Color Atlas of Cardiology: Challenging Cases 9741283608, 9789386322142

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Color Atlas of

Cardiology Challenging Cases

Color Atlas of

Cardiology Challenging Cases Editors Majid Maleki MD, FACC, FESC, FAPSC

Professor of Cardiology, Interventional Cardiologist, Echocardiologist, Cardiogenetic Research Center Rajaie Cardiovascular Medical and Research Center Iran University of Medical Sciences Tehran, Iran Affiliate Member of the Medical Devices Chair University of Ottawa Heart Institute

Azin Alizadehasl MD, FACC, FASE

Associate Professor of Cardiology Fellowship of Echocardiography Echocardiography Research Center Cardiogenetic Research Center Rajaie Cardiovascular Medical and Research Center Iran University of Medical Sciences Tehran, Iran

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Website: www.jaypeebrothers.com Website: www.jaypeedigital.com © Digital Version 2018, Jaypee Brothers Medical Publishers The views and opinions expressed in this book are solely those of the original contributor(s)/author(s) and do not necessarily represent those of editor(s) of the book. All rights reserved. No part of this publication may be reproduced, stored or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission in writing of the publishers. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. Medical knowledge and practice change constantly. This book is designed to provide accurate, authoritative information about the subject matter in question. However, readers are advised to check the most current information available on procedures included and check information from the manufacturer of each product to be administered, to verify the recommended dose, formula, method and duration of administration, adverse effects and contraindications. It is the responsibility of the practitioner to take all appropriate safety precautions. Neither the publisher nor the author(s)/editor(s) assume any liability for any injury and/or damage to persons or property arising from or related to use of material in this book. This book is sold on the understanding that the publisher is not engaged in providing professional medical services. If such advice or services are required, the services of a competent medical professional should be sought. Every effort has been made where necessary to contact holders of copyright to obtain permission to reproduce copyright material. If any have been inadvertently overlooked, the publisher will be pleased to make the necesUCT[CTTCPIGOGPVUCVVJGſTUVQRRQTVWPKV[

Inquiries for bulk sales may be solicited at: [email protected] Color Atlas of Cardiology: Challenging Cases First Edition: Digital Version 2018 ISBN 978-93-86322-14-2

Dedicated to Our dear patients, our family, and our mentors

Contributors Azin Alizadehasl MD, FACC, FASE

Mohammad Javad Alemzadeh-Ansari MD

Associate Professor of Cardiology Fellowship of Echocardiography Echocardiography Research Center Cardiogenetic Research Center Rajaie Cardiovascular, Medical and Research Center Iran University of Medical Sciences, Tehran, Iran

Assistant Professor of Cardiology Fellowship of Interventional Cardiology Cardiovascular Intervention Research Center Rajaie Cardiovascular Medical and Research Center Iran University of Medical Sciences, Tehran, Iran

Hamidreza Pouraliakbar MD Associate Professor of Radiology Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran

Majid Maleki MD, FACC, FESC, FAPSC Professor of Cardiology, Interventional Cardiologist, Echocardiologist Cardiogenetic Research Center Rajaie Cardiovascular, Medical and Research Center Iran University of Medical Sciences Tehran, Iran Affiliate Member of the Medical Devices Chair University of Ottawa Heart Institute

Sedigheh Saedi MD Assistant Professor of Cardiology Fellowship of Adult Congenital Heart Disease Rajaie Cardiovascular Medical and Research Center Iran University of Medical Sciences, Tehran, Iran

Preface There are lots of excellent books on cardiology and even many cardiology atlases. This book is distinguished from the others by emphasizing on the daily practice. The intended groups are all training residents, fellows and cardiologists who are doing daily practice. Also, this book is useful to those who are experienced, just as a reminder. This book is not an encyclopedic text or reference book in which you can find everything; instead, we think this book can serve you as a practical guide. The book provides an easy and ready access to key information on the diagnosis and treatment of cardiovascular conditions. Basic information about different aspects on cardiology is drawn from the personal experiences, clinical literature and professional authorities. The guide is designed as a digest for rapid reference, and it may not always include all information necessary for cardiac sciences. Also, less detail is given on areas, such as pathophysiology, anatomy, and physiology, which need access to specialized literature. Majid Maleki Azin Alizadehasl

Acknowledgments We are grateful to individuals and organizations that have provided advices and helped in bringing out this book. The principal contribution of this edition is from Sara Tayebi. We thank the contributing authors for their hard work. Importantly, this edition would not have been possible without an invaluable help and contribution of M/s Jaypee Brother Medical Publishers (P) Ltd, New Delhi, India, and also Parsian Publishing Company in Tehran, Iran. Finally, we wish to acknowledge the support and patience of our family members without which this book would not have been possible.

Contents Chapter 1 History and Physical Examination of the Heart

1

Majid Maleki

Chapter 2 Electrocardiography Challenging Cases

10

Mohammad Javad Alemzadeh-Ansari

Chapter 3 Chest X-ray Challenging Cases

61

Hamidreza Pouraliakbar

Chapter 4 Exercise Stress Testing

84

Sedigheh Saedi

Chapter 5 Clinical Points of Echocardiography in Daily Practice

88

Azin Alizadehasl

Chapter 6 Common Coronary Angiography: Views and Courses of Catheters

121

Sedigheh Saedi

Chapter 7 Cardiovascular Hemodynamic Study

134

Sedigheh Saedi Index

147

Abbreviations AF AI AI Ao AOC AOO AP ARVD AS ASD AV block AV AVNRT AVRT BBB CAD CVP CX D DCM ECG EDV EF EST ESV ET HCM HOCM IVC IVCT IVRT JVP LA LAD LAP LBBB LSB

: : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : :

Atrial fibrillation Aortic insufficiency Aortic regurgitation Aorta Aortic closing Aortic opening Accessory pathway Arrhythmogenic right ventricle dysplasia Aortic stenosis Atrial septal defect Atrioventricular block Aortic valve Atrioventricular nodal reentry tachycardia Atrioventricular reciprocating tachycardia Bundle branch block Coronary artery disease Central venous pressure Circumflex artery Diameter Dilated cardiomyopathy Electrocardiogram End-diastolic volume Ejection fraction Exercise stress testing End-systolic volume Ejection time Hypertrophic cardiomyopathy Hypertrophic obstructive cardiomyopathy Inferior vena cava Isovolumic contraction time Isovolumic relaxation time Jugular venous pulse Left atrium Left anterior descending Left atrial pressure Left bundle branch block Left sternal border

xvi

Color Atlas of Cardiology: Challenging Cases LSVC LV LVEDP LVOT MC METs MI MO MPI MR MS MV MVP PA PAP PAPVC PCWP PDA PHT PI PISA PMI PS PV PVC RA RAP RBBB RCA RCM RV RVEDP RVH RVOT S1 S2 S3 S4 SEP

: : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : : :

Left SVC Left ventricle LV end-diastolic pressure Left ventricular outflow tract Mitral closing Metabolic equivalents Myocardial infarction Mitral opening Myocardial performance index Mitral regurgitation Mitral stenosis Mitral valve Mitral valve prolapse Pulmonary artery Pulmonary artery pressure Partial anomalous pulmonary venous connection Pulmonary capillary wedge pressure Patent ductus arteriosus Pressure half-time Pulmonary insufficiency Proximal isovelocity surface area Point of maximal impulse Pulmonary stenosis Pulmonary valve Premature ventricular complex Right atrium Right atrial pressure Right bundle branch block Right coronary artery Restrictive cardiomyopathy Right ventricle RV-end diastolic pressure Right ventricle hypertrophy Right ventricular outflow tract First heart sound (mitral/tricuspid closing) Second heart sound (aortic/pulmonic closing) Third heard sound Fourth heard sound Systolic ejection period

Abbreviations STEMI SVC SVT TC TdP TEE TF TO TR TS TTE TV TVI VSD VT WPW

: : : : : : : : : : : : : : : :

ST-segment elevation myocardial infarction Superior vena cava Supraventricular tachycardia Tricuspid closing Torsades de pointes Transesophageal echocardiography Tetralogy of Fallot Tricuspid opening Tricuspid regurgitation Tricuspid stenosis Transthoracic echocardiography Tricuspid valve Time velocity integral Ventricular septal defect Ventricular tachycardia Wolff–Parkinson–White syndrome

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Chapter

1 History and Physical Examination of the Heart Majid Maleki

HISTORY A complete cardiovascular physical examination needs a detailed cardiac examination. We must guess what physical examination findings are predicted by taking good present and past medical history. The most common symptoms that should usually be asked are as follows: x x x x x x x x x x x

Dyspnea Palpitation Easy fatiguability Chest pain Cyanosis Edema Hemoptysis Vertigo Syncope General nonspecific symptoms It is recommended to consider the quality, quantity, timing, location, associated symptoms and precipitating factors of each symptom. For example regarding chest pain, it should be asked the location of the pain, its radiation, describing the pain, such as burning, stabbing and accompanying symptoms, such as shortness of breath, palpitation and so on. Or when you are taking history from a patient with cyanosis, it must be asked: x How long has been the duration of cyanosis? x Is it sudden or gradual? x Is it congenital or family type? (Figure 1) x And about accompanied symptoms.

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Color Atlas of Cardiology: Challenging Cases

Figure 1 Micrognathia in a patient with congenital heart disease

PHYSICAL EXAMINATION In spite of advanced technology in recent years in cardiovascular medicine, history taking and physical examination remain an important tool for general cardiologist, electrophysiologist, interventionist and echocardiologist. In summary, cardiac examination includes inspection, palpation and auscultation. You have to inspect jugular venous pulse (JVP) and point of maximal impulse. You also have to note to chest deformity, such as pectus excavatum or carinatum (Figures 2 and 3).

General Inspection Simple inspection can conclude different cardiac conditions. How does the patient look? Unwell, ill, cyanotic, pallor, sweatiness, cachectic, jaundice, ascites, edema…. Physical appearances can lead to awareness of certain cardiac pathologies It is also important to look at patient face, and teeth

History and Physical Examination of the Heart

Figure 2 Intercostals retraction in a child with congestive heart failure

A

B

C Figures 3A to C (A and B) Chest deformity and (C) bulging of left hemithorax in a patient with severe right ventricular enlargement

3

4

Color Atlas of Cardiology: Challenging Cases It must be remembered that there are many cardiac manifestations associated with different genetic abnormalities, such as: x Down syndrome: Atrioventricular septal defect x Turner’s syndrome: coarctation of the aorta x Ankylosing spondilitis: Aortic regurgitation x Marfan syndrome: Aortic regurgitation, aortic dissection, bicuspid aortic valve Cardiac conditions can be diagnosed by noting facial signs too. x x x x

Malar flush, redness around the cheeks (mitral stenosis) Yellow deposit of lipids at palms or around the eyes (xanthoma) Ring around the cornea (hyperlipidemia corneal arcus) Projection of the eyeball (Graves’ disease, atrial fibrillation) JVP can guide to guess the central venous pressure (CVP). It also gives you a view of probable cardiac abnormalities by looking at different parts of JVP, such as a,c,v,x and y wave. Many cardiac conditions, such as normal sinus rhythm, atrial fibrillation, ventricular tachycardia, complete heart block can be inferred. Also several cardiac abnormalities, such as tricuspid regurgitation, tricuspid stenosis, right ventricular dysfunction, cardiac tamponade and constrictive pericorditis, can be diagnosed by noting at JVP.

Jugular Venous Pulse (Figure 4) x Is it up or down? x Differential diagnosis of right sided heart failure, pulmonary emboli, acute dyspnea from pulmonary disease. x Large a wave in tricuspid stenosis, pulmonary stenosis, pulmonary hypertension x Absent a in atrial fibrillation x Canon a wave in complete heart block, VVI pace x Steep x and y descent in constrictive pericarditis x Large cv wave in tricuspid regurgitation x Kussmual’s sign: increased JVP on inspiration in constrictive pericarditis.

Palpation Point of maximal impulse (PMI), all kinds of lift and heave, accentuated heart sounds and pulse can be palpated and several cardiac abnormality can be diagnosed. Place your left hand over the chest to feel the heave (right ventricular hypertrophy) or thrill (Aortic stenosis, ventricular septal defect) (Figure 5).

Pulse One of the simplest and informative part of physical examation is taking the pulse. At the same time you can look for any abnormalities, such as clubbing fingers and peripheral signs of inflective endocarditis, such as Osler nodes, splinter hemorragia, etc. (Figures 6 to 8).

History and Physical Examination of the Heart

Figure 4 Elevated jugular venous pressure in dilated cardiomypathy in a patient with heroin addiction

Figure 5 How to palpate the chest pain for heave, lift, thrill etc.

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Color Atlas of Cardiology: Challenging Cases

A

B Figure 6 Clubbing fingers due to bacterial endocarditis

Figure 7 Clubbing fingers in complex cyanotic congenital heart disease

You must consider the following points with pulse taking: x Rate and rhythm of the pulse x The character and volume x Check for unequal volume of radial and femoral pulse (coarctation of aorta, Takayasu’s disease) x Check both radial simultaneously (aorta dissection, anomalous origin of subclavian artery, atherosclerosis...)

History and Physical Examination of the Heart

Figure 8 Severe cachexia in advanced heart failure

x Peripheral pulse should be checked for probable peripheral vascular disease, such as femoral, popliteal, posterior tibial and dorsalis pedis x Peripheral vascular disease is an important predictor of coronary artery disease.

Point of Maximal Impulse The PMI in usually palpable. It is related to left ventricular (LV) contraction. The PMI is usually located at the 5th or 6th intercostals space in midclavicular line. In 25% of normal people you cannot palpate PMI. The PMI duration is short and if it persists it may be sign of LV failure or left ventricular hypertrophy. Lift or heave means intense PMI.

Auscultation There are many physiologic and abnormal conditions which can make noises in the heart. Physiologic phenomenon, such as pregnancy and noncardiac conditions, such as anemia, hyperthyroidism and atriovenous fistula can make murmurs due to increased flow across normal heart valves. Any kind of abnormal valve closing or insufficiency, such as mitral, tricuspid (S1) aortic and pulmonic (S2) can produce abnormal sounds and murmurs, including abrupt halt of LV with consequent third and fourth heart sounds.

7

8

Color Atlas of Cardiology: Challenging Cases I recommend to listen to the heart from the point with the least intensity of the heart sounds, i.e. lower right sternal border and then to come up inch by inch until you reach to the apex with usually the highest intensity. When you describe auscultation features it is noteworthy to report it as following: x First heart sound characteristics (S1) x Second heart sound (S2) x Third and fourth heard sounds (S3, S4) x Abnormal and additional heart sounds, such as opening snap (mitral stenosis), pericardial sound (constrictive pericarditis), tumor plop (atrial myxoma) pacemaker sound and ejection or nonejection click x Normal or abnormal prosthetic valve sounds, such as metallic sounds, opening or closing click x Physiologic or abnormal murmur, including location, radiation, timing, intensity features of heart sounds.

Features of Heart Sounds S1, starts at the beginning of systole and its loudest location is at the apex or left sternal border (LSB). It is the result of closure of atrioventricular valves. It is important during heart sounds listening note their volume if it is normal, increased or diminished. Also splitting whether physiologic or abnormal should be reported (Tables 1 and 2) Table 1 Heart sounds in different cardiac conditions

Sounds S1 S2

Loud

Soft

Splitting

Mitral stenosis

Mitral regurgitation

A2

Hypertension

Aortic regurgitation Calcified Aortic Valve

Inspiration RBBB

P2

Pulmonary hypertension

PS/TF

ASD ( fixed) PS

S3

Normal in children MR, TR, LV failure, RV failure

S4

Hypertension, myocardial infarction, AS, HOCM Aortic stenosis, heart block

Opening snap

Mitral stenosis Tricuspid stenosis

Systolic click

AS, PS, MVP

ASD, atrial septal defect; HOCM, hypertrophic obstructive cardiomyopathy; LV left ventricular; MR, mitral regurgitation; PS, rulmonic stenosis; RBBB, right bundle branch block; RV, right ventricular; AS aortic stenosis; TF, tetralogy of Fallot; TR, tricuspid regurgitation

History and Physical Examination of the Heart Table 2 Cause of heart murmur and timing

Timing

Cause of murmur

Early systole

Acute MR, VSD, TR

Mid systole

AS (supravalvular and subvalvular) PS (supravalvular and subvalvular) ASD, dilated PA

Late systole

MVP, TVP

Holo systole

MR, TR, VSD

Early diastolic

AI, PI

Mid diastolic

MS, TS, MR, VSD

Late diastolic

Presystolic accentuation of MS Austin flint

Continuous

PDA, AV fistula, ruptured sinus of Valsalva, venous hum, ASD, coronary artery stenosis

AS, aortic stenosis; ASD, atrial septal defect; MR, mitral regurgitation; MVP, mitral valve prolapse; PDA, patent ductus arteriosus; PS pulmonic stenosis; TR, tricuspid regurgitation; TVP, tricuspid valve prolapse; VSD, ventricular septal defect

BIBLIOGRAPHY 1. 2. 3. 4.

Advantage of a new specific activity scale. Circulation. 1981;64:1227. Braunwald E, Perlof JK. Physical examination of the heart and circulation. Tenth edition; 2015. David T, Linker, (Editor) 1. Practical echocardiography of congenital heart disease; 2001. HURST, JW, Morris PC. The history, symptoms and past events related to cardiovascular disease. The heart lathed. Newyork. MC Graw-Hill; 2001.

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Chapter

2

Electrocardiography Challenging Cases

Mohammad Javad Alemzadeh-Ansari

INTRODUCTION Electrocardiogram (ECG) is the most important and often first diagnostic method in detection of cardiovascular disorders, such as cardiac rhythm disturbances, conduction system abnormalities, myocardial ischemia, cardiomyopathy, and pericarditis. Herein we describe the principles of normal ECG and then common ECG traces that a physician may meet with them in routine practice.

NORMAL ECG The clinical ECG is performed using 12 leads: three standard limb leads (leads I, II, and III), six precordial leads (leads V1 through V6), and three augmented limb leads (leads aVR, aVL, and aVF). The right pericardial leads can be used for assess right ventricular abnormalities and left posterior leads to detect acute posterolateral infarctions. Limb leads represent the potential difference between two limbs: lead I between the left arm (positive electrode) and right arm (negative electrode), lead II between the left leg (positive electrode) and right arm (negative electrode), and lead III between the left leg (positive electrode) and left arm (negative electrode). For augmented limb leads, the exploring electrode (positive input) is the right arm electrode for lead aVR, the left arm electrode for lead aVL, and the left leg electrode for aVF; and the reference potential for the these leads is formed by connecting the two limb electrodes that are not used as the exploring electrode. The exploring electrode (positive input) of precordial leads is placed on each precordial site (Table 1) and the negative input is the mean value of the potentials recorded at each of the three limb electrodes (Wilson central terminal).1 The waveforms and intervals of a standard ECG are displayed in Figure A. Normal values for durations of ECG waves and intervals were shown in Table 2. It should be mentioned that significant differences in ECG patterns may occur in a same individual between ECGs recorded days, hours, or even minutes.

Electrocardiography Challenging Cases Table 1 Location of pericordial leads on the chest

V1

Right sternal margin, 4th intercostal space

V2

Left sternal margin, 4th intercostal space

V3

Midway between V2 and V4

V4

Left midclavicular line, 5th intercostal space

V5

Left anterior axillary line, 5th intercostal space

V6

Left midaxillary line, 5th intercostal space

V7

Posterior axillary line, 5th intercostal space

V8

Posterior scapular line, 5th intercostal space

V9

Left border of spine, 5th intercostal space

V3R to V6R

Mirror image positions of left pericardial leads on the right side of the chest

Figure A The waves and intervals of a normal electrocardiogram Table 2 Normal values for durations of ECG waves and intervals

Duration (milliseconds)

Comment

P wave duration

7 mm tall and R/S in V1 >1), dominant S wave in V6 (>7 mm deep and R/S ratio 0.25 mV (“P pulmonale”), prominent initial positivity in lead V1 or V2 >0.15 mV are in favor to right atrial abnormality. Also, increased area under initial positive portion of the P wave in lead V1 to >0.06 mm-sec, rightward shift of mean P wave axis to more than +75 degrees, qR pattern in the right precordial leads without evidence of myocardial infarction, and low-amplitude (120 milliseconds in lead II, prominent notching of P wave, usually most obvious in lead II, and the interval between notches of >0.40 milliseconds (“P mitrale”) suggest the LA abnormality. Also, ratio between the duration of the P wave in lead II and duration of the PR segment >1.6, increased duration and depth of terminal-negative portion of P wave in lead V1 (P terminal force) so that area subtended by it >0.04 mm-sec, and leftward shift of mean P wave axis to between −30 and −45 degrees is in favor to LA abnormality (Figure 12). Mitral stenosis: Although the ECG is relatively insensitive for detecting mild mitral stenosis, but it does show characteristic changes in moderate or severe mitral stenosis. Left atrial enlargement is a principal electrocardiographic feature of mitral stenosis in patients with sinus rhythm. The left atrial enlargement correlate more closely with left atrial volume than with left atrial pressure. Also, it often regresses after successful percutaneous mitral commissurotomy.1 The major findings of significant mitral stenosis are listed in Table 3.

Electrocardiography Challenging Cases Table 3 Electrocardiographic findings in moderate-to-severe mitral stenosis

ECG change

Interpretation

Left atrial enlargement

In 90% of patients with sinus rhythm

Atrial fibrillation

Common in patients with longstanding MS

RV hypertrophy

Correlates with RV systolic pressure (about in 50% of patients with pressure of 70–100 mm Hg; and in all patients with pressure greater than 100 mm Hg)

Poor R wave progression

ECG 12

Figure 12 Note to a tall P waves in lead II (right atrial abnormality) and an abnormally large terminal negative component of the P wave in lead V1 (left atrial abnormality), and notched P wave in lead V5; suggesting biatrial abnormality. Also, RVH and right axis deviation was seen

Biatrial abnormality: ECG patterns findings include large biphasic P waves in lead V1 and tall and broad P waves in leads II, III, and aVF, and notched P wave in lead V5.

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Color Atlas of Cardiology: Challenging Cases

ECG 13

Figure 13 Note to low limb QRS voltage in the limb leads accomplish with relatively prominent QRS voltage in the pericordial leads, and poor R wave progression in pericardial leads; suggesting dilated cardiomyopathy (DCM). Also, presence of low-amplitude QRS complexes in lead V1 with a ≥3 increase in lead V2 is in favor to right atrium abnormality

Dilated cardiomyopathies (DCM): Presence of relatively low limb voltage (QRS voltage 7 mm tall), dominant S wave in V6 (>7 mm deep and R/S ratio 60 milliseconds (Figure 17).

Electrocardiography Challenging Cases

ECG 18

Figure 18 Note to rSR´ patterns in leads V1, S waves in leads I ≥40 milliseconds wide, early intrinsicoid (normal time to peak R wave) in leads V5 and V6, and late intrinsicoid (Prolonged time to peak R wave) in V1, suggest RBBB

Right bundle branch block (RBBB): The common diagnostic criteria for RBBB include QRS duration ≥120 milliseconds, rsr´, rsR´, or rSR´, patterns in leads V1 and V2, S waves in leads I and V6 ≥40 milliseconds wide, early intrinsicoid (normal time to peak R wave) in leads V5 and V6, and late intrinsicoid (Prolonged time to peak R wave) in V1 >50 milliseconds . In contrast to LBBB, RBBB is a common finding in the general population. RBBB pattern was seen in many persons without overt structural heart disease (Figures 18 and 19).

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Color Atlas of Cardiology: Challenging Cases

ECG 19

A

B Figure 19 ECGs from a patient with atrial tachycardia. Figure A showed 1:1 AV association, and after initiation of rate control, Figure B showed a varied AV conduction. In Figure B, AV conduction with aberrancy (RBBB morphology, Ashman phenomenon) is seen before the last beat

Electrocardiography Challenging Cases Atrial tachycardia: During this tachycardia the ectopic P wave precedes the QRS complex. By using the configuration of the P wave, such as axis and width, the site of origin of an atrial tachycardia could be distinguished.7 The PR interval depends on origin site of P wave formation and AV nodal conduction rate. Also, the ratio between P waves and QRS complexes depend on the rate of abnormal atrial impulse formation and the AV nodal transmission characteristics. The most common type of atrial tachycardia is paroxysmal (with sudden onset and offset). The other type of atrial tachycardia is incessant (permanent) which had persistent nature and the inability to control the rate. This form of atrial tachycardia more prone to developed the dilated cardiomyopathy (tachycardiomyopathy) (Figures 20 and 21).

ECG 20

Figure 20 Atrial tachycardia with 2:1 AV conduction. The atrial rate is about 230 beats/minute and ventricular rate is about 115 beats/minute. The p waves were positive in V1 and were negative in I, aVL leads

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Color Atlas of Cardiology: Challenging Cases

ECG 21

Figure 21 ECG from a patient with frequent episodes of palpitation. The first three beats are sinus, but after a premature atrial complex (blue arrow), an episode of atrial tachycardia begin. These episodes are repeat after some sinus beats

Electrocardiography Challenging Cases

ECG 22

Figure 22 Presence of atrial tachycardia accomplished with more than three P wave contours, irregular P-P intervals, and variable PR intervals; suggesting multifocal atrial tachycardia. This ECG was taken from an old male patient with chronic obstructive pulmonary disease

Chaotic (multifocal) atrial tachycardia: The main findings of this arrhythmia is atrial rates between 100 and 130 beats/minute, marked variation in P wave morphology (at least three P wave contours), totally irregular P-P intervals, and variable PR intervals. This arrhythmia is more in older patients with chronic obstructive pulmonary disease and congestive heart failure. Some drugs such as digitals or theophylline appear to be an unusual cause of this tachycardia (Figure 22).

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Color Atlas of Cardiology: Challenging Cases

ECG 23

Figure 23 Presence of the flutter waves which are negative in leads inferior leads and upright in V1; suggesting counterclockwise atrial flutter. The atrial rate is 300 beats/minutes and ventricular rate is 150 beats/minutes (twoto-one AV conduction)

Atrial flutter: This arrhythmia is a rapid form of atrial tachycardia sustained by a macro-reentrant circuit. Atrial flutter usually occurs in the right atrium and occasionally in the left atrium. During the more common “typical” type, the flutter circulates in a counterclockwise direction around the tricuspid annulus in the frontal plane (counterclockwise flutter); however, during the less common (10%) “atypical” type, the macro-reentry circuit rotates in a clockwise direction (down the intra-atrial septum and up the right atrial free wall). Other forms of atrial flutter can be observed in the setting of incisional scars from previous atrial surgery, previous atrial ablation, mitral annular flutter, idiopathic fibrosis in areas of the atrium, or other anatomic or functional barriers to conduction in the atria (Figure 23).

Electrocardiography Challenging Cases In counterclockwise atrial flutter, the flutter waves are negative in leads II, III, aVF, and V6 and upright in V1; whereas in clockwise atrial flutter, the flutter waves are upright in leads II, III, and aVF and often notched. In contrast to atrial tachycardia, lack of an isoelectric interval between flutter waves is seen because of evidence of continual electrical activity. The ventricular regularity and rate in this arrhythmia depend on AV transmission characteristics. If the AV conduction ratio was fixed, the regular QRS complexes are seen. If irregular QRS complexs was seen, it would because the wenckebach of AV conduction (group beating) or variable AV conduction ratio (irregular with no fixed pattern) (Figures 24 and 25).

ECG 24

Figure 24 Presence of the flutter waves which are negative in leads inferior leads and upright in V1; suggesting counterclockwise atrial flutter with varied AV conduction. Note the low ventricular response

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Color Atlas of Cardiology: Challenging Cases

ECG 25

Figure 25 Presence of notched flutter waves which are positive in leads inferior and negative in lead V1; suggesting The clockwise atrial flutter. Note to varied AV conduction

Electrocardiography Challenging Cases

ECG 26

Figure 26 In patient with atrial fibrillation (AF), the f waves can mimic atrial flutter waves in V1

Atrial fibrillation: This arrhythmia is considered as a most common tachyarrhythmia. The fibrillatory or f waves of atrirm are variable in amplitude, shape, and timing, although in lead V1, f waves sometimes appear uniform and can mimic flutter waves. The ventricular rhythm is irregularly irregular unless complicated by complete AV block or digitalis toxicity. However if ventricular responses were very rapid (>170 beats/min), it may appear to be regular (Figures 26 and 27).

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ECG 27

Figure 27 Note to presence of aberrant AV conduction with RBBB complex morphology (short cycle) after a long RR cycle in a patient with AF, suggest Ashman phenomenon (Phase 3 block)

Wolff–Parkinson–White (WPW) syndrome: Preexcitation, or the WPW abnormality on the ECG, occurs when the atrial impulse activates the ventricle earlier than would have occurred after normal conduction over the AV node (Figures 28 and 29). This premature activation is caused by accessory pathway. The basic features of electrocardiographic abnormalities in patients with the WPW including PR interval less than 120 milliseconds during sinus rhythm, QRS complex duration exceeding 120 milliseconds with a slurred, slowly rising onset of the QRS in some leads (delta wave) and usually a normal terminal QRS portion, and secondary ST-T wave changes that are generally directed in an opposite direction to the major delta and QRS vectors. The most common location of accessory pathway is left free wall (approximately 55%); other locations are posteroseptal (33%), right free wall (9%), and anteroseptal (3%).8 Presence of intermittent preexcitation during sinus rhythm and abrupt loss of conduction over the accessory pathway following intravenous administration of procainamide or with exercise suggest that the refractory period of the accessory pathway is long. These patients are not at risk for a rapid ventricular rate following atrial flutter or fibrillation development. Accessory pathway variants listed in Table 4. Atrioventricular reciprocating tachycardia (AVRT) may result in narrow (orthodromic) or broad (antidromic) QRS tachycardia in patient with accessory pathway. The most common tachycardia is orthodromic AVRT characterized by a normal QRS (