-normalization” of transmitral filling velocity pattern on Doppler echocardiography. 3) The muller maneuver109 is the converse of the Valsalva maneuver. It consists of forced inspiration against closed glottis i.e. with closed nose and firmly sealed mouth for about 10 s. This maneuver is less often used, as it is less useful. Effects on heart sounds and murmurs: As this maneuver exaggerates the inspiratory effort ● ●

S2 split is widened, RV S3 and S4 are accentuated and All right-sided murmurs are augmented.

4) Postural changes a) Sudden lying down from standing or sitting posture or sudden passive elevation of both legs: ●

●

It results in an increase of systemic venous return which initially augments the RV stroke volume followed by Increased LV stroke volume and LV size after several cardiac cycles.

Effects on heart sounds ● ●

Widening of S2 split in both phases of respiration Initially, RV S3 and S4 are accentuated and later after several cardiac cycles, LV S3 and S4 are accentuated.

Effects on the murmurs (i) Due to increased stroke volume of both RV and LV, following systolic murmurs are augmented: ● SM of PS, AS

416

CARDIOVASCULAR SYSTEM EXAMINATION

Fig. 21.43

| Auscultation in squatting position.

SM of MR, TR SM of VSD ● Functional systolic murmurs. (ii) Due to increased LVED volume and LV size ● SM of HOCM is diminished as the pressure gradient decreases. ● Mid systolic click and late SM of MVP are delayed and may be attenuated as there is little or no prolapse of the mitral leaflets. ● ●

b) Sudden standing or sitting up from supine position or sudden standing from squatting position: Physiological changes and effects on heart sounds and murmurs are opposite to that of sudden lying down position from standing or sitting position. But no changes occur in patients with true fixed S2 split. c) Squatting from standing posture: (see Fig. 21.43). It results in: ● ●

●

Increase of systemic venous return and stroke volume Increase of systemic vascular resistance due to the kinking of iliac arteries and reduction of distending pressure of gravity on the lower limbs vessels and Increase of systemic arterial pressure with a transient reflex bradycardia.

Effects on heart sounds: Due to increased venous return and stroke volume, S3 and S4 of both ventricles are accentuated. Effects on the murmurs (i) Due to increased venous return and stroke volume: Following murmurs become louder with right-sided events preceding left-sided events. ● SM of PS and AS ● DM of TS and MS.

CARDIAC AUSCULTATION

417

(ii) Increased LV size due to increased venous return and elevated arterial pressure results in: ● Decrease of LVOTO in HOCM causing decrease in the intensity of SM ● Little or no prolapse in patients with MVP hence, mid systolic click and late SM are delayed. (iii) Due to increase in aortic reflex: The inaudible DM of AR becomes audible and augmented. (iv) Due to elevated systemic vascular resistance, right to left shunt is decreased with increased pulmonary blood flow and immediate improvement in arterial oxygen saturation and thereby alleviates the symptoms and intensity of SM in patients with TOF. (v) Due to elevated systemic vascular resistance and systemic pressure, ● There is an increased regurgitant volume thereby resulting in the augmentation of SM of MR. ● Left-to-right shunt volume increases through VSD which results in a loud SM. d) Left lateral recumbent position causes closeness of the heart to the chest wall and a transient increase in heart rate. Effects on heart sounds ●

Accentuates S1, LV S3 and S4, and mitral OS.

Effects on the murmurs ● ●

●

Accentuates MDM of MS, Austin Flint murmur of AR and SM of MR. Accentuation and early occurrence of mid systolic click and late SM in MVP as a result of increased prolapse due to increased heart rate and inotropism. Occasionally, PVCs can occur and may help in differentiating SM of AS from that of MR.

e) Sitting up and leaning forward positions causes more closeness of the base of the heart to the chest wall. Effects on heart sounds and murmurs: ● ●

Loud P2 and split S2 are more clearly audible. Similarly, DM of AR and PR are more readily audible.

f) Knee-elbow position: This position brings closeness of the heart to the chest wall. Effects: Pericardial rub becomes more prominent due to increased friction between parietal and visceral pericardial layers. 5) Isometric exercise Methods: It is done by sustained handgrip (isometric handgrip exercise, (see Fig. 21.44). 1. Ideally by using calibrated handgrip device simultaneously by both hands 2. By pressing a hand ball simultaneously with both hands or 3. By simply making a hand grip with both hands simultaneously – Sustained the handgrip for 20–30 s – It should be simultaneously done by both hands

418

CARDIOVASCULAR SYSTEM EXAMINATION

Fig. 21.44

| Auscultation with sustained handgrip by both hands.

– Inadvertently doing Valsalva maneuver during handgrip must be avoided – It should be avoided in patients with ventricular arrhythmias and myocardial ischemia. Physiological effects: Isometric handgrip results in transient but significant increase in: ● ● ● ● ●

Systemic vascular resistance (SVR) Arterial pressure Heart rate Cardiac output LV filling pressure and size.

Effects on heart sounds ●

LV S3 and S4 is accentuated.

Effects on the murmurs110 ● ●

●

●

DM of MS becomes louder due to the increased cardiac output. Accentuation of DM of AR and SM of MR and VSD due to increased systemic vascular resistance. SM of AS is diminished as a result of reduction of pressure gradient across the aortic valve due to an increase in arterial pressure and SVR. As a result of increased LV volume and size, – SM of HOCM diminishes due to decreased pressure gradient – Mid systolic click and late SM of MVP are delayed due to decrease in prolapse.

6) Changes in cardiac cycle length due to arrhythmias (PVC and atrial fibrillation): During the compensatory pause, that follows a premature ventricular contraction or following a longer cycle lengths in atrial fibrillation, there is ● ●

An increase in the ventricular filling and ventricular size In addition, there is secondary augmentation of ventricular contractility of the next beat and transient elevation of the arterial pressure.

CARDIAC AUSCULTATION

S1

SM S2

S1 SM

S2

S1

SM

419

S2

Carotid pulse PVC

Fig. 21.45

S1

PSM

intensity of SM in aortic stenosis after compensatory pause fol| Increase lowing premature ventricular contraction (PVC).

S2

Fig. 21.46

S1

PSM

S2

S1

PSM

S2 PVC

S1

PSM

S2

| No change in the intensity of PSM of mitral regurgitation following PVC.

The same observations may be made during transient slowing of the sinus rate by light carotid sinus pressure. Effects on heart sounds and murmurs: (see Figs 21.45 and 21.46) ● ●

● ●

●

Varying intensity of S1 is observed especially with atrial fibrillation. SM of AS and PS accentuate due to  ventricular filling i.e. prolonging the preceding diastole and contractility.111 DM of AR becomes louder due to transient elevation in the arterial pressure. SM of HOCM is augmented due to  LVOTO as a result of ventricular contractility, which is associated with decreased volume in the pulse (Brokenbrough Braunwald sign).112 Mid systolic click and late SM of MVP are delayed because of decreased prolapse due to increase in ventricular filling and LV size.

420

CARDIOVASCULAR SYSTEM EXAMINATION

No change ●

SM of MR and VSD.

7) Pharmacological agents a) Amyl nitrate inhalation: Place amyl nitrate on a piece of gauze and ask the patient to take three or four deep breaths over 10–15 s. Physiological changes:105 ●

●

●

It induces marked vasodilatation (due to  SVR) with the reduction of systemic arterial pressure in first 30 s. After 30–60 s, it is followed by reflex tachycardia, increase in cardiac output and velocity of blood flow. However, the major auscultatory changes occur in the first 30 s after inhalation. Effects on heart sounds

● ●

●

S1 is augmented and A2 is diminished. Mitral and tricuspid OS become louder and A2–OS interval shortens as arterial pressure falls. S3 of either ventricle is augmented due to rapid ventricular filling, but S3 of MR origin diminishes. Effects on the murmurs (i) Due to increased cardiac output, following murmurs are augmented:

SM of AS and PS SM of TR ● All functional SM ● DM of MS and TS ● DM of PR. (ii) Due to  SVR, following murmurs are diminished: ● ●

SM of MR and small VSD (see Table 21.23) DM of AR ● Austin Flint murmur of AR ● Diastolic phase of continuous murmur of PDA ● SM in TOF as decreased SVR and arterial pressure increases right-to-left shunt and decreases the pulmonary blood flow. (iii) Due to  LV volume and size: ● LVOTO increases and SM is accentuated in HOCM. ● The degree of prolapse increases in MVP, and there is an early onset of mid systolic click and late SM, but softening of SM due to decreased resistance to LV ejection. ● ●

(iv) Though presently amyl nitrate inhalation at the bedside is not routinely practiced, its response is useful in distinguishing most of the common murmurs (see Table 21.23). ● SM of AS (which is augmented) vs SM of MR (which is diminished) ● SM of TR (which is accentuated) vs SM of MR (which is diminished) ● SM of PS (which is augmented) vs SM of TOF (which is diminished)

CARDIAC AUSCULTATION

421

Table 21.23 Useful maneuvers to differentiate similar murmurs Murmurs

Maneuvers

Maneuvers

1. SM of AS vs HOCM SM of AS SM of HOCM 2. SM of AS vs MR SM of AS SM of MR 3. SM of MR vs TR SM of MR SM of TR 4. SM of PS vs TOF SM of PS SM of TOF 5. SM of PS vs VSD SM of PS SM of VSD 6. DM of MS vs TS DM of MS DM of TS 7. DM of MS vs AFM of AR DM of MS Austin Flint murmur 8. Ejection sound (ES) of PS vs AS ES of PS ES of AS

Valsalva   Amyl nitrate   Respiration No change Inspiration Amyl nitrate   Amyl nitrate   Respiration Expiration Inspiration Amyl nitrate   Respiration Expiration No change

Squatting   Post PVC  No change

● ●

– – – – – – – – – – Inspiration

DM of MS (which is augmented) vs AFM of AR (which is diminished) EDM of AR (which is diminished) vs EDM of PR (which is augmented).

b) Methoxamine and phenylephrine: These vasopressor drugs are less commonly used because of the inconvenience of intravenous administration and greater care needed in titrating these drugs to achieve the desired effect. Methods ●

●

3–5 mg of methoxamine IV is administered which elevates arterial pressure by 20–40 mmHg for 10–20 min. But 0.3–0.5 mg of phenylephrine IV is preferred as it elevates the arterial pressure by 30 mmHg for only 3–5 min.

Physiological response: It is opposite to that of amyl nitrate inhalation. ● ● ●

It increases arterial pressure It causes reflex bradycardia and decreased contractility and cardiac output Hence, these drugs should not be used in patients with CHF and hypertension.

Effects on heart sounds and murmurs are opposite to those of amyl nitrate inhalation. ●

They are especially useful to elicit low intensity DM of AR and to verify AFM of AR, which are augmented.

422

CARDIOVASCULAR SYSTEM EXAMINATION Midsystolic Right sided

Left sided

S1

A2

S1

Holosystolic

Right sided

Left sided

S1

A2 P2

A2

S1

A2 P2

Early systolic

S1

S2

Late systolic

S1

Fig. 21.47

●

S2

| Classification of systolic murmurs.

However, there is no change in the intensity of the murmurs with these drugs in the following conditions: – SM of AS and PS (fixed ventricular outflow tract obstruction) – DM of PR and TS.

Systolic Murmurs Classification of SM Systolic murmurs are sub-classified according to their time of onset and termination as113 (see Fig. 21.47): ● ●

●

●

Early systolic murmurs (ESM) begin with S1 and confine to early systole. Mid systolic murmurs (MSM) begin after S1 and end before S2 (left-sided MSM before A2 and right-sided MSM before P2). Holosystolic or pansystolic murmurs (HSM/PSM) begin with S1, occupy all of systole and end with S2 (left-sided PSM end with A2 and right-sided PSM end with P2). Late systolic murmurs (LSM) begin in mid to late systole and end with S2.

1. Early systolic murmurs (ESM): The early systolic murmurs are high pitch, decrescendo in configuration, begin with S1 and end well before S2, usually at or before mid-systole. Causes: ESM are ‘regurgitant’ murmurs due to the retrograde flow from a high pressure cardiac chamber to a low pressure chamber and occur in: ● ● ●

Acute severe MR114 Acute TR with normal RV systolic pressure115 Small VSD or nonrestrictive VSD with PH.34

CARDIAC AUSCULTATION

423

i) Acute severe MR: The regurgitation occurs into a relatively normal sized LA with limited distensibility and as the LV-LA pressure gradient is abolished during late systole, termination of retrograde flow and abbreviation of systolic murmur occurs well before S2. It is often associated with expiratory S2 split, loud S4 with classic radiation of the murmur and a tall v wave in left atrial pressure tracing. Common conditions that produce acute MR are: ● ● ● ●

Spontaneous rupture of chordae tendineae of a myxomatous valve Subacute bacterial endocarditis of mitral valve Papillary muscle rupture or dysfunction secondary to acute myocardial infarction Disruption of mitral apparatus due to chest trauma.

ii) Acute TR: Due to low pressure gradient between RV-RA, the murmur is soft, medium pitched and abbreviated but as usual augments on inspiration. It is associated with RV S4 and tall v waves in jugular venous pulse. Acute TR occurs in: ● ● ● ●

Infective endocarditis in drug abusers Carcinoid heart disease RV infarction Damage of tricuspid valve during open heart surgery or chest trauma.

iii) Small VSD: The murmur is high pitched and abbreviated as ejection continues, ventricular size decreases, ventricular septum thickens which seals off the small defect in the septum and ceases the flow. This type of VSD may spontaneously close as the child grows. Early SM may also occur in non restrictive VSD with an elevated pulmonary vascular resistance which decreases or abolishes the late systolic shunting. 2) Mid systolic murmur (MSM): The mid systolic murmurs are high to medium pitched, crescendo-decrescendo in configuration, are often described as ‘diamond-shaped’ or ‘spindle-shaped’, and systolic ‘ejection’ in nature that begin after S1 and end before S2. ●

●

● ●

●

●

The MSM begins after the semilunar valve opens due to the rise in ventricular pressure and is due to flow across the LV or RV outflow tract that reflects the pattern of phasic flow across the LVOT or RVOT. As the flow proceeds, the murmur increases in crescendo and as the flow decreases, the murmur decreases in decrescendo (see Fig. 21.48). The intensity of the murmurs closely parallels changes in the cardiac output. Conditions such as exercise, fever, anxiety, pregnancy and thryotoxicosis; which increase the cardiac output and forward flow or conditions such as PVC, or associated AR and PDA that increase the stroke volume due to prolonged diastolic filling; increase the intensity of the MSM. Any condition such as CHF that decreases the cardiac output, or drugs that cause negative inotopism such as beta blockers or associated proximal lesions such as MS, MR and VSD will decrease the intensity of the murmur. The response of the murmurs to various bedside maneuvers which alter the flow and loading conditions of the heart (dynamic auscultation) and other auscultatory findings will help in the definitive diagnosis of the MSM.

424

CARDIOVASCULAR SYSTEM EXAMINATION

Aorta L. atrium L. ventricle

S1

Fig. 21.48

MSM

S1

of murmur to hemodynamics in aortic stenosis- mid systolic | Relationship murmur (MSM) is crescendo-decrescendo as the gradient is the greatest in the middle of the systole.

Causes of mid systolic murmurs (MSM) ●

●

●

●

Due to the obstruction to ventricular outflow tract: – AS – HOCM – PS. Functional: – Due to dilatation of aortic root – Due to dilatation of pulmonary trunk – Due to accelerated flow into the aorta or – Due to accelerated flow into the pulmonary artery. Innocent mid systolic murmurs: Due to flow across the normal ventricular outflow tracts. MSM in MR: Due to papillary muscle dysfunction.

1. Aortic stenosis (AS): AS could be acquired or congenital, and congenital could be valvular, subvalvular or supravalvular. i) Acquired aortic stensosis nd ● MSM is often harsh, medium pitched, and best heard at the 2 right intercostal space and apex. ● Depending upon the severity, it may have an early peaking and a short duration or late peaking and prolonged duration. ● Due to high velocity jet within the aortic root, the murmur conducts into the neck along the carotids. ● It is associated with pulsus parvus et tardus, soft or absent S with single S or 2 2 reverse S2 split and S4.

CARDIAC AUSCULTATION

425

Table 21.24 Systolic murmur of fixed vs dynamic aortic stenosis Bedside maneuvers

Fixed LVOTO (Aortic stenosis)

Dynamic LVOTO (hypertrophic obstructive cardiomyopathy)

1. 2. 3. 4.

No change Decreases Increases Decreases

May increase with expiration Increases Decreases Increases

Respiration Standing Squatting Valsalva

Associated AR is common which increases the intensity of the murmur. Systemic hypertension or coarctation of aorta if associated, obliterates the gradient and decreases the intensity of the murmur ● The elderly patients with aortic sclerosis or stenosis due to fibrocalcific changes usually have ‘Gallavardin dissociation’ i.e. two distinct mid systolic murmurs are audible—the noisy medium pitch murmur at the right base (due to turbulence caused by the high velocity jet within the aortic root) and high frequency musical murmur at the apex (due to periodic wake phenomenon caused by high frequency vibrations of the fibrocalcific aortic cusps).116 ii) Congenital valvular aortic stenosis nd ● MSM is best heard at the 2 right intercostal space. ● Associated systolic ejection sound is the hallmark of the congenital bicuspid AS, the intensity of which correlates well with the mobility of the valve and not with the severity of the obstruction. ● S may be normal or single. 2 ● S and associated AR are common. 4 iii) Congenital supravalvular stenosis ● ●

● ●

●

MSM is prominent in the 1st right intercostal space and over the right carotid. Characteristic elfin facies is common and right brachial and carotid are more prominent as compared to the left side. S2 is normal or single with S4 and associated AR is uncommon.

2. Hypertrophic obstructive cardiomyopathy (HOCM) ● ●

● ● ●

MSM is best heard at the apex and lower left sternal edge. It is associated with brisk arterial pulse (carotids) or pulsus bisferience with double or triple apex and S4. A2 is of normal intensity and S2 may be single or reversed split. Often, a late SM of MR is common due to the distorted mitral apparatus. Bedside maneuvers i.e. dynamic auscultation help in the definitive diagnosis of HOCM (see Table 21.24). 3. Pulmonary stenosis (PS): It could be valvular, infundibular or supravalvular. i) Valvular pulmonary stenosis could be congenital (often) or acquired usually with an intact ventricular septum.

426

CARDIOVASCULAR SYSTEM EXAMINATION ●

●

●

●

●

●

●

MSM is best heard at the left 2nd–3rd intercostal spaces which accentuates during inspiration and may be conducted to the left supraclavicular and left side of the neck. It begins with pulmonary systolic ejection sound which accentuates with expiration. But in severe PS, the ejection sound fuses with S1 and S4 appears. The murmur may have an early peaking with a short duration or a late peaking with a prolonged duration depending upon the severity of the obstruction (see Fig. 21.49). P2 becomes soft and S2 split widens with the increasing severity of stenosis. However, it is difficult to appreciate the widening split at the bedside as P2 becomes progressively fainter and A2 is lost in the murmur. Associated with prominent a waves in jugular venous pulse, left parasternal heave and RV S4 which increases with inspiration. Associated with PR in dysplastic pulmonary valve (as in Noonan’s syndrome) or when complicated with infective endocarditis. May have hypertelorism and moon face.

ii) Infundibular pulmonary stenosis is often associated with VSD (as in TOF, see Fig. 21.50). ●

The MSM is best heard at the 3rd left intercostal space. It becomes shorter with increased severity of the obstruction and may be accompanied by an ejection sound due to the dilated aorta.

S1 S1

S2

MSM

S2 MSM

Mild

Mild

A2 A2

PES S1

P2

MSM

S2

S1

S2

P2

MSM

Moderate Moderate

PES S1

MSM

A2

P2

A2

S1

S2

S2 Shortened MSM

Severe

Severe S4 PES

Fig. 21.49

A2

P2

systolic murmur (MSM) in pul| Mid monary stenosis—PES: pulmonary ejection sound.

AES

Fig. 21.50

A2

systolic murmur (MSM) in infundibu| Mid lar pulmonary stenosis as in tetralogy of Fallot—AES: aortic ejection sound.

CARDIAC AUSCULTATION

427

It shortens and decreases in intensity with amyl nitrate inhaltion. P2 is often absent. iii) Supra-valvular pulmonary stenosis or branch stenosis of pulmonary artery often has characteristics facies. ● It may be associated with supra-valvular AS. ● The murmur is less harsh, high pitched with varying intensity and is best heard at the upper left sternal border, infraclavicular region and laterally. ● In pulmonary artery branch stensosis, the murmur is heard more laterally with wide transmission to the right chest, back and both axillae. ● It may become continuous with severe branch stenosis. ● ●

4. Functional MSM: These are short and soft and usually are grade 3/6. (1) Due to dilatation of aortic root: Short soft MSM is best heard at the apex and is present in elderly subjects with dilated sclerotic aorta. (2) Due to dilatation of pulmonary artery i) Idiopathic pulmonary artery dilatation ● MSM is best heard at the pulmonary area and is often confused with ASD due to the presence of wide expiratory S2 split. ● However, X-ray chest PA and lateral views with no evidence of increased pulmonary blood flow and echocardiogram will help in the definitive diagnosis. ii) Dilated pulmonary artery secondary to pulmonary hypertension ● Functional MSM is identified by ‘the company it keeps’ i.e. associated prominent parasternal heave, prominent a wave in jugular venous pulse, loud P2 and RV S4. ● A high pitched EDM of PR is often present. (3) Due to increased flow into the aorta: Functional MSM due to increased cardiac output and flow into the aorta occurs in: ● ● ● ● ● ● ●

Pregnancy Thyrotoxicosis Anemia Fever Exercise and Peripheral arteriovenous fistula In significant AR, functional MSM is secondary to a large forward stroke volume and the murmur may be grade 4/6 associated with a thrill.

(4) Due to increased flow into the pulmonary artery: Functional MSM at the base occurs due to an increased flow into the dilated pulmonary trunk secondary to significant left-to-right shunt due to: ● ● ●

ASD: Wide fixed S2 is the hall mark of ASD. VSD: Holosystolic murmur along the left sternal border is usual. Straight back syndrome and pectus excavatum117 may be confused with ASD as expirartory S2 split is often audible. However, physical examination of the spine, thoracic cage and sternum and X-ray chest will confirm the diagnosis.

428

CARDIOVASCULAR SYSTEM EXAMINATION

5. Innocent MSM occurs without the evidence of physiologic or structural abnormalities in the cardiovascular system. They are always  grade 3/6 in intensity and with no radiation to carotids or axillae. They occur due to flow across the normal LVOT or RVOT. They are present in 30–50% of children. i)

ii)

Innocent MSM due to flow across the normal LVOT or Still’s murmur118 ● Still’s murmur is common in young children of 3–8 yrs of age and usually disappears by puberty. ● It is related to a small ascending aorta diameter with a concomitant high aortic blood flow velocity.119 ● It is a short medium frequency murmur and is ‘croaking’ or ‘buzzing’ in character. rd ● The murmur is best heard along the left sternal border at the 3 or 4th intercostal space. Innocent MSM due to flow across the normal RVOT or innocent pulmonary MSM ● It is also common in children, adolescents and young adults. ● The MSM is low to medium frequency with a blowing quality. ● It is best heard in the pulmonary area with radiation along the left sternal border.

6. MSM in MR:120 The MSM is usually due to the papillary muscle dysfunction as a result of ischemic heart disease with an early systolic competence of the mitral valve and midsystolic incompetence, followed by a late systolic decline in the regurgitant flow. Holosystolic murmurs (HSM) or pansystolic murmurs (PSM): (holos entire) A holosystolic or pansystolic murmur begins with S1, occupies all of the systole and ends with S2 on its side of origin. ● ●

It is high pitched, blowing in quality and plateau-like in configuration. HS murmurs are regurgitant murmurs produced by retrograde flow from a chamber of high pressure to a chamber of lower pressure.101 Causes of HSM

● ● ● ●

Chronic MR Chronic TR Restrictive VSD Aorto-pulmonary connection: AP window and PDA with PH (see Table 21.25). (1) HSM in chronic mitral regurgitation (MR)

●

●

●

The murmur in chronic MR is holosystolic as the LV pressure exceeds LA throughout the systole (see Fig. 21.51). The classical HSM of chronic MR is high pitched, blowing in quality, plateau-like in configuration with grade 3/6 in intensity, not accompanied by a thrill and with no or little variation in intensity with respiration or changes in cardiac cycle due to arrhythmias. It is best heard at the apex and radiates to: – The left axilla, angle of the left scapula and occasionally to the vertebral column with bone conduction from the cervical to the lumbar spine when the regurgitant jet is directed posterolaterally within the LA due to dominant involvement of anterior mitral leaflet (as in rheumatic etiology).

CARDIAC AUSCULTATION

429

Table 21.25 Differential diagnosis of holosystolic murmur Features

Mitral regurgitation

Tricuspid regurgitation

Ventricular septal defect

1. Best heard

Apex

Lower left sternal area

Left sternal border in 3rd–4th intercostal space No selective transmission

2. Selective transmission 3. Thrill

Radiation to axilla and back Rare (with chordal rupture) 4. Character High pitched, soft and blowing 5. Respiration No change 6. Accompanying Eccentric left features ventricular hypertrophy, S1, LV S3

No selective transmission Does not occur

Common

High pitched, soft and Medium pitched, rough and blowing harsh  During inspiration  During expiration Right ventricular Biventricular enlargement and hypertrophy, prominent may have signs of PH v in jugular venous pulse, signs of pulmonary hypertension (PH)

Aorta

LV

LA

HSM

S1

Fig. 21.51

S2

of holosystolic murmur (HSM) to hemodynamics in chronic | Relationship mitral regurgitation—the murmur is holosystolic as regurgitation persists to the end of the systole. LV, left ventricular pressure, LA: left atrial pressure, Aorta: aortic pressure.

●

– The left sternal edge, base and may even radiate into the neck when the direction of the intra-atrial jet is forward and medial against the interatrial septum due to the dominant involvement of posterior mitral leaflet. Often associated with muffled S1, a loud LV S3 is produced which is not a manifestation of heart failure, but occurs due to the hemodynamically significant MR. (2) HSM in high pressure tricuspid regurgitation (TR)

●

The murmur in TR is holosystolic when there is a substantial elevation of RV systolic pressure usually secondary to PH or PS. However in organic TR, the murmur is non pansystolic, lower in frequency and RV systolic pressure is normal (see Fig. 21.52).

430

CARDIOVASCULAR SYSTEM EXAMINATION

PA

RV

RA

HSM

S1

Fig. 21.52

S2

of holosystolic murmur (HSM) to hemodynamics in chronic | Relationship tricuspid regurgitation—the murmur is holo systolic as regurgitation persists to the end of the systole. RV: right ventricular pressure, RA: right atrial pressure, PA: pulmonary artery pressure.

●

●

●

●

Similarly, the murmur is soft, high pitched and blowing in quality with 3/6 in intensity. It increases its intensity with inspiration (Carvallo’s sign), but this augmentation is absent when associated with organic TR or severe RV failure. – In severe RV failure; the RV fails to take up an additional venous return with inspiration, fails to increase the cardiac output and thereby no augmentation of the HSM occurs. – Associated organic TS prevents any further increase in venous return into the RV and thereby HSM of TR fails to increase during inspiration. It is best heard at the lower left sternal border (tricuspid area) with no selective radiation. But the HSM may be heard to the right of the sternum and when the RV forms the apex, it may be heard at the apex in which case it may be mistaken for MR. It is associated with prominent v wave with a rapid y descent in jugular venous pulse that augments during inspiration, left parasternal heave and RV S3. (3) HSM in restrictive ventricular septal defect (VSD)

●

●

The murmur is holosystolic as the left ventricular systolic pressure and systemic vascular resistance (SVR) exceed right ventricular systolic pressure and pulmonary vascular resistance (PVR) from the onset to the end of systole. – The murmur is non pansystolic in large nonrestrictive VSD (0.8 cm2/m2), very small VSD and multiple VSDs. – VSD murmur is absent in Eisenmenger’s VSD and only pulmonary ejection systolic murmur may be present. Usually, the murmur is medium pitched, harsh in character, 4/6 grade in intensity and is associated with a thrill.

CARDIAC AUSCULTATION ●

●

431

It is best heard along the left sternal border in 3rd–5th intercostal spaces during expiration with no selective transmission. – However, in supracristal VSD, the murmur is best heard at the pulmonary area and may be conducted to infraclavicular area and left neck. It may be confused for PS. – In Gerbode’s defect (VSD of LV to RA), the murmur may be conducted to the right of the sternum. – VSD of L-TGA may be best heard at the apex and may be mistaken for MR. Valsalva maneuver and amyl nitrate inhalation decrease the intensity of the murmur.

(4) HSM in AP window and PDA with pulmonary hypertension: Rise in PVR abolishes the diastolic portion of the continuous murmur and HSM may only be audible.34 Late systolic murmurs (LSM) begin in mid to late systole and proceed up to the S2. ●

●

●

Mital valve prolapse is the prototype of LSM which is due to the prolapse of posterior mitral leaflet. The murmur is high pitched, sometimes has a musical quality (“whoop”4 or “honk”121), and is best heard at the apex frequently introduced by single or multiple non-ejection clicks. Bedside maneuvers which increase or decrease the LV volume and size alter the intensity and length of the murmur (see hemodynamic ausculatation) (see Table 21.26 and Fig. 21.53).

Diastolic Murmurs Diastolic murmurs are subclassified according to their time of onset and termination into: ● ●

Early diastolic murmur (EDM): It is confined to early diastole which begins with S2. Mid diastolic murmur (MDM): It begins at a clear interval after S2 and ends before S1.

Table 21.26 Systolic murmurs Early systolic murmur

Organic mid systolic murmur

1. Acute severe mitral regurgitation 2. Acute TR with normal RVSP 3. Small ventricular septal defect (VSD) 4. Nonrestrictive VSD with PH

1. Aortic stenosis 1. Severe aortic regurgitation 2. HOCM 2. PH 3. Pulmonary stenosis 4. MR (papillary muscle dysfunction)

Functional mid systolic murmur

3. ASD 4. VSD

5. Idiopathic PA dilatation 6. Hyperkinetic circulatory states 7. Still’s innocent murmur

Pan systolic murmur

Late systolic murmur

1. Mitral regurgitation 2. Tricuspid regurgitation 3. VSD

1. MVP

4. AP window and PDA with PH

432

CARDIOVASCULAR SYSTEM EXAMINATION ●

●

Late diastolic murmur (LDM) or presystolic murmur (PSM): It occurs in presystole immediately before S1. Pandiastolic murmur (PDM) or holodiastolic murmur (HDM): It begins with S2, occupy whole diastole and ends with S1.

EDM and PDM are regurgitant murmurs due to the retrograde flow across an incompetent semilunar valve, while MDM and LDM are filling murmurs due to an obstruction to the forward flow across an AV valve. 1) Early Diastolic Murmurs (EDM) These are SL valve regurgitation murmurs which begin with S2 (see Fig. 21.54). ●

●

They are high pitched reflecting the high velocity of the regurgitant blood flow from the great vessels. So also the shape and length (decresendo and short) of the EDM reflect the diastolic pressure gradient between the aorta or pulmonary artery and respective ventricle (see Fig. 21.55).

1. Acute MR 2. Acute TR

1. Small VSD 2. Nonrestrictive VSD with PH

Late SM

Early SM Systolic murmur (SM)

1. Chronic MR 2. Chronic TR Pan SM 1. Restrictive VSD 2. PDA with PH 3. AP window with PH

1. ASD 2. VSD 3. SB syndrome

Fig. 21.53

MVP

1. AS 2. PS 3. HOCM

MR due to PM dysfunction

Mid SM

Functional

1. Aortic root dilatation 2. PA dilatation 3. PH

Significant AR

Hyperkinetic states: 1. Pregnancy 2. Anemia 3. Thyrotoxicosis 4. Exercise 5. AV fistula

Innocent murmur: 1. Still’s murmur (child 3–8 yrs) 2. Pulmonary mid SM (child and young adults)

and causes of systolic murmurs—MR: mitral regurgitation, TR: tricuspid regur| Classification gitation, HOCM: hypertropic obstructive cardiomyopathy, AS: aortic stenosis, PS: pulmonary stenosis, VSD: ventricular septal defect, PDA: patent ductus arteriosus, ASD: atrial septal defect, PH: pulmonary hypertension, PM: papillary muscle dysfunction, PA: pulmonary artery, SB: straight back, AV: arteriovenous, AR: aortic regurgitation, AP: aorto-pulmonary.

CARDIAC AUSCULTATION

Right sided

Left sided

S1

Fig. 21.54

A2

433

S1

A2P2

| Early diastolic murmurs.

Aorta L. atrium L. ventricle

S1

Fig. 21.55

S2

EDM

of early diastolic murmur (EDM) to hemodynamics in aortic | Relationship regurgitation—EDM is due to diastolic pressure gradient.

Causes of EDM ● ●

Aortic regurgitation Functional pulmonary regurgitation (Graham Steell murmur).

i) EDM in aortic regurgitation ●

The murmur is decrescendo, soft high pitched and blowing in character. – However EDM of acute severe AR is medium-pitched as the velocity of the regurgitant flow is less rapid and relatively short as aortic diastolic pressure rapidly equalizes with the steeply rising diastolic pressure of unprepared and nondilated LV. – A “cooing dove” or musical diastolic murmur occurs due to the rupture or retroversion of an aortic cusp secondary to bacterial endocarditis or trauma122 and as a complication of syphilitic AR.123

●

●

EDM is best heard in sitting and leaning forward position during a held deep expiration along left sternal border in 3rd and 4th intercostal spaces (Neo aortic area) in AR of valvular origin, while the AR murmur due to aortic root etiology is usually best heard at the right 2nd intercostal space and to the right of the sternum. In AR of valvular origin, A2 is diminished or may even be absent due to an inadequate coaptation of the deformed cusps.

434

CARDIOVASCULAR SYSTEM EXAMINATION ●

●

Severe AR of valvular etiology is often associated with systolic ejection murmur in the aortic area without significant associated AS and Austin Flint murmur at the apex besides the classical peripheral signs. Prompt squatting and isometric handgrip bring out the faint EDM, while amyl nitrate inhalation decreases its intensity. So also, EDM of mild AR often disappears during later stages of pregnancy due to decreased peripheral vascular resistance (SVR) (see Fig. 21.56).

ii) EDM in functional pulmonary regurgitation: The pulmonary annulus cannot with stand high pressures unlike aortic annulus and the murmur occurs in the setting of severe PH when the pulmonary artery systolic pressure (PASP) is  systemic pressure. ●

●

Functional PR is usually secondary to: – Valvular lesions: such as severe MS or combined MS and MR with dominant MS, usually of rheumatic etiology. It rarely occurs in pure MR and almost never occurs with aortic valve disease. – Primary pulmonary hypertension. – Congenital heart disease (CHD) with left-to right shunt and severe PH which often means inoperability. – Eisenmenger’s syndrome. Rarely, Graham Steell murmur may occur in cyanotic CHD with increased pulmonary blood flow and severe PH as in TGA, DORV, single ventricle or TAPVC. – Sometimes occurs in ASD without PH due to the dilated pulmonary artery and increased pulmonary blood flow. – Rarely audible in end stage renal failure secondary to fluid overload and reflect correctible pulmonary hypertension (PH).124 The Graham Steell murmur is a high velocity regurgitant flow murmur which is usually short, high pitched and blowing in character beginning with loud P2. However, the murmur may be pandiastolic in severe PH when pulmomary artery diastolic pressure is 50 mmHg, as the length of the murmur reflects the duration of pressure difference between pulmonary artery and right ventricle in diastole. Chronic AR SEM

Acute AR EDM

ESM

EDM

Aortic area

S2

S1 SEM

S1 S3

AFM

Apex

Fig. 21.56

S1

S2 ESM

S1 S3 AFM

in chronic and acute aortic regurgitation (AR) auscultated at aor| Murmurs tic area and apex—SEM: systolic ejection murmur, EDM: early diastolic murmur, AFM: austin flint murmur.

CARDIAC AUSCULTATION ●

●

435

The murmur is best heard at the pulmonary area and often during inspiration, but may also be heard at the apex when the apex is formed by the right ventricle. However, most often it is helpful from the ‘company the murmur keeps’ i.e. loud P2, prominent a waves in jugular venous pulse and left parasternal heave.

2) Pandiastolic or Holodiastolic Murmurs In severe AR and PR, the murmur becomes pandiastolic, and the length of murmur reflects the duration of the pressure difference between aorta and LV in AR and PA and RV in PR during diastole. 3) Mid Diastolic Murmurs (MDM) MDM are diastolic filling murmurs that begin at a clear interval after S2 in rapid ventricular filling phase (see Fig. 21.57). ●

●

They are caused by the forward flow across the AV valves when the atrial pressure exceeds the declining ventricular pressure (see Fig. 21.58). They are low pitched and rumbling in character as the velocity of flow is relatively low.

S1

Fig. 21.57

S2

S1

| Mid diastolic murmur.

Aorta L. atrium L. ventricle

S1 (loud)

OS S2 MDM

Pre SM 0.07s

Fig. 21.58

of murmurs to hemodynamics in mitral stenosis—mid diastolic | Relationship murmur (MDM) and presystolic murmur (Pre SM) are due to diastolic pressure gradient across the mitral valve.

436

CARDIOVASCULAR SYSTEM EXAMINATION

Causes of MDM (see Table 21.27) i) Obstruction to the ventricular inflow ●

●

Obstruction to the LV inflow: MS, LA myxoma, Cortriatriatum, constriction around AV groove. Obstruction to the RV inflow: TS, RA myxoma, Carcinoid syndrome, Ebstein’s anomaly.

ii) Increased flow across the AV valve (diastolic flow murmurs) Increased flow across the mitral valve i.e. mitral diastolic flow murmurs: – Severe MR – Left-to-right shunts (post-tricuspid shunts): VSD, PDA, AP window, RSOV into RV – Hyperkinetic circulatory states: Anemia, pregnancy, thyrotoxicosis – Complete heart block. ● Increased flow across the tricuspid valve i.e. tricuspid diastolic flow murmurs: – Severe TR – Left-to-right shunts (pre-tricuspid shunts): ASD, RSOV into RA, LV to RA communication (Gerbode’s shunt), PAPVC, coronary artery to RA communication – Admixture lesions: TAPVC, single atrium. iii) Mechanisms that interfere with AV opening: ●

●

Mechanisms that interfere with mitral opening: – Severe AR (Austin Flint murmur)

Table 21.27 Etiology of mid diastolic murmurs LV inflow obstruction

RV inflow obstruction

1. Mitral stenosis 2. Left atrial myxoma

1. Tricuspid 1. Severe MR stenosis 2. Right atrial 2. VSD myxoma

3. Cor 3. Carcinoid triatriatum syndrome 4. Constriction 4. Ebstein’s around AV anomaly groove

Mitral diastolic flow murmurs

3. PDA 4. AP window

Tricuspid diastolic MV opening flow murmurs interference 1. Severe TR 2. ASD

PR with no pH

1. Severe AR (Austin 1. Organic Flint murmur) PR 2. Acute rheumatic carditis (Carey Coombs murmur)

3. RSOV in to right atrium 4. PAPVC

5. RSOV into 5. Coronary right ventricle artery to RA communication 6. Hyperkinetic 6. TAPVC circulatory states 7. Single atrium RSOV: rupture of sinus of Valsalva, PAPVC: partial anomalous pulmonary venous connection, TAPVC: total anomalous pulmonary venous connection.

CARDIAC AUSCULTATION

●

437

– Mitral valvulitis of acute rheumatic carditis: Carey-Coombs murmur. Mechanisms that interfere with TV opening: Severe PR with normal PA pressure producing right-sided Austin Flint murmur.

iv) PR with no PH 1) MDM in mitral stenosis is a decrescendo diastolic filling rumble occurring in the first rapid filling phase (see Fig. 21.59). i) Pitch: ● It is low pitched, rough and rumbling in character and sounds like a bullock cart slowly moving on a wooden bridge or the sound of a bowling ball racing down the alley. ● It is low pitched as the pressure gradient across the valve is low. ● However in a calcified immobile valve, a higher frequency murmur with less intensity not accompanied by a thrill is often the auscultatory finding. ii) Intensity: ● The intensity of the MDM correlates poorly with the severity of the obstruction, but the length of the murmur correlates well with the severity of the stenosis. ● However, the duration of the murmur is unreliable indicator of the severity in the following conditions: – Low cardiac output states such as severe RVF, severe PH where the murmur appears shorter due to lower LA pressure. – Associated hyperkinetic circulatory states such as anemia, pregnancy, thyrotoxicosis, anxiety where the murmur appears longer due to high cardiac output. – When associated with conditions with high LVEDP such as aortic valve disease, CAD systemic hypertension where the murmur becomes shorter due to obliteration of the transmitral gradient. – When associated with arrhythmias: In tachyarrhythmias, the murmur appears longer due to shortening of the diastole. Gentle carotid sinus massage may

PreSM

S1

S2 OS

PreSM

S1

MDM Mild MS

S1

S2 OS

PreSM

PreSM

S1

MDM

Severe MS A2 P2

Fig. 21.59

of mitral stenosis (MS)—MDM: mid diastolic murmur, PreSM: | Murmurs presystolic murmur.

438

CARDIOVASCULAR SYSTEM EXAMINATION

temporarily slow the heart rate, and thereby allow uncovering the potential length of the murmur. – In bradycardia, the murmur appears shorter as diastole is prolonged. – In atrial fibrillation, the duration of the murmur is variable as diastolic cycle lengths vary. However; if the murmur lasts upto S1 in longer cycles, it indicates the severity of the MS. iii) Site: ● The murmur is well localized and best heard just medial to the apex in left lateral position during expiration with the bell of the stethoscope. ● In patients with severe emphysema, the murmur is best heard only at the xiphisternum. iv) Introduction: ● The murmur is often introduced by a prominent OS (in mobile valve) and is associated with a loud S1, presystolic murmur (accentuation) and a diastolic thrill. ● However; in severe MS with severely calcified immobile valve, S is soft and no 1 thrill is palpable. ● The A –OS interval correlates with the level of LA pressure and thereby severity 2 of the stenosis may be clinically determined to some extent. v) Dynamic auscultation: ● The bedside maneuvers such as left lateral position, hand grip exercise and amyl nitrate inhalation enhance the MDM of MS. ● While the Valsalva maneuver diminishes the murmur. 2) MDM in tricuspid stenosis (TS) is often associated with MDM of MS and in the presence of atrial fibrillation. However, the commonest murmur of TS is presystolic with or without MDM. ●

●

●

●

●

●

The mid diastolic murmur of TS is earlier in onset and crescendo-decrescendo in configuration as RA systole occurs earlier than that of the left.125 Similarly; it is low pitched, rough and rumbling in character as the pressure gradient is low. However in RA myxoma, the murmur may be high pitched. Similarly, the murmur may be introduced by a high pitched OS, which usually follows mitral OS. The duration of the murmur also correlates with the severity of the TS. However; despite the presence of significant TS, the murmur is shorter in the following: – Associated MS with severe PH due to elevated RVEDP and – Ebstein’s anomaly due to associated ASD. The murmur is usually best heard in the tricuspid area during inspiration in right lateral position or with passive leg raising. TS is often accompanied by puffiness of the face, early edema of the legs, prominent a waves (in absence of atrial fibrillation) with no history of PND. 3) MDM due to increased flow across the AV valve (functional AV stenosis)

●

Augmented volume and high velocity flow across the normal or insufficient AV valves may result in short MDM.

CARDIAC AUSCULTATION ●

●

●

●

●

439

It is often accompanied by S3, especially in the presence of MR or TR but without presystolic murmur and S1 is usually diminished. The murmur occurs during rapid closing motion of the AV valve suggesting a ‘functional obstruction’ during rapid diastolic filling phase.126 The tricuspid diastolic flow murmurs are usually softer in character, relatively medium pitched and do not increase significantly during inspiration. The mitral diastolic flow murmurs in left-to-right shunts indicate that the pulmonary flow is atleast twice the systemic flow and are definite indication for hemodynamic evaluation and closure of the shunt. Short mid diastolic flow murmurs occur intermittently in complete heart block when atrial contraction coincides with the rapid filling phase.

4) Austin Flint murmur (AFM): Original AFM is an apical presystolic murmur described by A. Flint in1862 in patients with severe AR.127 (see Table 21.28) However, it could be mid diastolic and/or presystolic murmur best heard at the apex with most of the qualities of MDM of MS. ●

●

●

●

It is introduced by S3 rather by an OS and S1 is never accentuated but could be normal or diminished due to the premature closure of mitral valve. The bed side maneuvers such as isometric handgrip exercise that accentuate the AR murmur also increase the intensity of AFM, while amyl nitrate inhalation diminishes the murmur (MDM of MS is increased). In acute severe AR, presystolic component of AFM is lost due to the marked elevation of LVEDP. Right-sided AFM has been reported in association with severe PR due to PH.128

Pathogenesis of AFM: From the phonoechocardiographic, echo-Doppler and MRI studies, the AFM in AR is due to the combination of the following: (i) Regurgitant jet creating vibrations and turbulance in the following way: ● Collision of the regurgitant jet with mitral inflow producing the turbulence

Table 21.28 Differential diagnosis of mid diastolic murmur (MDM) of mitral stenosis and Austin Flint murmur of aortic regurgitation Features

MDM of mitral stenosis

1. Etiology

Organic mitral stenosis (rheumatic)

2. 3. 4. 5. 6. 7. 8. 9.

Austin Flint murmur

Severe aortic regurgitation (non rheumatic) Diastolic thrill Common Rare Introduce by OS LV S3 Presystolic murmur Usually present Absent in severe aortic regurgitation Amyl nitrate inhalation Increases Decreases/disappears Isometric handgrip Variable/increases Increases S1  (with calcified and immobile valve) Normal/diminished Atrial fibrillation Atrial fibrillation is common Usually sinus rhythm Signs of pulmonary Common Unlikely hypertension

440

CARDIOVASCULAR SYSTEM EXAMINATION

Regurgitant jet impinging on anterior mitral leaflet (AML) producing the vibrations of AML129 ● Regurgitant jet impinging on the myocardial wall producing the vibrations Increased mitral inflow velocity creating a flow rumble Due to rapid closing motion of the mitral valve leaflets during mid diastole and presystole similar to MR and high output states130 Due to narrowing of the valve orifice by the regurgitant jet and Incomplete valve opening during mid diastole and presystole.131 ●

(ii) (iii) (iv) (v)

5) MDM in organic pulmonary regurgitation (PR) ●

MDM is a feature of organic PR without PH as in: – – – – –

●

●

●

Pulmonary valve endocarditis Carcinoid syndrome Dysplastic pulmonary valve TOF with absent pulmonary valve or Surgical procedures on pulmonary valve e.g. post balloon dilatation for PS, post surgical valvotomy, after surgical repair of TOF.

It is a short crescendo-decrescendo murmur which begins well after P2 and ends well before the subsequent S1. It is heard best at the pulmonary area during inspiration and is accentuated in supine position or with passive leg raising.34 It is a low velocity retrograde flow and low pitched murmur often associated with a systolic ejection murmur secondary to large RV stroke volume and a diminished or absent P2. The murmur is absent in early diastole (as in AR) as the diastolic gradient is negligible and regurgitant flow is minimal. But as the RVEDP dips below the PADP in mid diastole, the regurgitant flow is maximum with maximum intensity of the murmur. Again, the late diastolic equilibration of pulmonary arterial and RV pressures eliminates the regurgitant flow and abolishes the murmur (see Fig. 21.60).

4) Late Diastolic or Presystolic Murmurs (LDM/PreSM) These occur in presystole immediately before S1. The presystolic murmur occurs in rapid ventricular filling phase which coincides with the atrial systole. Causes of presystolic murmurs: ● ● ●

AV obstruction: MS, TS Complete heart block Austin Flint murmur of moderate AR.

1) PreSM in mitral stenosis: ●

●

●

Presystolic murmur is a typical feature of rheumatic MS with sinus rhythm due to an increased mitral inflow as a result of LA contraction132 (see Fig. 21.61). However, presystolic accentuation may also be heard in patients of MS with atrial fibrillation especially during short cycle lengths.133 It is a crescendo low pitched murmur audible upto S1.

CARDIAC AUSCULTATION

441

20

PA

RV 0 MDM S1

Fig. 21.60

P2

S1

of mid diastolic murmur (MDM) to hemodynamics in organic | Relationship pulmonary regurgitation reflecting diastolic pressure gradient- pulmonary artery (PA), right ventricular (RV) pressures. MS

TS

PreSM

S2

S1

PreSM

S1

Fig. 21.61

S2

S1

systolic murmur (PreSM) | Pre in mitral stenosis (MS).

S1

Fig. 21.62

systolic murmur (PreSM) | Pre in tricuspid stenosis (TS).

2) PreSM in tricuspid stenosis: ●

● ●

The commonest murmur of TS is presystolic and typically occurs with sinus rhytm and even in the absence of MDM. The PreSM of TS is crescendo-decrescendo and relatively fades before S1. As usual, the murmur accentuates during inspiration (see Fig. 21.62).

3) PreSM in complete heart block (CHB): Short crescendo-decrescendo presystolic murmurs are occasionally heard in complete heart block when the atrial contraction falls in late diastole. However, the murmur in CHB is usually mid diastolic (see Table 21.29 and Fig. 21.63). Continuous Murmurs A murmur that begins in systole and continues without interruption through S2 into all or a part of diastole without change in the character of the murmur is defined as a continuous murmur.99 Continuous murmurs are usually generated by uninterrupted flow from a high pressure vascular bed into a low pressure vascular bed without phasic interruption

442

CARDIOVASCULAR SYSTEM EXAMINATION

Table 21.29 Etiology of diastolic murmurs Early diastolic murmur

Mid diastolic murmur

Pre systolic murmur

Pan diastolic murmur

1. AR 2. Functional PR (Graham Steell murmur)

1. LV inflow obstruction: MS 2. RV inflow obstruction: TS

1. MS 2. TS

1. Severe AR 2. Severe PR

3. Mitral diastolic flow murmurs: severe MR, left-to-right shunts (VSD, PDA) 4. Tricuspid diastolic flow murmurs: severe TR, left-to-right shunts (ASD, RSOV into RA, PAPVC) 5. Severe AR (Austin Flint murmur) 6. Acute rheumatic carditis (Carey Coombs murmur) 7. Organic PR

3. AR (Austin Flint murmur) 4. Complete heart block

RSOV: rupture of sinus of Valsalva, PAPVC: partial anomalous pulmonary venous connection.

between systole and diastole. They have to be differentiated from to and fro murmurs of VSD  AR, AS  AR, MS  MR (see Fig. 21.64). Causes of Continuous Murmurs: 1. Due to high to low pressure shunts (i) From systemic artery to pulmonary artery ● Aortic run off into pulmonary artery: PDA, AP window, truncus arteriosus with pulmonary artery stenosis, surgically created aortopulmonary anastomosis (Blalock, Waterston or Pott’s shunts). ● Bronchial collaterals (bronchial to precapillary pulmonary arterial anastomosis and resultant aortic pulmonary fistula): Pulmonary atresia, TOF.134 ● Anomalous left coronary artery from pulmonary artery (ALCAPA). (ii) From systemic artery to right heart: ● Aortic run off into right heart: RSOV into RA or RV. ● Coronary cameral fistula: Coronary artery fistula into RA or RV (LA). (iii) Other shunts: ● Left to right atrial shunts with mitral valve obstruction: Lutembacher’s syndrome (MS with ASD), mitral atresia with ASD, Post PTMC. ● Arteriovenous fistula. ● Venovenous shunts: Anomalous pulmonary venous drainage, porto-systemic shunt in cirrhosis of liver i.e. Cruveilheir Baumgarten syndrome. 2. Due to rapid blood flow ● ●

Cervical venous hum Mammary souffle

CARDIAC AUSCULTATION

1. AR 2. Functional PR (GSM)

1. AR (AFM) 2. CHB

Early DM

PreSM

Diastolic murmur (DM)

Organic PR Mid DM LV inflow obstruction: 1. MS 2. LAM 3. Cor at

1. MS 2. TS

Fig. 21.63

1. Severe AR 2. Severe PR

Holo DM

MD flow murmur: 1. Severe MR 2. Shunts: VSD, PDA, AP window, RSOV into RV 3. Hyperkinetic states: anemia, pregnancy, thyrotoxicosis 4. Complete heart block

RV inflow obstruction: 1. TS 2. RAM 3. Carcinoid syndrome 4. Ebstein’s anomaly MV opening interference: 1. Severe AR (AFM) 2. Acute Rh carditis (CCM)

443

TV opening interference: Severe PR with normal PA pressure (right-sided AFM)

TD flow murmur: 1. ASD 2. RSOV into RA 3. Gerbode’s shunt 4. PAPVC, TAPVC 5. CA to RA 6. SA

and causes of diastolic murmurs-VSD: ventricular septal defect, | Classification PDA: patent ductus arteriosus, ASD: atrial septal defect, PH: pulmonary hypertension, AR: aortic regurgitation, PR: pulmonary regurgitation, MR: mitral regurgitation, MS: mitral stenosis, TS: tricuspid stenosis, AP: aortopulmonary, RSOV: rupture of sinus of Valsalva, RV: right ventricle, RA: right atrium, PAPVC: partial anomalous pulmonary venous connection, TAPVC: total anomalous pulmonary venous connection, CA: coronary artery to right atrial communication, SA: single atrium, LAM: left atrial myxoma, RAM: right atrial myxoma, Cor at: Cor triatriatum, Rh: rheumatic, AFM: Austin Flint murmur, CCM: Carey Coomb’s murmur, GSM: Graham Steell murmur, PA: pulmonary artery, Pre SM: presystolic or late diastolic murmur, MD: mitral diastolic, TD: tricuspid diastolic.

● ● ●

Hyperthyroidism Hemiangioma Hyperemia of neoplasm: Hepatoma, renal cell carcinoma, Paget’s disease.

3. Secondary to localized arterial obstruction ● ● ● ● ● ●

Coarctation of aorta Branch pulmonary artery stenosis Carotid occlusion Femoral artery occlusion Celiac mesenteric artery occlusion Renal artery occlusion.

444

CARDIOVASCULAR SYSTEM EXAMINATION S1

S2

S1

Continuous murmur (PDA)

S1

MSM

S2

EDM

S1

To-Fro murmur (AS and AR)

Fig. 21.64

murmur in patent ductus | Continuous arteriosus (PDA) vs to and fro murmur i.e. mid systolic murmur (MSM) of aortic stenosis (AS) and early diastolic murmur (EDM) of aortic regurgitation (AR).

Fig. 21.65

murmur is best heard in infra| PDA clavicular and pulmonary areas during expiration.

Table 21.30 Continuous murmur of PDA Features

Findings

1. Proper name 2. Frequency 3. Character

Gibson’s murmur Combination of high and low Rough machinery, crescendo-decrescendo murmur peaking at S2 In left infraclavicular and pulmonary areas during expiration Augments the murmur Murmur decreases/disappears Diastolic component

4. Best heard 5. Isometric hand grip 6. Valsalva maneuver 7. Amylnitrate inhalation

1. Continuous Murmurs Due to High-to-Low Pressure Shunts 1) Continuous murmur in patent ductus arteriosus (PDA): The classic description of the PDA murmur was given by George Gibson in 1900 and hence also known as Gibson’s murmur.135 ●

●

●

●

●

It is classically described as a rough machinery murmur due to the combination of high and low frequency vibrations and associated thrill is common. It peaks at S2, after which it gradually wanes until it terminates before S1 (crescendodecrescendo murmur). The murmur is best heard in the left infraclavicular and pulmonary areas during expiration (see Fig. 21.65). The systolic component is widely audible, while the diastolic component is restricted to pulmonary and infraclavicular areas. Isometric hand grip increases the intensity and duration of the murmur and may bring out the diastolic component when it is not heard. The murmur decreases or disappears with Valsalva maneuver (see Table 21.30).

CARDIAC AUSCULTATION

445

Table 21.31 PDA with no continuous murmur 1. 2. 3. 4. 5. 6.

Young infants Very small ductus Very large ductus With pulmonary hypertension With Eisenmenger’ syndrome When associated with: (i) Preductal coarctation of aorta (ii) Aortic stenosis (iii) Large ventricular septal defect

The murmur is not continuous in the following conditions ●

●

●

●

In young infants (due to high pulmonary vascular resistance), when ductus is too small (valve-like) or too large (when equalization of pulmonary and systemic pressures occurs) the diastolic component may be very short or absent. So also in severe PH as the pulmonary vascular resistance increases, PADP approaches and reaches systemic levels, diminishing and finally abolishing the diastolic flow and diastolic component of the murmur. When associated with preductal coarctation of aorta (due to lower aortic pressure), AS (due to lower aortic pressure and elevated LVEDP), large VSD (due to equalization of pulmonary and systemic pressures), severe PH secondary to MS, peripheral pulmonary artery stenosis. When the equalization of pulmonary and systemic pressures occurs in Eisenmenger’s syndrome, the systemic flow across the shunt diminishes and finally ceases leaving the ductus silent (see Table 21.31).

2) Continuous murmur associated with bronchial collaterals: It is heard in the same location as that of PDA, but radiates widely especially over the posterior thorax. 3) Continuous murmur in anomalous origin of left coronary artery from pulmonary artery (ALCAPA): The murmur is continuous when the left-to-right shunt is large and is usually best heard at left sternal border. The child may have chest pain with ECG evidence of myocardial infarction. 4) Continuous murmur in RSOV (rupture of sinus of valsalva) ●

●

●

●

The murmur is usually continuous when RSOV occurs into RA or RV. It may be continuous when RSOV occurs into LA. But it is early diastolic when sinus of Valsalva aneurysm ruptures into LV. It also becomes early diastolic when PH supervenes with high RVSP which shortens or abolishes systolic flow and systolic component of the murmur. It is more of a superficial murmur with very prominent diastolic thrill, which is described as ‘purring of a cat’. It is maximally heard at the lower left sternal border or over the xiphoid corresponding to the fistulous tract.136 It is often well audible to the right of the sternum with no significant changes with respiration.

446

CARDIOVASCULAR SYSTEM EXAMINATION

5) Continuous murmur in coronary cameral fistula ● ●

●

●

●

In general, the murmur is soft, superficial and high pitched. In 90%, coronary artery (CA) fistula drains into right heart and resultant murmur is continuous. But in case of CA fistula draining into RV, the murmur softens during systole (when the systolic flow decreases due to compression of the fistula during RV contraction). The murmur is louder in systole as the pressure gradient is more in systole in case of CA fistula draining into RA or LA. The murmur is not continuous if it empties into LV. It may be purely diastolic or systolic and diastolic. Continuous murmur is also absent and may be silent if multiple coronary artery fistulas empty into pulmonary artery. Site

●

●

●

The murmur is best heard either left or right of the lower sternal area when CA drains into RA. It is maximally heard at left mid to lower sternal border or in subxiphoid region in CA draining into RV. In CA draining into LA, it is best heard in upper to mid left sternal border and may radiate leftward as far as the anterior axillary line.

6) Continuous murmur in left-to-right atrial shunts with MV obstruction ● ●

●

As in Lutembacher’s Syndrome, mitral atresia with ASD. Continuous murmur is also heard when a small ASD is produced following transseptal catheterization or percutenous transmitral commisurotomy (PTMC), due to high velocity flow across the septal defect especially if the mitral obstruction is not adequately relieved by the balloon valvuloplasty. The murmur increases during inspiration and decreases with Valsalva maneuver.

7) Continuous murmur in venovenous shunts ●

●

Total anomalous pulmonary venous drainage into a systemic vein (usually superior vena cava or innominate veins) may produce a continuous murmur (venous hum) usually heard in pulmonary or left infraclavicular areas.137 Portosystemic shunts: In portal hypertension usually secondary to cirrhosis of liver, tortuous collateral veins are seen radiating from the umbilicus (Caput medusae). A continuous murmur (venous hum) may be heard over these collaterals (CruveilheirBaumgarten syndrome) (see Fig. 21.66).

8) Continuous murmur in arteriovenous fistula ●

Arteriovenous fistulas could be congenital or acquired which give rise to continuous murmurs. – Congenital AV fistulas include coronary arterial fistula, RSOV, ALCAPA – Acquired AV fistulas include surgically created fistula for hemodialysis, posttraumatic or after catherization.

CARDIAC AUSCULTATION

Fig. 21.66

●

447

murmur is heard over the Caput medusae which is described | Aascontinuous Cruveilheir Baumgarten syndrome.

Systolic accentuation of the continuous murmur occurs in peripheral arteriovenous fistulas and is best heard over the site of the fistula. – Local compression may: (i) Decrease the intensity of the murmur by raising venous pressure and thereby reducing the AV pressure gradient. (ii) A baroreceptor-mediated reflex bradycardia may occur (Branham’s sign) and reflex tachycardia occurs on release (see Table 21.32).

2. Continuous Murmurs Due to Rapid Blood Flow High velocity blood flow through veins and arteries may cause a continuous murmur. 1) The Venous Hum was first recognized by Potain in 1867. ●

● ●

●

The normal flow of blood across the normal veins in the neck is noiseless. But increased velocity of blood flow gives rise to a continuous bruit over the neck veins which is known as cervical venous hum. It may be rough and noisy and typically louder in diastole.34 The venous hum is best heard in sitting posture with head rotated to the opposite side and chin upwards, placing the bell of the stethoscope at the base of the neck in between the two heads of the sternomastoid muscle and may be more prominent on the right side. Sometimes it may radiate below the clavicles and may be confused with the continuous murmur of PDA if not evaluated carefully (see Fig. 21.67). The murmur is abolished by the digital compression of the internal jugular vein with head in neutral position (see Fig. 21.68). – It is poorly heard in supine position, while – Anemia and thryotoxicosis initiate or reinforce the venous hum (see Table 21.33).

448

CARDIOVASCULAR SYSTEM EXAMINATION

Table 21.32 Continuous murmurs Due to high-to-low pressure shunts

Due to rapid blood flow

Due to localized arterial obstruction

1. PDA 2. AP window 3. Truncus arterosus with PA stenosis 4. Pulmonary atresia 5. Blalock, Waterston and Pott’s shunts 6. ALCAPA 7. RSOV into RA, RV 8. Coronay artery fistula into RA, RV 9. Lutembacher’s syndrome 10. Mitral atresia with ASD 11. Post PTMC with ASD 12. AV fistula 13. TAPVC into systemic veins 14. Portosytemic shunt

1. 2. 3. 4. 5.

1. Coarctation of aorta 2. Branch pulmonary artery stenosis 3. Carotid occlusion 4. Femoral artery occlusion 5. Renal artery occlusion 6. Celiac mesenteric artery occlusion

Cervical venous hum Mammary soufflé Hemangioma Hyperthyroidism Hyperemia of neoplasm (hepatoma, renal cell carcinoma, Paget’s disease)

RSOV: rupture of sinus of Valsalva, TAPVC: total anomalous pulmonary venous connection, PTMC: percutaneous transmitral commisurotomy, ALCAPA: anomalous left coronary artery from pulmonary artery.

Fig. 21.67

to elicit the venous hum| Maneuver patient’s chin is pulled to the left and

Fig. 21.68

upward stretching the neck.

to abolish the venous hum by | Maneuver digital compression of right internal jugular vein with head in neutral position.

Causes of cervical venous hum include: i) Physiological causes: Healthy children and young adults, later stages of pregnancy ii) Pathological causes: ●

● ●

Hyperkinetic circulatory states (due to  velocity and  viscosity of blood): Anemia, thyrotoxicosis, beriberi. Intracranial AV fistula with bruit over the skull. Compression of the jugular vein by the fascia or bony structures in the neck.

CARDIAC AUSCULTATION

449

Table 21.33 The venous hum Features 1. 2. 3. 4. 5.

Findings

Due to  flow into Character Initiated or  by Abolished by Best heard with bell of the stethoscope

Fig. 21.69

Internal jugular veins Rough, noisy, louder in diastole Anemia, thyrotoxicosis Digital compression of internal jugular vein In sitting posture with head rotated to opposite side with chin upward at the base of the neck

| Auscultation for mammary soufflé.

Probable mechanism of the venous hum: The laminar flow in internal jugular vein may be disturbed by the deformation of the vein at the level of the transverse process of the atlas during head rotation designed to elicit the hum.138 2) The mammary soufflé: (soufflé puff in French) This innocent continuous arterial murmur occurs in 10–15% of pregnant women during 2nd and 3rd trimesters and in early postpartum period in lactating mothers.139 ● ●

●

●

It is due to increased blood flow to the breast tissue. This medium to high pitched murmur is best heard over the breast on either side between 2nd and 6th anterior intercostal spaces with no significant change with respiration and may be confused with the continuous murmur of PDA or AV fistula.140 The mammary soufflé usually begins after S1 with a distinct gap and systolic component is the loudest. Light pressure with the stethoscope augments the murmur, whereas the firm pressure with the stethoscope or digital compression abolishes the murmur (see Fig. 21.69). Valsalva maneuver has no significant effect on the murmur. It disappears after the termination of lactation (see Table 21.34).

3. Continuous Murmurs Secondary to Localized Arterial Obstruction ●

Localized stenosis of systemic or pulmonary arteries produce a continuous murmur or bruit if the obstruction is critical (80%) with no adequate collaterals so that a

450

CARDIOVASCULAR SYSTEM EXAMINATION

Table 21.34 Mammary soufflé Features

Findings

1. Type 2. Cause 3. Occurs in

Continuous arterial murmur  Blood flow to breast tissue 10–15% of pregnant women in 2nd–3rd trimester and early post partum period Medium to high pitched Begins after S1 with a definite gap, with loudest systolic component Augments the murmur Abolishes the murmur No effect on the murmur Murmur disappears

4. Frequency of the murmur 5. Description 6. 7. 8. 9.

Light pressure over the breast Firm pressure over the breast Valsalva maneuver Termination of lactation

1. Cervical venous hum 2. Mammary soufflé 3. Hyperthyroidism 4. Hemiangioma 5. Hepatoma, renal cell carcinoma Continuous murmur (CM) Rapid blood flow

Localized arterial obstruction High to low pressure shunts

Aortic runoff into PA: 1. PDA 2. AP window 3. Truncus arteriosus with PA stenosis 4. After shunt surgery

Bronchial collaterals: 1. P At 2. TOF

Fig. 21.70

1. COA 2. Branch PA stenosis 3. CA occlusion 4. FA occlusion 5. RA occlusion 6. CMA occlusion

SA to PA:

ALCAPA

Other shunts: 1. Lutembachers syndrome 2. M At with ASD 3. Post PTMC 4. AV fistula 5. Anomalous PVD 6. CM syndrome SA to right heart: 1. RSOV into RA or RV 2. Coronary cameral fistula

and causes of continuous murmurs—PDA: patent ductus arte| Classification riosus, ASD: atrial septal defect, PA: pulmonary artery, M At: mitral atresia, P At: pulmonary atresia, TOF: tetralogy of Fallot, AP: aorto-pulmonary, PTMC: percutaneous transmitral commisurotomy, AV: arteriovenous, PVD: pulmonary venous drainage, CM syndrome: Cruveilheir-Baumgarten syndrome, RSOV: rupture of sinus of Valsalva, RA: right atrium, RV: right ventricle, COA: coarctation of aorta, CA: carotid artery, FA: femoral artery, RA: renal artery, CMA: celiac mesenteric artery, SA: systemic artery, ALCAPA: anomalous left coronary artery from pulmonary artery, after shunt surgery e.g. Blalock, Waterston and Pott’s shunts.

CARDIAC AUSCULTATION

●

●

●

●

451

continuous pressure gradient is produced throughout the cardiac cycle and often with systolic accentuation.141 With adequate collateral arteries, only systolic gradient persists with no diastolic gradient across the obstructed artery as the collaterals around the obstructed artery deliver adequate flow and hence only systolic murmur may be present.142 Continuous murmur in coarctation of aorta (COA) heard over the thorax is produced by rapid blood flow through tortuous intercostal collaterals. A continuous murmur may also be produced at the site of coarctation and the murmur is best heard over the back in the midline between the scapulae.143 Continuous murmurs may also be present in branch pulmonary artery stenosis or partial obstruction of a major pulmonary artery occluded by a massive pulmonary embolus. Other common causes of continuous murmur are carotid stenosis, femoral artery stenosis and renal artery stenosis which have characteristically louder systolic component (see Fig. 21.70).

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Grewe K, Crawford MH, O’Rourke RA. Differentiation of cardiac murmurs by dynamic auscultation. Curr Probl Cardiol 1988;13(10):671. Barlow JB. Perspectives on the mitral valve. Phildelphia, FA Davis, 1987. Nishimura RA, Tajik AJ. The Valsalva maneuver and response revsited. Mayo Clin Proc 1986;61(3):211–217. Schmidt DE, Shah PK. Accurate detection of elevated left ventricular filling pressure by a simplified bedside application of the Valsalva maneuver. Am J Cardiol 1993;71(5):462–465. Rotham A, Goldberger AL. Aids to cardiac auscultation. Ann Intern Med 1983;99:346. McCraw DB, Siegel W, Stonecipher HK et al. Response of the heart murmur intensity to isometric (hand grip) exercise. Br Heart J 1972;34(6):605–610. Henke RP, March HW, Huktgren HN. An aid to identification of the murmur of aortic stenosis. Am Heart J 1960;60:354–363. Brokenbrough EC, Braunwald E, Morrow AG. A hemodynamic technique for the detection of hypertrophic subaortic stenosis. Circulation 1961;23:189–194. Lembo NJ, Dell’Italia LJ, Crawford MH, et al. Bedside diagnosis of systolic murmurs. N Eng J Med 1988;318(24):1572–1578. Sutton GC, Craige E. Clinical signs of acute severe mitral regurgitation. Am J Cardiol 1967;20(1): 141–144. Rios JC, Massumi RA, Breesman WT et al. Auscultatory features of acute tricuspid regurgitation. Am J Cardiol 1969;23(1):4–11. Gallavardin L, Pauper-Ravault. Le soufflé du retre cissement aortique peut changer de timbre et devenir musical dans se propagation apexienne. Lyon Med 1925:523. deLeon AC Jr. “Straight back” syndrome. In: Leon DF, Shaver JA, eds. Physiologic Principles of Heart Sounds and Murmurs. Monograph 46. New York: American Heart Association;1975:197–208. Still GF. Common Disorders and Diseases of Childhood. London: Frowde;1909. Van Oort A, Hopman J, De Boo T et al. The vibratory innocent heart murmur in school children: A case-control Doppler echocardiographic study. Pediatr Cardiol 1994;15(6):275–281. Perloff JK, Harvey WP. Auscultatory and phonocardiographic manifestations of pure mitral regurgitation. Prog Cardiovasc Dis 1962;5:172–194. Rackley CE, Whalen RE, Floyd W et al. The precordial honk. Am J Cardiol 1966;17:509–515. Gelfand D, Bellet S. The musical murmur of aortic insufficiency: Clinical manifestations; Based on a study of 18 cases. Am J Med Sci 1951;221(6):644–654. Stembridge VA, Hejtmancik MR, Herrmann GR. Unusual musical murmurs of anerior cusp aortic regurgitation: Report of 10 cases. Am Heart J 1954;48(2):163–172. Perez JE, Smith CA, Meltzer VN. Pulmonic valve insufficiency: A common cause of transient diastolic murmurs in renal failure. Ann Intern Med 1985;103(4):497–502. Wooley CF, Fontana ME, Kilman JW et al. Tricuspid sounds: Atrial systolic murmur, tircupid opening snap, and right atrial pressure pulse. Am J Med 1985;78(3):375–384. Fortuin NJ, Craige E. Echocardiographic studies of genesis of mitral diastolic murmurs. Br Heart J 1973;35(1):75–81. Flint A. On cardiac murmurs. Am J Med Sci 1862;44:29–54. Green EW, Agruss NS, Adolph RJ. Right-sided Austin Flint murmur. Documentation by intracardiac phonocardiography, echocardiography and postmortem findings. Am J Cardiol 1973;32(3):370–374. Rahko PS. Doppler and echocardiographic characteristics of patients having an Austin Flint murmur. Circulation 1991;83:1940–1950. Fortuin NJ, Craige E. On the mechanism of the Austin Flint murmur. Circulation 1972;45(3): 558–570. Reddy PS, Curtiss EI, Salerni R et al. Sound pressure correlates of the Austin Flint murmur: An intracardiac sound study. Circulation 1976;53(2):210–217. Wood P. An appreciation of mitral stenosis: I. Clinical features. BMJ 1954;1(4870):1051–1063: contd. Criley JM, Hermer HA. Crescendo pre-systolic murmur of mitral stenosis with atrial fibrillation. N Eng J Med 1971;285(23):1284–1287.

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134. 135. 136. 137. 138. 139. 140. 141. 142. 143.

Ongley PA, Rahimtoola SH, Kincaid OW et al. Continuous murmurs in tetrology of Fallot and pulmonary atresia with ventricular septal defect. Am J Cardiol 1966;18:821–826. Gibson GA. Persistence of the arterial duct and its diagnosis. Edin Med J 1900;1:1–10. Craige E, Millward DK. Diastolic and continuous murmurs. Prog Cardiovasc Dis 1971;14: 38–56. Keith JD, Rowe RD, Vlad P et al. Complete anomalous pulmonary venous drainage. Am J Med 1954;16(1):23–38. Cutforth R, Wiseman J, Sutherland RD. The genesis of the cervical venous hum. Am Heart J 1970;80(4):488–492. Tabatznik B, Randall TW, Hersch C. The mammary soufflé of pregnancy and lactation. Circulation 1960;22:1069–1073. Hurst JW, Staton J, Hubbard D. Precordial murmurs during pregnancy and lactation. N Eng J Med 1958;259(11):515–517. Myers JD, Murdaugh HV Jr, McIntosh HD et al. Observations on continuous murmurs over partially obstructed arteries. Arch Intern Med 1951;10:361–367. Edholm OG, Howarth S, Sharpey-Schafer EP. Resting blood flow and blood pressure in limbs with arterial obstruction. Clin Sci 1951;10:361–367. Spencer MP, Johnston FR, Meredith JH. Origin and interpretation of murmurs in coarctation of aorta. Am Heart J 1958;56:722–736.

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23. The normal electrocardiogram

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24. Abnormal P, T and U waves

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25. Ventricular hypertrophy

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26. Intraventricular conduction defects

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27. Myocardial infarction and ischemia

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28. Pericarditis and myocarditis

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29. Drug effects and electrolyte abnormalities

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30. Arrhythmias

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INTRODUCTION INTRODUCTION BASIC CONCEPTS a) Electrophysiology of the Heart b) Electrocardiographic Instrument, Recording Electrodes and Lead

AND 459 461 461

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c) Precautions to be Taken for Recording an ECG REFERENCES

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INTRODUCTION The electrocardiogram (ECG) is a graphic record of the electrical potentials produced during heart beat. ECG of today is the product of a series of technological and physiological advances occurred over the past two centuries. ●

●

●

The existence of electricity in the animal (“animal electricity”) was first suggested by Edward Bancroft (1769, in torpedo fish)1 and substantiated by John Walsh (1773 in eel)2 and Luigi Galvani (1780 in dissected frog) (see Table 22.1). However; it was in 1842, when Carlo Matteucci, Professor of Physics at the University of Pisa first showed that an electric current accompanies each heart beat in a dissected frog,3 which was later confirmed by Rudolph von Koelliker and Heinrich Muller in 1856.4 First successful attempt to record an ECG in humans was made by Alexander Muirhead, a Telegraph engineer in 1869 at St. Bartholomew’s hospital, London, using Thomson Siphon recorder. Table 22.1 History of development of ECG Discovery/invention

Scientist

1. Animal electricity

Bancroft (1769), Walsh (1773) and Galvani (1780) Matteucci (1842), Koelliker and Muller (1856) Gabriel Lippmann (1872) Willem Einthoven (1901) Alexander Muirhead (1869) Augustus D Waller (1887) Willem Einthoven (1895)

2. Electric current accompanies each heart beat (frog) 3. Capillary electrometer 4. String galvanometer 5. Attempt to record ECG in humans 6. Recorded first human ECG 7. Naming of deflections in ECG as “PQRST”

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●

●

●

●

●

French Physicist Gabriel Lippmann invented (1872) capillary electrometer, a glass tube with a column of mercury beneath the sulphuric acid, for which he was awarded a Nobel Prize in 1908. British Physiologists John Burden Sanderson and Frederick Page in 1878 first recorded the heart’s electric current with a capillary electrometer which consisted of two phases from the ventricle of a frog.5 But it was in 1887 when Augutus D Waller, British Physiologist, at St. Mary’s Medical school, London, recorded the first human ECG with a Lippmann’s capillary electrometer and labeled the deflections as ‘V1’, ‘V2’ and the third wave which was later discovered as ‘A’.6 After witnessing the Waller’s demonstration in 1889, the Dutch Physiologist Willem Einthoven recorded ECG with an improved Lippmann’s electrometer in 1895 and named the deflections as “ABCD” and with a correction formula as “PQRST”7 as per the mathematical convention derived from the French Philosopher Descartes points on the curves (1662).8 His invention of string galvanometer later in 1901 provided a reliable and direct method for recording ECG, and by 1910 the string galvanometer emerged from the research laboratory in the clinic.9 Subsequent improvement of the instrument and better understanding of the ECG resulted in the wide use of ECG and has become an invaluable clinical tool for the detection and diagnosis of a broad range of cardiac conditions. Though at present not a sine qua non for the diagnosis of the heart diseases, it continues even 100 yrs after its inception to be the most commonly used cardiologic test – For the diagnosis of the cause of chest pain – As a reliable tool for the diagnosis of acute myocardial infarction and dictates the timely administration of life saving thrombolytic therapy – For the diagnosis and the management of cardiac arrhythmias – Can help with the diagnosis of the cause of breathlessness – For the diagnosis of pericarditis and – For assessing the electrolyte disorders, drug effects and toxicity (see Table 22.2).

A patient with an organic heart disorder may have a normal ECG and a perfectly normal individual may show non-specific ECG abnormalities. Hence, a patient should not be given an unwarranted assurance of the absence of heart disease solely on the basis of a normal ECG.

Table 22.2 Utility of ECG in the current era Diagnosis

Management

Assessment

1. 2. 3. 4.

1. Acute myocardial infarction 2. Cardiac arrhythmias

1. Electrolyte disorders 2. Drug effects and toxicity

Chest pain Acute myocardial infarction Pericarditis Cardiac arrhythmias

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BASIC CONCEPTS The basic concepts are described as follows: ● ● ●

Electrophysiology of the heart Electrocardiographic instruments, recording electrodes and leads Precautions to be taken for recording an ECG.

a) Electrophysiology of the Heart 1) The Conduction System of the Heart See Part-1: Basic anatomy and physiology: chapter 6. 2) The Contractile or Working Myocardial Cell See Part-1: Basic anatomy and physiology, chapter 7: a) b) c) d) e)

Sarcolemma—see p57 Intercalated discs—see p58 Sarcotubular system—see p59 Diadic cleft—see p60 Contractile proteins—see p61

3) Electrical Activity of the Heart a) Properties of the transmembrane potentials: see Part-1: Basic anatomy and physiology, chapter 8 b) Recording of the electrical potentials (electrogram) produced by the normal cardiac cell: (i) Resting cell: In a resting cardiac muscle cell, molecules dissociate into positively charged ions on the outer surface and negatively charged ions on the inner surface of the cell membrane, and the cell is in an electrically balanced or polarized resting state. If an electrode is placed on the surface of the resting cell, no deflection is recorded by the galvanometer as entire cell surface has zero potential due to high impedance of the cell membrane (see Fig. 22.1). (ii) Depolarization: When the cell is stimulated (S) by an excitatory electrical wave, the negative ions migrate to the outer surface of the cell and positively charged ions pass into the cell, this reversal of polarity is called depolarization. ●

●

●

If an electrode is placed so that the depolarization wave flows toward the electrode, a galvanometer will record a positive or an upward deflection. When a depolarization current is directed away from an electrode, a negative or downward deflection is recorded. If an electrode (E) overlies the mid portion of the cell (muscle strip), the deflection will be diphasic. The initial deflection is upward due to an advancing positive charge, while the second deflection is downward due to the effect of passing negative charge (see Fig. 22.2).

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Polarized resting state no deflection





Fig. 22.1

Electrical activity

Depolarization positive redeflection

| Electrical activity in resting cell and effect of depolarization.





E





E

Upward deflection S Current flow towards the electrode

Downward deflection S Current flow away from the electrode



E



Diphasic deflection S Electrode overlying the mid portion of a cell

Fig. 22.2

| Depolarization wave in a single cell. E: electrode, S: stimulation. 





E

 E

S Two muscle strips of equal size

Fig. 22.3

●

●

| Depolarization wave in two cells of equal size. E: electrode, S: stimulation.

If two cells (muscle strips) of approximately equal size are stimulated at a central point, a positive of equal magnitude is recorded at either end (see Fig. 22.3). If two cells (muscle strips) of different sizes (e.g. RV and LV) are stimulated at a central point, a large positive deflection is recorded over the large cell (muscle mass) and a small positive deflection followed by a deep negative deflection or entirely negative deflection is recorded over the smaller cell surface (muscle mass) (see Fig. 22.4).

INTRODUCTION AND BASIC CONCEPTS

 

463



 E

OR

S Two muscle strips of different sizes

Fig. 22.4

| Depolarization wave in two cells of unequal size. E: electrode, S: stimulation.





E

 E

S Depolarization towards the electrode

Fig. 22.5

E

Repolarization in the opposite direction

| Repolarization in the opposite direction of depolarization. E: electrode, S: stimulation.

 E



 E

S Depolarization towards the electrode

Fig. 22.6



E

E

 E

Repolarization in the same direction

| Repolarization in the same direction of depolarization. E: electrode, S: stimulation. (iii) Repolarization: During recovery period, positively charged ions return to the outer surface and negatively charged ions move into the cell. The electrical balance of the cell is restored; this process of return of the stimulated cell to the resting state is known as repolarization. ●

●

If the repolarization occurs in a direction opposite to that of depolarization, the deflection will be in the same direction as that produced by depolarization (see Fig. 22.5). If the repolarization occurs in the same direction as that of depolarization, the deflection will be opposite to that of depolarization (see Fig. 22.6).

c) Intracellular and extracellular ion concentrations: see Part-1: Basic anatomy and physiology, chapter 8.

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●

●

The transfer of the Na and K ions across the cell membrane plays an important role in generating cardiac electrical activity. Intracellular concentration of K is 30 times greater than extracellular K. Na concentration is 30 times less inside the cell as compared to outside. Because of this ionic composition, membrane of the resting cardiac fiber is in an electrically balanced or polarized state.

d) Origin and sequence of cardiac activation: see Part-1: Basic anatomy and physiology, chapter 8. e) Phases of cardiac action potential: see Part-1: Basic anatomy and physiology, chapter 8. f) The modifying transmission factors: These factors affect transmission of electrical activity of the heart throughout the body and are broadly grouped into four categories: (i) Cellular factors determine the intensity of the current flow. They include: ● ●

Intracellular and extracellular resistance Intracellular and extracellular ions: Lower ion concentrations reduce the intensity of the current flow by reducing the movement of the ions and by lowering the extracellular potentials.

(ii) Cardiac factors affect the transmission of current from one cardiac cell to another. These include: ●

●

Anisotropy: It is the property of the cardiac tissue to propagate more rapidly along the length of the fiber than transversely. Hence, the recording electrodes oriented along the long axis of a cardiac fiber register larger potentials than the electrodes oriented perpendicular to the long axis. Connective tissue between the cardiac fibers: It disrupts the effective electrical coupling between adjacent fibers. The waveforms recorded from fibers with little or no intervening connective tissue are narrow and smooth in contour, whereas those recorded from the fibers with abundant connective tissue (fibrosis) are prolonged and fractionated.10

(iii) Extracardiac factors include all tissues and structures that lie between the region of cardiac electrical activity and the body surface. These tissues alter the electrical activity due to differences in electrical resistances of the adjacent tissues i.e. electrical inhomogeneities within the torso. e.g. intracardiac blood has lower resistance of 162 -cm than the lungs (2150 -cm) ● ● ● ● ● ● ●

Ventricular walls Intracardiac and intrathoracic blood volume Pericardium Lungs Skeletal muscles Subcutaneous fat and Skin.

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Table 22.3 Factors modifying transmission of action potential Modifying factors 1. 2. 3. 4. 5. 6. 7.

Intracellular and extracellular resistance

Intracellular and extracellular resistance Intracellular and extracellular ions Anisotrophy Connective tissue between the cardiac fibers Electrical in-homogeneities within the torso Distance between the heart and recording electrode Eccentric location of the heart

Intracellular and extracellular ions

Cellular factors

Eccentric location of the heart

Cardiac action potential

Cardiac factors

Anisotrophy

Connective tissue between cardiac fibers

Fig. 22.7

Connective tissue between heart and recording electrode

Physical factors

Extacardiac factors

1. Ventricular walls 2. Pericardium

Intracardiac and intrathoracic blood volume

1. Subcutaneous fat 2. Skin

1. Lungs 2. Skeletal muscles

| Factors modifying cardiac action potential. (iv) Physical factors which affect the electrical activity are: ●

●

The distance between the heart and recording electrode is governed by ‘inverse square law’ i.e. amplitude of the electrical potential decreases in proportion to the square of the distance. All electrodes placed at a distance 15 cm from the heart may be considered to be equidistant from the heart in electrical sense as the amplitude of the electrical potentials recorded will be the same in all electrodes. Eccentric location of the heart i.e. the heart is located eccentrically more anteriorly so that the RV and anteroseptal portion of the LV are located closer to the anterior of the chest than other parts of the LV and atria. Hence, the ECG potentials and wave forms generated by the anterior regions of the heart are higher and greater than those generated by the posterior ventricular regions and atria.

As a result of all these factors, body surface potentials have amplitude of only 1% of the amplitude of transmembrane potentials (see Table 22.3 and Fig. 22.7).

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Table 22.4 Methods of ECG recording Methods 1. 2. 3. 4.

Standard method ECG monitoring Ambulatory ECG Telemetry

b) Electrocardiographic Instrument, Recording Electrodes and Lead 1) Electrocardiographic Instrument The two main types of apparatus used are: ● ●

String galvanometer Radio amplifier

String galvanometer records on the photographic paper which has to be developed. It requires experience to operate so as not to damage the valuable string. Radio amplifier is compact, light, easy to operate and has a direct writer. Many modern machines record multiple leads simultaneously. Other methods utilized clinically are (see Table 22.4): ●

●

●

●

Oscilloscopic viewing of the ECG i.e. ECG monitoring in coronary and intensive care units. This produces a constant ECG on a fluorescent screen with a facility to obtain the ECG tracing. Ambulatory ECG recording: A small ECG tape recorder is attached to the patient for continuous recordings for 24 hrs while the patient is ambulatory which can be reviewed later by the attending physician for arrhythmias or myocardial ischemia. Telemetry ECG: ECGs can be transmitted via telephone lines, for constant or temporary monitoring and interpretation by a physician many miles away from the patient. Computer facilities are available not only for ECG interpretation but also for the recognition and quantitation of arrhythmias.

2) Recording Electrodes and Leads These are as follows: ● ● ● ● ● ● ● ●

Bipolar standard or limb leads Bipolar chest leads Unipolar augmented limb leads Unipolar precordial or chest leads Monitor leads Unipolar esophageal leads The Mason-Liker modified standard leads Unipolar intracardiac leads.

The standard clinical ECG consists of 12 leads: 3 bipolar limb leads (I, II, III), 3 augmented limb leads (aVR, aVL, aVF) and 6 unipolar precordial leads (V1–V6). The bipolar

INTRODUCTION AND BASIC CONCEPTS

467

Connected to ECG I 

RA lead

LA lead II

RA lead Connected to ECG II  LL lead

Fig. 22.8

III

LA lead III Connected to ECG  LL lead

| Bipolar standard leads (I, II, III).

and augmented limb leads are oriented in the frontal or coronal plane of the body, while the precordial leads are oriented in horizontal or transverse plane of the body. (1) Bipolar standard or limb leads: These were introduced by Einthoven.11 These leads record the potential difference between the two limbs and consists of three leads: I, II and III with four electrodes: LA (left arm electrode), RA (right arm electrode), LL (left leg electrode), and RL (right leg electrode) which serves as a ground connection. The electrodes are usually placed just above the wrists and ankles or to the stump in the amputated limb. ●

●

●

Lead I represents the potential difference between LA (positive electrode) and RA (negative electrode) (LA-RA). This lead with aVL is oriented to the left lateral wall. Lead II represents the potential difference between LL (positive electrode) and RA (negative electrode) (LL-RA). Lead III represents the potential difference between LL (positive electrode) and LA (negative electrode) (LL-LA). Leads II and III with aVF are oriented to the inferior surface of the heart (see Fig. 22.8).

The relation between these three leads is expressed algebraically by Einthoven’s equation or equilateral traiangle:11 Lead II  Lead I  Lead III i.e. electrical potential recorded in Lead II equals the sum of electrical potentials recorded in Leads I and III. This equation is based on Kirchhoff ’s Law i.e. the algebraic sum of all potential differences in a closed circuit equals zero. Hence I II  III 0 or II I  III. (2) Bipolar chest leads: Presently, a special bipolar chest lead (Lewis lead) is sometimes used to amplify the atrial activity and thereby to clarify the mechanism of an atrial arrhythmia. The RA electrode is placed in the 2nd intercostal (IC) space to right of the sternum, the LA electrode is placed in the 4th IC space to right of the sternum, and tracing is recorded on lead I.

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BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

(3) Unipolar augmented limb leads: The unipolar leads (limb leads: VR, VL, VF; multiple chest leads: V and esophageal leads E) were introduced by Wilson.12 ● The unipolar leads represent the potentials in a given lead and not the differences in potentials as in bipolar leads. ● The unipolar lead system consists of a Wilson’s central terminal or indifferent lead and an exploring lead. The central terminal is formed by joining electrodes (RA, LA, and LL) together to 5000  resistor which is attached to negative terminal of the machine. ● In unipolar limb leads, the central terminal is connected to the RA electrode of the machine (which acts as negative terminal) and exploring lead (positive terminal) is connected to the LA electrode of the machine and the tracing is recorded on lead I. Although technically this system has two electrodes i.e. bipolar leads, it represents a unipolar lead since one of the potentials is zero (central terminal has zero potential). ● At present, only augmented limb leads (aVR, aVL and aVF, introduced by Emanuel Goldberger in 1942) are in vogue as the amplitude of the deflections is 50% more than the non-augmented leads (VR, VL and VF). ● To record aVR (a augmented, VR vector of right arm), the LA electrode (exploring lead) of the machine is placed on the right arm, while RA electrode of the machine (indifferent lead/central terminal through 5000  resistor) is placed on the left arm and left leg. This lead is oriented to the cavity of the heart and hence all deflections (P, QRS, and T) are normally negative. ● To record aVL (a augmented, VL vector of left arm), the LA electrode of the machine is placed on the left arm, while RA electrode of the machine (indifferent lead through 5000  resistor) is placed on the right arm and left leg. This lead is oriented to the anterolateral or superior surface of LV. ● To record aVF (a augmented, VF vector for left leg), the LA electrode of the machine is placed on the left leg, while the RA electrode (indifferent lead through 5000  resistor) of the machine is placed on the right arm and left arms. This lead is oriented to inferior surface of the heart (see Fig. 22.9). The unipolar limb leads bear a definite mathematical relationship to the standard bipolar leads. This relationship is derived from Einthoven’s formula: VR  VL  VF 0. I 2/3 (aVL aVR) aVR I  II/2 II 2/3 (aVF aVR) aVL I III/2 III 2/3 (aVF aVL) aVF II  III/2 Bipolar and unipolar leads are not of equal lead strength. An augmented lead is 87% of the lead strength of a bipolar lead. Therefore, the above equations must be corrected. When the strength (voltage) of an augmented unipolar lead is determined from the bipolar lead values, it is corrected by multiplying by 0.87, and when the strength (voltage) of a bipolar lead is determined from an augmented lead values, it is corrected by multiplying by 1.15 (100/87) (see Fig. 22.10). Hence, I 2/3 (aVL aVR) (1.15) aVR III/2 (0.87) II 2/3 (aVF aVR) (1.15) aVL I III/2 (0.87) III 2/3 (aVF aVL) (1.15) aVF IIIII/2 (0.87) To determine voltage of R waves in augmented leads from the actual measurements of R waves from standard leads from illustration Fig. 22.10.

INTRODUCTION AND BASIC CONCEPTS

T

LA lead RA lead

aVR

LA lead ead RA l

aVL

ECG Recording on lead l

T

469

ECG Recording on lead l

LL lead LL lead

Unattached

Unattached

T

aVF

RA lead

ECG

LA lead Recording on lead l LL lead Unattached

Fig. 22.9

| Augmented limb leads—aVR, aVL, aVF. 111 aVR = 2 1.3

I = 2/3 (aVL aVR)

I III 2

aVL =

10

3.5

1.7 1 11.3 aVR

3

0

I





16

0.5 aVL

6 5

2

1

2 III

11

II = 2/3 (aVF aVR)

  +9.6

III = 2/3 (aVF aVL)

+1.3 +3 aVF

aVF =

Fig. 22.10

II  III 2

| Relationship between unipolar and bipolar limb leads.

aVR [10  16/2] (0.87) 11.3 aVL [10 6/2] (0.87) 1.7 aVF [16  6/2] (0.87) 9.6 Similar method is to used to determine voltages of P and T waves. To determine voltage of R waves in standard leads from the actual measurements of R waves from augmented leads from illustration Fig. 22.10.

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I 2/3(1.7  11.3) (1.15) 10 II 2/3(9.6  11.3) (1.15) 16 III 2/3(9.6 1.7) (1.15) 6 Similarly, same equation is used for P and T waves. (4) Unipolar precordial (chest) leads also consist of a Wilson’s central terminal or indifferent lead, the negative terminal of which is attached to RA lead of the machine, while one end of the exploring electrode is attached to LA lead of the machine, and the other end is applied to the desired chest positions, producing multiple unipolar chest leads i.e. V lead (V1 to V6 in standard lead system and from V1 to V9, V3R 9R in extended lead system). The common precordial positions of the chest leads as per AHA recommendations 193813 and 1992,14 are as follows: th ● V : 4 intercostal space (ICS) at the right of the sternal border 1 th ● V : 4 ICS at the left of the sternal border 2 ● V : Equidistant between V and V 3 2 4 th ● V : 5 ICS in left mid-clavicular line. All subsequent leads (V5–V9) are taken in the 4 same horizontal plane as V4 i.e. in the 5th ICS ● V : Anterior axillary line 5 ● V : Mid-axillary line 6 ● V : Posterior axillary line 7 ● V : Posterior scapular line 8 ● V : Left border of the spine 9 ● V 3R-9R: Taken on the right side of the chest in the same location as the left sided leads V3–V9 (see Fig. 22.11). However, the usual routine ECG consists of only 12 leads: I, II, III, aVR, aVL, aVF, and V1–V6. The precordial leads are arbitrarily subdivided into: anterior leads: V1, V2, anteroseptal leads: V3–V4, lateral or apical leads: V5 and V6. Leads V1 and V2 tend to be oriented to RV, while leads V4–V6 tend to be oriented to LV. (5) Monitor leads: In coronary care unit, modified bipolar chest leads are used. For rhythm evaluation the positive electrode is placed in usual V1 position (modified CL1), the negative electrode is placed near the left shoulder, and a third electrode which serves as a ground electrode is placed at a more remote area of the chest (see Fig. 22.12). ● For monitoring ST-T changes (due to ischemia), the positive electrode is placed in V4 or V5 position. (6) Unipolar esophageal leads are useful in recording atrial complexes, which are greatly magnified at this location for exploring the posterior surface of the LV (see Fig. 22.13). Esophageal lead (E) is passed into the esophagus through the nares and is attached to V (chest) lead of the machine. The nomenclature of the lead is derived from the distance in cm from the tip of the nares to the electrode in the esophagus. e.g. E50: represents the esophageal lead at a distance of 50 cm from the nares. For more accurate localization of the position of the esophageal leads, fluoroscopy may be used. ●

● ● ●

Leads E15–25: These reflect the atria. Leads E25–35: These reflect the region of AV groove. Leads E40–50: These reflect the posterior surface of LV.

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Midclavicular line Anterior axillary line Midaxillary line

Horizontal plane of V4–6

V1 V2 V3V4 V5V6

V7

V8 V9

V9R V8R V7R

V6RV5RV4RV3R V2R V1R

Fig. 22.11

| Location of unipolar precordial leads.

E20 E30 E50 3

Fig. 22.12

1

| Monitoring leads.

2

Fig. 22.13

| Unipolar esophageal leads.

(7) Unipolar intracardiac leads: An electrode contained in a cardiac catheter is attached to the V (chest) lead. Care must be taken as currents as low as 10 A can induce ventricular fibrillation. They are used for: ● Clarification of an arrhythmia by amplifications of the waves of the atrial activity. ● Localization of the catheter tip when a floating pacemaker is inserted without fluoroscopic guidance at bed side in intensive care units. The nature of P waves and QRS complexes will identify the location of the catheter tip. ● Pericardiocentesis without fluoroscopic guidance, by attaching V lead to a pericardiocentesis needle under sterile conditions. When the needle strikes the epicardium, ST elevation will be recorded, which is an indication for withdrawal of the needle.

472

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY 1 small square represents 0.04 s (40 ms)

1 large square represents 0.2 s (200 ms)

R–R interval: 5 large squares represent 1 s

Fig. 22.14

● ●

● ● ● ● ● ● ●

| Relationship between the squares on the ECG paper and time.

Recording bundle of His potentials with special catheter electrodes in cardiac laboratory. Multiple intracardiac recordings with programmed stimulation in specialized electrophysiological laboratories which are of value in determining the site of ectopic activity, efficacy of the drug therapy and for identification of the accessory pathways. Orientatation of leads in routine ECG: Leads I and aVL are oriented to left lateral wall Leads II, III and aVF are oriented to inferior surface of the heart Leads V1 and V2 are oriented to RV Leads V4–V6 are oriented to LV Leads V1–V4 are considered to be anteroseptal leads Leads V5 and V6 are considered to be apical or lateral leads There is no lead which is oriented directly to the posterior wall of the heart.

3) The Electrocardiographic Grid The electrocardiographic paper on which ECG is recorded is a graph paper with horizontal and vertical lines present at 1 mm intervals. A heavier line is present at every 5 mm (large square). ● Time is measured along the horizontal lines: 1 mm 0.04 s, 5 mm 0.20 s, every 15th large square (a 3 s period) is marked by a vertical line on the upper border for quick assessment of heart rate (see Fig. 22.14). ● Voltage is measured along the vertical lines: 10 mm 1 mV. ● For routine ECG, the recording speed is 25 mm/s with usual standardization producing 1 cm or 10 mm deflection with 1 mV signal. c) Precautions to be Taken for Recording an ECG For good ECG record, following precautions should be taken: ● The procedure should be explained to the patient before hand in order to allay any fears or anxieties and ECG should be recorded in a comfortable bed/couch and patient must be completely relaxed as any muscular motions or twitchings can alter the record. ● There should be good contact between the skin and the electrode.

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473

Table 22.5 Precautions to be observed for recording ECG 1. 2. 3. 4. 5.

●

●

●

Prior procedural explanation Good skin and electrode contact Proper grounding of the patient and equipment Proper standardization of the equipment All electronic equipment should be away from the equipment

The patient and the machine must be properly grounded to avoid alternating current interference. The machine must be properly standardized so that 1 mV will produce a deflection of 1 cm. Incorrect standardization will produce inaccurate voltage of the ECG complexes which leads to faulty interpretation. Any electronic equipment such as electrically regulated infusion pump can produce artifacts in the ECG; hence they should not come in contact with the patient (see Table 22.5).

REFERENCES 1. Bancroft E. An essay on the natural history of Guiana, London: T Becket and PA de Hondt, 1769. 2. Walsh J. On the electric property of Torpedo: in a letter to Ben Franklin. Phil Trans Royal Soc 1773; 63:478–489. 3. Matteucci C. Sur un phenomena physiologique produit par les muscles en contraction. Ann Chim Phys 1842;6:339–341. 4. von Koelhker A, Muller H. Nachwels der negation Schwankung des Murkelstroms am naturlich sich Kontrahierenden Herzen, Verhand lungen der Physikalisch-Medizinischen Gesellschaft in Wurzberg 1856:528–533. 5. Burdon Sanderson J. Experimental results relating to the rhythmical and excitatory motions of the ventricle of the frog. Proc R Soc Lond 1878;27:410–411. 6. Waller AD. A demonstration on man of electromotive changes accompanying the heart’s beat. J Physiol (Lond) 1887;8:229–234. 7. Einthoven W. Ueber die Form des menschlichen Electrocardiograms. Arch fd Ges Physiol 1895;60: 102–123. 8. Descartes R. De Homine (Treatise of Man). 1662: Moyardum & Leffen, Leiden. 9. Einthoven W. Un nouveau Galvanometre. Arch Necri Sc Ex Nat 1901;6:625–633. 10. Spach MS, Dolber PC. Relating extracellular potentials and their derivatives to anisotrophic propagation at a microsopic level in human cardiac muscle. Circ Res 1986;58:356–371. 11. Einthoven W. The different forms of the human electrocardiogram and their significance. Lancet 1912(1):853–861. 12. Wilson NF, Johnston FE, Macleod AG et al. Electrocardiograms that represent the potential variation of a simple electrode. Am Heart J 1934;9:447–458. 13. Barnes AR, Pardee HEB, White PD et al. Standardization of precordial lead. Am Heart J 1938;15: 235–239. 14. Schlant RC, Adolph RJ, DiMarco JP et al. Guidelines for electrocardiography. A report of the American Collage of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Committee on Electrcardiography). J Am Coll Cardiol 1992;19:473–481.

■ ■ ■ CHAPTER 23

T HE N ORMAL E LECTROCARDIOGRAM WAVES 474 1. P Wave 474 2. Q(q) Wave 476 3. R(r) Wave 476 4. S(s) Wave 477 5. R(r) Wave 477 6. T Wave 477 7. U Wave 478 8. Ta Wave 478 INTERVALS 479 SEGMENTS 480 THE ELECTRICAL AXIS 481 1. The Hexaxial Reference System 481 2. Methods of Determination of Electrical Axis 482

EFFECT OF HEART POSITION ON ECG 1. Electrical Rotation of the Heart in Frontal Plane on Anteroposterior Axis 2. Electrical Rotation of the Heart in Horizontal Plane on Long Axis NORMAL ECG VARIANTS 1. Normal ECG in Infants and Children 2. Juvenile Pattern 3. Early Repolarization 4. Anxiety and Hyperventilation 5. Postprandial Response 6. Effect of Deep Respiration REFERENCES

484

484 485 486 486 487 487 489 489 489 489

The normal ECG consists of waves, intervals and segments (see Table 23.1). Capital letters (Q, R, S) are used for large waves of 5 mm, and small letters (q, r, s) refer to smaller waves of 5 mm in size (see Figs 23.1 and 23.2).

WAVES 1. P Wave It is the first deflection of the ECG which is small, smooth and rounded. i) The initial portion is due to RA depolarization and the late portion is due to LA depolarization. The duration of RA depolarization is 0.02–0.04 s and that of LA is 0.05–0.06 s. ii) The normal duration of P wave is 0.12 s (120 ms) and its amplitude is not 2.5 mm or 25% of the normal R wave in normal individuals, especially in limb leads. iii) It is best seen in lead II, but usually studied in lead V1 as initial and terminal components are clearly identifiable, in which it is normally diphasic. The terminal

THE NORMAL ELECTROCARDIOGRAM

475

R

Isoelectric line: horizontal level between cardiac cycles

ST segment

PR

T wave P

P QRS V = Vulnerable period

1

Phase

2

0

3 Phase 4 QT

Fig. 23.1

| Phases of action potential and normal ECG. I

aVL

V1

V4

II

aVI

V2

V5

III

aVF

V3

V6

Fig. 23.2

| Normal ECG. Table 23.1 Composition of normal ECG Waves

Intervals

Segments

1. 2. 3. 4. 5. 6. 7.

RR PP PR QRS QT VAT

PR ST J junction

P Q (q) R (r) S (s) R(r) T U

negative deflection should not exceed 0.03 s in duration and 1 mm in depth (see Table 23.2). iv) As the normal P wave is oriented to the left, inferiorly in frontal planes (I, II, III, aVR, aVL and aVF), left and slightly anteriorly in horizontal planes (V1–V6).

476

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 23.2 Characteristics of normal P waves Features

Findings

1. 2. 3. 4. 5.

0.12 s (RA: 0.02–0.04 s, LA: 0.05–0.06 s) 2.5 mm 0.03 mm-s 0 to 90 II and V1 leads

Duration Amplitude Terminal ve deflection in V1 Frontal plane axis Best seen

Table 23.3 Characteristics of normal q waves Features

Findings

1. Duration 2. Depth

0.04 s 3 mm, 25 % of the R wave amplitude in the same QRS complex Normal

3. QS in V1

●

● ●

It is upright in leads I, II, aVF, and V3 V6 with P axis in frontal plane between 0 and 90. Inverted in a VR and frequently in V1 and sometimes in V2. Upright, diphasic or inverted in leads III and aVL. – P wave is upright in lead III if P axis is  30, and inverted if 30. – P wave is upright in lead aVL if P axis is  60, and inverted if 60.

2. Q(q) Wave All the three waves of the QRS complex are due to ventricular depolarization. i) This wave is the initial negative deflection which is due to the initial depolarization of mid portion of left side of the interventricular septum from left to right and hence it is oriented rightwards and anteriorly. ii) It is a small wave of 0.04 s in duration and 3 mm deep i.e. 25% of the height of R wave in the same QRS complex in leads I, II, aVF and V4–V6 (see Table 23.3). ● A larger Q wave (0.04 s in duration or 25% of the R wave) may normally be seen alone in lead III (for diagnostic significance, abnormal Q must also be present in lead aVF) or aVL (for diagnostic significance, abnormal Q must also be present in lead I or in precordial leads). iii) A QS complex (entirely negative) is often a normal finding in V1 and occasionally in V2. 3. R(r) Wave It is the first positive deflection during ventricular depolarization. i) After activation of the mid portion of the septum, anteroseptal region of the RV is depolarized which is oriented rightwards, anteriorly and either superiorly or

THE NORMAL ELECTROCARDIOGRAM

477

inferiorly which results in r wave in V1–V2 (right precordial leads) and q wave in I, V5 and V6, with a duration of 0.03 s. ii) Then the major activation of both ventricles (major muscle mass) which is oriented to the left, inferiorly and posteriorly results in a large dominant R wave in leads I, II, and V4–V6 with a duration of 0.03–0.05 s. The upper limit of R wave amplitude is 1.5 mV in lead I, 1.0 mV in lead aVL, 1.9 mV in leads II, III and aVF, and 0.6 mV in V1. Among the precordial leads, the tallest R wave is commonly seen in V4. ● Lead aVF will record R wave when frontal mean axis is 0 to 90, RS or rs complex if mean axis is 0 and a negative deflection (S) if the mean axis is between 0 and 30. ● Lead aVL will record R wave when frontal mean axis is between 30 and 60, and a negative deflection (S) if the mean axis is 60 to 90. ● Lead III will record R wave when frontal mean axis is between 30 and 90, and a negative deflection (S) if the mean axis is between 30 and 30. 4. S(s) Wave It is the negative deflection of ventricular depolarization that follows the first positive deflection (R), with duration of 0.01–0.02 s. i) It is due to the activation of last portion of the ventricular mass (posterior basal portion of LV, pulmonary conus and uppermost portion of the interventricular septum). In leads I and V5–V6 , s is small as it is oriented rightwards. ii) S wave may be due to major activation of ventricles and may be due to a dominant wave in leads. ● aVR: S is most prominent and always dominant, and a maximum amplitude upto 1.6 mV may be seen. It is deepest in V2 lead among the precordial leads. ● aVF when the frontal mean axis is between 0 and 30. ● aVL when the frontal mean axis is 60 to 90. ● III when the frontal mean axis is between 30 and 30. 5. R(r) Wave It is the second positive deflection that may occur during ventricular depolarization following S wave. ●

●

If the activation of the last portion of the ventricular mass is oriented anteriorly, a small positive deflection r is recorded in leads V1–V2. The negative deflection which may occur following r is termed as the s wave.

6. T Wave It is the deflection produced by ventricular repolarization and coincides with the closure of the semilunar valves. ● ●

The T wave is usually asymmetrical. Its orientation is to the left and inferiorly with a mean frontal axis between 0 and 90. However, it may normally be oriented slightly superiorly with mean axis between 0 and 30, with similar QRS orientation.

478

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY ●

● ●

It should be at least one tenth or 10% of the R wave amplitude in the same complex. Normally, its amplitude is 6 mm in limb leads with tallest T wave in lead II, and 10 mm in precordial leads with tallest T wave in leads V2 and V3. It is upright in leads I, II, aVF, and V2–V6 and inverted in aVR. It may be upright, diphasic or inverted in leads III, aVL (analogous to P wave) and V1 (occasionally in V2). It is inverted in V1 in approximately 50% of women and in 33% of men (see Table 23.4).

7. U Wave ● ●

●

●

●

●

It follows T wave preceding the next P wave. It is normally smaller than T wave, and usually 0.2 mV or approximately 10% of T wave in amplitude and 0.08 s in duration, with same polarity as the preceding T wave (see Table 23.5). The interval from the end of the T wave to the apex of the U wave is 90–110 ms, and the interval from the end of the T wave to the end of the U wave is 160–200 ms. Sometimes, a notch in the T wave may be mistaken for U wave. However, the interval between the apices of a notched T wave is usually 0.15 s, while the interval between the apices of the T and U waves is usually 0.15 s.1 It is best seen in leads V2–V4 and II as a “hump on a camel’s back” ( prominent in precordial leads). It is due to slow repolarization of the Purkinje fibers.2 More recently, U wave is thought to be due to ‘M’ cells in deep subepicardium (also for J or Osborne wave of hypothermia).3

8. Ta Wave It is usually a small negative deflection following P wave due to atrial repolarization which is not usually seen in a standard 12-lead ECG. Table 23.4 Characteristics of normal T waves Features

Findings

1. Amplitude

1/10th of R wave in the same QRS complex, 6 mm in limb leads and 10 mm in precordial leads III, aVF, V1 0 to 90

2. Upright/diphasic/inverted 3. Frontal axis

Table 23.5 Characteristics of U waves Features

Findings

1. 2. 3. 4.

10% of T wave of the same complex (0.2 mV) 0.08 s 60 V2–V4 and II leads

Amplitude Duration Mean frontal axis Best seen

THE NORMAL ELECTROCARDIOGRAM 1 small square represents 0.04 s (40 ms) QT 0.40 s PR 0.20 s

479

1 large square represents 0.2 s (200 ms) QRS 0.10 s

R–R interval: 5 large squares represent 1 s

Fig. 23.3

| ECG intervals (PR and QRS).

INTERVALS 1. RR interval is the distance between the two consecutive R waves. ● In regular sinus rhythm, the RR interval in seconds divided by 60 will give the heart rate/min. ● In irregular rhythm, the number of R waves in a given period of time (e.g. 10 s) converted into the number per minute will give the ventricular rate/min. 2. PP interval is the distance between the two consecutive P waves. The heart rate can be calculated in regular sinus rhythm similar to RR interval. However, in irregular rhythm atrial rate per minute is computed similar to the ventricular rate. 3. PR interval is measured from the onset of P wave to the beginning of QRS complex. It measures the AV conduction time from the onset of atrial depolarization to the onset of ventricular depolarization which includes: ● ● ●

Depolarization of both atria, AV node conduction including normal conduction delay in AV node (about 0.07 s), And passage of impulse through the bundle of His and bundle branches.

The normal PR interval is 0.12–0.20 s.4 However, it must be correlated with heart rate as slower the heart rate, longer the PR interval. 4. QRS interval (duration of QRS complex) is measured from the onset of Q (q) wave or R (r) wave (if Q/q wave is not seen) to the termination of S wave (see Fig. 23.3). ● It measures the total ventricular depolarization time. ● The normal duration of QRS complex is 0.12 s, which is slightly longer in males and large and tall subjects than in females and small and short subjects.5 5. QT interval is measured from the onset of Q wave to the end of T wave. It measures the total duration of ventricular depolarization and repolarization which corresponds to the duration of ventricular action potential.

480

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 23.6 ECG intervals Features

Findings

1. 2. 3. 4.

0.12–0.20 s 0.12 s

0.42 s in men, 0.43 s in women 0.03 s in V1–V2 0.05 s in V5–V6

PR interval QRS duration QTc interval VAT

Intrinsic deflection (VAT) –

+ E

S

Fig. 23.4

| Ventricular activation time (VAT).

i) Corrected QT interval (QTc ): As the QT interval varies with the heart rate i.e. QT interval decreases as the heart rate increases, it should always be corrected by Bazett (1920) formula6: QTc QT/(R–R) where QTc is corrected QT interval, QT is the measured QT interval, RR is the measured RR interval. ● The QT is 0.42 s in men and 0.43 s in women. c ● The QT interval is slightly longer in the evening and at night during sleep due to influence of the autonomic nervous system.7 ii) QU interval: When the end of T wave overlaps the beginning of U wave especially in metabolic abnormalities, QT is designated as QT (U) or QU interval. iii) QT interval dispersion: The QT interval also varies from lead to lead, maximum in mid precordial leads (V2–V3) and normally the difference between the longest and shortest intervals in the leads should not be more than 0.05 s. This variation in QT interval duration from lead to lead is known as QT interval dispersion and increased QT interval dispersion indicates electrical instability and risk of occurrence of ventricular arrhythmias8 (see Table 23.6). 6. Ventricular activation time (VAT) is the time that the impulse takes to traverse the myocardium from endocardium to epicardial surface (see Fig. 23.4). It reflects the intrinsicoid deflection and is measured from the beginning of the Q wave to the peak of R wave. Normally, it should not exceed 0.03 s in V1–V2 leads and 0.05 s in V5–V6 leads.

SEGMENTS 1. PR segment is the portion of the ECG tracing from the end of the P wave to the onset of QRS complex and normally it is isoelectric.

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481

2. ST segment is the portion of the ECG tracing that lies between the end of the QRS complex and the beginning of the T wave. ● It represents the period when all parts of the ventricles are in depolarized state. But early repolarization may encroach on the ST segment to a variable degree. ● The point at which QRS complex ends and ST segment begins is the J or junction point. The ST segment from J point to the beginning of T wave is usually isoelectric, but may vary from 0.5 (depression) to 1 mm (elevation) in precordial leads.

THE ELECTRICAL AXIS The electrical axis may be defined as a vector or an electromotive force originating in the center of Einthoven’s equilateral triangle which has magnitude, direction and polarity.9,10 The mathematical symbol expressed is an arrow pointing in the direction of the net potential (positive or negative), while its length indicates the magnitude of the electrical force. The electrical axis is usually determined in the frontal plane from the limb leads by using the hexaxial reference system, derived from Einthoven’s equilateral triangle. 1. The Hexaxial Reference System It is composed of lead axis of six frontal plane limb leads. The lead axis of these leads is rearranged so that their centers overlay one another and these axes divide the plane into 12 segments, each subtending 30 (see Fig. 23.5). ● ● ● ● ● ●

The postive pole of lead I is designated as 0, and the negative pole as 180 The positive pole of aVF is designated as 90, and the negative pole as 90 The positive pole of lead II is designated as 60, and negative pole as 120 The positive pole of lead III is designated as 120 and negative pole as 60 The positive pole of aVR is designated as 150 and negative pole as 30 The positive pole of aVL is designated as 30 and negative pole as 150 Superior –120o –150o

–90o –60o –30o

aV R

L aV

I

Right

+120o

aVF +90o Inferior

Fig. 23.5

| The hexaxial reference system.

II

+150o

III

±180o

+60o

0o

+30o Left

482

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Determination of electrical axis is useful in minority of cardiac conditions as in ● ● ● ●

Fascicular blocks Ventricular hypertrophy especially RVH and biventricular hypertrophy Some forms of ventricular tachycardia and Some forms of congenital heart diseases.

2. Methods of Determination of Electrical Axis Axis of QRS complex, P wave and T wave can be determined by the following methods: 1. Equiphasic Method Identify a lead in which the net QRS amplitude is zero i.e. smallest or equiphasic QRS deflection from the six frontal leads, the mean QRS axis (vector) will be perpendicular to this lead axis, in which the net QRS deflection will be highest of all frontal leads. e.g. in Fig. 23.6, the net QRS amplitude is zero in lead I, therefore the lead aVF is perpendicular to this lead, and the mean QRS axis will be 90 if the net QRS complex in aVF is positive or 90 if the net QRS complex is negative as per the hexaxial reference system (see Fig. 23.5).

I

aVF

0o

+90o aVF

Fig. 23.6

| Determination of axis by equiphasic method.

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483

2. Classical Method9,11 i) The net amplitude of the QRS complex in any 2 (usually I and III) of the 3 standard limb leads are plotted along the axis of the 2 standard limb leads on the hexaxial reference system. The net amplitude of the QRS complex represents the net area of the QRS complex of the corresponding lead. The results are counterchecked by using Eithoven’s equation (II I  III). ii) Then perpendicular lines are drawn at these locations, and a line drawn from the center of the hexaxial reference system to the intersection of the perpendicular represents the approximate mean QRS vector and its angle is the mean QRS axis in frontal plane. e.g. in Fig. 23.7, the net amplitude of QRS complex in leads I and III is as follows: Lead I: R 6 mm, S 2 mm; 6 2 4 mm Lead III: R 2 mm, S 5 mm; 2–5 3 mm Therefore, the net QRS amplitude of 4 mm in lead I and the net QRS amplitude of 3 mm in lead III are plotted along the axis of leads I and III respectively as in Fig. 23.8. An angle of 15 is obtained with a line drawn from the center of the hexaxial reference system to the intersection of the perpendiculars, which is the mean QRS axis in frontal plane.

I: R 6 mm, S 2 mm

Fig. 23.7

III: R 2 mm, S 5 mm

| Determination of axis by classical method. 90o

120o

ABNORM AL LE FT AX IS DE VI o AT 90 IO 60o

N

30o

3 180o

ABNO

180o

15o 0o I

4

G

H

AX

IS

DE

120o III V IA

T IO

N

60o II

90o NO

L RA RMA

110o

Fig. 23.8

EV

RI

IA

TI

AL

ON

RM T

| Determination of axis by classical method.

NG

EO

X FA

IS

D

484

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

3. Simplified Method12 Examine QRS complexes in leads I and aVF. i) If QRS complexes are upright (positive) in both leads  axis in frontal plane is normal (0 to 110 in 40 years of age, 30 to 90 in 40 years of age). ii) If QRS complex is positive in lead I and negative in lead aVF  left axis ( 30 to 90) in frontal plane. iii) If QRS complex is negative in lead I and positive in lead aVF  right axis (110 to 180) in frontal plane. Similarly, the axis of P and T waves in frontal plane can be determined by above methods. Normal Electrical Axes in Frontal Plane. i) Mean QRS axis: For all age groups is 30 to 110, 40 years of age is 30 to 90, 40 years of age is 0 to 110. ii) Mean P wave axis: 0 to 90. P wave is inverted in lead III if P axis is 30. Also, it is inverted in lead aVL if P axis is 60. iii) Mean T wave axis: 0 to 90. iv) Mean U wave axis is 60. v) Left axis deviation (LAD): When the mean QRS axis in frontal plane lies between 30 and 90. Common causes of LAD are: ● LBBB ● Left anterior fascicular block (hemiblock) ● LVH ● Some forms of VT ● AV canal defect, tricuspid atresia ● Mechanical shifts causing a horizontal heart: Pregnancy, ascites. vi) Right axis deviation (RAD): When the mean QRS axis in frontal plane lies between 110 and 180. Common causes of RAD are: ● RVH ● Left posterior fascicular block ● Pulmonary embolism ● Lateral myocardial infarction ● Dextrocardia ● Mechanical shifts causing a vertical heart: Emphysema.

EFFECT OF HEART POSITION ON ECG The electrical rotation of the heart may occur in frontal plane on anteroposterior axis or in horizontal plane on long axis. It is doubtful whether true anatomical rotation of the heart occurs, and if it occurs it is very minimal. 1. Electrical Rotation of the Heart in Frontal Plane on Anteroposterior Axis Besides determining the QRS axis in frontal plane, the resemblance of QRS complex in precordial leads (V1 and V6) is sought in unipolar limb leads to determine the heart

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485

Table 23.7 Positions of the heart Features

Vertical

Horizontal

Intermediate

1. Mean QRS axis 2. QRS complex in aVF 3. QRS complex in aVL

75 to 110 Resemble V6 Resemble V1

30 to 0 Resemble V1 Resemble V6

15 to 30 Resemble V6 Resemble V6

Table 23.8 Electrical rotation of the heart Clockwise rotation

Counterclockwise rotation

1. LV complex in V7–V9 2. S waves of RV complex in V5–V6

1. LV complex in V2 2. ST elevation in V2–V4

position in frontal plane. There are three main electrical rotations of the heart in frontal plane. • Vertical heart • Horizontal heart • Intermediate heart. Vertical heart is merely a manifestation of an inferiorly directed mean QRS axis. ● ● ● ●

Mean QRS axis is 75 to 110. aVR records RV cavity complex (i.e. all inverted complexes, P, QRS, and T). aVF records LV epicardial complex (i.e. upright P and T, qR) resembling V6. aVL may record RV epicardial complexes (i.e. downward major QRS deflection) resembling V1 or sometimes RV cavity complex resembling aVR. Horizontal heart is merely a manifestation of left QRS axis deviation.

● ● ● ●

Mean QRS axis is 30 to 0. aVR records RV cavity complex. aVF records RV epicardial complex resembling V1. aVL records LV epicardial complex resembling V6.

Intermediate heart is merely a manifestation of QRS axis midway between vertical and horizontal heart. ● ● ●

Mean QRS axis is between 15 and 30. aVR records usually RV cavity complex. aVF and aVL record LV epicardial complex resembling V6 (see Table 23.7).

2. Electrical Rotation of the Heart in Horizontal Plane on Long Axis The rotation of the heart on long axis may be clockwise or counterclockwise depending on the appearance of the precordial leads, especially the transitional zone (see Table 23.8). In an average case, the transitional zone is in the V4 lead.

486

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Fig. 23.9

| Clockwise rotation with persistence of S waves till V . 6

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Fig. 23.10

| Counterclockwise rotation—LV complexes from V

3

onwards.

Clockwise rotation: The transitional zone is shifted to the left, so that the typical LV epicardial complexes do not appear until V7–V9, i.e. S waves (typical of RV epicardial complex) persist in V5 and V6 (see Fig. 23.9). If rotation is rightward, S waves will also be seen in lead I. If rotation is leftward or superiorly, S waves are also seen in leads II, III, and aVF. If rotation is posteriorly, all frontal plane leads record normal QRS complexes. Counter clockwise rotation: The transitional zone is shifted to the right, so that the typical LV epicardial complexes are seen early in V2 (see Fig. 23.10). ST elevation in V2–V4 is a common accompaniment. NORMAL ECG VARIANTS 1. Normal ECG in Infants and Children a) Normal ECG in Infants ● RVH pattern: In fetus, RV performs more work than LV and therefore, at birth or in infancy there is a relative hypertrophy of the RV resulting in electrocardiographic pattern simulating RVH i.e. tall R waves in V1 or V2 with RAD (see Fig. 23.11). However, there is no initial q wave and VAT in V1 is not prolonged.

THE NORMAL ELECTROCARDIOGRAM

487

V4

Fig. 23.11

I

aVR

II

aVL

III

aVF

V1

V2

V5

V3

V6

| ECG in a child with sinus tachycardia and tall R in V . 1

Table 23.9 Normal ECG variants in infants and children Features

Findings

1. R wave in V1 2. VAT in V1 3. T wave in V1–V4

Tall mimics RVH, normalizes after 5 yrs of age Normal Inverted after 4 days of birth May persist into 2nd decade of life If persist into 3nd decade of life: Juvenile pattern Shifts to left in children

4. Frontal QRS axis

T waves are upright or inverted in V1, upright in V2–V6 within first 2–4 days. T waves are normally inverted in V1–V4 after 4 days. b) Normal ECG in Children ● Tall R waves in V –V usually disappears after 5 yrs of age. 1 2 ● Inverted T waves in right precordial leads may persist into second decade of life. ● Frontal plane QRS axis gradually shifts to the left (see Table 23.9). ● ●

2. Juvenile Pattern Inverted T waves in V1–V4 may persist into third decade of life which is more common in Negroes, and more common in women than in men.13 3. Early Repolarization It is characterized by: ● ST segment elevation (usually 2 mm) in mid precordial leads with an upward concavity and relatively tall symmetrical upright T waves (see Fig. 23.12). J point may be prominent. ● Common in young adults especially athletes (see Table 23.10).

488

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY V4

Fig. 23.12

I

aVR

V1

II

aVL

V2

V5

III

aVF

V3

V6

repolarization in V –V –ST elevation with concavity upwards and tall | Early symmetrical upright T waves. 2

4

Table 23.10 Normal ECG variants-early repolarization Features

Findings

1. 2. 3. 4.

Elevation of 2 mm with concavity upwards More in slower heart rates Common in young adults, especially athletes More in men

ST segment in precordial leads Heart rate Age of the individual Sex

1. T↓ 2. QRS axis → left

RVH pattern

T↓

In infants

>In females

Juvenile pattern

In children

Normal ECG variants

Anxiety & hyperventilation 1. Prolong PR 2. ST ↓ and T ↓

Fig. 23.13 ●

●

RVH pattern disappears >5 years of age

Sinus tachycardia

Post prandial

ST ↓ / T ↓ or both

Early repolarization >In young males

At slower heart rates

| Normal ECG variants—ST: ST segment depression, T: inverted T waves.

More common at slower heart rates than rapid heart rates, in men than in women, and often in black men.14 This phenomenon is due to beginning of repolarization of a portion of the myocardium before depolarization is completed in other areas of the myocardium. Following moderate exercise or hyperventilation, the ST segment may return to the isoelectric line.

THE NORMAL ELECTROCARDIOGRAM

489

4. Anxiety and Hyperventilation ECG changes are: ● Sinus tachycardia, ● Prolonged PR interval, ● ST depression and T wave inversion in left precordial leads. 5. Postprandial Response Following a heavy meal especially high carbohydrate meal, ST depression or T wave inversion or both may occur. It is due in part to an intracellular shift of potassium in association with intracellular glucose metabolism. 6. Effect of Deep Respiration ● ●

With deep inspiration, the heart becomes more vertical and rotates clockwise. With deep expiration, the heart becomes more horizontal and rotates counter clockwise (see Fig. 23.13).

REFERENCES 1. Lepeschkin E. The U wave of the electrocardiogram. Mod Concepts Cardiovasc Dis 1969;38:39–45. 2. Surawicz B. U wave: Facts, hypotheses, misconceptions, and misnomers. J Cardiovasc Electrophysiol 1998;9(10):1117–1128. 3. Antzelevitch C, Sicouri S. Clinical relevance of cardiac arrhythmias generated by after-depolarization: Role of M cells in the generation of U waves, triggered activity and torasade de pointes L J Am Coll Cardiol 1994;23:239. 4. Chou TC. When is the vectorcardiogram superior to the scalar electrocardiogram? J Am Coll Cardiol 1986;8(4):791–799. 5. Surawicz B. Stretching the limits of the electrocardiogram’s diagnostic utility. J Am Coll Cardiol 1998; 32:483–485. 6. Bazett HC. An analysis of the time relations of electrocardiograms. Heart 1920;7:353–70. 7. Molnar J, Zhang F, Weiss JS, et al. Diurnal pattern of QTc interval: how long is prolonged? J Am Coll Cardiol 1996;27(1):76–83. 8. Franz MR, Zabel M. Electrophysiological basis of QT dispersion measurements. Prog Cardiovasc Dis 2000;42(5):311–324. 9. Einthovan W, Fahr G, de Waart A. Uber die Richtung und die manifeste Grosse der Potentialschwankungen in menchlichen Herzen und uber den Einfluss der Herzlage auf die From des Elecktrocardiograms. Arch Physiol 1913;150:275–315. 10. Barker JM. The Unipolar Electrocardiogram: A Clinical Interpretation. New York: Appleton-CenturyCrotts:1976. 11. Sodi-Palares D, Medrano GA, Bisteni A, et al. Deductive and Polyparametric Electrocardiography. Mexico: Instituto Nacional Cardiologia Mexico; 1970;36:136. 12. Castellanos A Jr, Lemberg L. A Programmed Introduction to the Electrical Axis and Action Potential. Oldsmart, FL: Tampa Tracings; 1974;34:114. 13. Vitelli LL, Crow RS, Shahar E, et al. Electrocardiographic findings in a health biracial population. Am J Cardiol 1998;81(4):453–459. 14. Haydar ZR, Brantley DA, Gittings NS, et al. Early repolarization: An electrocardiographic predictor of enhanced aerobic fitness. Am J Cardiol 2000;85(2):264–266.

■ ■ ■ CHAPTER 24

A BNORMAL P, T ABNORMAL P WAVES 1. Abnormal Sites of Atrial Activation 2. Dextrocardia 3. Left Atrial Enlargement or LA Abnormality 4. Right Atrial Enlargement or RA Abnormality 5. Biatrial Enlargement or Abnormality

490 490 491 491 493 494

AND

U WAVES

ABNORMAL T WAVES 1. Tall T Waves 2. Flat T Waves 3. T Wave Inversion ABNORMAL U WAVES 1. Large Prominent U Waves 2. Inverted U Waves (in Leads I, II, V5 and V6) REFERENCES

495 495 496 496 497 497 497 499

ABNORMAL P WAVES Abnormal P waves occur due to alteration in morphology, amplitude, duration or their absence. Abnormal P waves may be due to: ● ● ● ●

Abnormal sites of atrial activation Dextrocardia LA enlargement or LA abnormality RA enlargement or RA abnormality.

1. Abnormal Sites of Atrial Activation Shifts in the site of initial activation away from the SA node to other ectopic sites results in major changes in the pattern of atrial activation and therefore changes in the morphology of P waves.1 These shifts from the usual initial activation can occur: ● ●

As escape rhythms if the normal SA node pacemaker fails or As AV junctional or ectopic atrial rhythms if automaticity of ectopic site is enhanced.

The resulting P waves abnormalities includes: ●

●

Negative P waves in leads II, aVF, V4–V6 (in which P waves are normally upright) with upright P waves in aVR. Absent P waves in regular rhythm: in SA block and AV junctional rhythm; and absent P waves in irregular rhythm: consider atrial fibrillation.

ABNORMAL P, T AND U WAVES

Fig. 24.1

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

491

complexes in I are inverted and all complexes in aVR are | Dextrocardia—all upright with RV epicardial complexes in V . 6

●

Polymorphic P waves: 3 different P wave morphologies in the same lead, consider multifocal atrial tachycardia.

2. Dextrocardia ●

●

In true dextrocardia, there is reversal of the polarity of I axis and all deflections including P wave are inverted in leads I and aVL as P is oriented to the right, inferiorly and anteriorly, and all deflections including P wave are upright in aVR. The precordial leads V1–V6 reflect right ventricular epicardial complexes (i.e. loss of R waves in V4–V6). However, right precordial leads (V4R, V5R) record left ventricular epicardial pattern (see Fig. 24.1). In technical dextrocardia, the ECG in limb leads (I, aVL, aVR) mimics true dextrocardia due to interchange of RA and LA electrodes but depicts normal ECG pattern in the precordial leads.

3. Left Atrial Enlargement or LA Abnormality Anatomical or functional abnormality of LA alters the morphology, duration and amplitude of P waves in ECG, which is best seen in leads II and V1. Since the ECG changes of P waves could be due to increased atrial size (LAE), intra-atrial conduction defects or LV dysfunction, it is preferable to refer these changes as LA abnormality (LAA) than LA enlargement (LAE) (see Fig. 24.2). ECG criteria of LAA have low sensitivity but high specificity when correlated with echocardiographic findings. Following is the diagnostic criteria for LA abnormality (see Table 24.1). i) Duration ●

●

●

Duration of P wave of 0.12 s (2.5 mm) in lead II.2 Prolonged duration of P wave was present in 2/3rd of the patients with documented LAE.2 Ratio between the duration of P wave and duration of PR interval in lead II of 1.6 (Macruz index). Relative shortening of PR interval.

492

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY RAA

Normal

LAA

RA RA

LA

LA

LA

RA

II

RA RA

RA V1 LA

LA

LA

Fig. 24.2

wave abnormalities | Pabnormality (LAA).

in right atrial abnormality (RAA) and left atrial

Table 24.1 ECG suggestive of atrial enlargement Left atrial enlargement

Right atrial enlargement

1. P wave duration 0.12 s 2. Macruz index: 1.6 3. P mitrale 4. Morris index: 0.04 mm-s 5. Frontal P axis: 30 to 45 6. f waves 1 mm in atrial fibrillation

1. 2. 3. 4. 5.

P wave amplitude in II: 2.5 mm P initial force in V1: 0.06 mm-s P pulmonale Frontal P axis: 75 Right ventricular hypertrophy

ii) Morphology ●

●

Normal P wave is bullet shaped. If it is notched or is double-peaked like bent staple or camel humped appearance with a distance of 0.04 s between the notches in lead II, it is known as ‘P mitrale’ pattern and indicates LAE.3 However, it was observed in only 1/3rd of the patients with isolated MS proved at surgery.2

iii) P Terminal Force ●

●

●

●

Increased P terminal force or Morris index:4 It is derived by multiplying the depth (in mm) by duration (in seconds) of terminal negative portion of diphasic P wave in V1 and expressed in mm-s. If P terminal force is 0.04 mm-s (i.e. depth 1 mm and duration 0.04 s), it indicates LAE. The ECG diagnosis of LAE by Morris criterion was confirmed in 68% of cases at surgery.2 The combined P terminal force and P wave duration are correlated with echocardiographic LAE in 82%.5 The Morris index may also be positive in COPD with or without corpulmonale, and in patients with pectus excavatum and straight back syndrome.

ABNORMAL P, T AND U WAVES

Morris index: >0.04 mm-s

P duration >0.12 s-P mitrale

P initial force in V1: >0.06 mm-s

Tall P >2.5 mmP pulmonale P axis: >75°

Macruz index: >1.6 P axis: 30 to 45° f >1 mm in atrial fibrillation

493

Left atrial enlargement

Right atrial enlargement RVH

Abnormal P waves Tall peaked P in V1  notched P in V5 or V6 or II

Biatrial enlargement

Tall and wide P in limb leads

Diphasic P in V1

Fig. 24.3

| Abnormal P waves—diagnostic criteria of left, right and bi-atrial enlargement. iv) Frontal P Axis LAE is usually associated with leftward shift of mean P axis6 between 30 and 45. However, it lacks specificity and sensitivity, and it occurs only in 10% of the cases with LAE. v) In Atrial Fibrillation If the size of the fibrillatory f waves is 1 mm (coarse atrial fibrillation), is suggestive of LAE, which is correlated with roentgenographic and anatomic evidence of LAE.7 Fine f waves if they are 0.5 mm in size.7 4. Right Atrial Enlargement or RA Abnormality As in LAA, the P wave abnormality may be due to increase in RA size or may reflect a more vertical heart position within the chest due to pulmonary hyperinflation (as in COPD), hence the term RA abnormality (RAA) is preferred to RA enlargement (RAE). (see Fig. 24.3) Similarly, the criteria for RAA have low sensitivity but high specificity when correlated to echocardiographic findings. Following is the criteria for RAA. i) Amplitude Tall peaked P waves in lead II of 2.5 mm (250 V) (P pulmonale or church steeple appearance). P pulmonale was present in about 20% of patients with chronic corpulmonale.8 ii) Initial Positive Portion of Diphasic P Wave in Lead V1 ● ● ●

The amplitude of the initial positive deflection of P wave taller than 1.5 mm Duration of the initial positive deflection is greater than 0.04 s9 P initial force: 0.06 mm-s. This is derived by multiplying amplitude (in mm) by duration (in seconds) of initial positive deflection of the diphasic P wave.

494

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

iii) Frontal P Axis Rightward shift of mean P axis of greater than 75. iv) QRS Complex Abnormalities These may also suggest RAA ●

●

qR pattern followed by a tall R wave in V1 (suggestive of RVH) without the evidence of myocardial infarction.10 The qR pattern occurs due to an anatomical shift of the hypertrophied RV by an enlarged and dilated RA. Low amplitude QRS complexes (6 mm or 600 V) in lead V1 with a three fold or greater increase in lead V2. This has been attributed to a large volume of blood in RA that lies between the ventricles and precordial leads.

v) With Echocardiographic Correlation The best ECG predictors of RAE in the absence of complete RBBB11 were: ● ● ●

A P wave amplitude of 2.5 mm in V1, A QRS axis of 90, and An R/S ratio of 1 in V1.

The combined sensitivity of these criteria was 48% with 100% specificity.11 5. Biatrial Enlargement or Abnormality (i) Notched P wave in lead II: It is seen with initial component increased in amplitude and taller than the second component (P tricuspidale). It is frequently seen in tricuspid valve disease, and mitral valve disease with PH. (ii) Diphasic P wave in lead V1: Initial positive deflection is 1.5 mm in amplitude and second negative portion is wide (1 mm or 0.04 s) and deep (1 mm depth).12 (iii) A tall peaked P wave (1.5 mm): It is seen in V1 and a wide, notched P wave in limb leads (II) or in (precordial leads (V5 and V6).12 (iv) Increase in both amplitude (2.5 mm) and duration (0.12 s) of P wave: It occurs in limb leads12 (see Fig. 24.4 and Table 24.2).

V1

II

V5

Fig. 24.4

enlargement with diphasic P in V , notched P in V , and tall and | Biatrial wide P in II. 1

5

ABNORMAL P, T AND U WAVES

495

Table 24.2 Biatrial enlargement Precordial leads

Limb leads

1. Diphasic P in V1 2. Tall peaked P in V1 with notched P in V5 or V6

1. Notched P in II with tall peaked P in V1 2. Tall and wide P in limb leads

Table 24.3 Abnormal T waves Tall T

Inverted T

1. Hyperkalemia 2. True posterior wall myocardial infarction 3. Cerebrovascular accidents (CVA)

1. Myocardial ischemia or infarction 2. Ventricular hypertrophy 3. Drug effects 4. Pulmonary embolism 5. Bundle branch block 6. Wolff-Parkinson-White syndrome 7. Ventricular ectopics or paced beats 8. CVA

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Fig. 24.5

| Tall peaked T waves in precordial leads in hyperkalemia.

ABNORMAL T WAVES It could be due to the alteration in morphology (tall or flat T waves) or polarity (inverted T waves) (see Table 24.3). 1. Tall T Waves The criteria for tall T waves: When amplitude of T waves is 6 mm in limb leads or 10 mm in precordial leads. Following are the common causes: ●

Tall peaked narrow based tented T waves occur in most of the leads, but are more prominent in precordial leads and occur in hyperkalemia (serum level of 5.7–6.5 mEq/L) (see Fig. 24.5).

496

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY ●

●

●

Tall symmetrical T waves in V1–V2 with tall R waves occur in true posterior wall myocardial infarction. Tall symmetrical T waves in precordial leads can occur in hyperacute phase of anterior wall myocardial infarction. Tall T waves occasionally occur in patients with cerebrovascular accidents.

2. Flat T Waves These are usually not diagnostic unless associated with ST depression and have the same significance as that of ST depression. 3. T Wave Inversion T wave changes may be primary or secondary which may occur alone or may be associated with ST changes (elevation or depression). ●

●

●

There is abnormality in shape and duration of action potentials in primary T wave changes, while there is an alteration of sequence of depolarization in secondary T wave changes. Abnormal sequence of repolarization can occur both in primary and secondary T inversions. The ventricular gradient (QRS-T angle) may help in differentiating primary T wave inversions from obligatory secondary T wave inversions.13

QRS-T angle (ventricular gradient):13 The QRS-T angle is calculated by determining the mean QRS axis and T axis in frontal plane. QRS-T angle mean QRS axis-mean T axis, which is normally 60. In primary T wave inversion, QRS-T angle is wide (60) as T wave axis is directed away from the site of pathology. a) T Wave Inversion with ST Changes i) Primary T wave inversions are due to alterations in the duration or morphology of ventricular action potentials without changes in the activation sequence. Common causes are as follows: ● Myocardial ischemia or infarction ● Drug effects: Digitalis effect (associated with shortening of QT interval) ● Ventricular hypertrophy ● Pulmonary embolism (V –V ). 1 3 ii) Secondary T wave inversions are due to the alteration of ventricular activation (depolarization) without changes in action potentials. Common causes are: ● Bundle branch blocks ● Wolff-Parkinson-White syndrome ● Ventricular ectopics or paced beats. T wave vector deviates opposite to that of main QRS vector in LBBB, opposite to the slow terminal QRS component in RBBB and opposite to the delta wave in pre-excitation syndromes.

ABNORMAL P, T AND U WAVES

497

b) T Wave Inversion without Significant ST Changes (Mostly Primary T Wave Inversion) i) Deep T wave inversion of 5 mm: It is characteristics of ● Ischemia or post MI (localized to precordial or limb leads) ● Cardiomyopathy (in most of the leads) ● Apical cardiomyopathy (inverted giant T waves in V –V ) 2 4 ● Cerebrovascular accidents especially in subarachnoid hemorrhage (diffuse “CVA T wave pattern” associated with prolonged QT interval) ● Post Stokes-Adams syncope ● Myocarditis ● Pericarditis ● Cocaine and alcohol abuse ● Pancreatitis and gall bladder disease ● Pheochromocytoma 14 ● Idiopathic “global T wave inversion” in women without an apparent cause. ii) Minor T wave inversion of 5 mm: It may be found in all aforementioned conditions as well as in the following: ● Mitral valve prolapse ● Hyperventilation ● Postprandial (after a meal or cold drink) ● Pneumothorax ● Normal variant.

ABNORMAL U WAVES These could be: ● ●

Large prominent U waves taller than T wave or 1.5 mm in the same lead or Inverted U waves.

1. Large Prominent U Waves These are commonly seen in (see Table 24.4): ● ● ● ● ● ●

Hypokalemia (in mid precordial leads V2–V4, see Fig. 24.6) Digitalis use Quinidine use Hypercalcemia Intracranial hemorrhage Thyrotoxicosis.

2. Inverted U Waves (in Leads I, II, V5 and V6) These are commonly observed in: ●

Severe hypertension—with systolic or diastolic overload (see Fig. 24.7).

498

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 24.4 Abnormal U waves

I

Prominent U

Inverted U

1. 2. 3. 4.

1. CAD 2. Severe hypertension

Hypokalemia Digitalis use Intracranial hemorrhage Hypercalcemia

aVR

V1

V4 U

II

aVL

V2

V5 U

III

Fig. 24.6

aVF

V3

V6

| Prominent U waves in precordial leads (V –V ) in hypokalemia. 2

3

U V1

V4

V2

V5

V3

V6

U

U

Fig. 24.7

●

| Inverted U waves in V –V 4

6

in severe hypertension.

CAD – Acute ischemia (may be the only ECG finding). – Rarely, earliest sign of acute coronary syndrome.15 – Exercise-induced transient U wave inversion has been correlated with severe stenosis of LAD coronary artery.16 – Acute anterior wall MI: It usually has less ST elevation, better collateral circulation and a larger amount of stunned but viable myocardium.17

ABNORMAL P, T AND U WAVES

499

REFERENCES 1. Fitzgerald DM, Hawthorne HR, Crosseley GH, et al. P wave morphology during atrial pacing along the atrioventricular ring. J Electrocardiol 1996;29(1):1–10. 2. Saunders JL, Calatayud JB, Schulz KJ. Evaluation of ECG criteria for P wave abnormalities. Am Heart J 1967;74(6):757–765. 3. Thomas P, DeJong D. The P wave in the ECG in the diagnosis of heart disease. Br Heart J 1954;16(3):241–254. 4. Morris JJ Jr, Estes EH Jr, Whalen RE, et al. P wave analysis in valvular heart disease. Circulation 1964;29:242–252. 5. Velury V, Spodick DH. Axial correlates of PV1 in left atrial enlargement and relation to intraatrial block. Am J Cardiol 1994;73:998–999. 6. Gooch AS, Calatayud JB, Goran PA. Left hand shift of the terminal P forces in the ECG associated with LAE. Am Heart J 1966;71:727. 7. Thurmann M, Janney JG Jr. The diagnostic importance of fibrillatory wave size. Circulation 1962;25:991–994. 8. Fowler NO, Daniels C, Scott RC, et al. The electrocardiogram in cor pulmonale with and without emphysema. Am J Cardiol 1965;16:500–506. 9. Dines DE, Parker TW. Some observations on P wave morphology in precordial lead V1 in patients with elevated LA pressure and LA enlargement. Proc Staff Meet Mayo Clin 1959;34:401. 10. Sodi-Pallares D, Bisteni A, Herrmann GR. Some views on the significance of qR and QR type complexes in the right precordial leads in absence of MI. Am Heart J 1952;43:716–734. 11. Walder LA, Spodick DH. Global T wave inversion: long term follow up. J Am Coll Cardiol 1993;21(7):1652–1656. 12. Kaplan JD, Evans GT, Foster E, et al. Evaluation of electrocardiographic criteria for right atrial enlargement by quantitative two-dimensional echocardiograph. J Am Coll Cardiol 1994;23:747. 13. Surawicz B, Knilanu TR. Biatrial enlargement: Diagnostic criteria. In: Chou’s Electrocardiogrphy in Clinical Practice. 5th ed, WB Sanders Company, Philadelphia, Pennsylvania. 2001:39. 14. Wilson FN, Macleod AG, Barker PS, et al. The determination and significance of the areas of the ventricular deflections of the electricardiogram. Am Heart J 1934;10:46–61. 15. Jaffe ND, Boden WE. Spontaneous transient, inverted U waves as initial electrocardiographic manifestations of unstable angina. Am Heart J 1995;129(5):1028–1030. 16. Chikamori T, Kitaoka H, Matsumura Y, et al. Clinical and electrocardiographic profiles producing exercise-induced U waves inversion in patients with severe narrowing of the left anterior descending coronary artery. Am J Cardiol 1997;80(5):628–632. 17. Tamura A, Watanbe T, Nagase K, et al. Significance of negative U waves in the precordial leads during anterior wall acute myocardial infarction. Am J Cardiol 1997;79(7):897–900.

■ ■ ■ CHAPTER 25

V ENTRICULAR H YPERTROPHY 1.

LEFT VENTRICULAR HYPERTROPHY (LVH) ECG Changes Systolic and Diastolic Overload of the Left Ventricle Diagnostic ECG Criteria for LVH 2. RIGHT VENTRICULAR HYPERTROPHY (RVH)

500 500 501 502 507

ECG Changes Diagnostic ECG Criteria for RVH Types of RVH Systolic and Diastolic Overload of the Right Ventricle 3. BIVENTRICULAR HYPERTROPHY (BiVH) REFERENCES

508 510 511 512 513 514

1. LEFT VENTRICULAR HYPERTROPHY (LVH) ECG Changes LVH produces the following ECG changes: (i) Changes in QRS complex (ii) Changes in ST segment and T waves (iii) Changes in axis in frontal plane, and (iv) Other changes (i) Changes in QRS Complex ●

● ●

●

●

Increased amplitude of R waves in leads facing the hypertrophied LV (I, aVL, V5 and V6) and deeper S waves in leads overlying RV (V1 and V2). High QRS voltages and prolongation of QRS duration may be due to the increase in LV mass and the delay in conduction system.1 Besides transmission factors may also contribute i.e. lateral free wall lies closer to the chest wall due to LVH which causes increase in body surface potentials in accordance with the inverse square law. LVH may then be defined when LV mass index is 118 g/m2 in men and 104 g/m2 in women. There may be widening of QRS complex with an increase in QRS duration of 0.11 s. Notching of QRS complex may also be observed due to the fractionation of activation wave fronts as a result of ventricular hypertrophy. Deep (0.2 mV or 2 mm) and narrow (25 milliseconds) Q waves in leads facing the left side of the septum (V4–V6) in LV diastolic overload. An increase in VAT of 0.05 s in V5–V6. The VAT is usually prolonged with LV systolic overload than with LV diastolic overload.

VENTRICULAR HYPERTROPHY

Fig. 25.1

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

with tall R waves, ST segment depression and T waves inversion in V | LVH waves in V and V .

5

1

501

and V6, deeper S

2

(ii) Changes in ST Segment and T Waves ●

●

●

ST segment depression and asymmetrical inverted T waves in leads with tall R waves in LV systolic overload (see Fig. 25.1). Minimal ST segment elevation (usually 1 mm) with concavity upwards with tall symmetrical T waves and tall R waves in leads V5–V6 in LV diastolic overload with or without initial deep narrow Q waves. These repolarization changes reflect primary defect of repolarization that accompanies the cellular process of ventricular hypertrophy.

(iii) Changes in Axis in Frontal Plane ● ●

LAD may be present but usually it is  30. QRS-T angle is widened (60) especially in LV systolic overload.

(iv) Other Changes ●

●

Inverted U waves in left precordial leads, which is more common in LV diastolic overload2 (see Fig. 25.2). Presence of left atrial abnormality or LAE.

Systolic and Diastolic Overload of the Left Ventricle The concept of systolic and diastolic overload of the ventricle was introduced by Cabrera and Monroy in 1952.3 ●

●

●

The ECG pattern of systolic overload includes high voltage of R wave and secondary ST and T wave changes in precordial leads, which usually occurs in aortic stenosis, coarctation of aorta and systemic hypertension. (see Fig. 25.3) The ECG pattern of diastolic overload includes high voltage of R wave with prominent Q waves in precordial leads and ST segment is usually elevated (concavity upwards) with an upright peaked T wave, which usually occurs in AR, MR and PDA. (see Fig. 25.4) However, the clinical application of this concept is better correlated in young patients especially with congenital heart disease than in patients with advanced acquired heart disease.

502

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY I

II

III

aVR

aVL

aVP

V1

V2

V3

V4

V5

V6

U

U

U

X 1/2

Fig. 25.2

U

X 1/2

X 1/2

(voltage criteria and ST–T changes) with inverted U waves in precordial leads in severe | LVH hypertension.

I

II

III

aVR

aVL

aVF

T

T T V1

Fig. 25.3

V2

V3

V4

V5

V6

| Systolic overload of LV—LVH with ST depression (arrow) and T inversion in precordial leads. Diagnostic ECG Criteria for LVH Based on the ECG changes, several diagnostic criteria for LVH have been developed. However, echocardiography is taken as gold standard for diagnosis of ventricular hypertrophy as several necropsy studies have demonstrated the superiority of echocardiography over ECG to detect LVH4 (see Fig. 25.5A and 25.5B). Besides echocardiography is also a better noninvasive method for serial follow-up of changes during progression or regression of LVH.

VENTRICULAR HYPERTROPHY

II

I

III

aVR

aVL

503

aVF

T

T q

q V1

Fig. 25.4

V2

V3

V4

V5

| Diastolic overload of LV—LVH with prominent Q and upright T in V

V6 5

and V6.

LV RV

LVH RA

LA

|

Fig. 25.5A Apical 4 chamber echocardiographic view— Echocardiagraphy is superior to ECG for detecting left ventricular hypertrophy (LVH)—RV: right ventricle, LV: left ventricle, RA: right atrium, LA: left atrium.

Fig. 25.5B

representation of | Diagrammtic LVH.

(i) Sokolow-Lyon Voltage Criteria5 ● ● ●

S in V1  R in V5 or V6 35 mm (3.5 mV): sensitivity 55.6%, specificity 89.5% R in I  S in III 25 mm (2.5 mV): sensitivity 10.6%, specificity 100% R in aVL 11 mm (1.1 mV): sensitivity 10.6%, specificity 100%

504

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY ● ●

R in V5 or V6 26 mm (2.6 mV): sensitivity 25%, specificity 98% Largest R  largest S in precordial leads  45 mm is more sensitive with less specificity as compared to S in V1  R in V5 or V6.6

The voltage criteria may overdiagnose LVH in young adults (under 40 years),7 thinly built and obese individuals.8 Sokolow-Lyon grading system: Depending upon the associated repolarization changes, it is classified into four grades. The diagnostic sensitivity and specificity increase with higher grades: ● ●

● ●

Grade I: only have voltage criteria (as above) Grade II: voltage criteria  low amplitude T waves (10% of R wave in the same lead) Grade III: voltage criteria  biphasic T waves Grade IV: voltage criteria  inverted T waves

(ii) Romhilt-Estes Point Score System9 ●

●

●

● ● ●

Any of the following increased amplitude or depth criteria: 3 points – R or S waves in limb leads 20 mm (2.0 mV) – S wave in V1 or V2 30 mm (3.0 mV) – R wave in V5 or V6 30 mm (3.0 mV) ST–T segment changes (typical LV strain pattern) – Without digitalis therapy: 3 points – With digitalis therapy: 1 point LAE: 3 points – P terminal force in V1 of 4 mV-msec (1 mm depth with a duration of 0.04 s) LAD:  30: 2 points QRS duration of 0.09 s: 1 point Intrinsicoid deflection (VAT) in V5 or V6 0.05 s: 1 point

5 points are diagnostic of LVH, while 4 points suggest probable LVH. Sensitivity is 54% and specificity is 97%. (iii) Glassglow Scoring System It is modified Romhilt-Estes point score system which is as follows: ● ● ● ● ● ●

Any of the increased amplitude (R) or depth (S) criteria: 2 points ST–T segment changes: 1–4 points LAE: P terminal force of 4 mV-msec: 2 points LAD: 2 points QRS duration of 0.09 s: 1 point Intinisicoid deflection of 0.05 s: 1 point.

Definite diagnostic of LVH: 6 points, probable LVH: 5 points and possibility of LVH: 4 points.

VENTRICULAR HYPERTROPHY

505

(iv) Cornell Voltage Criteria10 R in aVL  S in V3  28 mm (2.8 mV) in men and 20 mm (2.0 mV) in women. Sensitivity is 36% and specificity is 95%. (v) Cornell Product (voltage–duration measurement)11 ● ●

Cornell voltage  QRS duration 2,436 Sum of voltages in all 12 leads  QRS duration 17,472

Sensitivity is 51% and specificity is 95%. (vi) Cornell Regression Equation10 To further increase the sensitivity, regression equation is devised which is as follows: 1/(1  e exp) where exp 4.558 0.093 (R in aVLS in V3) 0.306 T in V1 0.211 QRS duration 0.278 P terminal force in V1 0.859 (sex) where R, S, and T in mV; QRS duration in msec; P terminal force in mm-sec and sex 1 for men, 2 for women. LVH is present if exp is less than 1.55. (vii) Novacode Criteria12 ●

●

LV mass index (LVMI) can be calculated with the equation of the Novacode criteria which also enhances its sensitivity in the diagnosis of LVH. LVMI (g/m2) 36.4  0.010 R in V5  0.20 S in V1  0.28 S* in III  0.182 T(neg) in V6 0.148 T(pos) in aVR  1.049 QRS duration

where S*: amplitude of S, Q, or QS whichever is larger, neg and pos: amplitudes of negative and positive portions of T waves respectively. (viii) Seigel’s Total QRS Voltage Criteria ● ●

Sum of QRS voltages in all 12 leads 179 mm QRS voltage–duration product: voltage criteria  QRS duration 17,472.

(ix) The Hernandez Padial Voltage Criterion12 ● ●

Sum of QRS voltages in all 12 leads 120 mm It has high specificity and sensitivity for the diagnosis of LVH in systemic hypertension.

(x) Natural History Series-2 (1993)13 QRS duration 120 ms  1 of the following ● ●

R or S in the limb leads 20 mm S in V1 30 mm or R in V6 30 mm.

506

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 25.1 ECG diagnostic criteria of LVH Criteria

Sensitivity (%)

Specificity (%)

1. 2. 3. 4. 5. 6.

10.6–55.6 54 36 51 50 Low sensitivity

90–100 97 95 95 100 90

Sokolow-Lyon voltage criteria Romhilt-Estes point score system Cornell voltage criteria Cornell product Koito and Spodick criterion Talbot criterion

S V1R V5 35 mm R L1S L3 25 mm R aVL 11 mm R V5 or R V6 26 mm

1. R aVLS V3 28 mm in men 20 mm in women 2. Voltage  QRS  2,436

QRS 102 ms  1 of 1. R or S in limb lead 20 mm 2. S V1 or R V6  30 mm Natural history series-2

Cornell

Total QRS 120 mm

Sokolow-Lyon HernandezPadial R aVL 16 mm

Talbot

LVH criteria Seigel’s

Romhilt-Estes: 5p

1. ↑ amplitude or depth criteria: 3p 2. ST-T changes: 3 or 1p (with digitalis) 3. LAE: 3p 4. LAD: 2p 5. QRS  0.09 s: 1p 6. VAT: 1p

Fig. 25.6

Glassglow: 6p

Kaito and Spodick

1. ↑ amplitude or depth criteria: 2p 2. ST-T changes: 1–4p 3. LAE: 2p 4. LAD: 2p 5. QRS 0.09 s: 1p 6. VAT: 1p

R V6  R V5

Total QRS 179 mm

of the various diagnostic ECG criteria for left ventricular hypertrophy (LVH)—LAE: | Summary left atrial enlargement, LAD: left axis deviation, VAT: ventricular activation time, p: point.

(xi) The Talbot Criterion14 R in aVL 16 mm. It has high specificity (90%) even in the presence of myocardial infarction and ventricular block but has low sensitivity. (xii) The Koito and Spodick Criterion15 R in V6 R in V5. This criterion claims 100% specificity with a sensitivity of 50% (see Table 25.1 and Fig. 25.6). (xiii) Diagnosis of LVH in Left Bundle Branch Block (LBBB) The diagnosis of LVH in the presence of LBBB is difficult because LBBB can alter the amplitude of QRS complex in either direction.

VENTRICULAR HYPERTROPHY

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 25.7

| LVH with complete LBBB with S in V  R in V 2

6

507

is 45 mm.

(i) Kafka et al. criteria based on echocardiogram:16 ● R in aVL 11 mm (sensitivity: 24%, specificity: 100%) ● S in V  R in V or V 40 mm (sensitivity: 58%, specificity: 97%) 1 5 6 ● S in V 30 mm and S in V 25 mm (sensitivity: 75%, specificity: 90%) 2 3 ● Frontal QRS axis 40 (or S  R ) (sensitivity: 39%, specificity: 100%) 2 1 (ii) Klein et al. criteria also based on echocardiogram:17 ● S wave amplitude in V  R wave amplitude in V 4.5 mV (sensitivity: 86%, 2 6 specificity: 100%) (see Fig. 25.7) ● Presence of LAE and QRS duration of 160 ms supports the diagnosis. (xiv) Diagnosis of LVH in the Presence of Left Anterior Fascicular Block (LAFB) ●

● ●

LAFB can cause a false positive diagnosis of LVH based on voltage criteria without associated secondary ST-T changes. R in aVL 13 mm (sensitivity: 35%, specificity: 92%). S in II  maximum sum of R  S in any single precordial lead 3.0 mV (sensitivity: 96%, specificity: 87%).18

(xv) Diagnosis of LVH in Presence of Right Bundle Branch Block (RBBB) ●

●

Usual criteria for LVH has to be applied even though the presence of RBBB lowers the sensitivity and increases the specificity of the voltage criteria for the diagnosis of LVH. The combination of LAE or LAD with RBBB also suggests underlying LVH19 (see Fig. 25.8).

2. RIGHT VENTRICULAR HYPERTROPHY (RVH) The hypertrophy of the RV may occur in one or more of the regions of the RV: ●

The free wall of the RV

508

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Kafka: 1. R aVL 11 mm 2. S V1  R V5 or V6 40 mm 3. S V2 30 mm and S V3 25 mm 4. S L2 R L1 or axis 40°

LBBB

Klein: 1. S V2  R V6 45 mm 2. LAE and QRS 160 ms

Fig. 25.8

1. Usual criteria 2. LAE or LAD with RBBB LVH in presence of Left anterior fascicular block

RBBB

R aVL 13 mm SL2Sum of R and S in a precordial lead 30 mm

of the diagnostic ECG criteria of left ventricular hypertrophy (LVH) | Summary in presence of other conditions—LAE: left atrial enlargement, LAD: left axis deviation, LBBB: left bundle branch block, RBBB: right bundle branch block.

● ●

The right paraseptal portion The basal portion especially the right ventricular outflow tract.

ECG Changes The ECG changes in RVH are mainly due to increased mass (hypertrophied cell) and prolongation of the electrical action time of the RV. The ECG changes could be due to systolic (pressure) or diastolic (volume) overloads. Following are the ECG changes that occur in RVH: (i) (ii) (iii) (iv)

Changes in QRS complex Changes in ST segment and T wave Changes in frontal QRS axis and Other changes.

(i) Changes in QRS Complex ●

●

●

There is a progressive increase in the amplitude of R or R waves and progressive diminution of S waves in right oriented leads (V1 and V2) which is expressed as an R:S or R:S ratio of 1 with R or R waves 5 mm in amplitude. These changes indicate RV systolic overload and are often due to hypertrophy of RV free wall or combination of RV free wall and right paraseptal portion. Presence of small q in V1 resulting in qR pattern due to anatomical shift of the hypertrophied RV by an enlarged and dilated RA.20 Partial or complete RBBB pattern (rSr or rsR) in V1 due to RV diastolic overload as in ASD.

VENTRICULAR HYPERTROPHY ●

● ●

●

●

509

Deep S waves and abnormally small r waves in left oriented leads (I, aVL, V5–V6) with an r:S or R:S ratio of 1 in V5 or V6. VAT in V1 is  0.03 s. Evidence of RVH in COPD include: – Deep S waves in lateral precordial leads, – S1Q3T3 pattern, i.e. deep S in lead I (RS or rS), abnormal Q in lead III and inverted T wave in inferior leads including lead III and – RAD Evidence of RVH in pulmonary embolism which causes acute RV pressure overload, includes qR in V1 or V2, S1Q3T3 pattern (occurs in only 10%), ST segment and T changes in V1–V3, incomplete or complete RBBB and sinus tachycardia. Dominant hypertrophy of right basal portions of RV is uncommon and is characterized by deep S in V5–V6, tall R or qR in aVR, S1S2S3 syndrome (deep S waves in Leads I, II, III) and RAD.

(ii) Changes in ST Segment and T Waves Minimal ST segment depression with T wave inversion in right oriented leads (V1–V3) especially in the presence of RV pressure overload. (iii) Frontal QRS Axis There is a dominant RAD and widened QRS-T angle. (iv) Other Changes ●

●

Amplitude of U wave may be diminished or it may be inverted in right precordial and/or inferior leads in both RV systolic and diastolic overloads. Associated RAE (see Fig. 25.9) or RA abnormality is common.

I

II

III

Fig. 25.9

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

| RVH and RAE with peaked P, tall R, and inverted T waves in V and V . 1

2

510

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Diagnostic ECG Criteria for RVH (i) Natural History Series (1993)13 QRS complex duration 120 ms  1 of the following ● ● ●

R in V1 7 mm Frontal QRS axis: RAD of 110 rSR in V1 where R is 10 mm (in 1 year of age) or 15 mm (in 1 year of age)

(ii) Milnor Modified Sokolow and Lyon Criteria21 ● ●

QRS duration 0.12 s and frontal QRS axis of 110 to 180 R/S or R/S ratio in V11 with R or R amplitude 0.5 mV

(iii) Butler-Legger Criteria22 The sensitivity of this criteria varies from 66% to 79% with 97% in pulmonary arterial disease. ● ● ●

P wave amplitude of 0.25 mV in any of the leads: II, III, aVF, V1 or V2 R wave amplitude in lead I 0.2 mV A  R PL 0.7 mV, where A (Anteriorly directed deflection): Derived from R wave amplitude in lead V1 or V2. R (Rightward deflection): Derived from S amplitude in lead I or V6. PL (Posterolateral deflection): Derived from S amplitude in lead V1.

(iv) Other Criteria (a) QRS changes: ●

● ● ●

qR (has 10% sensitivity but highly specific23) or rsR (with R 10 mm) pattern in V1 R in V1 7 mm (0.7 mV) has sensitivity of 10%24 R/S in V1 1 with R 5 mm (0.5 mV) has sensitivity: 25% and specificity: 89%24 S in V5 or V6 7 mm (0.7 mV) has sensitivity: 17% and specificity: 93%24

(b) Frontal QRS axis: ●

RAD has sensitivity: 14% and specificity: 99%24

(c) S1Q3T3 pattern has sensitivity: 11% and specificity: 93%24 (d) S1S2S3 pattern has sensitivity of 10%24 (see Fig. 25.10 and Table 25.2) (e) Diagnosis of RVH in the presence of RBBB: Even though the mere presence of RBBB is suggestive of RVH, the presence of RBBB lowers the specificity and sensitivity of criteria for the diagnosis of RVH. ●

Barker and Valencia criteria: RVH is suggested with a specificity of 60% by the presence of R of 1.5 mV in V1 in complete RBBB and 1.0 mV in incomplete RBBB.25

VENTRICULAR HYPERTROPHY

QRS 120 ms1 of 1. R V1 7 mm 2. RAD 110° 3. rSR in V1 R 10 mm(1 year of age) 15 mm(1 year of age)

1. QRS 120 ms, axis: 110 to 180 2. R/S or R/S in V1 1 – R or R 5 mm

511

1. P 0.25 mV in L2, L3, aVF, V1 or V2 2. RL1 0.2 mV 3. RV1 or V2SL1 or V6 SV1 0.7 mV

Milnor modified Sokolow-Lyon

Natural history series

RVH criteria

1. S V5 or V6 7 mm 2. S1Q3T3 3. S1S2S3

Others

Fig. 25.10

Butler-Legger

of the various diagnostic ECG criteria of right ventricular hyper| Summary trophy (RVH)—RAD: right axis deviation.

Table 25.2 ECG criteria of RVH

●

●

Criteria

Sensitivity (%)

Specificity (%)

1. 2. 3. 4.

10 14 11 10

89–93 99 93

QRS changes Frontal QRS axis (RAD) S1Q3T3 pattern S1S2S3 pattern

Milnor criteria: Frontal QRS axis of 110 to 270 or R/S or R/S ratio in V1 1, provided R or R amplitude in V1 is 0.5 mV, with a specificity of 60%.21 However, the likelihood of RVH is increased if both RAD and R of 1.5 mV in V1 are present.

(f) Diagnosis of RVH in the presence of LBBB: It is difficult to diagnose RVH in presence of LBBB. However, it can be suspected when RAD is present in LBBB. Types of RVH RVH has been described in three types: ●

●

Type A RVH: Typical RVH pattern with tall R wave, small S wave, increased R/S ratio in V1, which is typically present in pulmonary hypertension, congenital PS, TOF. Type B RVH: Incomplete RBBB pattern, i.e. rSR pattern, characteristic of volume overload conditions, such as ASD, TR, PAPVC.

512

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

aVR

aVL

V4

V5

R

q

Fig. 25.11

Fig. 25.12

| Systolic overload of RV (qR pattern in V ). 1

I

II

III

V1

V2

V3

aVF

V6

| Diastolic overload of RV (rSR pattern in V ). 1

●

Type C RVH: Deep S wave, small r wave, and R/S ratio 1 in leads V5 or V6, typically present in patients with chronic lung disease.

Systolic and Diastolic Overload of the Right Ventricle The concept of systolic and diastolic overload of the ventricle was introduced by Cabrera and Monroy in 1952.3 ●

●

●

The ECG pattern of systolic (pressure) overload includes tall monophasic R wave or diphasic RS, Rs, or qR complex in lead V1 with T wave usually inverted, which typically occurs in PS, PH or TOF. (see Fig. 25.11) The ECG pattern of diastolic (volume) overload includes rSR pattern in V1, which is characteristic of ASD, PAPVC and TR. (see Figs 25.12 and 25.13) However, the hemodynamic correlation of the ECG overload pattern is more satisfactory in congenital than acquired heart diseases.

VENTRICULAR HYPERTROPHY AS, COA, systemic HTN

AR, MR, PDA

LVH (voltage criteria) with tall R and ST↓ and T↓ in precordial leads

Tall R, RS, Rs, or qR with T↓ in V1

Fig. 25.13

513

LVH (voltage criteria)— Tall R, prominent Q, T↑, ST↑ (slight) in precordial leads LV systolic overload

LV diastolic overload

RV systolic overload

RV diastolic overload

PS, PH, TOF

rSR in V1

ASD, PAPVC, TR

and diastolic overloads of left and right ventricles—LVH: left ventricular hypertrophy, | Systolic LV: left ventricular, RV: right ventricular, AS: aortic stenosis, AR: aortic regurgitation, MR: mitral regurgitation, COA: coarctation of aorta, HTN: hypertension, PDA: patent ductus arteriosus, PS: pulmonary stenosis, PH: pulmonary hypertension, TOF: tetralogy of Fallot, ASD: atrial septal defect, PAPVC: partial anomalous pulmonary venous connection, TR: tricuspid regurgitation, : upright or elevation, : inverted or depression.

3. BIVENTRICULAR HYPERTROPHY (BiVH) Hypertrophy of one ventricle may result in an apparent diminution of electrical activity of the other ventricle and hence there are no specific ECG diagnostic criteria for BiVH. i) Features of LVH with one of the following: ● ● ● ●

●

●

RAD (greater than 90) in presence LVH criteria (especially in precordial leads).26 Tall R waves in both right and left precordial leads especially when R/S in V1 is 1.23 Deep S waves in left precordial leads in the presence of LVH criteria. Large equiphasic QRS complexes (tall R and deep S) in mid precordial leads (V3–V4) which is known as Katz-Wachtel pattern or phenomenon, which is commonly present in congential heart diseases such as VSD or PDA with PH.27 R  S V3 or V4 should be 60 mm in children and 50 mm in others (see Fig. 25.14). R wave greater than Q wave in lead aVR, and S wave R wave in lead V5, with T wave inversion in lead V1 in conjunction with signs of LVH.28 Small s wave in V1 with criteria for RVH or LVH which is known as shallow s syndrome. ii) Left atrial abnormality (LAE) with one of the following:24

● ● ●

R/S in V5 or V6 is 1 S wave in V5 or V6 7 mm (0.7 mV) RAD of greater than 90

514

Fig. 25.14

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

I

II

III

V1

V2

V3

aVR

aVL

aVF

V3

V5

V6

Biventricular hypertrophy with equiphasic QRS complexes in V –V , tall R waves in V | deep S waves in V . 3

4

1

and

5

All the above criteria suggested for BiVH have low sensitivity with moderate specificity. Jain et al found that 25% had ECG findings compatible with BiVH, 36% had an LVH pattern and 20% had an RVH pattern in 69 patients of BiVH identified by echocardiography with sensitivity of 24.6% and specificity of 86.4%.29

REFERENCES 1. Xiao HB, Brecker SJ, Gibson DG. Relative effects of left ventricular mass and conduction disturbance on activation in patients with pathological left ventricular hypertrophy. Br Heart J 1994;71:548–553. 2. Kishida H, Cole JS, Surawicz B. U wave: a highly specific but poorly understood sign of heart disease. Am J Cardiol 1982;49(8):2030–2036. 3. Cabrera CE, Monroy JR. Systolic and diastolic loading of the heart. II Electrocardiographic data. Am Heart J 1952;43(5):669–686. 4. Surawicz B. Electrocardiographic diagnosis of chamber enlargement. J Am Coll Cardiol 1986;8(3): 711–724. 5. Sokolow M, Lyon TP. The ventricular complex in LVH as obtained by unipolar precordial and limb leads. Am Heart J 1949;37:161–186. 6. Romhilt DW, Bove KE, Norris RJ et al. A critical appraisal of the electrocardiographic criteria of left ventricular hypertrophy. Circulation 1969;40(2):185–195. 7. Manning GW, Smiley JR. QRS-voltage criteria for LVH in a normal male population. Circulation 1964;29:224–230. 8. Kitty SE, Lepeschkin E. Effect of body build on the QRS voltage of the electrocardiogram in normal men: its significance in the diagnosis of left ventricular hypertrophy. Circulation 1965;31:77. 9. Romhilt D, Estes EH Jr. A point score system for the ECG diagnosis of left ventricular hypertrophy. Am Heart J 1968;75(6):752–758. 10. Casale PN, Devereux RB, Kligfield P, et al. Electrocardiographic detection of left ventricular hypertrophy: Development and prospective validation of improved criteria. J Am Coll Cardiol 1985;6(3): 572–580.

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11. Molloy TJ, Okin PM, Devereux RB, et al. Electrocardiographic detection of left ventricular hypertrophy by the simple QRS voltage-duration product. J Am Coll Cardiol 1992;20(5):1180–1186. 12. Rodriguez Padial L. Usefulness of total 12-lead QRS voltage for determining the presence of left ventricular hypertrophy in systemic hypertension. Am J Cardiol 1991;68(2):261–262. 13. Micheal O’Fallon, Cynthia S Crowson, Linda J Rings, et al. Report from the second joint study on the natural history of congenital heart defects (NHS-2). Circulation 1993;87:4–15. 14. Talbot S, Kilpatrick D. Diagnostic criteria for left ventricular hypertrophy. In McFarlane PW, ed. Progress in Electrocardiology. London: Pittman Medical, 1979:534–541. 15. Koito H, Spodick D. Electrocardiographic RV6/RV1 voltage ratio for diagnosis of left ventricular hypertrophy. Am J Cardiol 1989;63:352–361. 16. Kafka H, Burggraf GW, Milliken JA. Electrocardiographic diagnosis of left ventricular hypertrophy in presence of left bundle branch block: An echocardiographic study. Am J Cardiol 1985;55(1): 103–106. 17. Levy D, Labib SB, Anderson KM, et al. Determination of sensitivity and specificity of electrocardiographic criteria for left ventricular hypertrophy. Circulation 1990;81:815. 18. Gertsch M, Theler A, Foglia E. Electrocardiographic detection of left ventricular hypertrophy in presence of left anterior fascicular block. Am J Cardiol 1988;61(13):1089–1101. 19. De Leonardis V, Golstein SA, Lindsay J Jr. Electrocardiographic diagnosis of right ventricular hypertrophy in presence of complete left bundle branch block. Am J Cardiol 1988;62:590–593. 20. Sodi-Pallares D, Bisteni A, Hermann GR. Some views as the significance of qR and QR type complexes in right precordial leads in absence of myocardial infarction. Am Heart J 1952;43(5): 716–734. 21. Milnor WR. Electrocardiogram and vectorcardiogram in right ventricular hypertrophy and right bundle branch block. Circulation 1957;16(3):348–367. 22. Behar JV, Howe CM, Wagner NB, et al. Performance of new criteria for RVH and MI in patients with pulmonary hypertension due to cor pulmonale and mitral stenosis. J Electrocardiol 1991;24:231. 23. Loperfido F, Digaetano A, Santarelli P, et al. The evaluation of left and right ventricular hypertrophy in combined ventricular over load by electrocardiography: relationship with echocardiography data. J Electrocardiol 1982;15(4):327–334. 24. Murphy MI, Thenabadu PN, de Soyza N, et al. Reevaluation of electrocardiographic criteria for left, right and combined cardiac ventricular hypertrophy. Am J Cardiol 1984;53(8):1140–1147. 25. Barker JM, Valencia F. The precordial electrocardiogram in incomplete RBBB. Am Heart J 1949; 38:376. 26. Soulie P, Laham JP, Papanicolis I, et al. Les principaux types electrocardiographiques de surcharge ventriculaire combinee. Arch Mal Coeur 1949;42:791. 27. Katz LN, Watchtel H. The diphasic QRS type of electrocardiogram in congenital heart disease. Am Heart J 1937;13:202. 28. Pagnoni A, Goodwin JF. The cardiographic diagnosis of combined ventricular hypertrophy. Br Heart J 1952;14(4):451–461. 29. Jain A, Chandna H, Siber EN et al. Electrocardiographic patterns of patients with echocardiographically determined biventricular hypertrophy. J Electrocardiol 1999;32(3):269–273.

■ ■ ■ CHAPTER 26

I NTRAVENTRICULAR CONDUCTION D EFECTS 1.

RIGHT BUNDLE BRANCH BLOCK (RBBB) 516 WHO/International Society and Federation for Cardiology (ISFC) Task Force Criteria for RBBB (1985) 517 Variants RBBB 518 2. LEFT BUNDLE BRANCH BLOCK 520 WHO/International Society and Federation for Cardiology (ISFC) Task Force Criteria 522

WHO/ISFC Task Force Criteria 3. FASCICULAR BLOCKS Left Anterior (Hemiblock) Fascicular Block Left Posterior (Hemiblock) Fascicular Block Multifascicular Blocks REFERENCES

523 523 524 526 527 531

An intraventricular conduction defect occurs as a result of an abnormality of conduction through one or more of the divisions of the intraventricular conduction system (RBB, LBB, left fascicular branches) distal to the bundle of His.

1. RIGHT BUNDLE BRANCH BLOCK (RBBB) Following are the ECG changes: ● ●

QRS duration 120 ms (0.12 s). Broad notched R waves (rsr, rsR, or rSR patterns) in right precordial leads (V1, V2, V3R). The wide R is 0.04 s. Sometimes, s is very small or even absent resulting in an rR complex (see Table 26.1). The spread of excitation from the SA node down to the AV node and through the bundle of His occurs normally. Also, the septal activation occurs normally from left to right producing a small initial r wave. As the RBB is blocked, the excitation next spreads down the LBB and LV myocardium producing an S or s wave. The impulses then pass around the blocked RBB into the RV myocardium (after the activation of LV has been completed) producing a wide R wave (0.4 s), resulting in a typical pattern of rsR, rSR, or rsr in right precordial leads. In addition, as the LV activation remains relatively intact, the initial portions of the QRS complex are normal, while delayed activation of the RV causes prolongation of QRS duration.

INTRAVENTRICULAR CONDUCTION DEFECTS

517

Table 26.1 ECG criteria for intraventricular conduction defects Right bundle branch block

Left bundle branch block

1. QRS duration 120 ms 2. Broad notched R waves  rsr, rsR, or rSR in V1, V2, V3, R and wide R 0.04 s 3. Wide and deep S 40 ms or longer than R in V6 and I

1. QRS duration 120 ms 2. Broad notched R waves or rsR in V5, V6, I, aVL

4. VAT in V1 50 ms, but normal in V5, V6 5. Mean QRS axis is not altered 6. Minimum secondary ST–T changes in V1, V2

●

●

●

3. q waves absent in left sided leads except aVL Small initial r (may be absent) and deep S waves in right precordial leads 4. VAT in V5, V6 0.06 s, but normal in V1, V2 5. Mean QRS axis is not altered. 6. Secondary ST–T changes in V5, V6, I, aVL

Wide and deep S waves in left precordial leads (V5 and V6), I, and aVL. As the septal and LV activation are normal, the normal initial small q followed by R waves in left oriented leads will occur. The wide and deep S waves in left oriented leads are due to delayed activation of the RV. There may be minimal depression of ST segment and secondary T wave inversion in right precordial leads as a result of abnormalities in conduction. T wave is usually opposite to the terminal deflection of the QRS complex, hence it is upright in Leads I, V5 and V6, and inverted in right precordial leads. In transitional precordial leads (V3 or V4), the T wave may be diphasic. The mean QRS axis in frontal plane is not altered by RBBB, and axis shifts occur when associated with fascicular blocks.

WHO/International Society and Federation for Cardiology (ISFC) Task Force Criteria for RBBB (1985) It includes:1 ● ●

● ●

QRS duration 120 ms. An rsr, rsR, or rSR pattern in Lead V1 or V2 (see Fig. 26.1) and occasionally a wide notched R wave. Wide S wave 40 ms or more than duration of R wave in leads I and V6. Normal R peak time in Leads V5 and V6, but 50 ms in V1.

There is a good correlation between the ECG findings of RBBB and the histopathological changes of the bundle branch.2 Many subjects with RBBB have no evidence of underlying heart disease, the incidence increasing with age, the incidence being 1.3/1,000 below 30 years of age, and the incidence being 2.0–2.9/1,000 between 30–44 years of age.3 The long and slender structure of the bundle makes it vulnerable to the processes associated with aging. RVH alone can cause an RBBB pattern (complete or incomplete) due to slow conduction in the hypertrophied or dilated RV.4 Besides, there is an increased incidence of RBBB among the populations at high altitude.4

518

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Fig. 26.1

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

| RBBB—rsR in V and V 1

2

with wide S in V5 and V6.

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 26.2

| Incomplete RBBB—rsR in V and QRS duration is 120 ms. 1

Variants RBBB a) Incomplete RBBB The conduction through right bundle branch and its ramification is still possible, but is delayed. ● ●

●

Duration of QRS complex is 120 ms (0.12 s) (see Fig. 26.2). With progressive delay in the conduction of RBB due to progressively increasing incomplete RBBB, there is a progressive diminution of s waves5 followed by slurring of the upstroke of the small s waves in V1, which may be only early sign of incomplete RBBB.6 Hence, a serial tracing become necessary. With progressively increasing block, the activation of the free wall of the RV occurs after the activation of the free wall of the LV producing a small r in V1 and V2, producing rsr or rSr pattern. As the delay increases, r becomes increasingly taller (producing rsR pattern) as a larger part of free wall of RV activation will occur after free wall of LV activation. However, R is not widened beyond 0.04 s. In complete RBBB, R is widened 0.04 s as conduction occurs through myocardium.

INTRAVENTRICULAR CONDUCTION DEFECTS

519

The WHO/ISFC task force criteria for incomplete RBBB are the same as for complete RBBB, except the QRS duration is 120 ms.1 Even though incomplete RBBB often occurs in normal subjects, the likelihood of an abnormality increases with increased QRS duration. Following criteria suggest no abnormality in the presence of incomplete RBBB7: ● ● ●

Amplitude of initial R 0.8 mV. Amplitude of r 0.6 mV. R/S ratio of 1.0.

The likelihood of developing a complete RBBB in 11 yrs follow up of male subjects with incomplete RBBB was 5.1% as compared to 0.7% of subjects without incomplete RBBB pattern; even though there was no demonstrable increase in cardiac deaths in a follow up of 20 years.8 Besides normal subjects, the pathological incomplete RBBB can also be present in the following conditions: ●

●

●

●

●

●

During atrial fibrillation, atrial flutter, supraventricular tachycardia (SVT) or atrial premature contractions (APC); incomplete (sometimes complete) RBBB is the most common pattern of aberrant intraventricular conduction as the RBB has the longest action potential and the longest refractory period. It can occur in massive pulmonary embolism or other forms of acute corpulmonale due to acute RV distension and conduction delay in the stretched myocardium or in the peripheral conducting system. It can occur in RVH (of any cause: corpulmonale, MS, congenital heart disease) due to slow conduction in the hypertrophied or dilated RV. Commonly occurs in ASD, Ebstein’s anomaly, arrhythmogenic RV dysplasia due to conduction delay in the myocardium or in the peripheral conducting system. Complete or incomplete RBBB frequently appears after CABG, heart transplantation and during right ventriculotomy. An rSr pattern is often present in patients with pectus excavatum and straight back syndrome, due to change in the position of the heart as a result of decrease in anteroposterior diameter of the chest.9,10

b) Brugada Syndrome It is a special form of incomplete or complete RBBB with persistent ST segment elevation in right precordial leads (V1 and V2) (see Fig. 26.3). It is a characteristic of young adults of Asian origin and the commonest cause of idiopathic ventricular fibrillation and sudden death.11 c) Arrhythmogenic Right Ventricular Dysplasia It is a type of RV cardiomyopathy involving inflow, outflow and apex of the RV, characterized by sudden death in young individuals. ECG characteristics are: ●

●

Incomplete or complete RBBB with epsilon wave (terminal notch in QRS) in V1 and V2 as a result of slowed intraventricular conduction (see Fig. 26.4). T waves inversion in V1–V3 (see Fig. 26.5).

520

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Fig. 26.3

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

| Brugada syndrome—RBBB pattern with ST elevation in V and V . 1

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 26.4

2

right ventricular dysplasia—epsilon wave (arrow head point| Arrhythmogenic ing to the notch) with T wave inversion in V and V . 1

2

2. LEFT BUNDLE BRANCH BLOCK Following are the ECG changes: ●

●

●

●

QRS duration 120 ms (0.12 s) due to delayed and anomalous activation of left septal mass and free wall of LV. Absent septal q waves in left oriented leads (V5, V6, I and aVL), instead a small initial r waves may be present due to septal activation in reverse fashion. Broad notched R waves or rsR (M-shaped QRS complex) in lateral precordial leads (V5, V6), I and aVL. Small initial r waves (may be absent) and deep wide S waves in right precordial leads (V1, V2) (see Table 26.1 and Fig. 26.6). The activation from SA node to AV node and bundle of His occurs in a normal fashion. Due to block in the LBB, the impulse cannot enter the left bundle system but enters the RBB and activates the septum from right to left in reverse fashion producing a small initial r wave (instead of the usual q waves) in left oriented leads and a

INTRAVENTRICULAR CONDUCTION DEFECTS

WHO/ISFC: 1. QRS 120 ms 2. rsr, rsR, or rSR in V1 3. Wide S 40 ms in I and V6 or S  R in I and V6 4. VAT in V1  50 ms

Fig. 26.5

521

RBBB complete or incomplete with ST ↑ in V1 and V2

Brugada syndrome

WHO/ISFC: 1. QRS 120 ms 2. Rest similar to complete RBBB

Complete

RBBB

Incomplete

RBBB complete or incomplete with epsilon wave and T ↓ in V1 and V2

Arrhythmogenic RV dysplasia

criteria for right bundle branch block (RBBB) and its variants— | Diagnostic VAT: ventricular activation time, RV: right ventricular.

V6

V1

Normal

R

R′ r

RBBB

q

T

S R

S T

LBBB T

S

Fig. 26.6

QRS complexes in V and V leads—in normal, right bundle branch block | (RBBB) and left bundle branch block (LBBB). 1

6

522

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

● ●

●

small initial q wave in right precordial leads (V1, V2). These initial very small waves (r in left oriented leads and q in right precordial leads) may not be seen in all conventional ECGs. As left bundle is blocked, the impulse next spreads down the right bundle branch activating RV in the normal fashion producing a small s wave in left oriented leads and small normal r waves in right precordial leads. Since the RV is relatively thin, the small s waves in left oriented leads may not go down the isoelectric line but may merely produce a notch in the subsequent R waves. Then the impulse passes around the blocked left bundle activating LV producing a wide R in left oriented leads and deep wide S wave in right precordial leads. This results in notched or slurred widened R or rsR pattern in V5, V6 and I and qrS or rS or QS pattern in V1 and V2. VAT in V5, V6 of 0.06 s. Secondary ST–T changes due to abnormal intraventricular conduction are discordant with QRS complexes i.e. ST segment depression and T wave inversion in leads with positive QRS complexes (i.e. in V5, V6, I and aVL) and ST segment elevation and upright asymmetrical T wave in leads with negative QRS complexes (i.e. in V1 V2). Usually, there is no QRS axis shift in frontal plane, and the superior axis shift occurs often in patients with preexisting left anterior fascicular block.

WHO/International Society and Federation for Cardiology (ISFC) Task Force Criteria It includes:1 ● ● ● ●

QRS duration of 120 ms. Broad and notched or slurred R waves in leads V5, V6 and aVL (see Fig. 26.7). Absent Q waves in left precordial leads with possible exception of lead aVL. The R peak time (VAT) in V5 and V6 is 60 ms and normal in V1 and V2.

Fig. 26.7

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

notched R (M-shaped) and absent q waves in V –V | LBBB—broad with rS pattern in V –V . 5

1

3

6

and aVL

INTRAVENTRICULAR CONDUCTION DEFECTS

Complete

WHO/ISFC: 1. QRS 120 ms 2. Broad and notched R in V5, V6 and aVL 3. Absent q in left precordial and I leads 4. VAT in V5 or V6 60 ms

Fig. 26.8

LBBB

523

Incomplete

WHO/ISFC: 1. QRS 100 ms but 120 ms 2. Rest similar to complete LBBB

| Diagnostic criteria of LBBB—VAT: ventricular action time.

Clinical Significance ●

●

●

●

The LBBB usually occurs in patients with structural heart disease associated with hypertrophy, dilatation or fibrosis of the LV myocardium, ischemic heart disease, cardiomyopathy and advanced valvular heart disease. It can occur as a result of toxic and inflammatory changes,12 hyperkalemia,13 or digitalis toxicity.14 Primary degenerative disease of the conducting system, the Lenegre disease15 and calcification of the cardiac skeleton, the Lev disease16 can also cause LBBB. The prevalence of LBBB in a general male population at 50 years of age was 0.4% and 80 years of age was 6.7%.17

Incomplete left bundle branch block is due to conduction delay in the left bundle branch system. It is suspected when ECG shows LVH with slight QRS widening and absent Q waves in left precordial leads and lead I. It has similar ECG features except QRS duration being 120 ms (0.12 s) and VAT 0.06 s. WHO/ISFC Task Force Criteria ● ● ●

QRS duration 100 ms but 120 ms.1 Prolongation of R peak time (VAT) 60 ms in left precordial leads. Absence of Q waves in leads V5, V6 and I (see Fig. 26.8).

3. FASCICULAR BLOCKS Immediately after its origin, the left bundle branch divides into two major divisions or fascicles (see Fig. 26.9): ●

●

The posterior fascicle which arises proximally spreads as a broad band of fibers over the inferior and posterior endocardium of the LV. The anterior fascicle which arises more distally spreads as a narrow band of fibers over the anterior and superior endocardium of LV.

524

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY Left posterior fascicle Bundle of His Left anterior fascicle Left septal fibers

Right bundle branch

Purkinje fibers

Fig. 26.9

| Divisions of left bundle branch.

Normally, the conduction spreads simultaneously through both the fascicles. However, in a fascicular block which is due to delay or interruption of conduction in one of the two major fascicles, the conduction will first proceed through the undamaged division, altering the normal direction of the mean QRS axis. Left anterior fascicular block is more common than left posterior fascicular block. Left Anterior (Hemiblock) Fascicular Block Due to block in the anterior fascicle, the conduction initially spreads through the posterior fascicle which directs the QRS vector: ● ●

Inferiorly producing r wave in inferior leads (II, III, aVF) (see Fig. 26.10) and To the right producing q waves in I and aVL reflecting normal left to right activation of the septum.

The anterior fascicle will then be activated via interconnecting Purkinje fibers distal to the site of the block orienting the QRS vector to: ● ●

The left producing R waves in I, aVL, resulting in a qR pattern in the same leads and Superiorly producing deep S waves in inferior leads resulting in an rS pattern in II, III and aVF, with deeper S in lead III than in lead II (see Fig. 26.11). Deep S waves are also present in V5, V6 resulting in an RS (from usual qRs) pattern.18

As there is an alteration in the sequence of LV activation only, the overall duration of QRS complex is not prolonged and is usually 120 ms (0.12 s) (see Table 26.2). The most characteristic ECG finding is the marked LAD usually of 45 to 90 due to the delayed activation of anterosuperior LV wall. The chronic obstructive pulmonary diseases, CAD and WPW syndrome are other common causes of LAD (see Table 26.3)

INTRAVENTRICULAR CONDUCTION DEFECTS Block in left anterior fascicle

Late left ventricular activation

Activation of left anterior fascicle distal to block via Purkinje fibers

aVL

aVR 2 3

1

Initial left ventricular activation via posterior fascicle

Fig. 26.10

525

III

I

aVF

II

anterior fascicle block—rS in II, III, aVF and qR in aVL with T inversion and a mean | Left frontal QRS axis of 60.

I

aVR

II

aVL

III

aVF

Fig. 26.11

anterior fascicular block—QRS complex 120 ms, rS in II, III, aVF and | Left prominent R in AVL with a mean frontal QRS axis of 60.

Table 26.2 Diagnostic criteria for left anterior fascicular block Features

Findings

1. QRS duration 2. QRS morphology 3. Frontal QRS axis

120 ms rS pattern in II, III, aVF and qR pattern in aVL 45 to 90

526

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 26.3 Causes of superior (left) axis deviation in frontal plane 1. Normal individuals20 2. Congenital heart diseases22 3. CAD: 4% of acute myocardial infarction21 4. COPD 5. WPW syndrome22 6. Degenerative disease of the conducting system

20 yrs of age in 5% AV canal defect, common atrium, tricuspid atresia, common ventricle with TGA, cTGA with left sided apex Anteroseptal or anterolateral myocardial infarction (MI) due to LAD occlusion. Can occur in inferior MI Especially with S1S2S3 ECG pattern – Lenegre disease15, Lev disease16

CAD: coronary artery disease, COPD: chronic obstructive pulmonary disease, WPW: Wolff-Parkinson-White, TGA: transposition of great arteries, LAD: left anterior descending artery.

Initial left ventricular activation via anterior fascicle

Activation of posterior fascicle distal to block via Purkinje fibers

Block in posterior fascicle

aVR

aVL 1

2 I

Late left ventricular activation

Fig. 26.12

III

aVF

II

posterior fascicular block—rS in I and aVL and qR in III, II and aVF with a mean frontal | Left QRS axis of 110.

There may be secondary T wave changes due to intraventricular conduction disturbances i.e. T wave inversion in I and aVL. Warner et al improved ECG criteria (1983)19 include: ● ●

Prominent R waves in aVL and aVR leads Peaking of R later in aVR than peaking of R in aVL.

Left Posterior (Hemiblock) Fascicular Block Due to block in the posterior fascicle, the conduction initially spreads through the anterior fascicle resulting in the QRS axis oriented to: ● ●

the left producing a small r waves (usually 4 mm) in I and aVL and superiorly producing q waves in inferior leads (II, III and aVF) (see Fig. 26.12).

INTRAVENTRICULAR CONDUCTION DEFECTS

Table 26.4 Diagnostic criteria for posterior fascicular block Features

Findings

1. QRS duration 2. QRS morphology

120 s rS pattern in I, aVL and qR pattern in inferior leads 120, exclusion of other factors causing RAD such as RVH

3. Frontal QRS axis

527

Table 26.5 Causes of right axis deviation (RAD) in frontal plane 1. Right ventricular hypertrophy (RVH) 2. Emphysema 3. Vertical heart 4. Extensive lateral wall myocardial infarction

The posterior fascicle will then be activated via interconnecting Purkinje fibers distal to the site of the block resulting in QRS vector oriented to: ● ●

●

the right producing deep S waves in I, aVL resulting in rS pattern in the same leads, inferiorly producing tall R waves in inferior leads, resulting in a qR pattern in II, III and aVF, and posteriorly producing deep S waves in V1 V2.

As there is only an alteration in the sequence of the LV activation, the overall duration of QRS is not prolonged and is usually 120 ms (0.12 s). The prominent feature is right axis deviation (RAD); QRS axis in frontal plane is 120 (see Table 26.4). The extensive lateral wall infarct, right ventricular hypertrophy and emphysema can also give rise to RAD (see Table 26.5). Similarly, there may be secondary T wave changes due to intraventricular conduction disturbances i.e. T wave inversion in inferior leads but upright T waves in I. WHO/ISFC Task Force Criteria ● ● ●

Frontal QRS axis 90 to 180.1 QRS duration 120 ms. A Q waves should always be present in lead III; it may be small or absent in leads II and aVF (see Fig. 26.20).

Left posterior fascicular block occurs in 0.2–0.4% of myocardial infarction (anterior and posterior)23 and is seldom recognized as an isolated finding in the absence of RBBB because: ● ● ●

It is short and thick It has a dual blood supply from LAD and PDA coronary arteries, and It is situated in the less turbulent LV inflow tract.

Multifascicular Blocks Conduction delay in more than one structural components of the specialized conduction system can occur. Conduction delay in any two fascicles is known as bifascicular block and delay in all three fascicles (RBB, LAF, LPF) is called trifascicular block. However, if block is present in all fascicles, conduction would fail and complete heart block would result. The multifascicular block: ● ● ●

Indicates advanced conduction system disease. Is a marker of advanced myocardial disease. Identifies the patients at risk for complete heart block.

528

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Bifascicular Blocks Following are the various types of bifascicular blocks: ● ● ●

RBBB with left anterior fascicular block (LAFB) RBBB with with left posterior fascicular block (LPFB) RBBB or LBBB with prolonged AV conduction (PR interval 0.2 s)

(i) RBBB with LAFB: It is common and is characterized by ECG pattern of RBBB and LAD i.e. QRS axis of  45 (see Figs 26.13 and 26.14). This type of bifascicular block occurs in: ● ● ●

●

4.8–7.0% of MI (anterior).21 Primary degenerative disease of the conducting system (Lenegre’s15 and Lev disease16). Aortic stenosis, when both fascicles may be involved due to extension of the fibrocalcific process of the aortic valve.24 It can also occur in congenital heart disease with endocardial cushion defects. Block in left anterior fascicle

Block in right bundle branch

Fig. 26.13

Fig. 26.14

| Bifascicular block—RBBB and LAFB. I

aVR

V1

II

aVL

V2

V5

III

aVF

V3

V6

| Bifascicular block (RBBB  LAFB)—RBBB with LAD.

V4

INTRAVENTRICULAR CONDUCTION DEFECTS

529

The patients of MI with bifascicular block may progress to complete AV block in 24–43%.21 (ii) RBBB with LPFB: It is rare and is characterized by ECG pattern of RBBB and RAD i.e. QRS axis of 120 (see Figs 26.15 and 26.16). ●

The causes of this type of bifascicular block are similar to RBBB with LAFB with CAD being the most commonest cause. Block in left posterior fascicle

Block in right bundle branch

Fig. 26.15

Fig. 26.16

| Bifascicular block—RBBB and LPFB.

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

| Bifascicular block (RBBB and LPFB)—RBBB with RAD.

530

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY ●

It occurs in 0.8% of acute myocardial infarction,21 which may also progress to complete AV block (in 2 of 21 patients over a mean period of 2 years follow up).25

Trifascicular Block It usually involves conduction delay in the right bundle branch plus ● ● ●

●

Conduction delay either in the main left bundle branch or Both left anterior and left posterior fascicles (see Fig. 26.17). The ECG findings are characterized by bifascicular block (most commonly RBBB  LAFB) and prolonged PR interval, which indicates the first degree AV block (see Figs 26.18, 26.19 and 26.20), but more likely represents an incomplete block in the third fascicle in this situation. A complete trifascicular block results in a complete AV block. Hence, His bundle recording is usually required for definitive diagnosis and for the site of the block. Block in left posterior fascicle

Block in right bundle branch

Fig. 26.17

Block in left anterior fascicle

| Trifascicular block.

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 26.18

block—RBBB and LPFB (QRS axis 120) with 1 AV block | Trifascicular (prolonged PR interval).

INTRAVENTRICULAR CONDUCTION DEFECTS

I

aVR

V1

V4

II

aVL

V2

V5

V3

V6

aVF

III

Fig. 26.19

531

| Trifascicular block—RBBB and LAFB (QRS axis 60) with 1 AV block (prolong PR interval). 1. QRS 120 ms 2. rS in II, III and aVF 3. qR in aVL 4. LAD 45ο to 90ο

Left anterior fascicular block (LAFB) RBBB  LAFB: RBBB with LAD  45ο

Fig. 26.20

RBBB  LAFB/ LPFB  ↑PR

Trifascicular block

Fascicular blocks

Bifascicular block

1. QRS 120 ms 2. rS in I and aVL 3. qR in II, III and aVF 4. RAD 90ο to 180ο

Left posterior fascicular block (LPFB) RBBB  LPFB: RBBB with RAD 120ο

criteria of fascicular blocks—RBBB: right bundle branch block, | Diagnostic LAD: left axis deviation, RAD: right axis deviation.

REFERENCES 1. Willems JL, Robles de Medina EO, Bernard R, et al. Criteria for intraventricular conduction disturbances and pre-excitation. World Health Organizational/International Society and Federation for Cardiology Task Force Ad Hoc. J Am Coll Cardiol 1985;5(6):1261–1275. 2. Lev M, Unger PN, Lesser ME, et al. Pathology of the conduction system in acquired heart disease. Complete right bundle branch block. Am Heart J 1961;61:593–614.

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BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

3. Hiss RG, Lamb LE. Electrocardiographic findings in 122,043 individuals. Circulation 1962;25: 947–961. 4. Horowitz LN, Alexander JA, Edmunds LH. Postoperative RBBB: identification of three levels of block. Circulation 1980;62:319–328. 5. Schamroth L, Myburg DP, Schamroth CL. The early signs of RBBB. Chest 1985;57:180. 6. Sodi-Pallares D, Medrano GA, Bisteni A, et al. Deductive and Polyparametric Electrocardiography. Mexico: Instituto National Cardiologia Mexico, 1970;36:136. 7. Tapia FA, Proudfit WL. Secondary R waves in right precordial leads in normal persons and in patients with cardiac disease. Circulation 1960;21:28–37. 8. Liao Y, Emidy LA, Dyer A, et al. Characteristics and prognosis of incomplete RBBB, an epidemiological study. J Am Coll Cardiol 1986;7:492–499. 9. DeLeon AC Jr, Perloff JK, Twigg H, et al. The straight back syndrome: clinical cardiovascular manifestations. Circulation 1965;32:193–203. 10. De Oliveira JM, Sambhi MP, Zimmerman HA. The electrocardiogram in pectus excavatum. Br Heart J 1958;20(4):495–501. 11. Brugada P, Brugada J. Right bundle branch block, presenting ST segment elevation and sudden death: A distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol 1992;20:1391–1396. 12. Brake CM. Complete LBBB in asymptomatic airmen. Aerospace Med 1969;40:781. 13. Cohen HC, Rose KN, Pick A. Disorders of impulse conduction and impulse formation caused by hyperkalemia in man. Am Heart J 1975;89(4):501–509. 14. Singh RB, Agraval BV, Somani PN. LBBB: a rare manifestation of digitalis intoxication. Acta Cardiol 1976;31:175. 15. Lenegre J. Etiology and pathology of bilateral BBB in relation to heart block. Prog Cardiovasc Dis 1964;6:409–444. 16. Lev M. Anatomic basis for atrioventricular block. Am J Med 1964;37:742–748. 17. Eriksen P, Hansson PO, Eriksson H, et al. BBB in a general male population: the study of men born 1913. Circulation 1998;98:2494–2500. 18. Rosenbaum MB, Elizari MV, Lazzari JO. The Hemiblocks. Oldsmar, FL: Tampa Tracings, 1970. 19. Warner RA, Hill NE, Mookherji S, et al. Improved electrocardiographic criteria for the diagnosis of left anterior hemiblock. Am J Cardiol 1983;51(5):723–726. 20. Ostrander LD. Left axis deviation: prevalence, associated conditions and prognosis. Ann Intern Med 1971;75(1):23–28. 21. Atkins JM, Leshin SJ, Blomqvist G, et al. Ventricular conduction blocks and sudden death in AMI: potential indications for pacing. N Eng J Med 1973;288(6):281–284. 22. Pryor R, Blount SG. The clinical significance of true left axis deviation: left intraventricular blocks. Am Heart J 1966;72(3):391–413. 23. Rizzon P, Rossi L, Baissus C, et al. Left posterior hemiblock in AMI. Br Heart J 1975;37(7): 711–720. 24. Thompson R, Mitchell A, Ahmed M, et al. Conduction defects in aortic valve disease. Am Heart J 1979;98(1):3–10. 25. Dhingra RC, Denes P, Wu D, et al. Chronic RBBB and left posterior hemiblock: clinical electrophysiologic and prognostic observations. Am J Cardiol 1975;36:867–879.

■■■

CHAPTER 27

M YOCARDIAL I NFARCTION AND I SCHEMIA 1.

2. 3. 4.

5.

MYOCARDIAL INFARCTION (MI) i. Depolarization Abnormalities ii. Repolarization Abnormalities iii. Other Changes Evolution of ECG Changes MYOCARDIAL ISCHEMIA NONSPECIFIC ST-T CHANGES LOCALIZATION OF ISCHEMIA OR INFARCTION i. Right Ventricular Infarction ii. Atrial Infarction PREDICTION OF THE SITE OF CORONARY ARTERY OCCLUSION i. Occlusion of Coronary Artery

533 534 535 540 540 541 542 542 543 543 545 546

ii. Coronary Artery Occlusion and ECG Correlation 546 6. ECG DIAGNOSIS OF MI IN BUNDLE BRANCH BLOCKS AND DURING RV PACING 552 i. MI in RBBB 552 ii. MI in LBBB 553 ECG Diagnosis of MI During RV Pacing 554 7. SENSITIVITY, SPECIFICITY, AND PROGNOSTIC VALUE OF THE ECG 555 i. The Sensitivity of the ECG 555 ii. Prognostic Value of ECG for MI 555 REFERENCES 556

The ECG remains a key investigation in the diagnosis of myocardial infarction and coronary syndrome. However, ECG findings vary depending upon the following factors: ● ● ● ●

Duration of the ischemic process (acute vs chronic) Extent of ischemia (transmural vs subendocardial) Its topography i.e. site of ischemia (anterior vs inferior–posterior or right ventricular) Presence of other underlying abnormalities (e.g. LBBB, WPW syndrome or pacemaker patterns) which can mask or alter the classic pattern.

1. MYOCARDIAL INFARCTION (MI) Histopathologically, an infarcted region consists of a central core of necrotic tissue, surrounded by a zone of injured tissue which in turn is surrounded by a zone of ischemic tissue, and as a result the ECG changes are as follows: ●

The myocardial necrosis results in depolarization abnormalities (QRS changes).

534

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY ●

●

The myocardial injury and ischemia cause repolarization abnormalities (injury is reflected by ST segment elevation and ischemia is represented by an inverted symmetrical T wave). Other changes: Ischemic U waves, increased QT dispersion.

As the electrode is situated some distance away from the heart, it subtends a relatively large area which includes all the zones of necrosis, injury and ischemia and consequently, it records all the ECG changes. i. Depolarization Abnormalities These often accompany the earliest repolarization abnormalities, which include: ● ●

Abnormalities of Q waves Abnormalities of R wave

Abnormalities of Q Waves i) ii)

iii)

iv)

v)

Small q waves are normally recorded in leads I, aVF, and V4–V6 which are 0.02 s in duration and q: R ratio is 25%. However; in myocardial infarction with necrosis of sufficient quantity, the forces of depolarization are lost in that area and mean electrical forces are directed away from the area of infarction resulting in: ● An abnormal Q wave (0.04 s in duration Q:R ratio of 25%) or ● QS complex in the leads overlying the infarct zone. Often, abnormal Q wave is followed by a small positive terminal r wave due to the late activation of the overlying viable myocardial tissue resulting in a Qr complex, while a totally negative QS complex indicates the absence of any viable myocardial tissue. In the past, abnormal Q waves were considered as markers of transmural myocardial infarction. However, abnormal Q waves occur as early as 2 hours and as late as 24 hours (mean of 9 hours) after the onset of symptoms of myocardial infarction, besides experimental and clinicopathological studies have shown that transmural infarcts can occur without abnormal Q waves and subendocardial infarcts can be associated with abnormal Q waves1 and hence myocardial infarction is better classified electrocardiographically as Q or non-Q wave infarction. Q wave infarctions tend to be larger than non-Q wave infarctions.2 Thrombolytic therapy is indicated in Q wave myocardial infarction, while it is of no benefit in non-Q wave myocardial infarction.

Abnormalities of R Waves There is a progressive loss of R wave amplitude in myocardial infarction. The diminution of R wave amplitude is recorded: ●

●

When the infarct is small and necrosis is insufficient to result in an abnormal Q wave. In the leads overlying periphery of the infarction.

MYOCARDIAL INFARCTION AND ISCHEMIA

535

ii. Repolarization Abnormalities These are the earliest and consistent ECG changes that occur during acute ischemia or infarction. Following are the repolarization abnormalities: ● ●

ST segment changes due to myocardial injury and T wave changes due to myocardial ischemia

ST Segment Changes The following changes occur in the electrical properties of the myocardial cells of the ischemic area. ● ● ● ●

Reduction of resting membrane potential. Shortening of duration of action potential resulting in early repolarization. Decrease in rate of rise (upstroke velocity) of the action potential (phase 0) and Decrease in the amplitude of action potential (phase 0).

The presence of one or more of these changes will establish a voltage gradient between normal and ischemic zones so that these currents of injury are directed towards the ischemic region resulting in primary ST segment elevation with convexity upwards in the surface ECG. ●

●

●

In dominant epicardial injury as in transmural infarction, the overall ST vector is directed to the outer (epicardial) layers resulting in ST segment elevation (and sometimes tall positive T waves-hyper-acute T waves) over the injury zone, and reciprocal ST segment depression in leads reflecting contralateral surface of the heart. In dominant subendocardial injury as in subendocardial infarction, the overall ST vector is directed towards the inner ventricular layer and the ventricular cavity resulting in ST segment depression in the overlying leads and ST elevation in aVR. However, currently MI is categorized depending upon the ST segment abnormalities into ST elevation MI (STEMI) and non-ST elevation MI (non-STEMI) as pathological Q waves most often develop after the onset of symptoms. An abnormal ST elevation of 1 mm in two or more contiguous leads is diagnosed as STEMI, an indication for thrombolytic therapy. However, there are many non-cardiac causes in which ST elevation can occur (see Table 27.1). ST elevation in myocardial infarction is usually associated with reciprocal ST depression in one or more of the standard 12 leads. i) In anterior MI, ST elevation is present in precordial leads. ● Absence of ST elevation in V may occur and has been attributed to protection 1 by the conal artery arising from right coronary artery (RCA).3 ● Reciprocal ST depression is nearly always present in leads III and aVF, and absence of reciprocal changes in aVF indicates occlusion of left anterior descending artery (LAD) distally4 (see Figs 27.1 and 27.2). ● In anteroseptal MI, ST elevation occurs in V –V 1 4 (see Figs 27.3 and 27.4), while in anterolateral MI, ST elevation mainly occurs in I, aVL, V5 and V6 (see Figs 27.5 and 27.6). ● ST elevation mainly in leads I and aVL and fewer changes in precordial leads occur in the occlusion of first diagonal branch of LAD, while ST elevation

536

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

RV

LV

Anterior wall infarct

Fig. 27.1

| Cross section through anterior wall infarct.

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 27.2

| Anterior wall MI with ST segment elevation in V –V . 1

RV

3

LV

Anteroseptal infarct

Fig. 27.3

| Cross section through anteroseptal infarct.

mainly in leads V1 and V2 with reciprocal depression in leads II, III, aVF, V5 and V6 occurs when main septal branch of LAD is occluded. ii) In apical or lateral MI, ST elevation occurs in leads V5 and V6 with reciprocal ST depression in leads III, aVF and occasionally in V1. iii) In inferior MI, ST elevation is present in II, III and aVF with reciprocal ST depression in leads I, aVL and one or more of precordial leads (V2–V3, see Figs 27.7 and 27.8,). ● Absence of reciprocal ST depression, but presence of ST elevation in V , RV MI 1 should be suspected.5

MYOCARDIAL INFARCTION AND ISCHEMIA

Fig. 27.4

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

MI with Q waves, ST elevation in V –V | VAnteroseptal –V . 1

1

4

537

and inverted T in I, aVL,

6

LV

RV

Anterolateral infarct

Fig. 27.5

Fig. 27.6

| Cross section through anterolateral infarct. I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Anterolateral Q MI with Q waves in aVL, V –V | inversion in I, aVL and V –V . 2

3

5

3

and ST elevation and T wave

538

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

| Sagittal view through inferior wall infarct.

Fig. 27.7

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 27.8

| Inferior wall MI with q in III, ST elevation in II, III, aVF and inverted T in aVL.

Presence of additional ST elevation in lateral precordial leads (V5, V6) or in leads I and aVL (Inferolateral MI) indicates the occlusion of left circumflex (LCx) coronary artery.6 iv) True posterior MI7 is characterized by: ● Tall R waves, ST depression and upright T waves in V and V , (see Figs 27.9 1 2 and 27.10) and ● Q waves and ST elevation in leads V –V . 7 9 ● However, posterior MI is often associated with inferior MI (see Fig. 27.11). v) LV MI involving papillary muscles (PM): Besides ST-T changes in LV leads, ST depression in inferior leads is associated with anterolateral PM infarction, while ST depression in lead I or aVL is seen in posteromedial PM infarction.8 ●

T Wave Changes Leads overlying the ischemic region record inverted symmetrical and pointed T waves, with frequently increased magnitude as T vector is directed away from the region of

MYOCARDIAL INFARCTION AND ISCHEMIA

Fig. 27.9

Fig. 27.10

Fig. 27.11

539

| Sagittal view through posteroinferior wall infarct.

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

MI with tall R and upright T waves in V –V . Tall R waves are not due to RVH, as there | isPosterior no RAD, no inverted T waves, and no evidence of RAE. 1

2

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Postero-inferior MI-tall R waves and upright and tall T waves in V with abnormal Q waves and | inverted T waves in inferior leads. 1

540

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

I

II

aVR

aVL

aVF III

Fig. 27.12

V1

V2

V3

V4

V5

V6

| Anterolateral non-Q MI-symmetrical inverted T waves in aVL and V –V . 1

6

myocardial ischemia. They are sometimes known as ‘coronary’ T waves, which are usually associated with lengthening of QT interval. Inverted T waves occur in: ● ● ● ●

Leads I, aVL, V5 and V6 in anterolateral infarction (see Fig. 27.12). Leads V1–V3 in anteroseptal infarction. Leads II, III and aVF in inferior infarction. Upright T waves occur in right precordial leads in posterior infarction.

iii. Other Changes Ischemic U Wave Changes Alterations in polarity or amplitude of U waves can occur in acute ischemia or infarction. ● ● ●

●

Negative U waves in anterior precordial leads in anterior MI. Negative U waves in leads III and aVF in inferior infarction. In severe LAD stenosis, transient inverted U waves in precordial leads appear on stress test.9 Inverted U waves may be the earliest ECG finding of acute coronary syndromes.10

Increased QT Interval Dispersion The difference of QT interval in various leads is known as QT interval dispersion. The increased QT interval dispersion i.e. the greater difference between maximum and minimum QT intervals (0.05 s) reflects: ● ●

A marker of arrhythmia risk after myocardial infarction11 and A marker of acute ischemia after atrial pacing.12

Evolution of ECG Changes ●

ST elevation and hyperacute T waves occur as the earliest sign of acute MI, typically followed by evolving T wave inversion from hours to days and sometimes by abnormal Q wave in the same leads from 2–24 hours.

MYOCARDIAL INFARCTION AND ISCHEMIA

541

Table 27.1 Other causes of ST elevation 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

●

●

●

●

●

Early repolarization Acute pericarditis Pulmonary embolism Myocarditis Acute aortic dissection17 Acute cor pulmonale Hyperkalemia Cardiac tumor After mitral valvuloplasty18 Pancreatitis and gallbladder disease19 Anaphylactic shock20 Septic shock Spinal cord injury at C5–C6 levels (i.e. lesions that completely disrupt cardiac sympathetic influences)21

ST segment returns to the isoelectric line after a period of hours to days (most often 2 weeks). In most cases, the initial ST elevation decreases markedly during the first 7–12 hours after the onset of chest pain.13 It resolved within 2 weeks in 90% of patients with inferior infarction and in 40% in patients with anterior infarction.14 However, the resolution of ST elevation is complete and much earlier with the thrombolytic therapy. The T wave inversion can resolve after days or weeks or may persist indefinitely with Q waves especially in large transmural infarction with fibrosis. During its evolution, “Pardee T” or “coronary T” may be observed i.e. inverted T wave with ST segment is isoelectric but shows an upward convexity. In leads showing ST segment depression, T waves become tall and symmetrical. Q waves may regress within 2 years. However in the present era of thrombolytic therapy, regression occurs earlier and more frequently, within 6–60 months in one or more leads in 77% of the patients.15 Complete normalization of ECG following Q wave infarction is uncommon but can occur with smaller infarcts with improved left ventricular ejection fraction (LVEF). Persistent ST segment elevation together with Q waves for several weeks occurs with severe LV wall motion abnormalities (akinesia or dyskinesia) or with the development of ventricular aneurysm. The el-Sherif sign i.e. rSR in mid precordial leads or I is another marker of ventricular aneurysm (see Table 27.1).

2. MYOCARDIAL ISCHEMIA Myocardial ischemia, which is expressed clinically as angina, is associated with the ECG changes consisting mainly of primary ST-T changes i.e. ●

ST segment depression of  1 mm in one or more leads. ST segment depression must be horizontal or downward sloping with duration of atleast 0.08 s, in order to differentiate it from the normal J point depression.

542

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Fig. 27.13 ●

●

●

●

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

| Non-STEMI—ST depression of  1 mm in I, aVL and V –V . 1

6

However in Prinzmetal variant angina due to coronary vasospam, there is transient ST segment elevation which resolves within minutes or is followed by T wave inversion which may persist for hours or days. ST segment depression of 1 mm in two or more leads in a patient with chest discomfort and abnormal cardiac enzymes (troponin or CK-MB) is diagnostic of nonSTEMI (see Fig. 27.13). T wave inversion in one or more leads: Due to a high grade stenosis of proximal LAD, severe ischemia may be associated with deep coronary T wave inversion in multiple precordial leads (V1–V4), which is described as LAD-T wave pattern.16 Other ECG changes include ischemic U waves and increased QT interval dispersion.

3. NONSPECIFIC ST-T CHANGES ST segment depression of 1 mm is found in many conditions, such as: ● ● ● ● ● ● ● ● ●

Myocarditis Pericarditis, constrictive pericarditis Cardiomyopathy Pulmonary embolism Subarachnoid or cerebral hemorrhage Drugs: Digoxin effect, ethanol abuse Hyperventilation After a drink of cold water Electrolyte imbalance.

4. LOCALIZATION OF ISCHEMIA OR INFARCTION ● ●

ECG leads are helpful in localization of ischemia or infarction. ECG changes in one or more of precordial leads (V1–V6): anterior.

MYOCARDIAL INFARCTION AND ISCHEMIA

543

Table 27.2 Incidence of RV infarction

●

● ● ● ●

Criteria

Incidence

1. Autopsy studies 2. Hemodynamic studies 3. Radionuclide studies

5–43% with a mean of 19% 15–20% About 40%

However, ECG changes in V1–V2 are usually designated as anterior ischemia or infarction while ECG changes in V1–V6 are designated as extensive anterior. ECG changes in one or more of precordial leads from V1 to V6 and leads I and aVL: anterolateral. ECG changes in V1–V4: anteroseptal. ECG changes in V5–V6: apical or lateral. ECG changes in II, III and aVF: inferior wall. ECG changes in II, III, aVF and V5–V6: inferolateral.

ECG changes of ST segment depression and tall R and T waves in V1–V2 are diagnostic of true posterior wall infarction. However, ST segment elevation is recorded in leads V7–V9. i. Right Ventricular Infarction RV infarction occurs in the presence of inferior wall infarction of LV and as such, ECG diagnosis of RV infarction offers special challenges. ● ●

●

Most pathological studies show the presence of RV infarct in 14–36%.22,23 The clinical diagnosis of RV infarction is only 20%, while with echocardiogram and nuclear studies it is about 40% (see Table 27.2). RV infarction usually causes loss of R wave in leads V3R and V4R. Elevation of ST segment in right precordial leads is the most important diagnostic sign. Hence, ST segment elevation in right chest leads, V1 and V3R–V6R (V3R and V4R are more sensitive) must be sought in the presence of inferior wall infarction.

Following are the Diagnostic Criteria for RV Infarction in presence of inferior wall infarction ●

● ● ● ● ●

ST segment elevation in V3R or V4R (Erhadt et al, 1976) with a sensitivity of 100% and specificity of 68%24 (see Figs 27.14 and 27.15). ST segment elevation in V6R and V7R (Anderson et al) with 100% sensitivity.22 ST segment elevation in V1–V3 (Geft et al25). ST segment elevation in V1 and ST segment depression in V2 (Mak et al26). ST segment depression in V2:  50% ST elevation in aVF (Lew et al27). ST segment elevation in lead III  ST elevation in lead II (Anderson et al22).

ii. Atrial Infarction The atrial infarction has been related to extensive ventricular myocardial infarction,28 and it is suspected when an atrial arrhythmia develops in a patient with a large ventricular infarction.

544

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Aorta PA LA

RA LV RV

Right ventricular infarct

Fig. 27.14

| Right ventricular infarct.

I

aVR

V 1R

V4R

II

aVL

V2R

V5R

III

aVF

V3R

V6R

Fig. 27.15

infarction with inferior wall MI—ST elevation in II, III, aVF and right pre| RV cordial leads (V R–V R). 3

6

Table 27.3 Characteristics of atrial infarction 1. 2. 3. 4. 5.

●

● ●

Atrial infarction occurs in 7–17%. Mostly associated with ventricular infarction. Right atrium and appendages are more involved. Aluminium phosphate poisoning mimics atrial infarction. Atrial arrhythmias, atrial rupture and thrombus formation are complications of atrial infarction.

It occurs in 7–17%. The right atrial infarction is more common and the atrial appendage is commonly affected (see Table 27.3). Isolated atrial infarction, which is rare, usually presents with CHF. The ECG changes of atrial infarct are found in poisoning with aluminium phosphate.

MYOCARDIAL INFARCTION AND ISCHEMIA

P

545

P

Ta

| Ta: small negative deflection following P wave due to atrial repolarization.

Fig. 27.16

II P↑

aVF

P↑

P↑

P↑

P↑

V2 P↑

V6

Fig. 27.17

P↑

P↑

P↑

P↑

of PTa (arrow ) is diagnostic of atrial infarction with changes in | Elevation morphology of P waves (a minor diagnostic criterion).

Following is the ECG diagnostic criteria proposed by Chi Kong Liu et al (1961)29 i) Major criteria: ● ●

●

Elevation of PTa of 0.5 mm in V5–V6 with a reciprocal depression in V1–V2. Elevation of PTa of 1.5 mm in any precordial lead or 1.2 mm in I–III with atrial arrhythmias. Elevation of PTa in I with reciprocal depression in II and III. (Ta: is a small negative deflection following P wave due to atrial repolarization (see Fig. 27.16), which is not usually seen in standard 12 leads ECG)

ii) Minor Criteria: Minor Criteria alone is not regarded as an evidence of atrial infarction. ● Abnormal P morphology: Irregular or notched (M or W) (see Fig. 27.17). ● PTa depression with reciprocal changes (see Fig. 27.18).

5. PREDICTION OF THE SITE OF CORONARY ARTERY OCCLUSION The ECG provides information about the site of occlusion of coronary arteries in patients with myocardial ischemia or infarction.

546

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

1. Tall R, ST↓ and upright T in V1–V2 2. ST↑ in V7–V9

ST↑ T↓ in I, aVL, V5–V6

ST↑ T↓ in II, III and aVF

Lateral with or without Q

Inferior with or without Q

Infarction

Posterior

1. ST↑ T↓ in precordial leads 2. ↓U waves in precordial leads

Fig. 27.18

Anterior with or without Q

1. PTa↑  0.5 mm in V5–V6 with ↓ in V1–V2 2. PTa↑  1.5 mm in any precordial lead or  1.2 mm in I–III with atrial arrhythmia 3. PTa↑ in I with ↓ in II–III 4. Irregular or notched P (M or W shape)

Atrial

Right ventricular

Inferior MI with 1. ST↑ T↓ in right precordial leadsV3R, V4R 2. ST↑ in III  II 3. ST↑ in V1 and ST↓ in V2

and diagnostic criteria of myocardial infarction—: inverted or depression, : elevation | Types or upright.

i. Occlusion of Coronary Artery ●

●

●

Occlusion of right coronary artery (RCA) causes inferior, posterior, inferoposterior, inferolateral, and RV MI. Occlusion of left circumference (LCx) causes posterior and lateral infarctions (posteroapical, posterolateral, posterobasal, posteroinferior, inferolateral or high lateral MI). Occlusion of the dominant LCx causes inferoposterior and posterolateral infarctions. Occlusion of left anterior descending (LAD) causes anteroseptal and anterior MI. Proximal LAD occlusion can also result in bundle branch block (BBB) and left anterior fascicular block.

ii. Coronary Artery Occlusion and ECG Correlation ●

●

Presence of abnormal Q waves in leads I, aVL, and V1–V4 associated with LAD occlusion, and in leads II, III and aVF associated with LCx or RCA occlusion.30 In anterior MI, ST elevation is less frequent in lead V1 than in leads V2 and V3. Absence of ST elevation in V1 in anterior MI suggests the presence of a large conal branch of RCA protecting the septum, conversely ST elevation in V1 suggests either absent or small conal branch of RCA.31

i) Predicting RCA or LCx Occlusion in Inferior Wall MI ●

●

ST segment elevation in III  II: RCA occlusion with a sensitivity of 99% and a specificity of 100%, while ST segment elevation in II  III: LCx occlusion with a sensitivity of 93% and a specificity of 100%. In inferior infarction, ST elevation in lead III  II, especially when combined with ST elevation in V1 is a powerful predictor of RCA occlusion proximal to acute marginal branch32 (see Fig. 27.19).

MYOCARDIAL INFARCTION AND ISCHEMIA

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 27.19

I

547

wall MI with ST elevation in III  II and ST elevation also in V –V | Inferior due to proximal right coronary artery occlusion. 1

aVR

2

V1 V4

II

III

Fig. 27.20

●

●

●

●

●

aVL

V2

V5

aVF

V3

V6

MI with ST elevation in II, III, aVF and V –V | Inferolateral artery occlusion. 5

6

in left circumflex

In inferior MI with ST elevation in lateral leads V5 and V6 or I and aVL is a sensitive and specific marker for LCx lesion33 (see Fig. 27.20). Inferior MI with ST depression in V1–V3 is more often associated with LCx occlusion (71%) than of RCA occlusion (40%).34 Similarly, reciprocal changes (i.e. ST segment depression) in aVL predict LCx occlusion, while reciprocal changes in V4–V6 predict multivessel occlusion35 (see Figs 27.21 and 27.22). Ratio of ST segment depression in V3 to ST segment elevation in III has 91% sensitivity and specificity.34 – 0.5 predicts proximal RCA occlusion (see Fig. 27.23) – 0.5 1.2 predicts distal RCA occlusion – 1.2 predicts LCx occlusion (see Fig. 27.24) Abnormal R in V1 consistent with posterior infarction is highly specific for LCx occlusion.33

ii) Predicting LAD Occlusion Site in Anterior Wall Infarction ●

The ECG criteria for localization of site of LAD occlusion are less sensitive (50–85%) but are more specific (90–100%).36,37

548

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

I

aVR

V1

II

aVL

V2

III

aVF

V3

Fig. 27.21

V4

V5

V6

Inferior wall MI with reciprocal ST depression in aVL and V –V | circumflex artery occlusion. 1

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 27.22

3

due to left

wall MI with reciprocal ST depression in I and aVL due to left circum| Inferior flex artery occlusion.

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 27.23

Inferior wall MI—ratio of ST depression in V to ST elevation in III is 0.5— | due to proximal right coronary artery occlusion. 3

MYOCARDIAL INFARCTION AND ISCHEMIA ●

●

●

●

549

LAD lesions proximal to the first septal branch (S1) have sensitivity of about 50% and specificity of 90–100%, while LAD lesions proximal to first diagonal branch (D1) have sensitivity of about 60% and specificity of 90%. LAD lesions distal to S1 have sensitivity of about 25% and specificity of 88%, while LAD lesions distal to D1 have low (about 10–20%) sensitivity but are highly specific (100%). In anterior MI, presence of reciprocal ST depression in inferior leads suggests a proximal LAD lesion. Similarly, ST elevation (also in leads I and aVL) is predictive of proximal (proximal to D1) LAD lesion.38 Type III LAD occlusion is recognized by the presence of ST depression with upright T waves in lead III.39

a) ST segment depression of 1 mm in inferior leads predicts proximal LAD occlusion (proximal to septal (S1) or diagonal (D1) branch). (i) Following are the ECG predictors of LAD occlusion proximal to S1 branch (see Fig. 27.25)

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 27.24

wall MI—ratio of ST depression in V | Inferior to left circumflex artery occlusion.

3

I

V1

II

V2

III

V3

aVR

V4

aVL

V5

aVF

V6

Fig. 27.25

to ST elevation in III is 1.2—due

wall infarction with reciprocal ST depression in inferior leads and V | Anterior in V (2.5 mm) and aVR—due to LAD lesion proximal to S .

5

1

1

and ST elevation

550

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 27.26

wall MI with reciprocal ST depression in inferior leads and ST ele| Anterior vation in I and aVL—due to LAD lesion proximal to D . 1

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 27.27

Anterior wall MI with Q waves and ST elevation in V –V but no reciprocal | ST depression in inferior leads—due to LAD lesion distal to S . 2

5

1

ST segment elevation in V1 of 2.5 mm ST segment elevation in aVR ● Associated with complete RBBB ● ST segment depression in V . 5 (ii) Following is the ECG predictor of LAD occlusion proximal to D1 branch (see Fig. 27.26) ● Abnormal Q waves in aVL ● ST segment elevation in I and aVL. (b) Absence of ST depression in inferior leads predicts mid to distal LAD occlusion (distal to S1 or D1 branch). (i) Following is the ECG predictor of LAD occlusion distal to S1 branch (see Fig. 27.27) ● Presence of abnormal Q waves in V –V 4 6 (ii) Following is the predictor of LAD occlusion distal to D1 branch (see Fig. 27.28) ● ST segment depression in aVL (see Fig. 27.29) ● ●

MYOCARDIAL INFARCTION AND ISCHEMIA

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 27.28

551

Anterior wall MI with ST elevation in V –V and ST depression in aVL but no | reciprocal ST depression in inferior leads—due to LAD lesion distal to D . 1

5

1

Proximal to S1: 1. ST↑ in V1 2.5mm 2. ST↑ in aVR 3. ST↓ in V5 4. MI  RBBB

Proximal to D1: 1. Abnormal Q in aVL 2. ST↑ in I and aVL

Proximal to D1 and S1

Distal to D1: ST↓ in aVL

Ant. MI with ST↓ of 1 in II, III and aVF

Ant. MI with no ST↓ in II, III and aVF

Proximal occlusion

RCA occlusion

LAD occlusion

1. ST↑ in V1 2. V3 ST↓: III ST↑ 0.5

Inf. MI with ST↑ in III  II

CAO

V3 ST↓: III ST↑ 0.5 to 1.2

Distal occlusion

MV occlusion

Distal to S1: Abnormal Q in V4–V6

Distal to D1 and S1

LCx occlusion

Inf. MI with ST↑ in II  III

Inf. MI with ST↓ in V4–V6

Inf. MI with ST↓ in aVL Inf. MI with V3 ST↓: III ST↑ 1.2 Inf. MI with ST↓ in V1–V3

Fig. 27.29

Inf. MI with ST↑ in I, aVL or V5–V6 Posterior MI-tall R in V1

coronary artery occlusion (CAO) from ECG—MV: multi-vessel, Ant.: anterior, Inf.: | Predicting inferior, RCA: right coronary artery, LAD: left anterior descending artery, LCx: left circumflex artery, : depression, : elevation, RBBB: right bundle branch block.

552

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

6. ECG DIAGNOSIS OF MI IN BUNDLE BRANCH BLOCKS AND DURING RV PACING The diagnosis of myocardial infarction is often difficult in patients with baseline ECG showing BBB pattern or a BBB develops as a complication of the infarction. i. MI in RBBB The RBBB primarily affects the terminal phase of ventricular depolarization, and hence diagnosis of MI is usually not impeded by its presence. The criteria for the diagnosis of MI (Q wave infarct) in the presence of RBBB are the same as in patients with normal conduction (see Figs 27.30 and 27.31). V1

V4

V2

V5

V3

V6

Fig. 27.30

MI and RBBB—ST elevation in V –V | Anterior precordial leads with RBBB pattern in V –V . 1

1

4

and inverted T waves in all

3

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 27.31

MI and RBBB—ST elevation and inverted T waves in III and aVF | Inferior with RBBB pattern in V . 1

MYOCARDIAL INFARCTION AND ISCHEMIA ●

●

553

RBBB occurs in 3–29% of patients with AMI,40 often accompanied by left anterior fascicular block41 and LAD is usually involved.42 The mortality rate is higher in patients with new onset RBBB than in those with old RBBB, in contrast to AMI patients with an old LBBB have higher mortality than in those with recent onset LBBB.42

ii. MI in LBBB The LBBB: ● ●

Affects both early and late phases of ventricular depolarization, Alters the sequence of repolarization, with ST segment and T wave vectors directed opposite to QRS complex, producing secondary ST-T changes.

These changes may mask and mimic the ECG findings of MI. Hence, the ECG diagnosis of MI in the presence of LBBB is more difficult and sometimes confusing. Following is the ECG diagnostic criteria of MI in presence of LBBB i) Based on GUSTO-1 trial (Global Utilization of Streptokinase and Tissue plasminogen activator for occluded coronary arteries) (Sgarbossa et al criteria, 1996)43 ● ST segment elevation of 1 mm with concordant (positive) QRS complex: 5 scores ● ST segment elevation of 5 mm with discordant (negative) QRS complex: 2 scores (see Fig. 27.32) ● ST segment depression of 1 mm in V , V , or V : 3 scores (Fig. 27.33) 1 2 3 For diagnosis, a total score of 3 is a must, which yields a sensitivity of 78% and specificity of 90%. ii) Other diagnostic ECG criteria which are less sensitive and specific are as follows: R wave regression from V1 to V444 ● QS pattern in V –V 1 4 ● Presence of Q waves in two contiguous precordial or limb leads. Abnormal Q wave should be 20 ms in V4 or 30 ms in V5, V6, II and III. ●

V1

V4

V2

V5

V3

V6

Fig. 27.32

| Anterior wall MI with LBBB—Discordant ST elevation in V –V . 1

3

554

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 27.33

wall MI and LBBB with Q waves and concordant ST segment eleva| Inferior tion in lead III and ST segment depression in V and V leads. 2

3

Table 27.4 Other ECG changes in patients of MI with LBBB 1. 2. 3. 4. 5.

● ●

●

● ●

Presence of abnormal Q waves Notching of S waves (Cabrera sign) Regression of R waves in precordial leads (V1–V6) Notching of R waves (Chapman sign) Left axis deviation (LAD)

Positive T wave in V5 or V6 Notching of 0.05 s in the ascending limb of S wave in V3 or V4–V5 (Cabrera sign) Notching of 0.05 s in the ascending limb of R wave in I, aVL, V5 or V6 (Chapman sign)45 Terminal prominent S wave in V5 or V6 LAD (see Table 27.4).

ECG Diagnosis of MI During RV Pacing Similar principles apply for the diagnosis of MI in the presence of RV pacing. i. Anterior wall MI during RV pacing: Similar to MI in presence of LBBB. ii. Inferior wall MI during RV pacing: RV pacing masks the inferior wall MI. Following are ECG criteria for diagnosis of inferior wall MI during RV pacing: ● ●

●

●

GUSTO-1 criteria46 QR or Qr pattern in inferior leads with a specificity of 100% but with low sensitivity (15%) Normally, RV pacing results in QS, R, or qR pattern in aVR, hence rS pattern in aVR is diagnostic with a specificity of 52% and sensitivity of 15%. Cabrera sign in III, aVF leads is insensitive (see Fig. 27.34).

MYOCARDIAL INFARCTION AND ISCHEMIA

1. ST 1 mm in concordant QRS: 5p 2. ST 5 mm in discordant QRS: 2p 3. ST¯ 1 mm in V1, V2 or V3: 3p

GUSTO-1 criteria: 3p

Other less specific criteria

MI in LBBB

1. R regression → QS in V1–V4 2. Ab Q in 2 leads— 20 ms in V4 or 30 ms in V5–V6, II, III 3. Upright T in V5 or V6 4. Prominent S in V5 or V6 5. Cabrera sign 6. Chapman sign

Fig. 27.34

555

Similar to LBBB

Ant. MI

MI in RBBB

RV pacing in

Same criteria without RBBB

Inf. MI

Others: 1. QR or Qr in II, III, aVF 2. rS in aVR 3. Cabrera sign in III, aVF

GUSTO-1 criteria

of myocardial infarction (MI) in bundle branch blocks (LBBB and RBBB) and | Diagnosis during right ventricular pacing—Ant.: anterior, Inf.: inferior, GUSTO: Global Utilization of Streptokinase and Tissue plasminogen activator for Occluded coronary arteries, p: point, Ab: abnormal.

7. SENSITIVITY, SPECIFICITY AND PROGNOSTIC VALUE OF THE ECG i. The Sensitivity of the ECG The sensitivity of the ECG for recognizing autopsy proven MI was 55–61%47, while incidence of the ECG missing the diagnosis of acute infarction is 6–25%.48,49 The overall incidence of false positive diagnosis of MI was 31%.50 ii. Prognostic Value of ECG for MI i) Q Wave Infarction It is associated with more serious prognosis. ● ● ●

●

Q wave infarcts are often larger than non-Q wave infarcts.51 During early stage, mortality is higher among the patients with Q wave MI.52 The patients with Q wave infarct if not revascularized, tend to recur which is associated with increased mortality rate.53 Deeper and wider Q waves in more leads together decrease the R wave amplitude which is associated with greater decrease in the left ventricular ejection fraction (LVEF).54

556

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

ii) Site of Infarction ● ●

●

Anterior MI is associated with higher early and late mortality rates than inferior MI.55 Inferior MI has more serious prognosis in presence of: – Reciprocal ST depression in leads V1–V456 – Complete AV block is associated with more serious prognosis56 – Extensive RV infarction due to large infarct size47 There is an increased incidence of cardiogenic shock, ventricular fibrillation and complete AV block in patients with RV infarction.

iii) Abnormal T Waves ●

●

●

Higher T wave amplitude is associated with better prognosis (lower 30 days mortality) in patients receiving thrombolytic therapy for acute MI.57 Patients with acute Q MI with ST elevation of 2 mm and positive T waves are associated with large infarct and low incidence of recurrent ischemia, while patients with ST elevation 2 mm and inverted T waves have smaller infarcts and higher incidence of recurrent ischemia.58 Persistence of inverted T waves in Q MI indicates the presence of transmural infarct with a thin fibrotic layer, while positive T waves indicate a non-transmural infarct containing viable myocardium.59

iv) Associated BBB It has adverse prognosis. ●

●

●

Presence of LBBB was associated with a 34% increase in the risk of in-hospital mortality rate.60 Presence of BBB was associated with 53% higher risk for a 30-day mortality in GUSTO-I trial.61 In TAMI trial, AV block was associated with 20% mortality compared to 4% without AV block.42

v) QT Dispersion Increased QT dispersion is an indication of arrhythmia risk in patients with MI and thereby affecting the prognosis.62

REFERENCES 1. Mirvis DM, Ingram LA, Ramanathan KB, et al. R and S wave changes produced by experimental nontransmural and transmural myocardial infarction. J Am Coll Cardiol 1986;8(3):675–681. 2. Baer FM, Theissen P, Voth E, et al. Morphologic correlate of pathologic Q waves as assessed by gradient-echomagnetic resonance imaging. Am J Cardiol 1994;74(5):430–434. 3. Ben-Gal T, Sclarovsky S, Herz I, et al. Importance of the conal branch of the right coronary artery in patients with anterior wall myocardial infarction: electocardiographic and angiographic correlation. J Am Coll Cardiol 1997;29(3):506–511.

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4. Engelen DJM, Gorgels APM, Cheriex EC, et al. ECG criteria differentiating between proximal versus distal occlusion of the left anterior descending coronary artery [abstracts]. J Am Coll Cardiol 1997;29:430A. 5. Wong CK, Freedman B, Bautovich G, et al. Mechanism and significance of precordial AT-segement depression during inferior wall AMI associated with narrowing of the dominant right coronary artery. Am J Cardiol 1993;71(12):1025–1030. 6. Bairey CN, Shah PK, Lew AS, et al. Electrocardiographic differentiation of occlusion of the left circumflex versus right coronary artery as a cause of inferior AMI. Am J Cardiol 1987;60(7):456–459. 7. Casas RE, Marriott HJL, Glancy DL. Value of leads V7–V9 in diagnosing posterior wall AMI and other causes of tall R waves in V1–V2. Am J Cardiol 1997;80:508. 8. Dabrowska B, Walczak E, Prejs R, et al. Acute infarction of the left ventricular papillary muscle: electrocardiographic pattern and recognition of its location. Clin Cardiol 1996;19(5):404–407. 9. Chikamori T, Kitaoka H, Matsumura Y, et al. Clinical and electrocardiographic profiles producing exercise-induced U waves inversion in patients with severe narrowing of the left anterior descending coronary artery. Am J Cardiol 1997;80(5):628–632. 10. Jaffe ND, Boden WE. Spontaneous transient, inverted U waves as initial electrocardiographic manifestations of unstable angina. Am Heart J 1995;129(5):1028–1030. 11. Schneider CA, Voth E, Baer FM, et al. QT dispersion is determined by the extent of viable myocardium in patients with chronic Q-wave myocardial infarction. Circulation 1997;96(11): 3913–3920. 12. Sporton SC, Taggart P, Sutton PM, et al. Acute ischemia: A dynamic influence on QT dispersion. Lancet 1997;349:306. 13. Zmyslinski RW, Akiyama T, Biddle TL, et al. Natural course of ST segment and QRS complex in patients with acute anterior MI. Am J Cardiol 1979;43(1):29–34. 14. Mills RM, Young E, Gorlin R, et al. Natural history of ST segment elevation after AMI. Am J Cardiol 1975;35(5):609–614. 15. Iwaski K, Kusachi S, Hina K, et al. Q wave regression unrelated to patency of infarct-related artery or left ventricular ejection fraction or volume after anterior wall AMI treated with or without reperfusion therapy. Am J Cardiol 1995;76:14. 16. de Zwaan C, Bar FW, Janssen JH, et al. Angiographic and clinical characteristics of patients with unstable angina, showing an ECG pattern indicating narrowing of left anterior descending coronary artery. Am Heart J 1989;117(3):657–665. 17. Hirata K, Kyushima M, Asato H. Electrocardiographic abnormalities in patients with acute aortic dissection. Am J Cardiol 1995;76(16):1207–1212. 18. Ludman PF, Hildick-Smith D, Harcombe A, et al. Transient ST segment changes associated with mitral valvuloplasty using Inoue balloon. Am J Cardiol 1997;79(12):1704–1705. 19. Patel J, Movahed A, Reeves WC. Electrocardiographic and segmental wall motion abnormalities in pancreatitis mimicking myocardial infarction. Clin Cardiol 1994;17(9):505–509. 20. Rich MW. Myocardial injury caused by an anaphylactic reaction to ampicillin/sulbactam in a patient with normal coronary arteries. Tex Heart Inst J 1998;25(3):194–197. 21. Lehmann KG, Shanding AH, Yusi AU, et al. Altered ventricular repolarization in central sympathetic dysfunction associated with spinal cord injury. Am J Cardiol 1989;63(20):1498–1504. 22. Anderson HR, Falk E, Nielsen D. Right ventricular infarction frequency, size and topography in coronary heart disease: a prospective study comprising 107 consecutive autopsies from a coronary care unit. J Am Coll Cardiol 1987;10:1223. 23. Wartman WB, Hellerstein HK. The incidence of heart disease in 2000 consecutive autopsies. Ann Intern Med 1948;28:41. 24. Erhardt LR, Sjogren A, Wahlberg I. Single right sided precordial lead in the diagnosis of right ventricle involvement in inferior myocardial infarction. Am Heart J 1976;91(5):571–576. 25. Geft HL, Shah PK, Rodriguez L, et al. ST elevation in leads V1 to V3 may be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol 1984;53(8):991–996. 26. Mak KH, Chia BL, Tan ATH, et al. Simultaneous ST segment elevation in lead V1 and depression in lead V2: A discordant ECG pattern indicating right ventricular infarction. J Electrocardiol 1994; 27(3):203–207.

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27. Lew AS, Laramee P, Shah PK, et al. Ratio of ST segment depression in leads V2 to ST segment elevation in lead aVF in evolving inferior acute myocardial infarction: an aid to the early recognition of right ventricular ischemia. Am J Cardiol 1986;57(13):1047–1051. 28. Medrano GA, de Micheli A, Osornio A. Interatrial conduction and STa in experimental atrial damage. J Electrocardiol 1987;20(5):357–363. 29. Liu CK, Greenspan G, Piccirillo RT. Atrial infarction of the heart. Circulation 1961;23;331–338. 30. Fuchs RM, Achuff SC, Grunwald L, et al. Electrocardiorphic localizations coronary artery narrowings: studies during myocardial ischemia and infarction in patients with one-vessel disease. Circulation 1984;60:1209. 31. Ben-Gal T, Herz I, Solodky A, et al. Acute anterior wall MI entailing ST segment elevation in lead V1: electrocardiographic and angiographic correlations. Clin Cardiol 1998;21:399. 32. Zimetbaum PJ, Krishnan S, Gold A, et al. Usefulness of ST segment elevation in lead III exceeding that of lead II for identifying the location of the totally occluded coronary artery in inferior wall myocardial infarction. Am J Cardiol 1998;81(7):918–919. 33. Herz I, Assali AR, Adler Y, et al. New electrocardiogrphic criteria for predicting either right coronary artery or left circumflex artery as the culprit coronary artery in inferior wall AMI. Am J Cardiol 1997;8:1343. 34. Kosuge M, Kimura K, Ishikawa T, et al. New electrocardiographic criteria for predicting the site of coronary artery occlusion in inferior wall acute myocardial infarction. Am J Cardiol 1998;82:1318–1322. 35. Birnbaum Y, Wagner GS, Barbash GI, et al. Correlation of angiographic findings and right (V1–V3) versus left (V4–V6) precordial ST segment depression in inferior wall acute myocardial infarction. Am J Cardiol 1999;83:143. 36. Engelen DJ, Gorgels AP, Cheriex EC, et al. Value of electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infraction. J Am Coll Cardiol 1999;34:389–395. 37. Karthik V, Manjunath CN, Srinivas KH, et al. Electrocardiographic localization of the occlusion site in left anterior descending coronary artery in acute anterior myocardial infraction. IHJ 2004;56(4): 315–319. 38. Birnbaum Y, Sclarovsky S, Solodky A, et al. Prediction of the level of left anterior descending coronary artery obstruction during anterior wall AMI by admission electrocardiogram. Am J Cardiol 1993;72(11):823–826. 39. Porter A, Sclarovsky S, Ben-Gal T, et al. Value of T wave direction with lead III ST segment depression in acute anterior wall MI: electrocardiographic prediction of a “wrapped” left anterior descending artery. Clin Cardiol 1998;21(8):562–566. 40. Moreno AM, Alberola AG, Thomas JG, et al. Incidence and prognostic significance of RBBB in patients with AMI receiving thrombolytic therapy. Int J Cardiol 1997;61(2):135–141. 41. Nimetz AA, Shubrooks SJ, Hutter AM, et al. The significance of BBB during AMI. Am Heart J 1998;21:2651. 42. Simons GR, Sgarbossa W, Wagner G, et al. Atrioventricular and intraventricular conduction disorders in AMI: a reappraisal in the thrombolytic era. PACE 1998;21:2651. 43. Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of LBBB. GUSTO-1 (Global Utilization of Streptokinase and Tissue plasminogen activator for Occluded coronary arteries). N Engl J Med 1996;334:481–487. 44. Barold SS, Falkoff MD, Ong LS, et al. Electrocardiographic diagnosis of myocardial infarction during ventricular pacing. Cardiol Clin 1987;5:403–417. 45. Chapman MG, Pearce ML. Electrocardiographic diagnosis of myocardial infarction in the presence of LBBB. Circulation 1957;16:558. 46. Sgarbossa EB, Pinski SL, Gates KB, et al. Early electrocardiographic diagnosis of myocardial infarction in the presence of ventricular paced rhythm. GUSTO-1 investigators: Am J Cardiol 1996;77(5):423–424. 47. Chou TC. Electrocardiography. In: Clinical Practice, 4th ed. Philadelphia: WB Saunders, 1996. 48. Levine HD, Philips E. An appraisal of the newer electrocardiography: correlations in one hundred and fifty consecutive autopsied cases. N Engl J Med 1951;245(22):833–842.

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49. Woods JD, Laurie W, Smith WG. The reliability of the electrocardiogram in myocardial infarction. Lancet 1963;2:265–269. 50. Gunnar RM, Pietras RJ, Blackaller J, et al. Correlation of vector cardiographic criteria for myocardial infarction with autopsy findings. Circulation 1967;35(1):158–171. 51. Krone RJ, Greenberg H, Dwyer EM, et al. Long term prognostic significance of ST segment depression during AMI. J Am Coll Cardiol 1993;22(2):361–367. 52. Klein LW, Helfant RH. The Q wave and non Q wave myocardial infarction: differences and similarities. Prog Cardiovasc Dis 1986;29(3):205–220. 53. Birnbaum Y, Chetrit A, Sclarovsky S, et al. Abnormal Q waves on admission electrocardiogram of patients with first myocardial infarction: prognostic implications. Clin Cardiol 1997;20(5):477–481. 54. Sevilla DC, Wagner NB, Pegues R, et al. Correlation of the complete version of the Selvester QRS scoring system quantitative anatomic findings for multiple left ventricular myocardial infarcts. Am J Cardiol 1992;69(5):465–469. 55. Stone PH, Raabe DS, Jaffe AS, et al. Prognostic significance of location and type on myocardial infarction: independent adverse outcome associated with anterior location. J Am Coll Cardiol 1988; 11(3):453–463. 56. O’Rourke RA. Treatment of RV infarction: thrombolytic therapy, coronary angioplasty, or neither? J Am Coll Cardiol 1998;37:882–884. 57. Hochrein J, Sun F, Pieper KS, et al. Higher T wave amplitude associated with better prognosis in patients receiving thrombolytic therapy for AMI (a GUSTO-1 substudy). Am J Cardiol 1998;81(9): 1078–1084. 58. Sclarovsky-Benjaminov F, Sclarovsky S, Birnbaum Y. The predictive value of the electrocardiographic pattern of acute Q-wave myocardial infarction for recurrent ischemia. Clin Cardiol 1995; 18(12):710–715. 59. Maeda S, Imai T, Kuboki K, et al. Pathologic implications of restored positive T waves and persistent negative T waves after Q wave myocardial infarction. J Am Coll Cardiol 1996;28(6):1514–1518. 60. Go AS, Barron HV, Rundle AC, et al. Bundle branch block and in-hospital mortality in AMI. Ann Intern Med 1998;129(9):690–697. 61. Sgarbossa EB, Pinski SI, Topol EJ, et al. Acute myocardial infarction and complete bundle branch block at hospital admission: characteristics and outcome in the thrombolytic era. J Am Coll Cardiol 1998;31(1):105–110. 62. Dnyaneshwar V Mulay, Syed M Quadri. QT dispersion and early arrhythmic risk in acute myocardial infarction. IHJ 2004;56(6):636–641.

■ ■ ■ CHAPTER 28

PERICARDITIS PERICARDITIS i. ECG Changes Due to Pressure Effects

560 560

AND

MYOCARDITIS

ii. ECG Changes Due to Superficial Myocarditis MYOCARDITIS REFERENCES

560 565 566

PERICARDITIS The ECG changes in acute pericarditis mimic early repolarization and acute anteroinferior infarction, which are believed to be related to an actual current of injury caused by: ● ●

The pressure of fluid or fibrin and Superficial myocardial inflammation (myocarditis).

The ECG changes in later stages are due to the progression to effusion, tamponade, or constriction. i. ECG Changes Due to Pressure Effects ●

●

Pressure on the myocardium produces a ‘current of injury’ manifested by deviation of the ST segment from the baseline. The ST elevation is due to current flowing from the epicardial surface to the thorax and back into the heart through atria and great vessels.1 The ST elecation is more common with less pronounced reciprocal ST depression. ST elevation occurs in 70% in leads I, II, V5 and V6, in 32–55% in leads III, aVL, aVF, V3, and V4, and reciprocal ST depression in 64%, usually in leads aVR and V1.2 The PR segment depression occurs in all leads except in aVR and occasionally in V1, in which PR segment is elevated. The depression of PR segment occurs in 80% and reflects abnormal atrial repolarization due to atrial inflammation. However, any PR segment depression 0.8 mV or elevation 0.5 mV suggests the presence of atrial injury.3

ii. ECG Changes Due to Superficial Myocarditis ● ●

Manifested by T wave inversion in all leads except aVR and V1. However in typical cases of pericarditis, the T wave inversion is incomplete and amplitude of the inverted T waves is relatively low, which gives rise to a diphasic

PERICARDITIS AND MYOCARDITIS

561

Table 28.1 ECG evolution of acute pericarditis Epicardial leads: I, II, aVF, aVL and V3–V6

Endocardial leads: aVR and V1

Stage

ST segment

T waves

PR segment

ST segment

T waves

PR segment

1. I

Elevated

Upright

Depressed

Inverted

2. Early II

Isoelectric

Upright

Isoelectric

Inverted

3. Late II

Isoelectric

Isoelectric

Isoelectric Isoelectric

Isoelectric Isoelectric

Isoelectric Isoelectric

Flat or upright Upright Upright

Elevated or isoelectric Elevated or isoelectric Isoelectric

4. III 5. IV

Flat or inverted Inverted Upright

Depressed or isoelectric Depressed or isoelectric Isoelectric

Isoelectric Isoelectric

(positive–negative) wave or a notched T wave, a characteristic ECG feature of acute pericarditis.4 Evolution of ECG Changes Four stages have been described in the evolution of acute pericarditis, which occurs in few hours to days, after the onset of pericardial pain5 (see Table 28.1). Stage I accompanies the onset of chest pain and comprises of: ●

●

●

ST segment (J–ST) elevation with concavity upwards and upright T waves, PR segment depressed or isoelectric usually in I, II, aVL, aVF, and V3–V6 (see Fig. 28.1). ST segment depression with inverted T waves and elevated or isoelectric PR segment occurs in aVR and V1, and sometimes in V2 lead. QTc is usually normal, but may be prolonged in postoperative pericarditis.

ST elevation in acute pericarditis should be differentiated from acute myocardial infarction (AMI) and early repolarization ●

●

The ST elevation is less pronounced, elevation 0.5 mV is uncommon in pericarditis as compared to early stages of MI, indicating that injury current is probably smaller with pericarditis than with AMI. – In MI, ST segment elevation has convexity upwards with frontal QRS axis usually 100 to 120, while in acute pericarditis, ST segment elevation has concavity upwards and frontal QRS axis is 30 to 60.6 – The reciprocal ST depression is less pronounced and in fewer leads than in AMI. In early repolarization which is often seen in young males (40 years of age), ST segment changes are accompanied by tall and peaked T waves, R–S slurring, ST segment/T wave ratio in V6 0.25, and no ST evolution. Tallest T wave is noticed in V4. Acute pericarditis is characterized by ST evolution, tallest T in V5 and ST segment elevation/T wave amplitude ratio in V6 0.25.7

The PR segment changes in acute pericarditis should be differentiated from atrial injury ●

Any PR segment depression 0.8 mV or elevation 0.5 mV suggests the presence of atrial injury.3

562

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 28.1

pericarditis—diffuse ST segment elevation (concavity upwards) and PR | Acute segment depression.

Stage II occurs several days later and ECG changes consist of: ●

●

●

In leads I, II, aVL, aVF, and V3–V6: Return of the ST segment to the baseline, i.e. becomes isoelectric. PR segment may become isoelectric or remains depressed. In late stage II, T waves become progressively flattened to inverted. Such transient normalized ECG is observed in 20% of the patients for a period of 1 to 5 days (average of 2.3 days).2 In leads aVR and V1: ST segment also becomes isoelectric. PR segment may also return to baseline or may remain elevated. In late stage II, T waves become progressively flattened to upright. The change in the ST segment usually occurs prior to the appearance of T wave inversion in the main leads, while in AMI; T waves become inverted before ST segment returns to the baseline.

Stage III is characterized by T wave inversion in I, II, aVL, aVF and V3–V6. ●

●

●

T wave inversion occurs in more leads, but less deep or less completely inverted than in AMI. This is not associated with loss of R wave voltage or appearance of Q waves, characteristic of evolution of myocardial infarction. The stage III has become less frequent due to effective early treatment with antiinflammatory agents.

Stage IV represents the reversion of T wave changes to normal, which may take weeks to months. ●

However, T wave inversion may occasionally persist indefinitely in patients with chronic inflammation due to tuberculosis, uremia or neoplastic pericardial disease.

ECG Variants in Pericarditis ● ● ●

Abnormal ECG changes appear in 90% of cases. However, all four stages are detected only in about 50%. Sinus tachycardia is common and may be present in the absence of other contributing factors such as fever or hemodynamic compromise.8

PERICARDITIS AND MYOCARDITIS ●

●

563

Other atrial arrhythmias are infrequent. VT, AV block and BBB are not the features of acute pericarditis. The variations of the ECG pattern are present in 50% of the cases and includes typical and atypical variants.

i) Typical ECG variants: ● ● ●

●

Absence of one or more stages of the ST segment and T wave changes. There may be rapid evolution of stage I directly to stage IV. There may be persistence of stage III (T wave inversion) indefinitely or for long periods due to chronic pericardial inflammation or presaging constrictive evolution. In stage I, ST segment may be isoelectric or depressed in III, aVL, and isoelectric in I.

ii) Atypical ECG variants: ●

● ●

●

●

Absence of any serial ECG changes due to rapid evolution or delayed recording or accompanying superficial myocarditis is of low grade or absent. There may be isolated PR segment depression without ST–T changes. There is appearance of ST segment changes in only a few leads which may be mistaken for myocardial ischemia. However in pericarditis, reciprocal ST changes are absent. Appearance of T wave inversion before the ST segment returned to the baseline is characteristic of MI. In stage III, there may be T wave inversion only in some leads, usually V3 or V4–V6.

ECG Changes During Progression of Pericarditis i) Pericardial effusion ● Low amplitude ECG (QRS amplitude 0.5 mV in limb leads and 1.0 mV in precordial leads) is seen in most of the cases (see Fig. 28.2). ● Low P wave voltage indicates massive effusion. ● There may be ST–T wave changes due to superficial myocarditis, which may persist or disappear after paracentesis.

Fig. 28.2

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

effusion—low voltage ECG with T with inversion in I, II, III, aVF, | Pericardial and V –V . 5

6

564

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY ●

Electrical alternans can occur in pericardial effusion due to the changes in cardiac position that result from rotational and pendular motion of the heart, which is normally restrained by the lungs and mediastinum.9 This motion of the heart has been termed as ‘cardiac nystagmus’.10 However, electrical alternans is characteristic of cardiac tamponade.

Other causes of low voltage ECG include: Cardiac causes: ● ● ●

Hypothyroidism (myxedematous myocardial involvement) Chronic constrictive pericarditis Diffus myocardial diseases: amyloidosis, scleroderma, cardiac neoplasm, myocardial fibrosis (due to chronic ischemic heart disease).

Non-cardiac causes: ● ● ● ●

Pleural effusion Emphysema Pneumothorax, and Excess epicardial or subcutaneous fat overlying the heart.

ii) Cardiac tamponade ●

Electrical alternans is pathognomonic of acute cardiac tamponade in 1/3rd of the cases. Alternans is usually limited to QRS complex (2:1 or 3:1 pattern), while T and P waves alternans are rare (see Fig. 28.3). It is critically related to heart rate and beta-blockers which slow the heart rate and make alternans disappear. I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 28.3

| Cardiac tamponade—sinus tachycardia with QRS electrical alternans.

PERICARDITIS AND MYOCARDITIS

I

↑P IAB

II

aVR

V1

V4

aVL

V2

V5

aVF

V3

V6

565

↓P III

Fig. 28.4

pericarditis—low voltage ECG with flat to inverted T waves and | Constrictive wide P waves (due to interatrial block: IAB, upright in I, inverted in III, and biphasic in V1–V2).

●

●

●

ECG changes of acute pericarditis of any stage can be found, but most ST segment deviations are absent and T waves are low to inverted. QRS-T voltage tends to decrease (usually due to reduced heart size), but the degree of changes is unrelated to the severity of tamponade. Acute hemorrhagic tamponade provokes bradycardia often of the AV junctional origin.

iii) Constrictive pericarditis (CP): ● ●

●

●

ECG changes include:

Low QRS voltage seen in 55–90%.11 Generalized T wave inversion, flattening or notching is most common ECG finding, which is seen in 90–100% of the cases11,12 (see Fig. 28.4). P waves may be wide and bifid (interatrial block) and sometimes resembling P mitral with P wave axis between 90 and 10. Atrial arrhythmias occur in CP, usually atrial fibrillation (23–36%) and occasionally atrial flutter (6–10%).11,12 The arrhythmias increase with chronicity and are related to long standing elevation of atrial pressures and atrial enlargement.

MYOCARDITIS Myocarditis is said to be present when the heart is involved in an inflammatory process often caused by any infectious agent. However, it is usually described during and after a wide variety of viral, rickettsial, bacterial and metazoal diseases. ECG abnormalities occur more frequently than clinical myocardial involvement, but are usually transient. ●

●

●

ST segment depression or T wave inversion or both in LV epicardial leads: commonest ECG findings in acute myocarditis13 (see Fig. 28.5). Prolongation of AV or intraventricular conduction: complete AV block is usually transient and resolves usually without any sequelae. Intraventricular conduction abnormalities are associated with more severe myocardial damage and worst prognosis.14 Lengthening of QTc interval.

566

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Fig. 28.5

| Acute myocarditis—T wave inversion in precordial leads.

1. Diffuse ST↑ 5 mm and concavity upwards 2. Diffuse depressed PR segment and T↓

Cardiac tamponade

1. QRS electrical alternans 2. Flat or T↓

Pericardial disease

Myocarditis

Constrictive pericarditis

1. ST↓ T↓ 2. ↑QTc 3. Atrial and ventricular arrhythmias

Pericarditis 1. Less reciprocal ST↓ 2. Axis: 30o to 60o 3. ST↑/T amplitude in V6: 0.25

1. Low voltage ECG 2. ST–T changes may persist

Fig. 28.6

Pericardial effusion

1. Low QRS voltage 2. Flat or T↓ 3. Af or Afl

diagnosis of pericardial diseases and myocarditis—Af: atrial fibrillation, Afl: atrial flutter, | ECG vent.: ventricular, QTc: increased corrected QT interval, ST: ST elevation, ST: ST depression, T: inverted T waves.

● ●

Various atrial and ventricular arrhythmias. QRS abnormalities that may mimic MI may also occur (see Fig. 28.6).

REFERENCES 1. Teh BS, Walsh J, Bell AJ, et al. Electrical current paths in acute pericarditis. J Electrocardiol 1993;26(4): 291–300. 2. Surawicz B, Lassiter KC. Electrocardiogram in pericarditis. Am J Cardiol 1970;26(5):471–474.

PERICARDITIS AND MYOCARDITIS

567

3. Charles MA, Bensinger TA, Glasser SP. Atrial injury current in pericarditis. Arch Intern Med 1973; 131(5):657–662. 4. Noth PM, Barnes HR. Electrocardiographic changes associated with pericarditis. Arch Intern Med 1940;55:291. 5. Spodick DH. ECG changes in acute pericarditis. Am J Cardiol 1974;33(4):470–474. 6. Kouvaras G, Soufras G, Chronopoulos G, et al. The ST segment as a different diagnostic feature between acute pericarditis and acute inferior myocardial infarction. Angiology 1990;41:207. 7. Spodick DH. Electrocardiographic abnormalities in pericardial disease. In: Spodick DH: the Pericardium: a comprehensive Text book, New York, Marcel Dekker, 1997:40–64. 8. Dressler N. Sinus tachycardia complicating and outlasting pericarditis. Am Heart J 1966;72(3): 422–423. 9. McGregor M, Baskind E. Electrical alternans in pericardial effusion. Circulation 1955;11(6):837–843. 10. Littman D. Alternation of the heart. Circulation 1963;27:280–291. 11. Dalton JC, Pearson RJ, White PD. Constrictive pericarditis: a review and long term follow up of 78 cases. Ann Intern Med 1956;45(3):445–458. 12. Wood P. Chronic constrictive pericarditis. Am J Cardiol 1961;7:48. 13. Chida K, Ohkawa S, Esaki Y. Clinicopathological characteristics of elderly patients with persistent ST segment elevation and inverted T waves: evidence of insidious or healed myocarditis? J Am Coll Cardiol 1995;25:1641. 14. Matsuura H, Palacios IF, Dec GW, et al. Intraventricular conduction abnormalities in patients with clinically suspected myocarditis are associated with myocardial necrosis. Am Heart J 1994; 127(5):1290–1277.

■ ■ ■ CHAPTER 29

D RUG E FFECTS

AND

E LECTROLYTE

A BNORMALITIES DIGITALIS Digitalis Effects Mechanism of Digitalis Induced Arrhythmias ELECTROLYTE ABNORMALITIES AND ECG CHANGES: HYPERKALEMIA Modification of Hyperkalemic Effects by Other Electrolytes

568 568 572 572 573

HYPOKALEMIA 574 Modification of Hypokalemic Effects by Other Electrolytes 575 HYPERCALCEMIA 576 HYPOCALCEMIA 577 HYPERMAGNESEMIA 578 HYPOMAGNESEMIA 578 REFERENCES 579

DIGITALIS It is an inotropic agent discovered by William Withering in 1785. It has a steroid nucleus with an , -unsaturated lactone ring attached to C-17 position. ●

●

●

Its positive ionotropic effect is by inhibition of the Na pump (Na, KATPase) which results in an increase in the cytolic Ca2 concentration through Ca channels and Calcium pump (Na–Ca Exchanger) of the sarcolemma. On oral administration, it is mainly absorbed in small and large intestines, and in general serum therapeutic level ranges 0.5–1.5 mg/L.1 Therapeutically, it is mainly used in CHF, and four types of supraventricular tachycardia (SVT)—paroxysmal SVT, atrial fibrillation, atrial flutter and Wolff-ParkinsonWhite (WPW) syndrome.

Digitalis Effects The effects of digitalis therapy are mainly classified into three groups—therapeutic, excessive and/or toxic, unequivocal toxic effects. Therapeutic Effects These are acceptable effects of digitalis which include: ●

ST segment is shortened and depressed with characteristic rounded, concave (scooped) configuration. With ST depression, T wave is ‘dragged’ downwards giving the appearance of T wave inversion and ‘inverted right mark’ appearance (see Fig. 29.1). The dragged T wave may become diphasic, with initial portion being negative and terminal portion being positive. However, decreased amplitude of T wave and shortened

DRUG EFFECTS AND ELECTROLYTE ABNORMALITIES

569

QT interval are the earliest ECG changes. These ST–T changes are usually more pronounced in leads with tall R waves or in inferior and left precordial leads, while it is less marked in right precordial leads. Shortening of QT interval with occasional appearance of prominent U waves. Prolongation of PR interval may also occur. Slowing of the ventricular response is used in atrial fibrillation or flutter, and conversion of atrial arrhythmias to sinus rhythm directly or indirectly may also occur.

● ● ●

Excessive or Toxic Effects Digitalis is known to induce every known arrhythmias but rarely atrial flutter and BBB. Suspect digitalis toxicity when both increased automaticity and impaired conduction are present at the same time. Non-paroxysmal junctional tachycardia: It is highly specific for digitalis excess or toxicity. Atrial tachycardia with block (careful attention to lead V1 distinguishes it from atrial flutter) (see Figs 29.2 and 29.3). Paroxysmal atrial tachycardia (PAT) with block occurs in about 73%.2 Second degree AV block usually of the Wenkebach type, while Mobitz type II 2nd degree AV block is rare (see Fig. 29.4). Complete AV block in digitalis toxicity is uncommon (see Fig. 29.5) and as a rule is associated with narrow QRS complexes, since the level of block is proximal to the His bundle bifurcation. SA block can also occur. Atrial fibrillation accounts for 10% of the arrhythmias induced by digitalis (see Fig. 29.6).

●

●

●

● ●

I

II

III

V1

V2

V3

Fig. 29.1

V1

Fig. 29.2

aVR

V4

aVL

V5

aVF

V6

effect—ST depression with dragging of T waves resulting in charac| Digitalis teristic ‘inverted right mark’ and shortened QT interval.

P

R

P R

| Digitalis toxicity—atrial tachycardia with 1:1 conduction.

570

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

V1

P

P

P R

P

P R

aVF

Fig. 29.3

| Digitalis toxicity—atrial tachycardia with 2:1 AV block. V1

P

P

P

P

P

V4

Fig. 29.4

degree 2:1 AV block with regular atrial rate of 86/min, ventricular | Second rate of 43/min and ST depression in V due to digitalis toxicity which is not 4

common.

P

Fig. 29.5

P

AV block with normal QRS complex and blocked premature atrial | Complete contractions (arrow) due to digitalis toxicity which is also not common.

DRUG EFFECTS AND ELECTROLYTE ABNORMALITIES

571

V1

Fig. 29.6

| Atrial fibrillation occurs in 10% of digitalis toxicity.

V1

V6

Fig. 29.7

| Ventricular bigeminy—definite evidence of digitalis toxicity.

Fig. 29.8

ventricular tachycardia with slight irregularity—strong evidence | Bidirectional of digitalis toxicity.

Unequivocal Toxic Effects Presence of ventricular arrhythmias is the definite evidence of digoxin toxicity. ●

● ●

● ●

Ventricular premature contractions (VPC) are the earliest and most common manifestations of digitalis toxicity with least specificity. Ventricular bigemini and multifocal VPCs (see Fig. 29.7). Ventricular tachycardia (VT): VT with exit block and bi-directional VT strongly suggests digoxin toxicity3 (see Fig. 29.8). Ventricular fibrillation (VF): Digitalis induced VF is rarely recorded in humans. AV dissociation strongly indicates digitalis toxicity (see Table 29.1).

572

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 29.1 ECG in digitalis toxicity 1. 2. 3. 4. 5. 6.

Non-paroxysmal junctional tachycardia Second degree AV block (Mobitz type I) Sinoatrial (SA) block Ventricular premature contractions (VPCs) especially bigeminy and multifocal Ventricular tachycardia (VT) especially with exit block and bi-directional VT Atrioventricular (AV) dissociation

1. ST↓ 2. ↓T amplitude 3. T dragged down → ‘inverted right mark’ appearance

1. VPCs—multifocal and bigeminy 2. Bi-directional VT Unequivocal

Therapeutic effects 4. Prolonged PR 5. Decreased QTc with occasional U waves

Fig. 29.9

3. AV dissociation

Digitalis

Toxic effects

Excessive/toxic 1. NP junctional tachycardia 2. PAT with AV block 3. Atrial fibrillation

4. 2° AV blockWenkebach type 5. SA block

and toxic effects of digitalis—VPCs: ventricular premature con| Therapeutic tractions, VT: ventricular tachycardia, NP: non-paroxysmal, PAT: paroxysmal atrial tachycardia, ST: ST depression, T amplitude: decreased T amplitude.

Mechanism of Digitalis Induced Arrhythmias ●

● ● ●

Enhanced automaticity, reentry or delayed after depolarization results in atrial tachycardia with block, non-paroxysmal junctional tachycardia, VPCs, VT, bi-directional VT, ventricular fibrillation or flutter. Depression of the pacemaker causes SA node arrest. Depression of the conduction results in SA block and AV block. AV dissociation results in suppression of the dominant pacemaker with passive escape of lower junctional focus or inappropriate acceleration of a subsidiary pacemaker (see Fig. 29.9).

ELECTROLYTE ABNORMALITIES AND ECG CHANGES: HYPERKALEMIA It is associated with a distinctive sequence of ECG changes. The correlation between plasma K and ECG is less reliable, but there is a good correlation between plasma K levels and surface ECG in experimental hyperkalemia.

DRUG EFFECTS AND ELECTROLYTE ABNORMALITIES

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Fig. 29.10

573

| Hyperkalemia—tall tented T waves in II, aVF and V –V . 2

●

●

● ●

●

6

At a plasma level of about 5.7 mEq/L: T wave is tall, peaked (tented) and often symmetrical with a narrow base ( 0.20 s)4 and a normal or decreased QTc interval, which is best seen in Leads II, III, and V2–V4 (see Fig. 29.10). At a plasma level of about 7.0 mEq/L: There is reduction in the amplitude of P wave, intra-atrial conduction delay, prolongation of PR interval, and QRS begins to widen. At a plasma level of about 8.4 mEq/L: P wave is no longer recognizable. At a plasma level of 9–11 mEq/L: – QRS complex is uniformly widened, with prolongation of both initial and terminal portions, resulting in a pattern that may resemble RBBB, LBBB, left anterior or left posterior fascicular block or a combination of the four. – In RBBB pattern due to hyperkalemia, initial phase of QRS complex is prolonged, while in conventional RBBB, only the terminal portion of the QRS complex is delayed. – Similarly in LBBB pattern due to hyperkalemia, terminal portion of the QRS complex is delayed, while in conventional LBBB, only the initial portion of the QRS complex is prolonged. – Occasionally hyperkalemia induces ST elevation in right precordial leads (V1–V2) stimulating MI, known as the ‘dialyzable current of injury’, which disappears after appropriate treatment5 (see Fig. 29.11). At a plasma level of 12 mEq/L: SA block, AV block (Wenkebach-type I or Mobitz type II), junctional or ventricular escape rhythms may be present. However, it eventually leads to asystole sometimes preceded by undulating ventricular flutterfibrillation (see Table 29.2).

Modification of Hyperkalemic Effects by Other Electrolytes ●

Hypocalcemia frequently accompanies hyperkalemia in patients with renal insufficiency, which aggravates AV and intraventricular conduction disturbances and facilitates the appearance of ventricular fibrillation.

574

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

V1

V4

V2

V5

V3

V6

Fig. 29.11

Advanced hyperkalemia—tall and peaked T waves (best seen in V ) and | elevated ST segment in V (‘dialyzable current of injury’), widened QRS 3

1

complexes and flat P waves. Table 29.2 ECG in hyperkalemia 1. 2. 3. 4. 5. 6.

●

●

Tall tented T waves with narrow base Reduced P wave amplitude, which eventually disappears Prolonged of PR interval Normal or decreased QTc interval Widened QRS complex resembling RBBB or LBBB ECG changes best seen in II, III, V2–V4 leads

Hypercalcemia with hyperkalemia may also present in some patients with renal insufficiency due to the overzealous therapy with calcium or associated secondary hyperparathyroidism which may counteract the effects of hyperkalemia and prevent ventricular fibrillation. Similarly, hypernatremia may counteract the effects of hyperkalemia, while hyponatremia may augment the effects of hyperkalemia on AV and intraventricular conduction disturbances.

HYPOKALEMIA ECG also serves as a reasonably satisfactory guide to serum K levels in hypokalemia and there is a reasonable correlation between plasma K level 2.3 or 3.0 mEq/L and ECG changes. The ECG changes are a reflection of the K gradient across the cell membrane and hence indicate the ratio of extracellular and intracellular K. Hypokalemia is characterized by: ●

●

●

Gradual depression of ST segment, decrease of T wave amplitude (flattening of T wave) with occasional T wave inversion. Prominent upright U waves, best seen in V2–V4 due to prolonged repolarization of Purkinje fibers (see Fig. 29.12). Sometimes, the sinus beat that follows the VPC shows a prominent U wave and may be the only ECG clue to hypokalemia. QT interval is usually normal; QU interval is prolonged4 that may predispose to torsades de pointes.

DRUG EFFECTS AND ELECTROLYTE ABNORMALITIES

I

aVR

575

V4

V1

U II

V2

aVL

V5

U III

Fig. 29.12

V3

aVF

with ST segment depression, prominent U waves (amplitude | Hypokalemia more than T waves) especially in V –V . 2

●

V6

3

Hypokalemia also predisposes to various tachyarrhythmias similar to antiarrhythmic drugs including quinidine and digitalis: – Ectopics: supraventricular (22%) and ventricular ectopics (28%).6 – Similar to digitalis toxicity: nonparoxysmal atrial tachycardia with AV block and AV dissociation due to a combination of increased automaticity of ectopic pacemakers and AV conduction disturbance. – Serious ventricular arrhythmias including VT, torsades de pointes and ventricular fibrillation in patients with severe hypokalemia.7

Hypokalemia which frequently occurs in AMI and predisposes to arrhythmias is due to: ●

●

Intense sympathetic stimulation by the circulating epinephrine that shifts K into the skeletal muscle and liver.8,9 Due to treatment with thiazide diuretics7 or administration of sodium bicarbonate during resuscitation.10

Surawicz et al attempted quantitative analysis of ECG pattern of hypokalemia and proposed a diagnostic criteria.11 ● ● ●

ST segment depression of 0.5 mm U wave amplitude of 1 mm U wave amplitude  T wave amplitude in the same lead.

The ECG was considered to be ‘typical’ of hypokalemia if three of the above features were present in two leads. It was considered ‘compatible’ with hypokalemia if two of the above features or one related to the U wave were present. When serum K level was 2.7 mEq/L, the ECG was typical in 78% and compatible in 11% (see Table 29.3). Modification of Hypokalemic Effects by Other Electrolytes ST segment is prolonged in hypokalemic patients with hypocalcemia, without affecting its arrhythmogenic effects.6

576

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 29.3 ECG in hypokalemia 1. 2. 3. 4. 5.

Prominent upright U waves Normal QT interval Gradual ST depression Decrease amplitude/flattening of T waves Best seen in V2–V4

Normal

Hypercalcemia

I

I

II

II

III

III

QT 0.36 s QTc 0.41

Fig. 29.13

QT 0.26 s QTc 0.36

| Hypercalcemia—QT interval is shortened.

HYPERCALCEMIA The serum Ca2 level affects the duration of phase 2 of the action potential which determines the duration of ST segment and thereby affects the duration of QT interval. This was initially recognized by Carter and Andrus in 1922.12 ●

●

Hypercalcemia shortens the phase 2 action potential thereby shortening the QT interval (see Fig. 29.13). QT interval correlates reasonably with serum Ca2 level, if other known factors affecting QT interval, such as age, sex, heart rate, myocardial disease, drugs and other electrolytes are eliminated.4 Of the three intervals—QT, Q-oT (Q to the onset of T wave), Q-aT (Q to the apex of the T wave), Q-aT interval has greatest accuracy and correlates best with the Ca2 level.13

DRUG EFFECTS AND ELECTROLYTE ABNORMALITIES ● ●

●

577

ST segment is shortened and occasionally depressed with T wave inversion.14 Severe hypercalcemia (serum Ca2 15 mg/dl) is often associated with T wave changes—flattened, notched or inverted.15 Cardiac arrhythmias are uncommon in patients with hypercalcemia. However, ventricular fibrillation, second or third degree AV blocks have been reported in severe hypercalcemia.16,17

HYPOCALCEMIA It prolongs phase 2 action potential duration thereby: ●

●

●

Prolonging the QT interval and ST segment (see Fig. 29.14). Similarly, Q-aT is more accurate and correlates best with serum Ca2 level. Hypocalcemia may be associated with hypokalemia, in which case ECG also shows ST segment depression, T wave inversion and prominent U waves. Hypocalcemia is often associated with hyperkalemia in chronic renal disease, in which case ECG also reveals prolonged ST segment and tall tented T waves (see Table 29.4).

Hypocalcemia

Normal

I

I

II

II

III

III

QT 0.48 s QTc 0.52

Fig. 29.14

| Hypocalcemia—QT interval is prolonged.

QT 0.36 s QTc 0.41

578

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 29.4 Hypercalcemia and Hypocalcemia Hypercalcemia

Hypocalcemia

1. Shortened QT interval 2. Shortened ST segment 3. T wave changes with severe hypercalcemia

1. Prolonged QT interval 2. Prolonged ST segment 3. Prominent U waves when associated with hypokalemia 4. Tall tented T waves when associated with hyperkalemia

4. Arrhythmias-vent fibrillation and AV blocks in severe hypercalcemia

1. ST↓, flat T 2. U 1mm amplitude and T 3. ↑QU interval 4. Atrial and ventricular arrhythmias

1. ↓QT (Q-aT) 2. Shortened ST 3. T changes

Hypercalcemia (Ca↑)

Hypokalemia (K↓) Electrolytes

1. Tall tented T 2. Flat P 3. Prolonged PR 4. Widened QRS → resemble bundle branch blocks 5. ST↑ in V1–V2 (DCI) 6. 2° AV block 7. SA block

Fig. 29.15

Hyperkalemia (K↑)

Hypocalcemia (Ca↓)

1. ↑ QT (Q-aT) 2. Prolonged ST segment 3. Associated with K↑ and K↓

electrolyte abnormalities and ECG changes—DCI: dialyzable current of injury, Q-aT: | Common Q to the apex of T wave interval, ST: ST elevation, ST: ST depression.

HYPERMAGNESEMIA There are no specific ECG characteristics due to mild to moderate isolated abnormalities in serum Mg2 levels. Hence, ECG effects of hypermagnesemia may be dominated by the Ca2 levels. However, severe hypermagnesemia (serum Mg level 15 mEq/L) can cause AV and intraventricular conduction disturbances which may culminate in complete heart block and cardiac arrest.18

HYPOMAGNESEMIA It is usually associated with hypocalcemia or hypokalemia and as such isolated hypomagnesemia may not be recognized on ECG. It can potentiate certain digoxin toxic arrhythmias.

DRUG EFFECTS AND ELECTROLYTE ABNORMALITIES

579

Thus, the serum electrolyte imbalance (hyperkalemia, hypokalemia, hypercalcemia and hypocalcemia) causes distinctive ECG changes (see Fig. 29.15).

REFERENCES 1. Wirth KE. Relevant metabolism of cardiac glycosides. In: Erdmann E, Greeff K, Skou JC, eds. Update in Cardiac Glycosides, 1785–1985. New York: Springer-Verlag; 1986:257–262. 2. Lown B, Wyatt NF, Levine HD. Paroxysmal atrial tachycardia with block. Circulation 1960;21: 129–143. 3. Rosenbaum MB, Elizari MV, Lazzari JO. Mechanism of bi-directional tachycardia. Am Heart J 1969;78(1):4–12. 4. Vander Ark CR, Ballantyne F III, Reynolds EW Jr. Electrolytes and the electrocardiogram. Cardiovasc Clin 1973;5:269–294. 5. Levine HD, Wanzer SH, Merrill JP. Dialyzable currents of injury in potassium intoxication resembling acute myocardial infarction or pericarditis. Circulation 1956;13(1):29–36. 6. Davidson S, Surawicz B. Ectopic beats and atrioventricular conduction disturbances in patients with hypopotassemia. Arch Intern Med 1967;120(3):280–285. 7. Redleaf PD, Lerner IJ. Thiazide-induced hypokalemia with associated major ventricular arrhthmias. Report of a case and comment on therapeutic use of bretylium. JAMA 1968;206(6):1302–1304. 8. Brown MJ, Brown DC, Murphy MB. Hypokalemia from beta 2-receptor stimulation by circulating epinephrine. N Engl J Med 1983;309:1414–1419. 9. Vick RL, Todd EP, Luedke DW. Epinephrine induced hypokalemia: relation to liver and skeletal muscle. J Pharmacol Exp Ther 1972;181(1):139–146. 10. Thompson RG, Cobb LA. Hypokalemia after resuscitation from out-of-hospital ventricular fibrillation. JAMA 1982;248(21):2860–2863. 11. Surawicz B, Braun AH, Crum WB et al. Quantitative analysis of the electrocardiographic pattern of hypopotassemia. Circulation 1957;16(5):750–763. 12. Carter EP, Andrus EC. QT interval in human electrocardiogram in absence of cardiac disease. JAMA 1922;78:19–22. 13. Nierenberg DW, Ransil BJ. Q-aTc interval as a clinical indicator of hyperkalemia. Am J Cardiol 1979;44:243–248. 14. Lind L, Ljunghall S. Serum calcium and the ECG in patients with primary hyperparathyroidism. J Electrocardiol 1994;27(2):99–103. 15. Ahmed R, Yano K, Mitsuoka T et al. Changes in T wave morphology during hypercalcemia and its relations to the severity of hypercalcemia. J Electrocardiol 1989;22(2):125–132. 16. Voss DM, Drake EH. Cardiac manifestations of hyperparathyroidism, with presentation of a previously unrelated arrhythmia. Am Heart J 1967;73:235. 17. Crum WD, Till HJ. Hyperparathyroidism with Wenckebach’s phenomenon. Am J Cardiol 1960; 6:836. 18. Agus ZS, Morad M. Modulation of cardiac ion channels by magnesium. Annu Rev Physiol 1991; 53:299–307.

■■■

CHAPTER 30

A RRHYTHMIAS 1.

SINUS NODAL DISTURBANCES AND ARRHYTHMIAS i. Sinus Tachycardia ii. Sinus Bradycardia iii. Sinus Arrhythmia iv. Sinus Pause or Sinus Arrest v. Sinoatrial (SA) Exit Block vi. Wandering Pacemaker vii. Sick Sinus Syndrome (Bradycardia–Tachycardia Syndrome) viii. Sinus Node Reentry Tachycardia 2. ATRIAL ARRHYTHMIAS i. Premature Atrial Contractions (PACs) ii. Atrial Tachycardias (AT) iii. Atrial Flutter (Afl) iv. Atrial Fibrillation (Af) 3. AV JUNCTIONAL ARRHYTHMIAS i. AV Junctional Escape Beats ii. AV Junctional Rhythm iii. AV Junctional Premature Beats or Premature AV Junctional Beats iv. AV Junctional Tachycardia v. AV Nodal Reciprocating (Reentrant) Tachycardia (AVNRT)

580 580 581 581 582 583 583

584 585 586 586 587 589 593 598 598 599

600 601

4. PRE-EXCITATION SYNDROME (PES) Accessory Pathways (AP) i. Concealed Accessory Pathways ii. Pre-Excitaion Syndrome 5. NARROW QRS TACHYCARDIA i. Irregular tachycardia ii. Regular tachycardia 6. VENTRICULAR ARRHYTHMIAS i. Premature Ventricular Complexes (PVCs) or Ventricular Premature Beats (VPBs) ii. Ventricular Tachycardia (VT) iii. Idioventricular Rhythm (IVR) iv. Ventricular Flutter (Vfl) and Ventricular Fibrillation (Vf) 7. WIDE QRS TACHYCARDIA i. Regular Wide QRS Tachycardia ii. Irregular Wide QRS Tachycardia 8. HEART BLOCK AV Block REFERENCES

606 607 608 609 622 622 622 622

622 630 640 641 642 642 643 644 644 655

603

1. SINUS NODAL DISTURBANCES AND ARRHYTHMIAS i. Sinus Tachycardia In normal sinus rhythm, the heart rate is between 60 and 100 beats/min. ●

A sinus rhythm of 100 beats/min with constant PR interval and normal P wave is defined as sinus tachycardia (see Fig. 30.1). Sinus tachycardia is usually nonparoxysmal, which is accelerated and terminated gradually.

ARRHYTHMIAS

Fig. 30.1

●

● ●

●

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

581

| Sinus tachycardia—sinus rhythm with a rate of 110/min.

It is common in infancy and early childhood and is the normal reaction to a variety of physiological or pathophysiological stresses such as exercise, anxiety, fever and anemia. It is due to the accelerated phase 4 diastolic depolarization of sinus nodal cells. Inappropriate sinus tachycardia: It is a persistent increase in resting heart rate unrelated to or out of proportion with the level of physical, emotional, pathological or pharmacological stress. The cause is multifactorial, but main mechanisms are (i) Enhanced automaticity of the sinus node,1 and (ii) Abnormal autonomic regulation of the sinus node with excess symapathetic and reduced parasympathetic tone.2 Postural orthostatic tachycardia syndrome (POTS): It is a part of wide spectrum of autonomic dysfunction (other spectrum being orthostatic hypotension).3 POTS is said to be present when the heart rate increases by 30 beats/min of the baseline heart rate or 120/min within 10 minutes of upright tilt in the absence of postural hypotension.

ii. Sinus Bradycardia A sinus rhythm of 60 beats/min with normal P wave contour occurring before each QRS complex with a constant PR interval is defined as sinus bradycardia (see Fig. 30.2). ● ●

It frequently occurs in healthy young adults, particularly well trained athletes. It is due to decrease sinus node discharge, resulting from excessive vagal or decreased sympathetic tone (see Table 30.1).

iii. Sinus Arrhythmia It is defined as the variation in sinus rhythm between the longest and shortest cycle (P–P or R–R intervals) on a resting ECG exceeding 0.12 s or the maximum cycle length minus minimum cycle length divided by minimum cycle length exceeding 10% (see Fig. 30.3). ●

P wave morphology is normal with a constant PR interval (120 ms) since the focus of discharge remains within the sinus node.

582

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

V5

Fig. 30.2

| Sinus bradycardia at a rate of 50/min.

Table 30.1 Sinus tachycardia and sinus bradycardia Condition

Common causes

Salient ECG findings

1. Sinus tachycardia Infants and early childhood fever, Sinus rhythm of 100 beats/min, anemia, exercise, anxiety, acute myocardial normal P waves and constant infarction (AMI), heart failure PR interval 2. Sinus bradycardia Well-trained athletes, AMI (inferior MI) Sinus rhythm of 60 beats/min, normal P waves and constant PR interval

P

Fig. 30.3

● ●

P

P

P

P

P

P

P

P

| Sinus arrhythmia—varying P–P interval (non-respiratory).

It is due to rhythmic fluctuation in vagal tone mediated through Bainbridge reflex. It is of two types: respiratory form and non-respiratory form. – Respiratory or phasic sinus arrhythmia: Cycle length (P–P interval) shortens during inspiration and lengthens with expiration. Breath holding eliminates the cycle length variation. – Non-respiratory or non-phasic sinus arrhythmia: It is characterized by variation in P–P interval unrelated to respiratory cycle, and may be the result of digitalis toxicity.

● ●

It is most common in children and decreases with advancing age. The loss of sinus rhythm variability is a risk factor for sudden cardiac death, which can also occur in patients with acute intracranial lesions4 (see Table 30.2).

iv. Sinus Pause or Sinus Arrest It is due to a disorder of impulse formation as a result of slowing or cessation of spontaneous sinus nodal automaticity (see Fig. 30.4). ● ●

It is recognized by a pause in the sinus rhythm. Sinus node can be involved by degenerative fibrotic changes, MI, digitalis toxicity or excessive vagal tone.

ARRHYTHMIAS

583

Table 30.2 Sinus arrhythmia Common causes

Salient ECG findings

Children and acute intracranial lesions 1. Variation of RR or PP interval of 0.12 s due to fluctuation in vagal tone 2. Normal P waves and constant PR interval

Fig. 30.4

sinus bradycardia and sinus arrest which resulted in ventricular | Progressive escape rhythm.

v. Sinoatrial (SA) Exit Block It is due to a conduction disturbance during which an impulse formed within the sinus node fails to depolarize the atria or depolarizes with delay. It is recognized by a pause due to the absence of normally expected P wave. ●

●

●

●

●

First degree SA exit block: It cannot be recognized by ECG as SA node discharge is not recorded. Second degree SA exit block type I (Wenkebach): P–P interval progressively shortens prior to the pause and the duration of the pause is 2 P–P cycles (see Fig. 30.5). Second degree SA exit block type II: The duration of pause equals approximately two, three or four times the normal P–P cycle consistent with 2 : 1, 3 : 1, or 4 : 1 SA exit block (see Fig. 30.6). Third degree SA exit block: It can present as complete absence of P waves, but is difficult to diagnose with certainty without sinus node electrograms. Acute myocarditis or infarction involving the atrium, excessive vagal tone, and drugs such as quinidine, procainamide or digoxin can produce SA exit block (see Table 30.3).

vi. Wandering Pacemaker It indicates shift of dominant pacemaker from sinus node to the latent pacemakers usually atrial or AV junctional tissue. Only one pacemaker at a time controls the rhythm in contrast to AV dissociation. ●

There is a change in the contour of the P wave i.e. it becomes inverted or merged with the QRS complex (leads I, II), and there is cyclical increase in R–R interval with gradual shortening of PR interval (120 ms) (see Fig. 30.7).

584

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

PR

PR

PR

PR pause

Fig. 30.5

degree type I SA exit block—shortening of P–P interval followed by | Second a pause and the duration of the pause is less than twice the shortest cycle length. The cycle after the pause exceeds the cycle before the pause. PR interval is normal and constant.

P

Fig. 30.6

P

P

P

PR

P

degree type II 2 : 1 SA exit block—Pause is twice the basic P–P inter| Second val. PR interval is normal and constant.

Table 30.3 Sinoatrial exit block Common causes

Salient ECG findings

1. AMI involving atria 2. Increased vagal tone 3. Drugs: quinidine, digoxin, procainamide

Pause due to absence of expected P wave, 2nd degree exit block is usually recognized

P

Fig. 30.7

●

P'

P'

R P'

R

R

R

P

R

R

R P

P'

pacemaker—varying P wave contour (inverted P to upright P) | Wandering and gradual shortening of PR interval.

Often, it occurs in young individuals particularly athletes and is due to an augmented vagal tone.

vii. Sick Sinus Syndrome (Bradycardia–Tachycardia Syndrome) It is due to sinus node dysfunction with SA and AV conduction abnormalities, which may manifest as persistent sinus bradycardia interspersed with sinus arrest or SA exit

ARRHYTHMIAS

Afl

Fig. 30.8

585

Afl

sinus syndrome—Bradycardia interspersed with intermittent sinus | Sick arrest and junctional escape beats (dots), followed by tachycardia with a short spell of atrial flutter (Afl).

Table 30.4 Sick sinus syndrome Common causes

Salient ECG findings

1. Drugs: digitalis, quinidine, beta blockers

Sinus bradycardia interspersed with sinus arrest, SA exit block or paroxysms of atrial flutter or fibrillation

2. Hyperkalemia 3. Ischemia or AMI, pericarditis, cardiomyopathy, collagen disease, surgical injury

Abrupt termination of SNRT

SNRT aVR aVL P'

P'

P

P

P'

P'

P

P

I V1

Fig. 30.9

P'

P'

P

P

node reentry tachycardia (SNRT) and its abrupt termination—P wave | inSinus SNRT similar to sinus P wave.

block, or paroxysms of rapid regular or irregular atrial tachyarrhythmias (usually atrial flutter or fibrillation) (see Fig. 30.8 and Table 30.4). More than one of these can be recorded in the same patient on different occasions. viii. Sinus Node Reentry Tachycardia It accounts for 5–10% of SVT. ●

●

The rate is usually slower than other causes of SVT with a range of 80–200 beats/min, and an average of 130–140 beats/min (see Fig. 30.9). P waves are identical to sinus P waves.

586

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

2° type II: 1. Pause: 2, 3 or 4 times P–P cycle 2. Constant PR 1. P similar to sinus P 2. PR shorter 3. RP longer

2° type I: 1. P–P progressively↓ 2. Pause: 2 P–P cycles 3. Constant PR

SA exit block (SAEB)

SNRT

Sinus tachycardia

Wandering pacemaker

Sinus nodal disturbances and arrhythmias

SB interspersed with Sa, SAEB, Af or Afl

Sick sinus syndrome

Sinus arrhythmia

SB: Sinus bradycardia

Sinus arrest (Sa)

1. 60/min 2. Normal P 3. Constant PR

Pause in sinus rhythm

1.  100/min 2. Normal P 3. Constant PR

Fig. 30.10

1. Varying P contour 2. Gradual PR↓ 3. Cyclical RR↑

1. P–P  0.12s 2. Max CL–Min CL/Min CL = 10%

diagnosis of sinus nodal disturbances and arrhythmias—SNRT: sinus node reentry | ECG tachycardia, Af: atrial fibrillation, Afl: atrial flutter, Max CL: maximum cycle length, Min CL: minimum cycle length.

●

● ●

PR interval is related to tachycardia rate, but generally RP interval is longer with a shorter PR interval. Vagal maneuvers and adenosine can slow and terminate the tachycardia. They are usually initiated and terminated abruptly by a premature atrial contraction. (see Fig. 30.10).

2. ATRIAL ARRHYTHMIAS i. Premature Atrial Contractions (PACs) It is a common atrial arrhythmia occurring in about 0.4% normal individuals5 (see Fig. 30.11). ●

●

It can occur in fevers, emotional stress, thyrotoxicosis, alcohol, and tobacco, or caffeine consumption. PAC is characterized by P wave that occurs before the next expected sinus impulse with its contour differing from that of sinus P wave. – If premature atrial focus is high in the atrium, the premature P waves are upright and if the premature atrial focus is low in the atrium, P waves are inverted. – When PACs occur early in the cardiac cycle, P are superimposed on T waves (hence the admonition “search the T for P”), which deforms the T waves slightly.

ARRHYTHMIAS

V1

Fig. 30.11

P R

P R

R

P

587

R

atrial contractions (P)—with PR of 120 ms and short RP | Premature interval.

– However often such PACs are blocked before reaching the ventricle and can be misinterpreted as a sinus pause or sinus exit block. – Early occurring PACs may trigger atrial tachycardia, Afl or fibrillation. ●

●

●

Usually, PAC initiates a ventricular complex with a normal or basic QRS configuration (In BBB, the basic QRS complex will be wide and slurred and PAC will like wise initiate a QRS complex of BB type). PR interval of the conducted PAC is usually prolonged (120 ms) i.e. it follows the general rule: “RP interval is inversely related to the PR interval”. Thus a short RP interval produced by an early PAC is followed by a long PR interval. The PACs have less than fully compensatory pauses (the duration of the pause after PAC is less than twice the PP interval) as the premature P wave resets the sinus cycle early. – However, occasionally fully compensatory pause can occur due to delay in the reset of the sinus cycle. – Rarely, an interpolated PAC may occur, in which the pause after the PAC is very short and the interval bounded by normal sinus initiated P waves on either side of the PAC is slightly longer than or equal to one normal PP interval. – PACs that follow every sinus beat cause atrial bigeminy (see Table 30.5).

ii. Atrial Tachycardias (AT) They are classified into focal atrial tachycardia and multifocal atrial tachycardia. a) Focal Atrial Tachycardia ●

●

● ●

Focal atrial tachycardia constitutes 10–15% (but more in children) of the SVTs with an atrial rate of 150–200 beats/min (see Table 30.6). P wave contour is different from that of the sinus P wave. A positive or biphasic P wave in aVL and a negative or biphasic P wave in V1 favors RA origin, while a positive P in V1 and a negative P wave in lead I or aVL favors LA origin. Negative P waves in inferior leads are suggestive of a caudal origin, while positive P waves in these leads suggest a cranial origin6 (see Fig. 30.12). PR interval is influenced by the tachycardia rate. It has the capability of developing AV block without interrupting the tachycardia (atrial tachycardia with block), i.e. as the atrial rate increases, AV conduction becomes impaired.

588

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 30.5 Premature atrial contractions (PACs) Common causes

Salient ECG findings

1. Alcohol, tobacco or caffeine consumption 2. Fevers 3. Thyrotoxicosis 4. Digitalis toxicity 5. Ischemia 6. CHF 7. COPD

1. Premature P is different from sinus P wave, which may be upright or inverted depending upon the site of origin 2. Slightly deforms the T wave when it superimposes on it 3. PR is usually 120 ms with short RP interval 4. PAC initiates normal or basic QRS complex 5. Compensatory pause is not full 6. It can trigger atrial tachycardia, atrial flutter or atrial fibrillation

Table 30.6 Focal atrial tachycardia Common causes

Salient ECG findings

1. Alcohol ingestion

1. P wave differs from the sinus P wave and may be inverted or upright depending upon the site of origin 2. Atrial rate is 150–200/min 3. It has the capability of developing AV block without interruption i.e. as atrial rate increases AV conduction becomes impaired 4. Due to abnormal automaticity or micro-reentry

2. Digitalis toxicity 3. MI 4. COPD 5. Surgical atriotomy scar

I

aVR

V1

V4

II

aVL

V2

V5

aVF

V3

V6

P

III P

Fig. 30.12

●

P

atrial tachycardia—inverted P most obvious in II, III and aVF leads | Focal with narrow QRS complexes at a rate of 150/min.

The mechanism of focal tachycardia could be due to an abnormal automaticity or micro-reentry and both varieties are amenable for catheter ablation (see Table 30.7). Clinically, it may present as paroxysmal or persistent (incessant) AT. Automatic AT tends to be incessant especially in children.

ARRHYTHMIAS

589

Table 30.7 Differential diagnosis of automatic and reentry atrial tachycardia (AT) Automatic (ectopic) atrial tachycardia

Reentry atrial tachycardia

1. Morphology of P is similar in all leads 2. ‘Warm-up’ (gradual acceleration of the rate of tachycardia) and ‘cool-down’ are present 3. Vagal maneuvers (carotid sinus massage) do not terminate AT, but can produce AV block 4. Resetting of AT by a premature stimulus

1. Initial P differs from the subsequent P 2. Warm-up and cool-down are absent

5. Pacing cannot terminate the AT 6. Occurs in digitalis toxicity (usually AT with AV block), MI, COPD, alcohol ingestion

II

Fig. 30.13

P' R

P' R

3. Vagal maneuvers do not terminate AT and can produce AV block 4. Premature stimulus does not reset AT, but may terminate the AT 5. Pacing may suppress the AT 6. Less common and may be due to atrial fibrosis (with pulmonary disease) or surgical atriotomy scars

P'

R

R P'

P'

R

atrial tachycardia—varying P waves and PR interval with defi| Multifocal nite isoelectric base line.

b) Multifocal Atrial Tachycardia (MAT) or Chaotic Atrial Tachycardia (CAT) ● ●

●

●

●

It is characterized by usual atrial rates of 100–130 beats/min. The rhythm is irregular with totally irregular PP intervals and may be confused with atrial fibrillation; however the rate is usually not excessively rapid. There are multifocal premature beats, atleast three different P wave morphologies with changing PR interval in one lead and isoelectric base line between P waves (see Fig. 30.13). This tachycardia commonly occurs in older patients with COPD and CHF. Unusual causes include digoxin toxicity and theophylline administration. It has been suggested that MAT is the result of DAD (delayed after depolarization)— trigger induced automaticity7 (see Table 30.8).

iii. Atrial Flutter (Afl) It is a rapid regular atrial tachyarrhythmia with: ● ●

Usual atrial rate of 250–300 beats/min. Most common AV conduction ratios (i.e. the ratio of flutter wave to conducted ventricular complexes) are 2:1 and 4:1 and most often occurs in an even number e.g. 2:1, 4:1, (see Fig. 30.14); while 3:1 or 5:1 ratios are rare. But alternating 2:1 and 4:1 ratios

590

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Table 30.8 Multifocal atrial tachycardia Common causes

Salient ECG findings

1. Older patients with COPD, CHF 2. Rarely in digitalis toxicity, aminophylline administration

1. Atrial rate: 100–130/min 2. Totally irregular rhythm and may be confused with atrial fibrillation 3. Atleast three different P waves with varying PR interval in one lead and isoelectric base line between P waves 4. Due to delay after depolarization

II Afl

Fig. 30.14

Afl

Afl

Afl

| Atrial flutter (Afl) with 4 : 1 and 2 : 1 block.

Table 30.9 Atrial flutter (Afl) Common causes

Salient ECG findings

1. Mitral valve disease 2. Congenital heart disease

1. Atrial rate: 250–350/min 2. Regular saw toothed flutter waves without isoelectric base line in between them 3. Even number AV conduction (2 : 1 and 4 : 1 commonest) 4. Best visualized in II, III, aVF, and V1 leads

3. 4. 5. 6. 7. 8.

Cardiomyopathy CAD (less frequent) Surgical atriotomy scar Pericariditis Thyrotoxicosis Alcohol ingestion

●

●

●

are common generating a bigemini pattern. In young children and rarely in adults, 1:1 AV conduction may occur. The ventricular response becomes irregular with the occurrence of Wenckebach phenomenon. Regular saw toothed flutter waves without an isoelectric interval in between flutter waves (vs multifocal AT) are best visualized in leads II, III, aVF, or V1 (see Table 30.9). The combination of abrupt slowing of the ventricular rate and an increased rate of atrial flutter during carotid sinus massage strongly supports the diagnosis of Afl. Occasionally, carotid sinus massage will cause atrial flutter to convert to atrial fibrillation (Af ) and very rarely sinus rhythm follows.

ARRHYTHMIAS

591

Incidence and Etiology ●

● ●

●

The overall incidence of Afl is 0.37%. It is more common in men (2.5 times). It increases markedly with age, from 5/100,000 in 50 yrs old to 587/100,000 in 80 years old.8 It occurs in 25–35% of patients with Af.9 It is associated with underlying atrial abnormalities secondary to mitral valve disease, congenital heart disease, cardiomyopathy, and less frequently in CAD. It may occur in thyrotoxicosis, alcoholism, pericarditis, following surgery for congenital heart disease (especially TOF, TGA, or ASD).10 However, lone atrial flutter (no structural heart disease or precipitating cause) can also occur (though rare).6

Types of Afl Atrial flutter can be classified depending upon the electrophysiological and clinical properties. a) Electrophysiological classification a) Depending upon the mechanism: Afl is a macro-re-entrant AT and depending upon the re-entry circuits used, it is grouped into cavotricuspid isthmus (CTI) dependent Afl and non cavotricuspid isthmus (NCTI) dependent Afl. CTI-dependent Afl: They are all amenable for catheter ablation, and rapid overdrive pacing can terminate the arrhythmia. Depending upon the re-entry circuits, CTIdependent Afl has the following varieties: ● ● ● ●

Counterclockwise reentry or typical Afl Clockwise reentry or atypical Afl Double wave reentry Afl Lower loop reentry Afl

Counterclockwise reentry atrial flutter is the commonest and others are less common or rare. (i) Counterclockwise reentry or common or classic or typical Afl:11 ●

●

The CTI-dependent Afl is caused by a macro re-entrant right atrial circuit around the tricuspid annulus, i.e. the impulse travels in counterclockwise direction down the RA free wall inferiorly to atrial septum, from there it travels through the isthmus bounded by crista terminalis (i.e. the area between SVC and IVC), coronary sinus os on one side (forming the posterior barrier) and tricuspid annulus on the other side (forming the anterior barrier) and Afl is known as common or classic or typical Afl. Counterclockwise Afl is characterized by dominant negative flutter waves in inferior leads and a positive flutter deflection in V1 with transition to a negative deflection in V6 at the rate of 250–350 beats/min.

(ii) Clockwise reentry or atypical or reverse typical Afl:12 ●

In this CTI-dependent Afl, the re-entrant circuit travels in the opposite direction i.e. clockwise direction.

592

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY ●

This type of Afl is characterized by positive flutter waves in inferior leads, wide and negative flutter waves in V1 with transition to positive waves in V6.

(iii) Double wave reentry Afl:13 ● ●

In this arrhythmia, two flutter waves simultaneously occupy the usual flutter pathway. This arrhythmia is transient, usually terminating within three to six complexes, but may rarely deteriorate into Af.

(iv) Lower loop reentry Afl:14 ●

In this arrhythmia, the re-entry wave front circulates around the IVC due to conduction across the crista terminalis, and unusual ECG patterns occur.

Non-cavotricuspid dependent Afl or incisional macro-re-entry Afl:11 ●

●

● ●

●

●

It is caused by macro-re-entry circuits that do not use CTI. They are less common and most related to an atrial scar, which creates conduction block and a central obstacle for reentry. It is common in patients with prior cardiac surgery involving the atrium such as repair of congenital heart disease ASD, MV surgery, or atrial maze procedure. The resulting arrhythmia is known as “lesion-related or incisional macro-re-entry AT”. CTI-dependent Afl is also common in patients with prior atrial surgery and may coexist with incisional macro-reentrant atrial tachycardias. The flutter waves on ECG usually differ from that of CTI-dependent flutter, but can resemble typical patterns. However, definitive diagnosis requires intracardiac mapping. It is also amenable to catheter ablation but recurrences are more common than CTIdependent Afl.

b) Depending upon the atrial rate and ability to entrain and interrupt Afl with atrial pacing: Two types have been described:15 Type I Afl (common or classic): In type I, the atrial rate is 250–320/min with a mean of 300/min. It can be entrained and interrupted by atrial pacing. Type II Afl (uncommon): In type II, usual atrial rate is 320–350/min, but it may occasionally be as fast as 450/min. It cannot be entrained and interrupted by atrial pacing. It may occur as the fore runner for chronic atrial fibrillation (see Fig. 30.15). Clinical classification: Clinically, Afl is classified as paroxysmal (brief), persistent and chronic form and therapeutic approaches are influenced by the clinical pattern. ●

●

●

Paroxysmal Afl is common with type I Afl and have high success rate of reversion to sinus rhythm. Persistent Afl occurs in chronic heart diseases, thyrotoxicosis or pulmonary embolism. Chronic Afl occurs in the setting of advanced heart disease and with type II atrial flutter, which is often a forerunner of chronic Afl (see Table 30.10 and Fig. 30.16).

ARRHYTHMIAS

593

iv. Atrial Fibrillation (Af) a) Incidence: ●

●

●

Af is the most common sustained cardiac arrhythmia encountered in clinical practice with an overall incidence of 0.4–2% which is associated with an increased morbidity and mortality. It is found in 1% of persons older than 60 years to more than 5% of patients older than 69 years.16 As per Framingham data, the overall chance of developing Af over a period of two decades in patients older than 30 years is 2%.17 V5

AfI

Fig. 30.15

AfI

AfI

AfI

| Atrial flutter (Afl-type II).

Table 30.10 Types of atrial flutter (Afl) Depending upon the mechanism

Depending upon the atrial rate

Clinical classification

1. Cavotricuspid isthmus (CTI) dependent i) Counterclockwise reentry Afl ii) Clockwise reentry Afl iii) Double wave reentry Afl iv) Lower loop reentry Afl 2. Non-CTI dependent

1. Type I: 250–320/min 2. Type II: 320–350/min

1. Paroxysmal 2. Persistent 3. Chronic

Clockwise (Typical): ve Afl in II, III, aVF and V6; ve Afl in V1

Counter clockwise (Typical): ve Afl in II, III, aVF and V6; ve Afl in V1

Type I: 1. 250–320/min 2. Atrial pacing abolishes

Incisional macro reentry: Related to atrial scar, more recurrences

Depending upon the mechanism

Classification of Afl

Paroxysmal: 48 hours Clinical Persistent: 2 days to weeks Chronic: monthsforerunner to chronic Af

Fig. 30.16

Depending upon the atrial rate

Type II: 1. 320–350/min 2. Atrial pacing cannot abolish 3. Forerunner to chronic Af

| Classification of atrial flutter (Afl)—fl: flutter waves, Af: atrial fibrillation.

594

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

b) Etiology ●

●

●

A history of CHF, valvular heart disease and stroke, left atrial enlargement, abnormal mitral or aortic valve function, hypertension and advanced age have been found to be independent risk factors for prevalence of Af. Af was found in 29% of patients with isolated MS, 16% in isolated MR, 52% in patients with combined MS and MR, and in only 1% of patients with aortic valve disease.18 Af also occurs in CAD (5–17%, especially with CHF, atrial infarction, post CABG); cardiomyopathy, thyrotoxicosis (look for thyrotoxicosis in recent onset Af ), alcohol intake (holiday heart syndrome) and drugs such as digoxin and sympathomimetics.

c) Mechanism of Af The genesis of Af is explained by multiple-wavelets hypothesis of Moe (1962):19 Af involves several simultaneous and consistently shifting wave fronts that twist, block and split to form new wave fronts. The rhythm is sustained when the number of wavelets is large enough so that the probability of all wave fronts dying out at the same time is low. This hypothesis was substantiated by Allessie et al in 198520 (see Fig. 30.17). Persistence of Af depends on the: 1. Mass and width of excitable tissue i.e. size of the atria. Larger the size, easier is to sustain Af. 2. Electrical wave length of the atria which is equal to conduction velocity  effective refractive period. Electrical wave length is 12–16 cm for the normal sinus rhythm. ● Vagal stimulation, sympathetic stimulation and alcohol ingestion (through sympathetic stimulation) decreases the effective refractory period of the atria and thereby decreasing the electrical wave length of the atrial tissue. Shorter wave lengths of the atria predisposes to Af. ● In Af, the electrical wave length of the atria averages 7.8 cm.

Multiple wavelets

Fig. 30.17

| Genesis of atrial fibrillation.

ARRHYTHMIAS

Vagal stimulation

Size of atria

LAE/RAE

Electrical heterogeneity of atria

Sustenance of Af

Electrical wave length of atria

Advanced age

Genesis of Af

Electrical refractiveness of atria

595

Vagal stimulation

Multiple wavelets

Alcohol ingestion

Fig. 30.18

Sympathetic stimulation

| Mechanism of atrial fibrillation (Af)—LAE: left atrial enlargement, RAE: right atrial enlargement. 3. Electrical heterogeneity of the atria: Presence of IVC, SVC orifices in RA and pulmonary veins in LA causes electrical heterogeneity of the atria which facilitates the breakup of the wave fronts into new ones that are necessary to sustain Af. ●

●

Vagal stimulation decreases the atrial refractoriness non-uniformly, resulting in electrical heterogeneity which facilitates the sustenance of atrial fibrillation. Advanced age facilitates the electrical heterogeneity of the atria (see Fig. 30.18).

d) ECG Features Af is a totally irregular atrial rhythm characterized by: ●

●

●

●

●

●

Grossly disorganized atrial activity which results in fibrillatory (f) waves that are totally irregular and vary in size and shape from beat to beat with the absence of normal P waves, and are best seen in leads V1, II, III and aVF. The atrial rate ranges from 400–600/min with variable ventricular response due to variable AV conduction resulting in irregularly irregular ventricular rhythm (irregular RR interval). Hence, in the absence of discernible atrial activity (f waves), a grossly irregular ventricular rhythm still suggests the presence of Af. Aberrant conduction tends to occur when a long ventricular cycle is followed by a short cycle, the short cycle terminated by an aberrantly conducted beat, which is referred as Ashman phenomenon21 (see Fig. 30.19). A series of short cycles, if short enough may generate runs of aberrantly conducted beats mimicking VT. In Af, if the ventricular cycle length prolongs, then VPC may occur. This phenomenon is known as “rule of bigeminy”. The ventricular rate in Af is usually 120–180/min, but can accelerate to 200/min in the presence of WPW syndrome with conduction down the accessory pathway. The QRS complex during Af will be similar to that recorded during sinus rhythm, usually a narrow QRS complex. However, a wide QRS complex occurs if associated with BBB or antidromic variety of WPW syndrome (antegrade conduction over the accessory pathways) or Ashman phenomenon. Wide QRS complex in Af results in irregular wide QRS tachycardia.

596

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

V1

R

R

R

R

ACB

Fig. 30.19

phenomenon in atrial fibrillation—long–short cycle sequence | Ashman’s ending in an aberrantly conducted beat (ACB with RBBB pattern).

Table 30.11 Atrial fibrillation (Af) Common causes

Salient ECG findings

1. Valvular heart disease 2. CHF

1. Irregular atrial rhythm 2. Absence of normal P waves, but presence of fibrillatory (f) waves 3. Atrial rate 400–600/min with variable ventricular rate (usually 120–180/min) 4. Usually initiates narrow QRS complex, but wide QRS if associated with BBB or antidromic WPW syndrome or Ashman phenomenon 5. Best seen in V1, II, III, and aVF

3. Hypertension 4. Advanced age

5. Cardiomyopathy 6. CAD 7. Thyrotoxicosis 8. Alcohol intake 9. Drugs: digitalis, sympathomimetics

●

Lone Af: Af occurring in the absence of identifiable cause is known as “lone Af ” and carries a good prognosis22 (see Table 30.11).

e) Classification Based on ECG criteria ● ● ●

Coarse Af: Size of waves similar to flutter waves (i.e. 1 mm) (see Fig. 30.20). Fine Af: Size of f waves 1 mm (see Fig. 30.21). Discernible Af: No visible f waves, but gross irregularly irregular ventricular complexes.

Clinical classification: ●

●

It is helpful from therapeutic point of view.

Paroxysmal Af: It could be short standing (lasting from seconds to 1 hour) or long standing (lasting from 1 hour to 48 hours). Spontaneous termination of Af can occur. It is further grouped into: – Group I: First episode of Af – Group II: Recurrent attacks of Af in untreated individuals – Group III: Recurrent attacks of Af in treated individuals. Persistent Af: It lasts for 2 days to weeks and self termination is unusual, but reversion to sinus rhythm should be the aim of therapy.

ARRHYTHMIAS

R

Fig. 30.20

R

R

f

R

f

R

f

f

597

f

| Atrial fibrillation (coarse)—f waves 1 mm in size. R

R

R

R

V1

Fig. 30.21

| Atrial fibrillation (fine). Table 30.12 Types of atrial fibrillation ECG classification

Clinical classification

1. Coarse Af 2. Fine Af 3. Discernible Af

1. Paroxysmal 2. Persistent 3. Chronic or permanent

Coarse Af—f 1 mm

VPC occurs if vent. cycle length ↑→ ‘Rule of bigeminy’

Based on ECG

Due to modifications Aberrantly conducted beat in short cycle → ‘Ashman phenomenon’

Fine Af—f 60–130/min 2. Narrow QRS 3. Wenckebach conduction can occur in digitalis toxicity

1. Heart rate of 110–250/min 2. Narrow QRS or typical BBB pattern 3. AV dissociation often occurs

Paroxysmal

Nonparoxysmal

1. In 50% P is undetected in ECG 2. In 50% P occurs before, during or after QRS producing pseudo-r in V1 and pseudo-s in II, III, aVF 3. P ↓in II, III, aVF 4. R P normal P–P 3. PR is < 0.12 s if P precedes QRS 4. Normal QRS complex

AVJ rhythm— 35–60/min

AVJA

AVNRT

AVJ premature beats

1. P occurs before, during or after QRS 2. P ↓in II, III, aVF; upright in V2,V2; isoelectric or ↓in I, V6 3. Usually normal QRS complex

1. Heart rate of 140–250/min 2. Often initiated by premature atrial impulse with↑ PR 3. Narrow QRS complex

features | Diagnostic tachycardia.

of AV junctional arrhythmias (AVJA)—AVNRT: AV nodal reentrant

4. PRE-EXCITATION SYNDROME (PES) ●

The pre-excitation syndrome is due to the presence of extra nodal accessory pathways which can occur in the following form: – Concealed form – Manifest form producing Wolff-Parkinson-White (WPW) syndrome

ARRHYTHMIAS ●

● ●

607

The presence of concealed accessory pathways account for 30% of the patients with apparent SVT, while the reported incidence of manifested PES is 0.15–0.25% of the general population24 with a higher prevalence of 0.55% in the first degree relatives of the patients with accessory pathways.25 The PES is found in all age group, more common in males. Majority of the individuals with PES have normal hearts, but is also found in congenital heart diseases such as Ebstein’s anomaly (5–10%26), MVP (7%27) and cardiomyopathies (DCM and HCM-4% in HCM28). It is also reported in cardiac tumors (rhabdomyoma) and tuberous sclerosis.29 Other congenital heart diseases in which PES has been reported include ASD, TGA, tricuspid atresia, VSD, TOF and COA.30

Accessory Pathways (AP) These represent the developmental abnormality of AV ring and consist of small fibers resembling normal myocardium that can act as pathways of conduction. They are classified on the basis of their location along the mitral and tricuspid annulus. AP have their atrial site of origin along the mitral and tricuspid annulus, tend to ramify prior their insertion into the ventricular myocardium (either LV or RV). a) Location On the basis of their location, they are classified into left sided (or left ventricular) and right sided (or right ventricular): ● LV free wall (left lateral): The accessory pathways located in the LV free wall are the commonest (56%). ● RV free wall: The accessory pathways in the RV free wall constitutes 21%. ● Interventricular septum (IVS): The accessory pathways inserted into the IVS constitute 24%, Posterior septal wall: 18%, anterior septal wall: 2%, and mid septum: 4%. ● 10–15% have multiple pathways. Patients with Ebstein’s anomaly often have right sided multiple accessory pathways in the posterior septum or the posterolateral wall. b) Types Three types of accessory pathways have been described: ● Kent bundle i.e. atrioventricular accessory pathway is the usual or commonest accessory pathway, bypassing the AV node and extending from the atrium to the ventricle (see Fig. 30.39). Kent bundle is also found in monkeys, dogs and cats. ● James bundle i.e. atriohisian accessory pathway is the uncommon pathway bypassing the AV node and extending from the atrium to His bundle, which gives rise to Lown-Ganong-Levine (LGL) syndrome (see Fig. 30.40). ● Almost all Mahaim fibers are right sided and consist of (i) nodoventricular/ nodofascicular accessory pathway extending from AV node to the ventricle (nodoventricular) or RBB (nodofascicular) (see Fig. 30.41) and (ii) fasciculoventricular accessory pathway extending from His bundle or bundle branches to the

608

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY Atrium

Atrium

AV node

AV node

His

His

Ventricle

Ventricle AVAP

Fig. 30.39

|

Fig. 30.40 Atrioventricular accessory pathway (AVAP) from atrium to ventricle.

accessory pathway (AHAP) | Atriohisian from atrium to His bundle.

Atrium

Atrium

AV node

AV node

His

His

Ventricle

Ventricle NVAP

Fig. 30.41

AHAP

FVAP

accessory pathway | Nodoventricular (NVAP) from AV node to ventricle.

Fig. 30.42

accessory pathway | Fasciculoventricular (FVAP) from His bundle or its branches to ventricle.

ventricle (see Fig. 30.42). However, Mahaim fibers are atriofascicular pathways (also known as Brechenmacher tract), usually located in the RV free wall connecting anterolateral wall of RA, close to the lateral tricuspid annulus and apical region of the RV or distal RBB.31 They constitute approximately 8% of the accessory pathways and due to the presence of nodal tissue in these fibers, they display decremental conduction (antegrade or retrograde) which is not characteristic of other accessory pathways.32 i. Concealed Accessory Pathways ●

●

The patients with concealed accessory pathways are capable of only retrograde conduction from the ventricle to the atrium. Hence, these are not apparent in the ECG during sinus rhythm as typical ECG manifestations of PES/WPW syndrome are absent. However, it can still participate in the reentrant circuit to produce an AV reciprocating tachycardia (AVRT), and paroxysmal supraventricular tachycardia (PSVT) in which: – Tachycardia rate is unusually faster (200/min), – QRS complex is normal and

ARRHYTHMIAS

●

●

609

– Inverted P waves occur after QRS complex on the ST segment or early T wave especially in inferior and lateral leads. In majority of the patients, the accessory pathways are located in LV free wall and in the posteroseptal area. The treatment is similar to AVNRT and PES and is amenable to catheter ablation.

ii. Pre-Excitaion Syndrome It is a manifest form of presence of accessory pathways. It occurs when the atrial impulse activates whole or some part of the ventricle (antegrade conduction) or when the ventricular impulse activates whole or some part of the atrium (retrograde conduction) earlier than expected if the impulse traveled through normal conduction system (i.e. SA node-atrium-AV node-His bundle-ventricle). The activation of ventricle or atrium is possible only in the presence of accessory pathways. PES can present with sinus rhythm i.e. WPW syndrome or with tachyarrhythmias. a) PES With Sinus Rhythm—WPW Syndrome ECG manifestations ●

In patients with accessory pathways, the impulse may be conducted only through normal route i.e. atrium-AV node-His bundle-ventricle (concealed accessory pathways), only through accessory pathways (giving rise to full pre-excitation) or simultaneously through normal route and accessory pathways (resulting in fusion beats, i.e. delta waves). – With increasing conduction through accessory pathways, the QRS complex widens and PR and HV intervals shorten as in WPW syndrome, and with increasing conduction through normal route as during exercise, PR and HV intervals lengthen and QRS complex shortens. – Increasing pre-exctitation results in progressive shortening of PR interval and widening of QRS complex without change in the interval from P to the end QRS complex is known as concertina effect which usually occurs in intermittent PES (see Fig. 30.43).

●

Short PR interval 120 ms with a normal P wave. The duration of PR interval equals the duration of P wave or its initial portion especially in fully pre-excited complexes. R II R P

P NC

Fig. 30.43

R

R

R

R P

P

P

P APC

pre-excitation syndrome with concertina effect. The first com| Intermittent plex (NC) is conducted through normal AV node pathway alone, the sixth through accessory pathway alone (APC, fully pre-excited), while the rest are due to progressive pre-exctation without change in the P-end QRS interval.

610

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY ●

●

Wide QRS complex 120 ms with a delta wave in its initial portion, and normal terminal portion. A normal q wave is seldom found in pre-excited complexes and presence of q waves in V6 virtually excludes the PES.33 Delta wave, a fusion beat is due to the depolarization of ventricle in part by the wave front traveling along the normal conduction route with a normal physiological AV delay (i.e. atrium-AV node-His bundle-ventricle) and in part by the wave front traveling along the accessory pathway (i.e. atrium-AP-ventricle). The delta wave represents the ventricular activation from atrium through accessory pathway. – Duration of delta wave is 0.02–0.07 s. In PES, delta waves should be present in all leads. However, they become isoelectric and are overlooked in those leads which are perpendicular to initial QRS forces. – Negative delta waves resemble abnormal Q waves of myocardial infarction (MI). Hence, negative delta waves in right precordial leads mimic anterior MI (see Fig. 30.44), in aVL stimulate lateral MI (see Fig. 30.45) and in inferior leads they mimic an inferior MI (see Fig. 30.46). The large upright delta wave and positive QRS complex in V1 may simulate true posterior MI or RBBB or RVH (see Fig. 30.47).

I

aVR

V1

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 30.44

d

V4

syndrome with short PR interval and negative delta waves in right | WPW precordial leads simulating anterior MI.

I

aVR

II

aVL

III

aVF

Fig. 30.45

d

d

V1

V4

V2

V5

V3

V6

syndrome with short PR interval and negative delta waves in aVL | WPW simulating lateral MI.

ARRHYTHMIAS

611

d I

d

II

III

d

Fig. 30.46

aVR

V1

V4

aVL

V2

V5

V3

V6

aVF

d

syndrome with short PR interval and negative delta waves in inferior | WPW leads simulating inferior MI.

d

I

aVR

V1

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 30.47

V4

syndrome (type A) with short PR interval, upright delta waves and | WPW positive QRS complexes (tall R) in V simulates true posterior MI or RVH. 1

– Tall R waves in V1 and V2 simulating RVH, RBBB or posterior infarction is described as type A WPW syndrome. Negative QRS complex and delta waves in V1 and upright in V5, V6 simulating LBBB is described as type B WPW syndrome (see Fig. 30.48). ●

Secondary ST–T changes that are generally directed opposite to that of delta waves may be found, but are more common with tachyarrhythmias. The altered sequence of ventricular activation in these patients results in secondary repolarization abnormalities. As the duration of QRS complex increases, the T wave becomes more negative.

612

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

d

aVR

V1

II

aVL

V2

V5

III

aVF

V3

V6

I

Fig. 30.48

d

syndrome (type B) with short PR interval, negative QRS complexes | WPW and delta waves in V and upright in V simulating LBBB. 1

6

V1

aVR

I

V4

d

d

V4

d

II

d

V2

aVL

d

V5

d

III

Fig. 30.49

aVF

d

V3

d

V6

syndrome with left lateral accessory pathway—short PR interval, | WPW positive delta waves and QRS complex in V and isoelectric or negative 1

delta waves in I, aVL and V5.

Localization of accessory pathways during sinus rhythm:34 Accessory pathways located in the LV (left sided) have positive (ve) delta wave and QRS complex in V1  further. (i) the presence of isoelectric or negative delta waves in I, aVL, V5, and V6 localizes accessory pathway in left lateral wall (see Fig. 30.49). (ii) while early QRS transition i.e. in V2, V3: localizes accessory pathway in the septum  and if negative delta wave and QRS complex are also present in II, III and aVF, indicates the presence of accessory pathway in the left posteroseptal wall (see Fig. 30.50).

ARRHYTHMIAS

Fig. 30.50

V1

V4

aVL

V2

V5

aVF

V3

V6

I

aVR

II

III

R

613

syndrome with left posteroseptal accessory pathway—short PR | WPW interval, positive delta waves and QRS complex in V with negative delta 1

waves in inferior leads and early QRS transition in V2.

V4

I

aVR

V1

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 30.51

d

d

syndrome with RV free wall accessory pathway—short PR interval, | WPW negative delta waves and QRS complex in V with left axis ( 30) and late 1

QRS transition in V5.

Accessory pathways located in the RV (right sided) have negative ( ve) delta wave and QRS complex in V1,  further. (i) LAD and late QRS transition i.e. in V5, V6, localizes accessory pathway in RV free wall (see Fig. 30.51). (ii) While early QRS transition, i.e. in V2, V3, localizes accessory pathway in the septum  ●

●

If negative delta wave and QRS complex are also present in II, III and aVF; accessory pathway is located in the right posteroseptal wall (see Fig. 30.52) or If axis is inferior, accessory pathway is located in the right anteroseptal wall (see Figs 30.53 and 30.54).

614

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

V1

aVR

I

V4

d

aVL

II

V2

V5

V3

V6

d

aVF

III

d

Fig. 30.52

syndrome with right posteroseptal accessory pathway—short PR | WPW interval, negative delta waves and QRS complex in V and inferior leads 1

with early QRS transition in V3 simulating LBBB.

I

aVR

V1

d

Fig. 30.53

V4 d

II

aVL

V2

V5

III

aVF

V3

V6

syndrome with right anteroseptal accessory pathway—short PR, nega| WPW tive delta waves, and QRS complex in V with inferior QRS axis. 1

b) PES with Tachyarrhythmias The tachycardias, which occur in PES include: ●

●

Reciprocating or reentry tachycardia i.e. AVRT (80%), which can be orthodromic (90–95%) or antidromic (5–10%) Af (15–30%) which may degenerate into VF35

ARRHYTHMIAS

615

Lead V1 Negative delta and QRS complex

Positive delta waves and QRS complex

Right ventricle

Left ventricle

Negative delta waves and QRS in II, III, aVF

Left axis

Posteroseptal

RV free wall

Fig. 30.54

Inferior axis

Negative delta waves and QRS in II, III, aVF

Isoelectric or negative delta waves in I, aVL, V5, and V6

Anteroseptal

Posteroseptal

Lateral

| Localization of accessory pathways in WPW syndrome (PES with sinus rhythm).

Fig. 30.55

AVRT—antegrade conduction of reentrant impulse through | Orthodromic normal route and its retrograde conduction through accessory pathway producing narrow QRS tachycardia.

● ●

Afl (5%) and VT (uncommon)

Orthodromic AVRT: It is due to the antegrade conduction of reentrant impulse from the atrium to the ventricle through normal conduction route and its retrograde conduction from ventricle to the atrium through the accessory pathway, which results in narrow QRS SVT (see Fig. 30.55). The ECG characteristics are ●

Tachycardia in PES is often initiated by premature atrial or ventricular complexes (see Fig. 30.56).

616

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

II

P′

Fig. 30.56

| Orthodromic AVRT initiated by a premature atrial complex (P). RPR aVR

V1

II

aVL

V2

V5

III

aVF

V3

V6

I

R R

V4

P

Fig. 30.57

AVRT—Narrow QRS tachycardia at a rate of 186/min. P waves | Orthodromic after QRS complex on the depressed ST segment with RP interval PR interval.

●

●

●

● ● ● ●

Regular rate of 150–250 beats/min (usually faster than AVNRT). Delta waves no longer observed and duration of QRS complex is normalized. Short PR interval of 120 ms. RP interval is 70 ms and shorter than PR interval (see Fig. 30.57).36 (PR is RP when retrograde pathway is slow as in antidromic AVRT). P waves occur after, not during QRS complex. Inverted P waves in II, III and aVF with positive P waves in aVR and aVL (in posteroseptal pathway) or inverted P waves in I (in left lateral pathway).36 Presence of QRS alternans, i.e. alteration of R wave amplitude during tachycardia.37 Secondary ST–T changes, i.e. ST segment depression and T wave inversion are common. Sudden onset and termination. Adenosine, beta blockers, calcium channel blockers and digitalis prolong the conduction and refractive period of AV node, while quinidine, procainamide and disopyramide (Class IA sodium channel blockers) prolong the conduction and refractive period of accessory pathway and help in differentiating narrow QRS tachycardias.

Localization of accessory pathway during AVRT: It may be done on the basis of secondary ST–T changes, and localization of inverted P waves. ●

●

ST segment depression of 2 mm in V4–V6: Accessory pathway is located in the left lateral wall (sensitivity: 64%, specificity: 60%) (see Fig. 30.58). Inverted or notched T wave in V2: Accessory pathway is located in the anteroseptal wall (sensitivity and specificity: 100%).

ARRHYTHMIAS

I

aVR

617

v4

V1

V5 R R II R R

aVL

R R V2

T III

aVF

V6

V3

T

Fig. 30.58

T

T

AVRT—Narrow QRS tachycardia at a 180/min with upstroke | Orthodromic slurring of QRS complex and alteration of R wave amplitude suggest orthodromic AVRT, while ST segment depression of 2 mm in V4–V6 and inverted T waves in V5–V6 localizes to left lateral accessory pathway.

●

●

T wave inversion in II, III, and aVF: Accessory pathway is located in the right posteroseptal wall (sensitivity: 63%, specificity: 84%). Negative P waves in II, III and aVF with upright P waves in aVR and aVL: Accessory pathway is located in the posteroseptal wall; while negative P waves in I localize the accessory pathway to the left lateral wall.

Antidromic AVRT (i) It constitutes 5–10% of AVRT and is due to the antegrade conduction of reentrant impulse from the atrium to the ventricle along the accessory pathway and its retrograde conduction from the ventricle to the atrium through normal conduction route, produces a wide QRS tachycardia (see Fig. 30.59). (ii) One third of these patients may have multiple accessory pathways with a high incidence of atrial and ventricular fibrillation. (iii) The accessory pathways are located far away from AV node and no patient with a posteroseptal accessory pathway has antidromic AVRT.38 (iv) QRS morphology is similar to fully pre-excited complex. (v) In rare type of antidromic AVRT (see Fig. 30.60), two or more accessory pathways are used both for antegrade and retrograde conduction, also resulting in wide QRS tachycardia (see Table 30.16). WPW syndrome with Af and Afl: Wolf, Parkinson and White (1930) mentioned atrial fibrillation in their original description of the syndrome. If the ventricular rate is unusually rapid (200/min) during Af, wide QRS complex pre-excitation should be suspected as this is possible only in the presence of a short effective refractive period of

618

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Fig. 30.59

AVRT—antegrade conduction of reentrant impulse along the | Antidromic accessory pathway and retrograde conduction through normal route producing wide QRS tachycardia. V4 I

aVR

II

aVL

V1

V5 V2

III

V6

aVF V3

Fig. 30.60

| Antidromic AVRT—wide QRS tachycardia at a rate of 250/min.

the accessory pathway. The occurrence of Af is facilitated by the presence of reentrant tachycardia. ●

●

The QRS complexes are wide as the atrial impulses are conducted to the ventricles through the accessory pathway during Af and Afl in most cases. The QRS complexes are wide due to an aberrant ventricular conduction (see Fig. 30.61).

Ventricular fibrillation may develop in patients of WPW syndrome due to rapid ventricular rate during Af and Afl or due to the presence of multiple accessory pathways.

ARRHYTHMIAS

619

Table 30.16 Etiology and characteristics of AVRT Common cause

Orthodromic AVRT

Antidromic AVRT

1. Can occur in structurally normal heart 2. Ebstein’s anomaly

1. Constitutes 90–95% of AVRT

1. Constitutes 5–10% of AVRT

2. Sudden onset and termination

2. Regular tachycardia, unless associated with Af or Afl with variable AV conduction 3. Wide QRS complexes

3. MVP 4. Cardiomyopathies (DCM and HCM) 5. Cardiac tumors (rhabdomyoma) and tubersclerosis 6. Other CHD: ASD, VSD, tricuspid atresia, TGA, TOF, COA

3. Regular rate of 150–250/min 4. Short PR (120 ms) 5. RP 70 ms and shorter than PR

6. P waves after QRS complex

7. Absent delta waves and normalization of QRS complex 8. R wave alternans 9. Often associated with secondary ST–T changes

Fig. 30.61

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

syndrome with atrial fibrillation—wide QRS tachycardia at an irregular | WPW rate of about 200/min. There is slurring of the upstroke of QRS complexes after long pauses.

WPW syndrome with Af may be mistaken for VT. However, very rapid (200/min) and gross irregularity of the ventricular response occurs during Af rather than during VT. WPW syndrome with Afl, the rhythm is regular with AV conduction of 2 : 1 or 1 : 1 and may be mistaken for paroxysmal VT. However, the AV conduction of 1 : 1 in Afl is rare in the absence of accessory pathways.

620

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

I R

aVR

V1

V4

S

aVL

II

III

Fig. 30.62

aVF

V2

V5

V3

V6

tachycardia (Nodoventricular) at a rate of 186/min, LBBB pattern | Mahaim QRS complex with 30 axis, late QRS transition, R in I and rS in V . 1

c) Mahaim Tachycardia ●

●

●

A sinus impulse may travel from RA to AV node with normal delay, but is followed by premature excitation of basal part of the ventricle as the impulse travels through Mahaim fibers resulting in a delta wave with normal PR interval. However, no preexcitation (no delta wave) is generally apparent during sinus rhythm due to slow conduction and decremental properties of this pathway. But ECG may reveal short PR interval, narrow QRS complex with delta wave, late QRS transition (as accessory pathway is located in RV) and decremental conduction. During pre-excitation tachycardia, the absence of retrograde conduction in these pathways produces only an antidromic AVRT, and is characterized by anterograde conduction from the atrium to the ventricle over the accessory pathway and retrograde conduction from the ventricle over the RBB-His bundle-AV node to the atrium, producing: – – – –

●

●

LBBB pattern with superior axis (0 to 75) Late QRS transition (positive QRS complex after V4) R in I and rS in V1 (see Fig. 30.62) RP longer than PR interval, as a result of longer A-V interval (due to long conduction time over the accessory pathway) and shorter V-A interval.

A delay in retrograde conduction due to RBBB, increases the length of the tachycardia circuit i.e. prolongs the V-A interval and tachycardia can become incessant.39 PR interval is normal; HV interval is shortened with slight ventricular pre-excitation manifested by slurring of the initial QRS complex in pre-excitation due to fasciculoventricular Mahaim fibers. No specific arrhythmias have been associated with this accessory pathway.

ARRHYTHMIAS

621

d) Lown-Ganong-Levine (LGL) Syndrome It is characterized by short PR interval with normal P wave and normal QRS complex with short A–H interval (see Fig. 30.63). The atriohisian pathway may be demonstrated anatomically, but it is insignificant in the genesis of tachycardia. e) Permanent form of AV Junctional reciprocating Tachycardia (PJRT) ●

●

●

●

It is an incessant form of narrow QRS SVT with short PR interval but RP interval exceeding PR interval (similar to atrial tachycardia) (see Fig. 30.64). It is usually due to the presence of posteroseptal accessory pathway (most often in the right ventricle).40 Tachycardia is usually initiated by a premature complex or lengthening of PR interval and is maintained by orthodromic conduction, i.e. antegrade conduction over the normal AV conduction route and retrograde conduction along the accessory pathway. It does not respond to vagal stimulation (i.e. carotid sinus massage). I

aVR

V1

II

aVL

V2

V5

V3

V6

PR

PR

III

Fig. 30.63

V4

PR

aVF

| LGL syndrome with short PR interval and normal QRS complexes. R

R P

R PR

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 30.64

form of AV junctional reciprocating tachycardia (PJRT)—Narrow | Permanent QRS tachycardia with short PR interval and RP interval  PR interval.

622

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

5. NARROW QRS TACHYCARDIA The QRS duration is 120 ms and consists of: i. Irregular tachycardia It includes: ● Atrial fibrillation ● Atrial flutter with variable AV conduction ● Atrial tachycardia with variable AV block or Wenkebach block ● Multifocal atrial tachycardia (MAT). ii. Regular tachycardia It consists of: ● Sinus tachycaradia ● Atrial flutter with fixed AV conduction ● Atrial tachycardia ● AVNRT ● AVRT (orthodromic). Differential diagnosis: The AVRT can be differentiated from other common regular narrow QRS tachycardia by the presence of delta waves and P wave morphology and its relation with RP and PR intervals (see Table 30.17, Figs 30.65 and 30.66). The intravenous adenosine and vagal stimulation have different responses among the various causes of regular narrow QRS tachycardia (see Figs 30.67 and 30.68). The presence of delta wave is the most characteristic feature of WPW syndrome. The typical AVRT has to be differentiated from other causes of narrow QRS tachycardia, while the antidromic AVRT, WPW syndrome with Af and Mahaim tachycardia with their characteristic features can be differentiated from the ventricular tachycardia (see Fig. 30.69). 6. VENTRICULAR ARRHYTHMIAS Ventricular arrhythmias include: ● Premature ventricular complexes or Ventricular premature beats ● Ventricular tachycardia (VT) ● Ventricular flutter/fibrillation i. Premature Ventricular Complexes (PVCs) or Ventricular Premature Beats (VPBs) PVCs are also known as ventricular premature contractions (VPCs). ● They are the commonest ventricular arrhythmias occurring in 0.8% of normal individuals of 16 years to 50 years age. ● They can occur in 33% of men and 15% of women with exercise.

ARRHYTHMIAS

623

Table 30.17 Differential diagnosis of narrow QRS regular tachycardia Features

AVRT

AVNRT

AT

1. Rate (not much useful 150–250/min for differential diagnosis)

Less than AVRT

Usually  180/min

2. P waves

P waves after, not during QRS complex, P in II, III, aVF with P in aVR, aVL (in posteroseptal AP), P in I (in left lateral AP)

In 50% not detected. In 50% occurs before, during or after QRS  pseudo-r in V1 or pseudo-s in II, III, aVF P in II, III, aVF

P in I, aVL and P in V1 in left AT. P or biphasic in V1, aVL and P or biphasic in aVL in right AT

3. Atrial rate faster than ventricular rate

No

No

Yes

4. RP–PR intervals

i) RP is 70 ms and RP  PR

i) RP is 70 ms and RP  PR

i) RP is 70 ms and usually PR ii) But RP may be PR iii) Varying PR in MAT

ii) RP  PR in PJRT

ii) May be 70 ms and RP  PR in atypical form

5. Delta waves

May be present

Absent

Absent

6. QRS alternans

Present

Absent

Absent

i) May be present ii) Usually present with septal accessory pathways

i) Usually absent ii) May be present

No effect or terminate

No effect or terminate Does not terminate, but may cause transient AV block

7. ST–T changes i) ST 2 mm ii) T inversion

8. Vagal stimulation (carotid sinus massage)

● ●

i) Usually absent ii) Usually absent

They can occur in AMI, during fibrinolytic therapy, CHF, cardiomyopathy and MVP. They can be provoked by a variety of medications (digitalis), electrolyte imbalance, and excessive use of tobacco, caffeine or alcohol.

ECG Recognition PVC is characterized by: ●

●

The premature occurrence of wide bizarre QRS complex (duration usually 120 ms) with ST segment and large T wave opposite in direction to the abnormal QRS complex i.e. when QRS complex is upright, ST segment is depressed and T wave is inverted; and when QRS complex is negative, ST segment is elevated and T wave is upright. However, the QRS complex of the PVC may be narrow when it arises from the ventricular septum or fascicles, which is known as a fascicular beat. PVCs arising from the anterior fascicle resemble RBBB with left posterior fascicular block and those arising from the posterior fascicle resemble RBBB with left anterior fascicular block.

624

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

R

R OR P'

P'

Typical AVNRT: RP is < 70 ms and < PR. P waves may occur before, during or after QRS complex

R

R

P'

P'

AVRT: RP is >70 ms but < PR. P waves usually after, not during QRS complex

R

R

R

OR P P'

PJRT: RP is >70 ms > PR. P waves are inverted in inferior leads

R P

P'

Atrial tachycardia: RP < or > PR. P waves may occur before or after QRS complex

Fig. 30.65

Atypical AVNRT: RP may be >70 ms & > PR. P waves are inverted in inferior leads

fl

fl

fl

fl

Atrial flutter with flutter (fl) waves usually inverted in inferior leads

wave morphology and its relation with RP and PR intervals in narrow QRS tachycardia— | PAVNRT: AV nodal reentrant tachycardia, AVRT: AV reentry tachycardia, PJRT: permanent form of AV junctional reciprocating tachycardia.

●

●

●

PVC is not preceded by premature P wave, but may be preceded by a non-conducted sinus P wave. Retrograde conduction of ectopic ventricular impulse to the atrium often occurs resulting in retrograde P wave which is usually hidden in the ventricular complex, but occasionally atrial capture occurs and inverted P wave is observed following PVC. PVC is usually followed by a full compensatory pause, i.e. the interval between the sinus P wave immediately before the PVC and the first sinus P wave after the PVC is equal to twice the sinus cycle length (see Fig. 30.70). However; in bigeminy i.e. interpolated PVC, it is less than full, but long enough for PVC to occur. The bigeminy disappears when the heart rate increases as the long diastolic (RR) intervals shorten as per the “rule of bigeminy.” Occurrence of PVCs after long RR intervals and their disappearance when the RR intervals shorten is known as the “rule of bigeminy”39 (see Fig. 30.71). PVCs usually have fixed coupling interval, i.e. the interval between the normal QRS complex and the premature QRS complex (variation does not exceed 0.08 s).41 Variable coupling interval occurs due to parasystole (see Table 30.18).

ARRHYTHMIAS

625

Narrow QRS tachycardia (QRS duration ventricular rate Yes

No

Atrial flutter or Atrial tachycardia

Analyze RP interval

Short (RP shorter than PR)

Fig. 30.66

Long (RP longer than PR)

Atrial tachycardia (AT) PJRT Atypical AVNRT

RP 70 ms

AVNRT

• AVRT • AVNRT • Atrial tachycardia

| Differential diagnosis of narrow QRS tachycardia—AVRT: AV reentry tachycardia, AVNRT: AV nodal reentrant tachycardia, PJRT: permanent form of AV junctional reciprocating tachycardia. Regular narrow QRS tachycardia

IV Adenosine

Fig. 30.67

No change in rate

Gradual slowing then reaccelaration of rate

Sudden termination

Persisting AT with transient high grade AV block

1) Inadequate dose 2) Consider VT (fascicular or high septal origin)

1) Sinus tachycardia 2) Focal AT 3) Nonparoxysmal junctional tachycardia

1) AVNRT 2) AVRT 3) Focal AT 4) SNRT

1) Atrial flutter 2) AT

to IV adenosine in regular narrow QRS tachycardia and its differential diagnosis— | Response AVRT: AV reentry tachycardia, AVNRT: AV nodal reentrant tachycardia, AT: atrial tachycardia, SNRT: sinus node reentry tachycardia.

626

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Regular narrow QRS tachycardia No effect or may terminate

AVNRT

Vagal stimulation (carotid sinus massage)

AVRT

No effect

Does not terminate, but cause transient AV block

No effect, but may ↑ AV block and reveal fl waves more clearly

Atrial flutter

PJRT AT

Fig. 30.68

of vagal stimulation (carotid sinus massage) on regular narrow QRS | Effect tachycardia and its differential diagnosis—AVRT: AV reentry tachycardia, AVNRT: AV nodal reentrant tachycardia, AT: atrial tachycardia, PJRT: permanent form of AV junctional reciprocating tachycardia, fl waves: flutter waves.

1. Normal P 2. Short PR: 120 ms 4. Delta waves 5. Secondary ST–T changes

1. Normal P 2. Short PR: PR 3. P′ inverted in II, III, aVF LGL synd PJRT

Wide QRS tachycardia

PES

Narrow QRS tachycardia AVRT

Mahaim tachycardia

1. RP > PR 2. LBBB pattern QRS complex 2. Late QRS transition 3. R in I, rS in V1

Fig. 30.69

WPW synd with Af

1. Irregular ventricular rate of > 200/min 2. Wide QRS with slurring of upstroke after long pauses

Antidromic AVRT

1. Regular rate of 150–250/min 2. Wide QRS similar to fully preexcited complex

4. P waves after, not during QRS 5. No delta waves 6. Normaliztion of QRS 7. QRS alternans 8. Secondary ST–T changes

1. Regular rate of 150–250/min 2. Short PR 3. RP >70 ms, but 0.03 sec

Notch or slur

q S >0.06 sec

Fig. 30.82

of monmorphic LBBB pattern VT—r 30 ms, notching of | Characteristic S and r to nadir of S 60 ms in V with qR in V . 1

Fig. 30.83

6

I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

VT with LBBB pattern and inferior axis arising from RVOT at | Monomorphic a rate of 210/min.

LBBB Pattern VT occurs in: Bundle branch reentry tachycardia associated with dilated cardiomyopathy. It is a form of monomorphic sustained VT, characterized by retrograde conduction over the LBB and antegrade conduction over RBB producing LBBB contour with frontal axis of about 30. RVOT tachycardia is characterized by LBBB QRS morphology with an inferior axis and is often found in individuals with structurally normal hearts (see Fig. 30.83). Two types of RVOT tachycardia has been described—repetitive monomorphic VT and exercised induced VT. ●

Repetitive monomorphic VT are often non-sustained and benign. It is often due to early or delayed after depolarizations (see Fig. 30.84).

ARRHYTHMIAS

Fig. 30.84

●

635

| Repetitive monomorphic VT with LBBB pattern at a rate of 160/min.

Paroxysmal VT or exercised induced VT is also referred as catecholamine-sensitive tachycardia that are usually suppressed by  blockers and calcium channel blockers.

Arrhythmogenic RV dysplasia (ARVD) is characterized by LBBB contour with RAD and inverted T waves in right precordial leads. It occurs predominantly in young males. However in sinus rhythm, ECG exhibits complete or incomplete RBBB with T wave inversions in V1–V3.49 ●

●

●

●

RBBB pattern VT: It is characterized by monophasic R or biphasic qR, Rs or Rr in V1, R/S 1 in V6 with a frontal QRS axis between 90 to 90 (see Fig. 30.85).50 This type of VT occurs as Variant form of bundle branch reentry tachycardia with antegrade conduction over the LBB and retrograde conduction over the RBB. Idiopathic LV tachycardia has RBBB morphology with a superior axis originating near the posterior fascicle of the LBB at the inferior basal septum, hence sometimes referred as fascicular tachycardia (see Fig. 30.86). It can be paroxysmal and can be sustained once initiated. It is sensitive to verapamil. Generally, the prognosis is good. Isthmus tachycardia is similar to LVOT tachycardia found in patients with MI. The site of origin is between the basal inferior septum and the mitral annulus (see Table 30.20).

(ii) Multiform or polymorphic or pleomorphic VT: QRS contours vary randomly and from the management point of view, these are subclassified into: – Polymorphic VT with normal QT interval – Polymorphic VT with prolonged QT interval ●

Polymorphic VT with normal QT interval: It is most frequently caused by acute ischemia or MI and rarely arrhythmogenic RV dysplasia. – Idiopathic polymorphic VT or familial catecholaminergic polymorphic VT has

normal QT interval. – It is usually initiated during sinus tachycardia by PVC with a short coupling interval. – It is poorly tolerated and tends to quickly degenerate into VF. ●

● ●

Polymorphic VT with prolonged QT interval: Torsades de pointes (TDP) is the classical example (see Fig. 30.87). It was originally described as a syndrome characterized by prolonged QT interval.51 It is characterized by QRS complexes of changing amplitude that appears to twist around the isoelectric line.

636

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

aVF

R

R

V1

V2

V3

V4

V5

V6 S

Fig. 30.85

S

V sign in monomorphic VT with RBBB pattern (monophasic R in V | Vandanddeep S in V ). 1

6

1

6

● ●

●

●

●

●

It is frequently non sustained occurring with a rate of 200–250/min. It is often the late onset PVC that initiates TDP and is usually due to early after depolarization (see Figs 30.88 and 30.89). Females are more susceptible for the development of TDP than males in the ratio of 3:1.52 The clinical conditions known to predispose TDP are congenital long-QT syndrome, antiarrhythmic drugs which prolong QT interval (class IA: quinidine is the commonest, class IC: propafenone, class III: sotalol, ibutilide, dofetilide and amiodarone— amiodarone is the least cause), bradycardia, hypokalemia, and hypomagnesemia. Poisoning with organophosphorus compounds,53 intracranial hemorrhage54 and hypothyroidism55 are the other predisposing conditions. IV magnesium is the initial treatment of choice for TDP from an acquired cause followed by temporary ventricular or atrial pacing.56

(c) Depending upon the polarity of the QRS complex Bidirectional VT: It is an uncommon VT in which polarity of the QRS complex varies in alternate complexes.

ARRHYTHMIAS I

aVR

V1

V4

II

aVL

V2

V5

III

aVF

V3

V6

Fig. 30.86

637

VT with RBBB pattern arising from left posterior septum at a | Monomorphic rate of 210/min.

Table 30.20 Therapeutic classification of monomorphic VT Type depending upon the drug sensitivity 1. Adenosine sensitive VT 2. Verapamil sensitive VT 3. Catecholamine or Propranolol sensitive VT 4. Undifferentiated VT i.e. usually not responding to any drug

●

● ●

Origin and onset

ECG pattern

Mostly RVOT Post fascicle of LBB at the inferior septum Exercise induced from RV or LV Paroxysmal exercise induced usually from RV

LBBB contour with inferior axis RBBB contour with superior axis LBBB contour (if from RVOT) or RBBB contour (if from LV) LBBB contour with inferior axis

It is characterized by RBBB pattern alternating its polarity from ( 60 to 90) to (120 to 130) It has a regular rhythm with a ventricular rate of 140–200/min. It is due to severe digitalis toxicity (and indicates poor prognosis) and severe myocardial disease (see Fig. 30.90).

(d) Narrow QRS VT and Fascicular VT: VT arising from the fascicles may have a narrow QRS complex ( 110 ms) and diagnosis is established by the presence of AV dissociation, fusion beats and HV interval shorter than during the sinus rhythm.57 However, VT originating from the fascicles may have usual characteristics of VT. VT of left anterior fascicle is suggested by RBBB pattern with inferior axis and VT of left posterior fascicle is suggested by RBBB pattern with superior axis58 (see Fig. 30.91).

638

BASIC INVESTIGATIONS: CLINICAL ELECTROCARDIOGRAPHY

Fig. 30.87

| Polymorphic VT with prolonged QT interval—Torsades de pointes.

Fig. 30.88

or end diastolic PVC—also high risk for initiating polymorphic VT | Late especially Torsades de pointes.

SB PVC

Fig. 30.89

TDP

| Late onset PVC initiating Torsades de pointes (TDP)—SB: sinus beat.

Localizing the Site of Origin of VT 1. LV origin of VT: RBBB pattern of QRS complex. ● ●

q in I and V6 is associated with anterior origin of VT.59 R in I, V1 and V2 is associated with posterior origin of VT.59

ARRHYTHMIAS

639

V2

Fig. 30.90

RVOT tachycardia: inferior axis

ventricular tachycardia usually occurs in severe digitalis toxi| Bidirectional city or severe myocardial disease.

BBB reentry tachycardia: +30° axis

ARVD: RAD & T↓ in V1, V2

LBBB pattern: 1.V1-r >30 ms, r-S >60 ms and slurring of S 2.V6-qR or qS

1. Short CI PVC initiates 2. Acute ischemia/MI 3. Poorly tolerated→Vf

Nonsustained upto 30 s

Sustained: >30 s Monomorphic

Normal QT

VT

Polymorphic

Bidirectional

↑QT (TDP)

Variant BBB reentry tachycardia Isthmus tachycardia Idiopathic LV tachycardia

Fig. 30.91

RBBB pattern: 1. V1–R or qR, Rs, Rr 2. V6–R/S