Mastering the 12-Lead EKG [2 ed.] 0826181937, 9780826181930

Citation preview

Mastering the 12-Lead EKG

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David A. Roberts, MSPAS, RN, PA-C, has been in healthcare for the past 20 years. He spent the first 10 years practicing as a registered nurse in a cardiac intensive care unit and working as a physician extender for a cardiologist. He also maintains certifications in basic and advanced cardiac life support and has been an ACLS and PALS instructor. Since 2007, Roberts has been a practicing PA after obtaining his master’s degree in Physician Assistant Studies at Bethel University in Tennessee. Currently, he works in a rural emergency department, Dyersburg, Tennessee; is a former assistant professor at Bethel University, where he taught EKG interpretation and pathophysiology; and is vice president of Tennessee Academy of Physician Assistants. He also serves as a peer reviewer for article submissions to the Journal of the American Academy of Physician Assistants, hosts EKG workshops, and gives lectures at multiple state conferences.

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Mastering the 12-Lead EKG Second Edition

David A. Roberts, MSPAS, RN, PA-C

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Copyright © 2021 Springer Publishing Company, LLC All rights 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 Springer Publishing Company, LLC, or authorization through payment of the appropriate fees to the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400, fax 978-646-8600, [email protected] or on the Web at www.copyright.com. Springer Publishing Company, LLC 11 West 42nd Street New York, NY 10036 www.springerpub.com http://connect.springerpub.com/home Acquisitions Editor: Jaclyn Koshofer Compositor: S4Carlisle Publishing Services ISBN: 978-0-8261-8193-0 ebook ISBN: 978-0-8261-8194-7 Instructor’s PowerPoints ISBN: 978-0-8261-8195-4 Answers to Case Studies and Exercises ISBN: 978-0-8261-8196-1 DOI: 10.1891/9780826181947

Instructor’s Materials: Qualified instructors may request supplements by emailing [email protected] Supplementary Answers to Case Studies and Exercises are available from springerpub.com/12leadekg 19 20 21 22 23 / 5 4 3 2 1 The author and the publisher of this Work have made every effort to use sources believed to be reliable to provide information that is accurate and compatible with the standards generally accepted at the time of publication. The author and publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers’ use of, or reliance on, the information contained in this book. The publisher has no responsibility for the persistence or accuracy of URLs for external or third-party Internet websites referred to in this publication and does not guarantee that any content on such websites is, or will remain, accurate or appropriate. Library of Congress Cataloging-in-Publication Data Names: Roberts, David A., author. Title: Mastering the 12-lead EKG / David A. Roberts. Description: Second edition. | New York : Springer Publishing Company, [2021] | Includes bibliographical references and index. Identifiers: LCCN 2019042295 | ISBN 9780826181930 | ISBN 9780826181947 (ebook) Subjects: MESH: Electrocardiography--methods | Heart Diseases--diagnosis Classification: LCC RC683.5.E5 | NLM WG 140 | DDC 616.1/207547--dc23 LC record available at https://lccn.loc.gov/2019042295

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Dedicated to my big beautiful family: Angie, Zach, Sam, Julia, Malachi, Evan, and Abigail “The journey of a thousand miles begins with a single step.” —Lao Tzu

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Contents Contributors ix Peer Reviewer xi Preface xiii 1

1.

Anatomy and Physiology of the Heart

2.

Electrical Conduction System of the Heart

3.

Waves of the EKG

21

4.

The 12-Lead EKG

35

5.

Heart Rate and Rhythm

6.

Sinus Rhythms

7.

Supraventricular Arrhythmias

8.

Atrial Fibrillation and Atrial Flutter

9.

Wolff–Parkinson–White Syndrome

49

67 101 145 181

199

10.

Ventricular Arrhythmias

11.

Atrioventricular Blocks

229

12.

EKGs and Pacemakers

255

13.

EKG Artifacts

14.

EKG Axis Interpretation

15.

Bundle Branch Blocks

16.

Ventricular Hypertrophy

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viii Contents

17.

Causes of ST Elevation and Depression on the EKG

18.

Ischemia Detection on the EKG

19.

Infarction Detection on the EKG

20.

Electrolytes, Medications, and Disease on the EKG

Appendix: Rhythm Summary Index 495

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Contributors Thomas T. Alleva, MSPAS, PA-C Emergency Medicine Physician Assistant, Emergency Medical Care Facilities, P.C., Jackson, Tennessee Marisa Berger, PA-S Physician Assistant Student, Physician Assistant Program, Bethel University, Paris, Tennessee Daniel Patrick Brown, MSPAS, PA-C Assistant Professor, Physician Assistant Studies, Physician Assistant Program, Bethel University, Paris, Tennessee Elizabeth Capelle, PA-S Physician Assistant Student, Physician Assistant Program, Bethel University, Paris, Tennessee Taylor Clark, PA-S Physician Assistant Student, Physician Assistant Program, Bethel University, Paris, Tennessee Gabrielle K. Dykema, PA-S Physician Assistant Student, Physician Assistant Program, Bethel University, Paris, Tennessee Jordan P. Gaucher, PA-S Physician Assistant Student, Physician Assistant Program, Bethel University, Paris, Tennessee Kelsey A. Maher, PA-S Physician Assistant Student, Physician Assistant Program, Bethel University, Paris, Tennessee Ashleigh McCoy, PA-C Physician Assistant Student, Physician Assistant Program, Bethel University, Paris, Tennessee Kaleb Naseman, PA-S Physician Assistant Student, Physician Assistant Program, Bethel University, Paris, Tennessee Paige Stoneburner, PA-S Physician Assistant Student, Physician Assistant Program, Bethel University, Paris, Tennessee James W. Truett Jr, MD Tennessee

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Emergency Physician, West Tennessee Healthcare, Jackson,

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Peer Reviewer Allison Rusgo, MHS, MPH, PAC Assistant Clinical Professor, Physician Assistant Department, Drexel University College of Nursing and Health Professions, Philadelphia, Pennsylvania

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Preface I know what you are thinking . . . another EKG textbook? Is it really necessary? As an instructor, I wanted to provide my students with a book that didn’t require any previous EKG experience to understand it. I wanted them to learn a systematic approach to EKG interpretation that would solidify their knowledge and help them make sure they don’t miss a thing. I needed them to practice and then practice some more. I needed them to be able to connect this new skill to their future practice as a medical provider. And when it was all said and done, I wanted them to have a mastery of advanced EKG topics that would allow them to go above and beyond in providing excellent care to their patients. But after years of unsuccessfully searching for a book that would meet my students’ needs, I decided to write one myself. Mastering the 12-Lead EKG, Second Edition, provides a concise, easy to read, yet COMPREHENSIVE look at EKG interpretation. You will begin learning foundational anatomy and physiology and finish with recent important 12-lead EKG topics overlooked by many other texts. I’m a down-to-earth kind of guy and I like to write that way, too. You will find the writing easy to follow with lots of images that help you understand the material. To master EKG interpretation, you must use a SYSTEMATIC APPROACH. This text teaches a newly developed method that has been proved to enhance retention of the material and makes sure that you don’t miss anything. This type of algorithmic method was first introduced by Dr. M. Mirtajaddini in the Journal of Electrocardiography. With Dr. Mirtajaddini’s permission, my take on this systematic approach is woven through each chapter and illustrates the step-by-step method. Readers of Mastering the 12-Lead EKG, Second Edition, are clinicians or soon-to-be healthcare providers. You must be able to use the information you gather from the electrocardiogram to make clinical decisions, some of which will be required to save patients’ lives. This text provides you with CLINICAL CONNECTIONS, providing brief descriptions of symptoms, potential causes of EKG findings, and treatment options that should be considered. The text also touches on the anatomy and pathophysiology behind the disease processes, allowing you to develop a deeper understanding of the material. At the end of each chapter, you’ll find questions about foundational concepts, and most importantly, hundreds of opportunities to PRACTICE your interpretation skills. You will start with basic rhythm strip interpretation and advance to 12-lead EKGs using real-life case studies. Detailed answers with explanations of important concepts are provided online.

ABOUT ME What business do I have writing an EKG textbook? I have been in healthcare for the past 20 years. During that time, EKG interpretation has been a significant part of my career. I spent the first 10 years in healthcare practicing as a registered nurse. Most of that time was

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xiv Preface

spent in a cardiac intensive care unit and working as a physician extender for a cardiologist. Interpreting EKGs, including rhythm strips and 12 leads, was part of my daily routine. In 2007, I obtained my master’s degree in Physician Assistant Studies at Bethel University. I have spent the last 8 years working in emergency medicine where EKG interpretation continues to be a critical part of my job. In 2011, I began teaching EKG interpretation in the PA program at Bethel University in Paris, Tennessee, and am now teaching full time in the emergency department at Dyersburg Regional Medical Center in Tennessee. I live in West Tennessee with my big, beautiful family. I have been married to my high school sweetheart for over 20 years. We have six awesome and energetic kids who love their two goldendoodles. Thanks for purchasing this book. I hope you find it a valuable resource for years to come. — David A. Roberts

Qualified instructors may obtain access to the supplementary material (PowerPoints) by emailing [email protected] Supplementary Answers to Case Studies and Exercises are available from springerpub .com/12leadekg

GOT AN EKG? I love to collect EKGs. If you have a fun EKG or story you want to share, please send it my way. You can email it to [email protected].

ACKNOWLEDGMENT Special thanks to Bethel PA class of 2020 Bethel PA class of 2021

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Chapter

1

Anatomy and Physiology of the Heart Knowledge of the anatomy and physiology of the heart is foundational to our understanding of the EKG.

IT’S GREEK TO ME Learning to interpret an EKG is a lot like learning a new language. Several years ago, I had the opportunity to learn Koine Greek. I was attending church with a college professor who taught the subject at a local university. He offered to take a few men under his wing and help us tackle the language. At first, we learned the alphabet, the names of the letters, and how to pronounce them. Then we began to see them put together to create words, each with their own meaning. Soon those words were strung together to make sentences we could read … at least sometimes, and understand the important messages the author was trying to communicate.

Instead of a new alphabet, EKGs confront us with humps and bumps of different shapes and sizes, all with their own unique meaning. And when we put the humps and bumps together, they tell us an important message that, with lots of practice, we can read. Better yet, we can act upon the information we gain from our interpretation to benefit our patients.

THE EKG The electrocardiogram was invented in 1903 by the Dutch physician Willem Einthoven. Since its inception, the EKG has proved itself to be a useful tool for detecting several pathologic

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conditions of the heart. The EKG is considered the gold standard for detecting abnormal heart rhythms and conduction problems, but it can also be utilized to diagnose conditions such as a myocardial infarction (MI) and enlargement of the heart muscle. It can even add support for things like electrolyte abnormalities, intracranial bleeds, and hypothermia! The 12-lead EKG has become an essential part of the workup for patients who present with potential cardiac disease. It is inexpensive, noninvasive, and usually readily accessible. The only caveat is that the provider must be able to read the EKG’s message and know what to do with the information. Although EKG interpretation is considered a basic skill, many providers are not adequately prepared, and this can spell disaster for our patients. The goal of this book is to make you into a master EKG interpreter. You will learn how and why the EKG displays the waveforms it does for each condition. I will share with you some tricks of the trade I have learned along the way and help you watch out for things that trip providers up. You will also be able to build clinical connections to your EKG interpretation: risk factors, symptoms, and potential treatment options that are worth considering. The only way to get proficient at EKG interpretation is practice, and lots of it. This book provides you with ample opportunities to put your skills to use, so make sure you take advantage of it. Now let’s get started.

THE HEART The EKG tells us vital information about the heart. Although the EKG is a tracing of the heart’s electrical activity, it helps us see much more than that. We can obtain information about many structures of the heart such as the pericardium, myocardium, and coronary arteries. If the EKG is going to tell us information about these structures, we need to make sure we have a solid understanding of what they are and how they work. A few years ago, I was asked by my son’s teacher to give a talk to her elementary school class about the heart. I explained to them the heart’s structure was a lot like a house. The outside of the “house” is protected by a fence (pericardium). The house itself is a walled structure (myocardium) with four rooms (chambers), two upstairs (atria) and two downstairs (ventricles). The upstairs and downstairs are separated by doors that open and close (atrioventricular [AV] valves). The right and left sides of the house were separated by a wall (interatrial and interventricular septum). The house also has front and back doors that open up to the outside (the semilunar valves). The heart even has its own electrical wiring (electrical conduction system) and plumbing systems (coronary arteries, great vessels).

The heart is a powerful muscle about the size of your fist that sits in the anterior chest behind the sternum. About two-thirds of the heart sits to the left of the sternum, while the remainder sits to the right. Because the heart sits closer to the left, as you will soon see, we place most of the chest EKG wires on the left side of the chest.

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3

The heart works day and night to pump blood throughout our body. In fact, it serves as two pumps. The right side of the heart pumps deoxygenated blood to our lungs to pick up oxygen before returning to the left side of the heart, where it will be pumped out into the rest of our body’s circulation.

Pericardium The outside of the heart is covered by a tough double layer sac called the pericardium. Just like a fence, the pericardium surrounds the outside of the heart offering some protection. It limits the heart’s motion in the chest, prevents it from overfilling when there is too much blood volume, and provides some shock absorption in case of a jarring event like tripping over your shoelaces. The outer fibrous pericardium anchors the heart to surrounding structures such as the great vessels, diaphragm, and pleural membrane that covers the lungs. The inner serous pericardium has two layers, which fold to create a potential space called the pericardial cavity. The two layers of the serous pericardium include the outer parietal layer, which is fused to the fibrous pericardium, and the inner visceral layer, which fuses to the heart muscle (myocardium). The visceral layer that attaches to the heart is also called the epicardium and is considered the outer layer of the heart wall.

Conditions such as a viral illness or an autoimmune disease such as rheumatoid arthritis can cause inflammation of the pericardium to occur. This is called pericarditis. This often results in sharp pleuritic chest pain that causes the patient to seek medical attention. Pericarditis can sometimes be identified on the EKG. The pericardial cavity contains a serous fluid that functions as a lubricant. There is typically between 20 and 50 mL of pericardial fluid in this space. Inflammatory conditions such as a rheumatoid arthritis or a traumatic injury to the chest can lead to an overaccumulation of fluid. This is called a pericardial effusion. If the effusion is large or the fluid accumulates rapidly, it can prevent the heart from filling and pumping effectively. This condition is dangerous and is called pericardial tamponade. When tamponade occurs, the stroke volume (amount of blood ejected from the heart with each contraction) is reduced, resulting in a drop in cardiac output (Heart Rate × Stroke Volume = Cardiac Output). A significant drop in cardiac output means that the body is not getting the nutrients it needs to survive. If left untreated, this type of obstructive shock can

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lead to cardiac arrest and death. Pericardial effusion and tamponade can cause abnormal findings on the EKG tracing that we will discuss in a later chapter.

THE HEART’S LAYERS Three layers make up the heart’s wall. The outermost layer is called the epicardium. This is the same tissue as the visceral layer of the pericardium mentioned above. In other words, it’s a different name for the exact same thing. Because it sits on the outermost layer of the heart, you can think of it as the siding on the outside of the house. The middle layer of the heart is the myocardium. This is the thick muscular wall of the heart made of involuntary striated muscle. Thankfully, it is very resistant to fatigue. When the myocardium contracts, it pumps blood through the heart’s chambers and the body’s systemic circulation. Think of this as the middle part of the wall that is made up of studs and insulation. The innermost layer is called the endocardium. It lines the inside of the heart providing protection for the heart’s chambers and valves. Think of this as the sheetrock that covers the wall inside the house.

MYOCARDIUM Now that you have been introduced to the heart’s layers, let’s spend a little more time discussing the myocardium. This amazing muscle makes up the majority of the heart and is key to keeping us alive. Several abnormalities of the myocardium can be detected on the EKG, so it is important that we have a good understanding of it. Remember that the heart serves as two pumps: a right side that sends blood to our pulmonary circulation and a left side that pumps blood to the rest of our body. The pressures in the systemic circulation are much higher than the pressures required for blood to travel through the pulmonary circulation. Bodybuilders who train by lifting heavy weights look a little different from the rest of us. Think of Arnold Schwarzenegger back in his prime. As he lifted heavier and heavier weights, his body adapted, and his muscles continued to get bigger. The same is true of the myocardium. Because of higher pressures in the systemic circulation, the left ventricle has to overcome more “weight.” This results in a left ventricle that is larger than the right ventricle. This is an important concept to keep in mind for later. As you will see, the larger the muscle, the greater the electrical activity it will have. If the myocardium must overcome elevated pressures for prolonged periods, such as with systemic hypertension, the muscle will continue to abnormally enlarge the size of its cells in an attempt to compensate. We call this type of enlargement hypertrophy. The enlarged myocardium can be detected on the EKG. For the myocardium to pump blood, it must contract. And to contract, the cells (myocytes) of the myocardium must depolarize (internal electrical charge becomes positive). Normally the wave of depolarization is started by the electrical conduction system of the heart, principally the sinoatrial (SA) node. Once it begins, the wave of depolarization will spread quickly in all directions from cell to cell through the gap junctions. This happens fast so that the myocardium can function as a single unit, providing a succinct and coordinated contraction.

The waves we see on the EKG depict electrical conduction through the myocardium.

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ST

5

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Although normal depolarization of the myocardium is started by the electrical condition system, there are times that a random area of the myocardium can initiate the impulse. This leads to abnormal beats and rhythms that we call ectopy. Ectopy can be caused by things such as an overactive sympathetic nervous system. So the Starbuck’s venti coffee you had this morning or the stress over your next pharmacology examination could cause the myocardium to fire abnormally. Fortunately, the most common types of ectopic beats rarely cause more than a temporary “skipping” sensation in the chest. However, more serious problems can cause ectopy that poses a real danger. The myocardium can be damaged if it does not receive adequate blood supply from the coronary arteries. When the myocardium lacks sufficient oxygen (hypoxic), we call this ischemia. When the lack of nutrients persists and causes cell death of the heart muscle, we call it an MI. Damage to the myocardium can put people at risk for serious and life-threatening ectopic rhythms that were initiated by the irritable ischemic myocardium. It’s a good thing you are learning EKG interpretation, so you can detect these abnormalities and save patient’s lives.

MA

1: ANATOMY AND PHYSIOLOGY OF THE HEART

E KG

THE CORONARY ARTERIES The coronary arteries are the only “plumbing” system, and they provide blood and nutrients to the myocardium. There are three main arteries, each with branches that stretch out over the surface to ensure the myocardium gets the resources it needs to function. Needless to say, occlusions of the coronary arteries can lead to cell damage or death. And, as already mentioned, damage to the myocardium can cause life-threatening arrhythmias to occur.

An EKG is the quickest way to detect a possible occlusion of a coronary artery and the arrhythmias it can cause.

The Left Main The left main coronary artery (LMCA) originates from the aorta above the cusp of the aortic valve. And as its name suggests, it is the main route that supplies blood to the left side of the heart. The LMCA is a short artery, typically measuring between 10 and 15 mm in length (Boztosun, Aung, Olcay, & Kirma, 2008). Soon after arising from the aorta, the LMCA branches into two distinct coronary arteries—the left anterior descending (LAD) and the left circumflex (LCX). An occlusion of the left main would prevent blood from flowing

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through both of these major coronary arteries. Some folks call an acute occlusion of the LMCA a widow maker. Because of its high mortality rate, it unfortunately has turned more than one spouse into a widow.

The Left Anterior Descending The LAD branches off the short left main. It then travels down the anterior interventricular grove and supplies the anterolateral myocardium, apex, and interventricular septum. It typically provides blood for 45% to 55% of the left ventricle. The LAD gives rise to two types of arterial branches: septals and diagonals. To diagnose an MI caused by an occlusion of the LAD, we typically look to the septal and anterior (V1–V4) leads of the EKG. Much more on MIs and these leads later.

The Left Circumflex The LCX also originates from the left main. From there it travels within the posterior atrioventricular (AV) groove toward the inferior interventricular groove. The LCX usually has one to three large obtuse marginal (OM) branches. These arterial branches supply the lateral wall of the left ventricle. Depending on whether or not the LCX is the dominant artery for the left side of the heart (some people have a larger LCX than others), it can provide between 15% and 50% of the blood supply to the left ventricle. An acute MI of the LCX can often be suspected on finding certain abnormalities in the lateral leads of the EKG (V5–V6, I, aVL).

The Right Coronary Artery The right coronary artery (RCA) arises above the right cusp of the aortic valve and travels down the right AV groove. The RCA provides blood supply to the right ventricle as well as the posterior and inferior portions of the left ventricle. In about 70% of the population, the RCA also provides blood supply to the SA node, the primary pacemaker of the heart. Branches off the RCA include the acute marginal (AM) and the posterior descending artery (PDA). The inferior leads (II, III, aVF) of the EKG can provide information about an acute occlusion of the RCA.

THE HEART VALVES There are two types of valves or “doorways” in the heart: the semilunar (front/back doors) and the AV valves (upstairs/downstairs doors). The valves keep the blood moving in the right direction. They open, allowing the blood to flow through, then close, preventing the blood from returning to where it just came from. The closing of the valves creates the S1 and S2 heart sounds we hear during the physical examination. Valves can fail to do their job. They may become leaky, allowing blood to flow in the wrong direction (regurgitation). This can lead to enlargement of the myocardium due to increased pressures within the heart’s chambers. Valves can also become stiff (stenotic) and more difficult to open. This requires an increase in the strength of the myocardial squeeze in order to get the valve open. If prolonged, this too can result in hypertrophy of the myocardium. As mentioned above, hypertrophic myocardium can be detected on the EKG.

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7

The Semilunar Valves The aortic and pulmonic valves are known as the semilunar valves. They are called semilunar because both have three leaflets, which look like half-moons. The aortic and pulmonic valves serve as the “front/back doors” of the heart that go to the aorta and pulmonary artery, respectively. Their closure creates the S2 heart sound.

The Atrioventricular Valves The AV valves are so named because they separate the atria from the ventricles. Now that’s not hard. The tricuspid valve has three cusps and separates the right atrium from the right ventricle. The mitral valve has two cusps and separates the left atrium from the left ventricle. I was taught the saying “I will tri to do right.” This may help you remember that the tricuspid valve is on the right side of the heart. If the tricuspid valve is on the right, that must mean that the mitral valve is on the left. The closing of the AV valves creates the S1 heart sound.

Cardiac Skeleton Although the AV valves have a very important job in preventing backflow of blood, they have another very important role. The AV valves are surrounded by a fibrous skeleton that serves as an electrical insulator. This fibrous tissue is called the cardiac skeleton.

Much like the covering of an electrical wire that prevents you from getting shocked, the AV valves stop electrical conduction from going on a nonstop flight from the atria to the ventricles. If the conduction wasn’t halted by the cardiac skeleton, the atria and ventricles would contract at the same time. The atria need time to fill the ventricles before they contract to pump blood out of the heart. The cardiac skeleton also prevents the depolarization of the ventricles from circling back to the atria causing them to depolarize prematurely.

THE HEART CYCLE Deoxygenated blood arrives via the vena cava and dumps into the right atrium. The right atrium fills with blood until the pressure rises high enough to begin pushing open the AV

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valves. Once the tricuspid valve opens from the increased pressure, the blood from the right atrium begins passively filling the right ventricle. Approximately 70% of the blood that enters the ventricles is from passive filling alone. The atria then contract (atrial systole) forcing additional blood volume into the ventricles. Now we are ready for the ventricles to do their work. The right ventricle contracts (ventricular systole), and blood is pumped out of the heart through the pulmonic valve. It’s called the pulmonic valve because this blood is now on its way through the pulmonary artery to the lungs to be oxygenated. Even though it carries deoxygenated blood, it is called an artery because it carries blood away from the heart.

Source: Graph from OpenStax College. (2014). Anatomy & physiology. Retrieved from https://cnx.org/contents/[email protected]:IsP5aaud@3/Cardiac-Cycle

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After traveling to the lungs, oxygenated blood then arrives to the left atrium from the pulmonary veins. The same cycle occurs as above. The pressure increases in the atria until the AV valves are forced open. Atrial systole then pushes the remaining blood volume into the ventricles. Upon ventricular systole, the left ventricle forces open the aortic valve pushing oxygenated blood into the aorta and beyond.

FINAL THOUGHTS There you have it, a quick review of some of the anatomy and physiology of the heart. It is foundational to our understanding of the EKG. After all, the EKG is giving us valuable insight into many of these structures. But we are not done yet. In the next chapter, we will dig deeper into the anatomy and physiology of the heart’s electrical conduction system. This is where the real magic happens. Before we move on, don’t worry if some of the EKG terms or concepts don’t make sense to you yet. We will continue to unpack these topics as we go along. Just like learning a new language, we are laying a foundation to build on. Now, on to the electrical conduction system.

TAKE-HOME POINTS • Knowledge of the anatomy and physiology of the heart is foundational to the understanding of the EKG. • The EKG can detect abnormalities associated with several structures of the heart. For example: ▪ Pericarditis—an inflammation of the pericardium ▪ Pericardial effusion—an overaccumulation of fluid in the pericardial space ▪ Hypertrophy—cellular enlargement of the myocardium caused by systemic hypertension or ▪ Poorly functioning heart valves (regurgitation or stenosis) ▪ Ischemia and infarction—hypoxia or death of the myocardium caused by ▪ Coronary artery occlusion

EXERCISES Fill in the Blanks 1. The _____________ ventricle is larger than the ______________. 2. Waves on the EKG depict electrical conduction through the __________________. 3. The ________________ electrical insulates the atria from the ventricles. 4. An EKG is the quickest way to detect a possible ___________ of a coronary artery and the ____________ it can cause. 5. Approximately _________% of the blood that enters the ventricles is from passive filling alone.

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Thought Questions Describe the cardiac skeleton and why it is important.

Define depolarization.

Define myocyte.

REFERENCES Boztosun, B., Aung, S. M., Olcay, A., & Kirma, C. (2008). The longest documented left main coronary artery. International Journal of Cardiology, 126(1), e17–e18. doi:10.1016/j.ijcard.2006.12.088 OpenStax College. (2014). Anatomy & physiology. Retrieved from https://cnx.org/contents/ [email protected]:IsP5aaud@3/Cardiac-Cycle

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Electrical Conduction System of the Heart To be able to interpret an EKG and really understand it, you must be familiar with the electrical conduction system, its parts, and how they work together.

THE ELECTRICAL CONDUCTION SYSTEM The anatomy and physiology of the heart are foundational to our understanding of the EKG. Now it’s time to dive even deeper into the inner workings of the heart. To be able to interpret an EKG and understand it, really understand it, you must be familiar with the electrical conduction system, including its parts and how they work together.

Special Cells The electrical conduction system is made up of special cells that can generate an impulse and efficiently carry that impulse where it needs to go. Cells of the conduction system that have the ability to generate a wave of depolarization are called pacemakers. They are able to create an electrical current that repeats itself over and over without an external stimulus. Although there is a primary pacemaker called the sinoatrial (SA) node, pacemaker cells can be found throughout the conduction system and myocardium.

The cardiac cell with the fastest depolarization at any given time will function as the dominant pacemaker.

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In other words, the first one to take off from the starting line gets to be the pacemaker. Depending on the condition of the heart, the pacemaker may change from beat to beat or remain the same indefinitely. There is also a specialized conduction system that carries current from the atria into the ventricular myocardium. This acts as the “electrical wiring” of the heart. Conduction fibers help to accelerate and synchronize depolarization of the myocardium, providing for coordinated contraction of the ventricles.

MYOCARDIAL DEPOLARIZATION AND REPOLARIZATION Electrical activity transmitted through the conduction system spreads out into and through the myocardium. When the impulse arrives at a resting myocyte, it causes an action potential to occur. This is where positively charged ions (sodium, potassium, calcium) enter through the cell membrane and result in a positive charge to the cell’s interior. When the cell goes from a negative to positive charge, it has been depolarized. Depolarization continues to spread in all directions through the myocytes by way of gap junctions.

Depolarization of the myocyte should cause a mechanical response to occur. This process is called electromechanical coupling. Once depolarization occurs, the contractile proteins slide over each other, shortening the cell, and making it contract. The process of depolarization and contraction of the myocardium is called systole.

Source: Illustration from OpenStax College. (2014). Anatomy & physiology. Retrieved from https://cnx.org/contents/ [email protected]:MCgS6S0t@3/Cardiac-Muscle-and-Electrical-Activity

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After an action potential develops, the myocyte is unable to depolarize again for a period of time. This phase is called the refractory period. There are two parts to the refractory period: absolute and relative. During the absolute refractory period, the myocardium cannot depolarize regardless of the strength or number of stimuli it receives. The myocardium is tired, and irrespective of how great the bribe, it’s not ready to go. However, during the relative refractory period, the myocardium is vulnerable. If strong enough, a stimulus can win over the myocardium and cause depolarization to occur early. When the refractory period is completely over, the cell is able to receive a normal impulse, depolarize, and contract.

Source: Illustration from OpenStax College. (2014). Anatomy & physiology. Retrieved from https://cnx.org/contents/[email protected]:MCgS6S0t@3/Cardiac-Muscle-and-Electrical-Activity

Once the heart has become active, it needs to return to its resting state called diastole. Positive ions are moved out of the cell and the interior returns to its baseline negative charge. This is called repolarization. When repolarization occurs, the myocytes relax and everything is back to square one.

PARTS OF THE CONDUCTION SYSTEM The SA Node Now it’s time to discuss the individual parts of the electrical conduction system. Let’s begin where normal conduction of the heart begins, at the SA node.

The SA node is the heart’s primary pacemaker. It is a densely packed bundle of cells located in the upper posterior wall of the right atrium just under the epicardium. The SA node is made up of a central core of pacemaking cells and an outer layer of transitional cells that spread its impulse into the right atrium. Most often, the SA node gets its blood supply from the right coronary artery (55%) but can also be supplied by the left circumflex (45%). Both the parasympathetic (vagus nerve) and sympathetic nervous systems (T1–T4, spinal nerves) innervate the SA node. When stimulated by the vagus nerve, the SA node’s inherent pacing rate (chronotropy) decreases and the force of contraction (inotropy) is diminished. There is also a reduction in the speed of electrical conduction through the

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heart (dromotropy). The vagus nerve can be stimulated by activities such as coughing, holding your breath and bearing down, or jumping into a pool that is a bit too cold for comfort. The SA node has an opposite response when it is stimulated by the sympathetic nervous system. The heart rate increases along with the heart’s force of contraction. Things like an amp of epinephrine, someone jumping out from behind a wall to startle you, or your morning coffee can increase sympathetic activity. The SA node has a superpower called automaticity. It is able to spontaneously depolarize without any external stimulus. This extraordinary ability is one reason it can function as the primary pacemaker of the heart. This function is not completely understood but occurs in part due to the “funny current” (I(f)), a gradual increase in the resting membrane potential by sodium and potassium influx. Spontaneous release of calcium from the sarcoplasmic reticulum into the intracellular space also leads to depolarization of the SA node (Johnson, Johnson, & Rhodes, 2020). Although other cells have the gift of automaticity, under normal circumstances the SA node generates its impulse faster than all the other cells with pacemaker potential. Its inherent pacing rate is around 60 to 100 beats per minute, but it can be influenced by the autonomic nervous system. Its faster inherent rate allows it to dominate over others that want to be pacemakers. This phenomenon is called overdrive suppression. After the wave of depolarization leaves the SA node, it continues to spread throughout the myocardium and conductive system. When the impulse reaches other potential pacemakers, they depolarize. Once depolarized, the cells with pacemaker ability are suppressed until their refractory period has expired. Because the SA node is located in the upper right atrium, the wave spreads downward and to the left atrium. The depolarization of the atrium is seen on the EKG as a small amplitude wave called a P wave.

The Atrioventricular Node The cardiac skeleton prevents the wave of atrial depolarization from continuing nonstop to the ventricles. Because the electrical impulse is impeded by this fibrous tissue, there must be a path that allows conduction to proceed through the remainder of the myocardium.

Under normal circumstances, the atrioventricular (AV) node is the sole route allowing atrial depolarization to reach the ventricles. The AV node is a bundle of densely packed cells similar to those found in the SA node. It sits in the posterior inferior region of the interatrial septum near the opening of the coronary sinus. This area is also known as the triangle of Koch, a space defined by the tendon of Todaro (1) posteriorly, the tricuspid valve (2) anteriorly, and the opening of the coronary sinus (3) at the base. These landmarks are utilized during cardiac surgery to avoid damage to the nodal tissue. The right coronary artery supplies the AV node the majority of the time (90%).

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Just like the SA node, the AV node is affected by the sympathetic and parasympathetic nervous systems. When stimulated by the sympathetic nervous system, conduction through the AV node speeds up and the refractory period shortens. Vagal stimulation primarily by the left vagus nerve, on the other hand, slows conduction through the AV node and lengthens the refractory period, thus decreasing the ventricular rate. Conduction through the AV node is relatively slow due to a calcium-mediated action potential, which takes longer than those propagated by sodium channels. Once the impulse reaches the AV node, there is a slight delay before depolarization is allowed to reach the ventricles (~0.12 second). The AV node wants the depolarization wave to stop, have a cup of coffee, and smell the roses before moving on. This trait, called decremental conduction, gives the atria time to contract completely before depolarization of the ventricles. The AV node has two separate pathways. One conducts relatively fast and the other is a bit more sluggish. The anteriorly located pathway has a quicker conduction speed but has a longer refractory period. The speed through the posterior pathway is slower, but it has a faster recovery time. Because there are two pathways with unique conduction and recovery speeds, abnormal rhythms such as AV nodal reentry tachycardia can occur. More on that later. The AV junction, an area just superior to the AV node that extends to the bifurcation of the bundle of His, also has the superpower of automaticity. This allows it to serve as a backup pacemaker if the SA node fails to do its job. Its inherent pacing rate is set around 40 to 60 beats per minute. Because of its slower inherent rate, it shouldn’t unnecessarily take over as the primary pacemaker. However, if a wave depolarization fails to reach the AV node in time, it will act as pacemaker. This transition of power is called downward displacement of the pacemaker.

HIS-PURKINJE SYSTEM Bundle of His After slowed conduction through the AV node, the wave of depolarization reaches the bundle of His, which conducts very rapidly by use of sodium channels. This part of the electrical conduction system, named after the German cardiologist Wilhelm His, is the

bridge from the AV node to the ventricular electrical conduction system. The top part of the bundle has fibers that are similar to those of the AV node. The bottom half of the bundle has fibers that are more like the fascicles of the bundle branches that lie below. If potential pacemakers above the bundle of His fail to work, it may take over as the primary pacemaker. Its rate of depolarization leads to ventricular rates near 40 to 50 beats per minute.

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Source: Wilhelm His Jr. Photogravure, 1913, after Nicola Perscheid, 1907. (1913). Retrieved from https://wellcomecollection.org/works/jkfv4qrh. Credit: Wellcome Collection. CC BY.

The Bundle Branches Two main branches come off the bundle of His. One was created to service the right ventricle and the other for the left. Both follow along the septal surface of each respective ventricle. After separating from the bundle of His, the left branch quickly separates into two distinct fascicles, one anterior and the other posterior. The right branch, however, remains a single fascicle until reaching the end of the distal interventricular septum. The right bundle has a longer refractory period than the left bundle. This just means it takes longer to recover from depolarization. If called on too early, it can fail to do its job. Occasionally, one or multiple fascicles can fail to carry the impulse through the ventricles. We call this a fascicular or bundle branch block. Yep, we’ll get to that, too. When serving as a backup pacer for the heart, it often leads to ventricular rates around 20 to 40 beats per minute.

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Purkinje Fibers At the end of each bundle branch, the conductive tissue is composed of Purkinje fibers. The Purkinje cells have more mitochondria and can conduct an action potential quicker than the other conductive cells. This allows for synchronized contraction of the ventricles. Purkinje cells can also act as a pacemaker if pacing fails to occur from an area above in a timely manner. Their inherent rate is between 15 and 40 beats per minute. If your patient is relying on the Purkinje fibers as a pacemaker, that patient is in trouble. These patients are often very sick and need urgent intervention.

FINAL THOUGHTS The electrical conduction system is an amazing creation. When working properly, it keeps our hearts beating in rhythm. It keeps the atria and the ventricles working in sync as an efficient pump. It knows when to speed up and slow down. It even has a backup system in place in case parts fail. We need it to keep our heart beating day after day, year after year. Now that we have this under our belt, it’s time to learn some EKG!

TAKE-HOME POINTS • To be able to interpret an EKG and understand it, really understand it, you must be familiar with the electrical conduction system including its parts and how they work together. • Parts of the electrical conduction system include: ▪ SA node—the heart’s primary pacemaker ▪ AV node—the only way for atrial depolarization to reach the ventricles in normal circumstances ▪ Bundle of His—the bridge from the AV node to the ventricles ▪ Left and right bundle branches—two left fascicles and a single right fascicle ▪ Purkinje fibers—provide for rapid conduction of the ventricles • Pacemaker cells can generate a wave of depolarization without an external stimulus. • The autonomic nervous system can affect the speed of conduction and the length of the refractory period.

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EXERCISES Label the diagram:

Complete the chart with the inherent rate of each: SA Node AV Node Bundle of His Purkinje Fibers

Fill in the Blanks: 1. Action potential: A reversal in the cell’s electrical potential. This occurs when __________________ charged ions enter through the cell membrane and result in a ________________ charge to the cell’s interior. 2. Depolarization: Cell goes from a _______________ charge to a __________________ charge. 3. Repolarization: Cell returns to its baseline ____________________ charge and the myocytes are able to ______________.

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4. Electromechanical coupling: When _______________ causes contractile proteins to ___________ and cause the myocardium to _______________. 5. Systole: The process of depolarization resulting in _____________ of the myocardium. 6. Diastole: When the myocardium repolarizes and the heart returns to its _______________ state. 7. Absolute refractory period: During this time, the myocardium is unable to _________________, regardless of the number or strength of stimuli. 8. Relative refractory period: If the myocardium receives a strong enough stimulus during this time, it may _______________. 9. Automaticity: The ability to depolarize without any external stimulus. It is a characteristic of all _______________ cells. 10. Overdrive suppression: The ability of a faster pacemaker to ________________ over other potential pacemakers. 11. Decremental conduction: The slight delay at the __________ that allows time for the atria to contract before depolarization continues to the ___________________. 12. Downward displacement of the pacemaker: When the _________ pacemaker is at a level below the SA node. This occurs because the SA node failed to depolarize, or another pacemaker depolarized faster than it should have.

REFERENCES Johnson, F., Johnson, R. A., & Rhodes, S. A. (in press). Pathophysiology of the heart. In: N. Tkacs, L. Herrmann, & R. Johnson (Eds.), Advanced physiology and pathophysiology. New  York, NY: Springer Publishing Company. OpenStax College. (2014). Anatomy & physiology. Retrieved from https://cnx.org/contents/ [email protected]:MCgS6S0t@3/Cardiac-Muscle-and-Electrical-Activity Wilhelm His Jr. Photogravure, 1913, after Nicola Perscheid, 1907. (1913). Retrieved from https:// wellcomecollection.org/works/jkfv4qrh

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Waves of the EKG The EKG is made up of humps and bumps created by depolarization and repolarization of the myocardium.

PEP TALK There is a lot of information here. Focus on learning what each of the waves, intervals, and segments represent and their normal appearance. The rest of the material will be useful to you as you make your way through the rest of the book. You can refer back to this chapter as needed for little nuggets of information. We are laying a solid foundation we can build on.

TIME TO MIND YOUR PS AND QS Now that you are familiar with the anatomy of the heart and its electrical conduction system, we are ready to discuss the waves of the EKG. The EKG is made up of humps and bumps created by depolarization and repolarization of the myocardium. These two processes,

depolarization and repolarization, are the only activities represented on the EKG. By looking at the individual parts of the EKG, we can begin to read the story it is trying to tell us.

THE EKG PAPER If the EKG is only showing us two things, depolarization and repolarization, how can we get so many different sizes and shapes of these humps and bumps? Good question.

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The width of the waves tells us the time it takes for the depolarization or repolarization to occur. The wider the hump, the longer it took to complete. The narrower the bump, the shorter the duration. Easy enough. The height of each wave is derived from the amount of energy traveling through the myocardium at that moment in time. The larger the wave, the greater the amount of energy pointing in a given direction. The smaller the wave, the less the energy. The duration and amplitude of the waves are an important part of our interpretation of the EKG. To help us determine these values, the waves are printed on special graph paper with lines and boxes. When looking at the graph, time is measured from left to right, and amplitude is measured vertically. Each small box on the EKG paper measures 1 mm2. Because the paper moves at a standard speed of 25 mm/second, the width of one small box equals 0.04 second. The lines between every five small boxes are shaded darker. This creates a larger box that represents 0.20 second (0.04 second × 5 = 0.20 second). With typical calibration of the EKG machine, the height of every small box is equal to 0.1 mV. Ten small boxes (two large boxes) are equal to 1 mV. Calibration can be adjusted if the QRS complexes have large amplitudes and are making other leads difficult to read.

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ELECTRODES To obtain an EKG, you have to use electrodes. Electrodes are simply stickers or patches applied to the skin. They come in different shapes and sizes, but the purpose remains the same—to conduct electricity traveling from the myocardium through the body and bridge it to wires that are connected to the EKG machine. To conduct electricity, the electrodes have a conductive gel applied to the back. Often the wires are connected to the electrodes by clipping or snapping to them. Poorly attached electrodes will cause artifact that can make an EKG difficult to interpret. Occasionally, the skin surface must be prepped for the electrodes to attach properly. A hairy-chested man may need a bit of a trim. Electrodes also have a difficult time attaching to moist skin. In a patient who is diaphoretic, the skin will need to be dried, and the electrodes may need to be replaced periodically.

THE FOUR LAWS To create the waves and complexes we see on the EKG, the electrodes are assigned a positive or negative polarity by the EKG computer. Using the four laws below, the computer is able to take in the information it receives from the electrodes and create waves for us to interpret. Here are the four laws:

– – –

+ + +

1. A wave of depolarization flowing toward a positive electrode will record a positive wave. 2. A wave of depolarization flowing away from a positive electrode will record a negative wave. 3. A wave of depolarization moving perpendicular to a positive electrode will record a biphasic wave. 4. All the effects caused by repolarization have the reverse effect on the waves. For example, a wave of repolarization moving away from a positive electrode will result in a positive wave.

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THE WAVES, INTERVALS, AND SEGMENTS Not only did Einthoven invent the EKG, he is responsible for the names of the EKG waves that we continue to use today. Instead of starting at the beginning of the alphabet, Einthoven chose to use letters from the middle (PQRST). The 15th-century mathematician Descartes used letters near the end of the alphabet to represent variables or unknowns. Einthoven followed a similar tradition. He didn’t know if more waves would later be discovered that would occur before the P wave or after the T wave. By using the middle of the alphabet, other waves could be added without disrupting the naming pattern. Now let’s talk about what each of these waves means.

The P Wave The P wave represents depolarization of the atrial myocardium. After the SA node fires, the wave of depolarization spreads anteriorly in the right atrium, across the intraatrial septum, and on to the left atrium where the depolarization is directed posteriorly. Because the depolarization begins in the right atrium, the first half of the P wave represents right atrial depolarization. The second half of the P wave represents the spread of depolarization through the left atrium. Sometimes a small notch can be seen at the peak of P waves in normal EKGs as the depolarization goes from the right atrium to the left. When present, it is usually best detected in the anterior leads (V1–V6). This concept is also demonstrated in lead V1, where a biphasic (goes above and below baseline) P wave is often seen. The first upright portion of the P wave represents the anterior depolarization of the right atrium, followed by the inverted portion of the P wave that represents the posterior depolarization of the left atrium.

V1 and the Biphasic P Wave

As the right atrium depolarizes, the wave of electricity moves toward the chest, creating a positive wave. As the left atrium depolarizes, the wave moves toward the patient’s back, creating an inverted wave. Just remember the four laws of the EKG.

Normal P wave duration ranges from 0.07 to 0.12 second. If the P wave is abnormally prolonged, it could be due to an enlargement of the left atrium. Normal amplitude/height of the P wave is less than 2.5 mm or 0.25 mV. Amplitudes larger than normal can indicate enlargement of the right atrium. Atrial repolarization is at such a low amplitude that it is typically not seen and therefore not represented on the EKG.

The PR Interval The PR interval is the period from the beginning of the P wave to the beginning of the QRS complex. The isoelectric period (flat line) that follows the P wave is the time it takes for depolarization to make its way through the AV node. The normal duration of the PR interval is 0.12 to 0.20 second. Remember that the conduction is slowed at the AV node (decremental conduction) to allow time for the atria to contract and fill the ventricles. When measuring, look for the lead with the widest P wave and QRS complex.

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The QRS Complex The QRS complex depicts the depolarization of the ventricles. Because of the complexity and varying nature of ventricular depolarization, the QRS complex can have many different shapes or what we call morphologies. The myocardium of the ventricles is about three times larger than the atria, and therefore, the electrical activity is greater. This is why the QRS complex that represents the ventricles has a larger amplitude/size than the P wave that represents the atria. Because the QRS complex can take on multiple shapes, rules have been established to help us name and recognize common patterns. Here are the rules.

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1. Q wave: When the initial deflection is negative before the R wave, the deflection is called a Q wave. 2. R wave: The first positive deflection is called an R wave. 3. S wave: A negative deflection, following an R wave, is called an S wave. 4. QS wave: If there is only one wave, and it is entirely negative, it is called a QS wave. 5. R‘ (R prime): If there is more than one positive deflection above the baseline, the second is called an R‘. 6. S‘ (S prime): If there is more than one negative deflection, the second is called an S‘. 7. Capital letters (QRS) are used to designate waves of relatively large amplitude, while 8. Small letters (qrs) are used to describe waves with relatively small amplitudes. 9. To earn a letter, the deflection must cross the isoelectric baseline. 10. If the deflection does not cross the baseline, it is simply noted as notched. Normal duration of the QRS complex ranges from 0.07 to 0.10 second, but sometimes can reach 0.11 second in healthy individuals. It too should be measured in the lead with the widest QRS complex. Often this is one of the precordial leads, such as V2 or V3.

The J Point The J point is the “junction” where the QRS complex meets the ST segment. When the ST segment is isoelectric and has a sharp contrast between the final deflection of the QRS complex, the J point can be easy to determine. However, when the ST segment is sloped, or the QRS complex is wide, the J point can be more difficult to locate. In those circumstances, try to find the point where the wave becomes more horizontal than vertical.

The ST Segment The ST segment represents the first phase of ventricular repolarization. It begins at the J point, which is found at the end of the QRS complex, and ends at the beginning of the T wave. Normally the ST segment should be isoelectric, or flat, equal with the TP interval mentioned below. However, there are times that slight elevation of the ST segment above the baseline is considered normal. There are no less than 16 different causes for ST segment elevation, one of which is a myocardial infarction, so learning to interpret this part of the EKG is very important.

The T Wave The T wave represents the second phase of ventricular repolarization. It is an upright wave that follows the ST segment in all leads, except aVR and V1, where it is typically inverted just like the P waves. Abnormalities of the T wave can signal problems like electrolyte abnormalities, myocardial ischemia, or a pulmonary embolism. Taller than it should be, consider hyperkalemia. Inverted where it shouldn’t be, consider myocardial ischemia.

The U Wave The U wave is not always present, but when it is, it is a small hump that follows soon after the T wave. It usually appears when the rate is slower than 65 beats per minute. Normally it is pointing in the same direction as the T wave, but not always. The origin of the U wave

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is not fully understood, but one possibility is delayed repolarization of the Purkinje fibers. An abnormally large U wave could be due to hypokalemia.

The QT Interval The QT interval is measured from the beginning of the QRS complex to the end of the T wave. This measures the duration for both ventricular depolarization and repolarization. If a U wave is present and connected to the T wave, it should be included in the measurement. Obtaining the measurement of the QT interval is important. When abnormally prolonged or shortened, it places the patient at risk of life-threatening arrhythmias such as torsades de pointes and ventricular fibrillation. If the corrected QT (QTc) interval is greater than 440 ms in women or 460 ms in men, it is considered prolonged. If it is over 500 ms, the patient is at increased risk for a deadly arrhythmia called torsades de pointes. A QTc less than 350 ms is considered abnormally short. When just “eyeballing” the QT interval, it should be less than half the RR interval. The best methods for obtaining an accurate QTc measurement are discussed in a later chapter. They involve calculating square roots, ugh. The good news is the EKG calculates this important measurement for you and is usually reliable.

The Isoelectric Baseline, the TP Interval When something is isoelectric, it lacks a net electrical charge. So it should make sense that the isoelectric baseline is seen when there is no electrical activity in the myocardium. Because there is no electrical activity, the line is flat. The baseline is found between the T wave and the P wave. Other intervals, such as the PR interval and ST segment, can be compared to the TP interval to see if they deviate from their expected isoelectric position.

The R-R Interval The R-R interval is a measurement taken from the peak of one QRS complex to the peak of the next. This can be used to determine the regularity and rate of the ventricles. Noting irregular R-R intervals can help us to identify abnormal rhythms such as atrial fibrillation. As mentioned above, the R-R interval also helps in the calculation of the QTc.

The P-P Interval The P-P interval is just what it says. It is the measurement from the peak of one P wave to the peak of the next. This helps us to determine the regularity and rate of the atria. P waves that occur earlier than expected can clue us in to certain arrhythmias like a premature atrial complex.

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How to Measure Measuring all of these waves, segments, and intervals takes time. To a new EKG student, it will feel like grunt work, but it must be done. As can be seen, each interval holds some significance in our interpretation. After you have looked at hundreds of EKGs, you will eventually develop gestalt. In other words, you will be so familiar with what normal looks like that abnormally long intervals or segments that aren’t isoelectric when they should be will stick out. It will get easier and faster, but all these things need to be evaluated on every EKG. If you skip something, you will inevitably miss something. Measure the intervals. It will pay dividends in the end. So how does one measure all these things? Calipers are handy devices that can be used to measure the height and width of waves, complexes, and intervals. Place one tip of the caliper at the beginning of a segment and the other at the end. Move the calipers so that one side lines up with a dark line of a large box on the EKG paper. This will make it a little easier to count the number of small boxes included in each segment. Take the number of small boxes and multiply it by 0.04 second to obtain the duration. Then note if it is within the normal range for that segment. Wash, rinse, and repeat for each. If you don’t have a pair of calipers handy, don’t fret. A scrap piece of paper or index card can do the trick. Line up the interval with the end of the paper and make a mark where it ends. Pick it up and move it to a dark line, then count the small boxes. Piece of cake. In fact, don’t tell anyone, but this is how I usually do it.

FINAL THOUGHTS There you have it. Your first real chapter on EKG. There is a lot here to digest, but you can do it. After you know what each wave, interval, and segment represent, begin memorizing the normal and abnormal heights and durations for each. Now, go and practice!

TAKE-HOME POINTS • The EKG is made up of humps and bumps created by only two processes: depolarization and repolarization of the myocardium. • The waves, intervals, and complexes include ▪ P wave—depolarization of the atrial myocardium ▪ PR interval—from the beginning of the P wave to the beginning of the QRS complex. The time it takes for the atria to depolarize and the decremental conduction through the AV node ▪ QRS complex—depolarization of the ventricles ▪ J point—the junction where the QRS complex meets the ST segment ▪ ST segment—first phase of ventricular repolarization ▪ T wave—second phase of ventricular repolarization ▪ TP interval—no electrical activity, the isoelectric baseline ▪ U wave—delayed repolarization of the Purkinje fibers ▪ QT interval—duration of both ventricular depolarization and repolarization • The EKG is printed on graph paper so that the duration and amplitudes can be measured.

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EXERCISES 1. Write the four laws of the EKG. 1.

2.

3.

4.

2. Using the laws for depolarization, complete the following equations by drawing the correct wave form.

– – –

+ + +

3. Complete the following table: Wave/Interval

Normal Duration/Amplitude

P Wave PR Interval QRS Complex ST Segment QT Interval

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4. Name the QRS complexes using nomenclature rules:

On each of the following EKGs: Measure: PR duration, QRS duration Label at least one: P wave, ST segment, QT interval, T wave Name the QRS complex with the correct nomenclature

1.

PR duration _______________________

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QRS duration _______________________

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2.

PR duration _______________________

QRS duration _______________________

3.

PR duration _______________________

QRS duration _______________________

4.

PR duration _______________________

QRS duration _______________________

5.

PR duration _______________________

QRS duration _______________________

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6.

PR duration _______________________

QRS duration _______________________

7.

PR duration _______________________

QRS duration _______________________

8.

PR duration _______________________

QRS duration _______________________

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9.

PR duration _______________________

QRS duration _______________________

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10.

PR duration _______________________

QRS duration _______________________

REFERENCE Frease, M. (n.d.). EKG images. Retrieved from http://floatnurse-mike.blogspot.com

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Chapter

4

The 12-Lead EKG The 12-lead EKG provides a panorama of the electrical activity of the heart and is an essential first-line tool for making lifesaving diagnoses.

THE FOG Are you feeling it yet? The Fog. Hopefully you started your journey to learn EKG interpretation with an air of excitement. But as we progress, you may begin to feel a weight pushing down on your shoulders. Your eyes glaze over. A sense of panic is rising up in the distance. You say to yourself, “Can I do this?” Yes! You can! You may always feel one step behind. That’s normal. But if you look two steps back, you see those topics are now well in hand. Hang in there, you’ve got this.

REVIEW In this chapter, we dive deeper into the creation of waves we see on the EKG. By placing multiple electrodes on the skin, we can get several views of the heart’s electrical activity. These views, or leads, provide an electrical panorama that allows us to interpret the direction of the electrical current flowing through the myocardium.

INTRODUCTION TO THE 12-LEAD EKG Vectors The heart is a three-dimensional object. When depolarization occurs, it flows out like a wave in all directions. The surface EKG displays the average of the electrical activity. This is called the mean vector, also known as the electrical axis. In other words, the direction with the most energy at a given moment is what we see displayed on the EKG.

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Using a single EKG lead only gives us the mean vector from its unique vantage point. There are times when one lead may be sufficient for the job. When continuously monitoring a patient in the emergency department or ICU, one lead may be enough to tell us what rhythm the patient is in and alert us if a problem is occurring. However, when only one lead is used, a lot of information, sometimes very significant information, is being left on the table.

The 12 Leads Have you ever bought anything of value on eBay? You want the seller to provide you with multiple pictures of the item from various angles. One picture just won’t do. How do I know that the other side doesn’t have a scratch or ding in it? I need more pictures, so I don’t miss something important. This concept is even more valuable when we are talking about the condition of our patient’s heart. So, in order to get a more complete picture of the heart’s electrical activity, it has become commonplace to use the 12lead EKG. It was developed gradually over several decades by physicians who discovered new and useful leads. It is devised of 12 separate pictures of the heart’s electrical activity, each providing its own unique perspective.

The EKG is an essential first-line tool for making critical lifesaving diagnoses. Using multiple leads provides us with the ability to see and treat conditions such as a myocardial infarction. When only one lead is used, we can easily miss this and other deadly dilemmas. Being able to recognize abnormalities on the 12 leads and intervene allows us to save lives. Each picture is called a lead. To obtain this information, an electrode is placed on each arm, the left leg, and six locations across the chest. The EKG machine is connected to the electrodes by wires. The computer then assigns each wire either a positive or negative polarity. It uses the information to calculate the difference in the electrical signal between two or more electrodes. The computer then uses that data to create the tracing for each individual lead. A different combination of electrodes is used to record each lead of the EKG.

Electrode Placement So where do we put the electrodes to obtain the standard 12-lead EKG? When it comes to placement of the limb electrodes, there is some flexibility. The upper extremity leads can be placed anywhere on the arm below the shoulder where it meets the torso. From the deltoid to the fingertip, the picture will remain the same. They are often placed on the wrist out of convenience, but anywhere on the arm will do. The same is true for the lower extremity leads. They can be placed anywhere on the leg below the groin and the picture is essentially unchanged. The final location is usually based on the area of most convenience, and least hair. Although there is some flexibility, limb electrodes should never be placed on the torso. Even though this practice is incorrect, it has become the routine in some clinical settings. In a study completed by Jowett et al. in the Postgraduate Medical Journal, placing the limb electrodes on the chest caused five inferior myocardial infarctions to disappear and made other patients appear to have significant abnormalities that were not truly present.

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Proper electrode placement is critically important for an accurate 12-lead EKG. Chest lead placement requires more precision. There are designated areas on the chest to place each of the six precordial electrodes/leads. They are as follows: • V1—fourth intercostal space to the right of the sternum • V2—fourth intercostal space to the left of the sternum • V3—between V2 and V4 • V4—fifth intercostal space in the midclavicular line • V5—between V4 and V6 • V6—fifth intercostal space in the midaxillary line

Failure to place leads correctly will provide faulty information. In fact, it can cause the interpreter to diagnose a myocardial infarction when one is not present, or worse yet, miss the diagnosis. Electrodes should be placed under breasts. Do not use nipples or other landmarks on the chest to determine proper placement. Use the rules above and you will be in good shape. Each wire attached to the EKG machine is labeled with the proper electrode it should be connected with. Failure to attach the wires appropriately can lead to some strange and confusing findings on the EKG. Improper placement of the wires and/or electrodes has led to more than one patient unnecessarily being sent to the emergency department for evaluation.

The Four Laws Before we move on, this is a good opportunity to review the four laws.

– – –

+ + +

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1. A wave of depolarization flowing toward a positive electrode will record a positive wave. 2. A wave of depolarization flowing away from a positive electrode will record a negative wave. 3. A wave of depolarization moving perpendicular to a positive electrode will record a biphasic wave. 4. All the effects caused by repolarization have the reverse effect on the waves. For example, a wave of repolarization moving away from a positive electrode will result in a positive wave.

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THE LIMB LEADS Bipolar Leads The three bipolar, or limb, leads (I, II, III) are created using the electrodes placed on the arms and the left leg. Each lead uses just two of these wires, thus the name BI-polar. The diagram here shows what is known as Einthoven’s triangle, named after the inventor of the EKG who developed it. It shows lead placement (RA, LA, LL) and the polarity (+, −) of each of the bipolar limb leads. For example, lead I is created by taking the difference of the electrical activity detected at the right arm from the electrical activity at the left arm. It can be expressed as Lead I = LA − RA. A similar expression can be used for the other bipolar leads: Lead II = LL − RA, Lead III = LL − LA. Now imagine a camera sitting at the positive pole of each of these leads. Lead I has a “camera” sitting on the left arm and looking in toward the heart. Any wave of depolarization headed toward the left arm will be recorded as a positive deflection on the EKG. Lead II looks up from the bottom left of the heart. Any wave of depolarization headed in its direction will also record a positive deflection on the EKG.

RA = Right Arm, LA = Left Arm, LL = Left Leg

Augmented Leads The three augmented leads (aVR, aVL, aVF) were created later by Dr. Emanuel Goldberger in 1942. They use the same electrodes as the bipolar leads, but the computer augments the voltage it receives and gives another distinct picture of the electrical conduction through the myocardium. For example, aVR is created by assigning the right arm a positive polarity. The two remaining limb electrodes, the left arm and the left foot, are averaged to create a new imaginary negative electrode that sits between the two. See the images below for a visual explanation of the augmented and bipolar leads.

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Hexaxial Diagram The bipolar and augmented leads read the electrical activity of the heart in the frontal plane. They can be combined to form what is called the hexaxial diagram. This diagram is much like a map that demonstrates the placement of each of these leads and the direction from which they view the heart. Each of the leads is assigned a degree of orientation (based on a 360° circle). We use this understanding of the hexaxial diagram to help find the electrical axis in Chapter 18, Ischemia Detection on the EKG.

Knowledge of the hexaxial diagram is critical to a deep understanding of the 12-lead EKG. Leads that sit near each other on the hexaxial diagram can be grouped together. We call aVL and lead I the lateral leads because they view the heart from the left/lateral side of the chest. Leads II, III, and aVF are grouped together as the inferior leads because they view the heart from the bottom side. aVR—well, he is kind of a loner—looks at the heart from the top right. These terms (inferior, lateral) will reappear throughout the text.

I and aVL = Lateral Leads II, III, and aVF = Inferior Leads

THE CHEST LEADS The six chest/precordial leads (V1, V2, V3, V4, V5, V6) are placed on the chest and read the electrical activity in the horizontal plane. They were introduced by Dr. Frank Wilson in 1934. They are considered UNI-polar leads, with each of the electrodes serving as a positive pole. The precordial leads start on the right side of the heart and work their way around to the left. Each lead gradually provides a slightly different perspective as they work their way around the heart. V1 and V2 read the right side of the heart and are considered the right chest leads. V5 and V6 read the left side of the heart and are called the left or lateral chest leads.

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When these 12 leads are grouped together, they make up the 12-lead EKG. Each lead provides its own valuable perspective on the action. It is important to understand these fundamentals in order to have a firm grasp on the picture the EKG is providing.

It is worth your time to memorize and understand the hexaxial diagram and the placement of the chest leads.

V1, V2: Right Chest Leads V3, V4: Strictly Anterior V5, V6: Left Chest Leads

Posterior and Right-Sided Leads Occasionally, additional leads are required to obtain useful information and to make an accurate diagnosis. The 12 standard leads of the EKG do not obtain a direct picture of the posterior myocardium. If an injury to the posterior myocardium is suspected, additional leads can, and should, be placed on the back near the left scapula for additional information. These leads are referred to as V7, V8, and V9.

The standard 12-lead EKG also does a less than adequate job displaying information about the right ventricle. When there is concern for a right-sided myocardial infarction, additional leads can be placed over the right side of the chest which mirror those typically placed on the left. These leads are called V1R, V2R, V3R, V4R, V5R, and V6R. We consider both the posterior and right-sided leads in more detail when we discuss myocardial infarction.

12-Lead Layout Although different brands of EKG machines are in use, the information provided by each remains fairly consistent from one to another. At the top of the printed 12-lead EKG, you will find information such as patient name, age, and gender, and the date and time of the

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EKG. It generally includes the name of ordering provider and indication for the EKG. It also provides objective information such as the rate; duration of PR, QRS, and QT intervals; and the axis of the P wave, QRS complex, and T wave.

The EKG machine also provides its own computer-generated interpretation of the 12 leads. It gives its suggested impression of the rhythm and may also make mention of abnormalities such as myocardial infarction or bundle branch blocks. Use caution when looking at the computer’s interpretation. It is not a substitute for your well-trained brain. It often overcalls abnormalities and has been known to miss serious and life-threatening conditions. I recommend you only use it after you have made your own interpretation to see if it provides support for your diagnosis or helps you to see something you may have missed.

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Just like a basic rhythm strip, the 12 leads are placed on graph paper with markings that designate passage of time and voltage. The 12 leads are generally found in the same place. On the left side of the page are the limb leads. On the right side are the precordial leads. As you read the EKG from left to right, you will see that every few beats the lead changes. This is indicated by the lead name on the paper and is the reason the waves and complexes suddenly have a different appearance.

When looking at the 12 leads, each wave/complex that is seen above or below that wave/ complex is occurring at the same moment in time. The waveforms only vary in appearance because of the different perspective of each lead. When there is artifact or another situation

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in which it may be difficult to interpret a lead, it may be helpful to refer to other leads that show that same moment in time to gather more information. Typically, a “rhythm strip” is found below the 12 leads. It provides an entire page of the same rhythm strip. It is often lead II because it has the most direct view of the normal depolarization of the atria and ventricles, but can be any lead. Some 12 leads have more than one rhythm strip.

FINAL THOUGHTS The use of 12 leads (or more) provides a wealth of valuable information. Monitoring a patient’s rhythm with a single lead is appropriate, but to get the most out of this incredible invention we must use multiple leads. This, of course, means more information to learn. But it’s going to be fun. If I haven’t already made myself clear, make sure you understand the information in this chapter. Build a strong foundation; it will make everything else easier.

TAKE-HOME POINTS • The 12-lead EKG is an essential first-line tool for making critical lifesaving diagnoses. • Proper electrode placement is critical for obtaining an accurate and reliable EKG. • The hexaxial diagram is composed of the limb and augmented leads. Understanding this diagram is important for a deep understanding of the 12-lead EKG. • Additional leads can be used to better see the right and posterior sides of the heart. • Don’t trust the EKG computer. It can find problems that don’t exist and miss serious and life-threatening conditions.

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EXERCISES 1. Draw Einthoven’s triangle with lead names and polarities of each.

2. Draw the hexaxial diagram. Keep drawing until you can do it from memory.

3. Define electrical axis.

4. The bipolar and augmented leads read electrical activity in the ________________ plane and the chest/precordial leads read the heart’s electrical activity in the __________________ plane.

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5. Correctly label the 12 leads. Place a square around the objective information the computer provided: Rate, duration, intervals, etc. Place a circle around the computer interpretation of the rhythm.

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On each of the following EKGs: Measure the PR duration, QRS duration. Label at least one P wave, ST segment, T wave. Name the QRS complex with the correct nomenclature. When more than one lead is present, repeat labeling and nomenclature once for each.

1. PR duration _______________________

QRS duration _______________________

2.

QRS duration _______________________

PR duration _______________________

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3.

PR duration _______________________

QRS duration _______________________

4. PR duration _______________________

QRS duration _______________________

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5.

PR duration _______________________

QRS duration _______________________

6.

PR duration _______________________

QRS duration _______________________

REFERENCES Frease, M. (n.d.). EKG images. Retrieved from http://floatnurse-mike.blogspot.com Jowett, N., Turner, A., Cole, A., & Jones, P. (2005). Modified electrode placement must be recorded when performing 12-lead electrocardiograms. Postgraduate Medical Journal, 81, 122–125. doi:10.1136/ pgmj.2004.021204

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Chapter

5

Heart Rate and Rhythm Evaluating the RATE and RHYTHM are the first two steps you should complete on every EKG.

INTRODUCTION There are five major categories of interpretation that should be completed on every EKG: 1. Rate 2. Rhythm 3. Axis 4. Hypertrophy 5. Ischemia/infarction In this chapter, we focus on the first two categories: how to calculate an accurate rate and learn some foundational concepts that will help you analyze and narrow down the source of the rhythm.

WHAT IS THE RATE? Calculating the rate is important for multiple reasons. Rhythms that are too slow or too fast may need urgent treatment. Medications or even electrical shock may be required to improve the rate and the patient’s hemodynamic status. Rates should be checked for both the atria and ventricles. Believe it or not, the rates are not always identical. When the atria and ventricles have different rates, it can be a sign of a block within the atrioventricular (AV) node or His bundle or clues to abnormal rhythms such as atrial flutter. Noting the rate provides a valuable clue regarding the source of the rhythm. Most rhythms have a rate range into which they fall. For example, atrial flutter with a 2:1 AV ratio

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often has a ventricular rate of 140 to 160 beats/minute. Junctional escape rhythm often has a ventricular rate of 40 to 60 beats/minute.

The EKG Computer Most textbooks would never admit this, but I’ll let you in on a little secret. The EKG computer’s calculation of the heart rate is usually very reliable. You won’t hear me brag on the computer and its interpretations very often. You must take everything it tells you with a grain of salt. Although fairly trustworthy, artifact, large T waves, or spikes created by artificial pacemakers (pacing spikes) can fool the computer and cause it to report an inaccurate rate (see image below). Usually there is a large discrepancy and it is obvious to the interpreter. But sometimes it is not so clear. Therefore, to be a consummate EKG interpreter, you need to be able to calculate the rate by utilizing the markings on the EKG paper.

Manual Rate Calculation

Pacing spikes can confuse the EKG machine and cause it to report an inaccurate rate.

There are several ways to determine the rate without using the computer’s calculation. They range from using a factory-produced ruler to counting the number of small blocks (1 mm) between the P-P or R-R intervals. These calculations get you in the neighborhood of the correct rate, which is all that is required for most clinical purposes. If a rhythm strip is available, this is usually the easiest place to start your evaluation of both the rate and the rhythm. Having a prolonged look at one lead, especially when first starting to interpret EKGs, can be extremely helpful. If the rhythm strip is full of artifact or unavailable, you can always use the other leads.

Count-Off Method The count-off method was described in Dubin’s Rapid Interpretation of EKGs. By memorizing six numbers and this technique, you can quickly calculate the rate of most rhythms.

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Know these numbers by heart: 300, 150, 100, 75, 60, 50. Say them out loud, three at a time. Repeat it over and over until you can do it from memory. Now let’s learn what to do with those numbers.

The count-off method: 300, 150, 100, 75, 60, 50.

Look for a QRS complex that lands on or very near a heavy shaded line. This will make things a little easier. Starting with the QRS that you selected, count off the numbers you learned each time you reach another heavy line: 300, 150, 100. . . . Continue counting off until you reach the next QRS complex (see image). When counting off in the example below, the next QRS complex falls between 100 and 150. It appears to be closer to 100. Maybe the rate is 115 or so. The count-off method gets us in the neighborhood, which is good enough for most clinical situations.

The 300 Method This is the exact same technique as the count-off method, but by a different name. It explains the math behind the madness for those who have a need to understand why the count-off method works. It also helps you determine the rate if it is less than 50 beats/ minute (75, 60, 50, then what?). The duration between two heavy shaded lines is 1/300 of a minute (0.20 second). If there are 3 heavy lines before the next QRS complex, you perform the calculation like this: 300/3 = 100 beats/minute. If there are 7 heavy black lines before the next QRS, then use the formula 300/7 = 43 beats/minute.

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The 1,500 Method The 1,500 method is very similar to the 300 method. However, instead of counting the number of large boxes, you count the number of small boxes. You may have guessed it; each small block is equivalent to 1/1,500 of a minute (0.04 second). Because we are using the smaller boxes, we can calculate a more accurate rate. Using the same example, we can see that there are 14 small blocks between the QRS complexes. Now it’s time to calculate: 1,500/14 = 107. As you can see, the 1,500 method gives us a more accurate answer than the count-off/300 method.

The 1,500 method: 1,500/14 small boxes = 107 beats/ minute.

The 6-Second Method Sometimes the rhythm is irregular. That means the distance between the QRS complexes will vary. Taking a measurement between one set of QRS complexes will give you a totally different rate than using another. So how do we calculate the rate in those situations? The 6-second method. The 6-second method utilizes math, too. Using a 6-second strip of time, count the number of QRS complexes that occur. Multiply that number by 10 and you have your rate (e.g., 6 beats in 6 seconds, 6 beats × 10 = 60 beats/minute).

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This method works great if you have a telemetry strip, like the ones above and below, with 1-second marks noted by small lines above or below the grid paper (every five large boxes). Simply count out six spaces and you have a 6-second duration in which to count complexes.

The above rhythm is irregular. There are eight QRS complexes in the 6-second strip. 8 × 10 = 80 beats/minute.

12-Lead EKGs usually don’t have these wonderful little marks. In order to use the 6-second method on a 12-lead EKG, you’ll have to count 30 large boxes first (0.20 second × 30 = 6 seconds). I’m not lying—it’s a pain. But if you have doubts about the computer’s calculations,

the 6-second method is the only manual technique that can be used to properly calculate the rate of an irregular rhythm.

RHYTHM To properly analyze the rhythm, you must follow a systematic approach. Below you will learn why

determining the regularity of the rhythm and duration of the QRS complex is key to your rhythm interpretation. These are just the first of a few important steps required to make the final diagnosis of the EKG rhythm. Other steps will include looking for P waves and measuring intervals such as the PR. We will dive into this in later chapters.

Steps to evaluating rhythm:

1. Regularity 2. QRS width 3. P waves 4. Intervals

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IS THE RHYTHM REGULAR OR IRREGULAR?

Just like your favorite music, the heartbeat has a tempo and rhythm to it. Sometimes the rate is slow like an ’80s love ballad by Journey or fast enough to bang your head to like Metallica. Am I showing my age? It also has rhythm. Often it’s nice and regular, something you can easily tap your foot to. But sometimes it’s irregular, like jazz, where tapping your foot to it is not easy, or even possible. Noting the regularity or irregularity of a rhythm is another valuable way to narrow down the potential rhythm choices in your differential diagnosis. Rhythms such as atrial fibrillation are always irregular. If you have a regular rhythm, you can quickly rule it out. There are a few ways to evaluate the regularity of the rhythm.

AT FIRST SIGHT Sometimes it just takes a quick glance and it is obvious that the R-R intervals are irregular. Other times the irregularity of a rhythm may be difficult to see without closer inspection. Atrial fibrillation is a well-known irregular rhythm. When the rate is slow, eyeballing atrial fibrillation may be sufficient to see irregular intervals between the QRS complexes. But when the rate is fast, the variation between QRS complexes diminishes, and the irregularity is more difficult to spot at first sight.

March It Out When you can’t tell by taking a quick look, the best way to determine if the rhythm is regular is to “march out” the intervals. When evaluating the ventricles for a regular response, inspect the R-R intervals. This can be done easily with a pair of calipers or even a spare sheet of paper. Measure the first R-R interval. Check each subsequent interval and see if they match in duration. See if you can spot any irregularity. Occasional irregularities can occur and may point toward an aberrant beat such as a premature ventricular contraction. Persistent irregularities may indicate an irregular rhythm such as atrial fibrillation.

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Marching out the R-R intervals on this EKG strip reveals that each interval is the same. The rhythm is regular.

Atrial fibrillation is an irregular rhythm. When the rate is fast, the irregularity may be difficult to “eyeball.” Measuring and comparing each R-R interval quickly reveals the rhythm is irregular.

If you are questioning the regularity of atrial depolarization, evaluate the P-P intervals. Again, measure each interval to see if they are the same duration. Is a single P wave occurring early? Maybe it’s an abnormal beat called a premature atrial contraction.

Narrow QRS (0.12 second) = Ventricular Rhythm or Aberrant Ventricular Conduction

IS THE QRS NARROW OR WIDE? Narrow Evaluating the rate and regularity of a rhythm can reduce the list of possible arrhythmias you need to consider. The width of the QRS complex is another incredibly useful piece of information for narrowing the differential even further. This is because

all narrow complex rhythms are supraventricular in origin, but not all supraventricular rhythms have a narrow complex. If the QRS complex is narrow (0.12 second/>3 small blocks). Because of the delay in depolarization, contraction of the right and left ventricles is not simultaneous. Thus, ventricular arrhythmias often have a decrease in stroke volume. When the weaker contraction is combined with fast ventricular rates that fail to allow for the ventricles to fill with blood the patient can quickly decompensate.

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The QRS complex is 0.20 second (5 small blocks). Because it is greater than 0.12 second, it is considered a wide QRS. This rhythm originates in the ventricles. You may also notice that the P wave is missing.

ALGORITHM A study was published by Dr. M. Mirtajaddini of Kerman, Iran, in the Journal of Electrocardiology in 2017. Despite having received EKG training, a group of graduated medical students from the United States could only identify 57% of life-threatening conditions on the EKG. Because of poor performance, an algorithm was developed to help identify arrhythmias. Two groups were trained, one with the algorithm and the other without. Once the training was completed, the group who used the algorithm recognized 93% of life-threatening arrhythmias on an examination. Those who trained without the algorithm scored only 62%. With Dr. Mirtajaddini’s permission, I have reproduced his algorithm in the Appendix. As can be seen, determining the rate and regularity of the rhythm along with the width of the QRS are important first steps in interpreting every EKG. I encourage you to mark the page and refer to it often. It has been proved to improve students’ retention of the material and examination scores. And I know how much you care about examination scores.

FINAL THOUGHTS Memorize these three steps. Start every EKG interpretation by asking yourself the following questions: 1. What is the rate? 2. Is the rhythm regular or irregular? 3. Is the QRS narrow or wide? You will see these questions at the end of every chapter. The list will slowly grow longer, providing you with a systematic method for interpreting a 12-lead EKG. Memorize these steps and you will be well on your way to mastering this important skill. That does it for this chapter. The next several chapters focus on the most common rhythms you will see in practice and continue to build on the knowledge you have obtained. Remember that noting the rate and regularity along with the width of the QRS complex will be a big help. Now let’s get to it.

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TAKE-HOME POINTS • Five major categories of interpretation that should be evaluated on every EKG: ▪ Rate ▪ Rhythm ▪ Axis ▪ Hypertrophy ▪ Ischemia/infarction • Determining the rate can help you narrow down your rhythm differential diagnosis: ▪ Should be calculated for both atria and ventricles ▪ Can use any method you want, unless the rhythm is irregular • Evaluating the rhythm requires you to inspect the ▪ Regularity ▪ QRS width ▪ P waves ▪ Intervals

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EXERCISES 1. List the numbers used in the count off method each time you reach the next heavy line. 300, 150, __________, 75, ____________, 50 2. If the rhythm is irregular, you must use the _____________________ method to correctly calculate the rate. 3. The QRS complex is considered narrow when less than ______________ second. 4. When the rate is ________________ it can be difficult to eyeball irregularity; be sure and “_________________” the R-R and P-P intervals. 5. Write the first three questions you should answer in your systematic approach to interpreting an EKG. 1.

2.

3.

On each of the following EKGs: Answer the first three questions you should ask yourself when interpreting every EKG: What is the rate? Is the rhythm regular or irregular? Is the QRS narrow or wide?

1.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

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Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

3.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

4.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

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5.

Rate: ______________

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Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

6.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

7.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

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8.

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Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

9.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

10.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

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11.

Rate: ______________

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Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

12.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

13.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

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14.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

15.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

16.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

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17.

Rate: ______________

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Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

18.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

19.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

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20.

Rate: ______________

Rhythm: Regular or irregular ______________

QRS: Narrow or wide ______________

REFERENCES/RESOURCES Dubin, D. (2016). Rapid interpretation of EKG’s: Dr. Dubin’s classic, simplified methodology for understanding EKG’s (6th Ed.). Tampa, FL: Cover Publishing. Mirtajaddini, M. (2017). A new algorithm for arrhythmia interpretation. Journal of Electrocardiology, 50(5), 634–639. doi:10.1016/j.jelectrocard.2017.05.007

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Chapter

6

Sinus Rhythms When atrial depolarization originates from the sinoatrial (SA) node, we call it a sinus rhythm.

HEART RHYTHMS It’s time to discuss heart rhythms! Over the next several chapters, you will be introduced to common rhythms you will see as a healthcare provider. Learning the definitions, concepts, and treatments are important, but it is much more valuable to be able to identify the rhythm when you see it. You cannot appropriately treat your patient if you are unable to first determine the rhythm. Make that your top priority as you read through the next several chapters. This will take time and practice, so be sure to dedicate yourselves to both. It is important to determine the rate, regularity, and width of the QRS complex when interpreting the rhythm. We will revisit those concepts with each rhythm and discuss the finer details that set each rhythm apart.

THE FOUR LAWS Before we get started, it may help to review the four laws:

– – –

+ + +

1. A wave of depolarization flowing toward a positive electrode will record a positive wave. 2. A wave of depolarization flowing away from a positive electrode will record a negative wave. 3. A wave of depolarization moving perpendicular to a positive electrode will record a biphasic wave. 4. All the effects caused by repolarization have the reverse effect on the waves. For example, a wave of repolarization moving away from a positive electrode will result in a positive wave.

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SINUS RHYTHMS Under normal circumstances, the heart is paced by the SA node. The SA node, which is the primary pacemaker of the heart, is a spindle-shaped structure that lies high in the posterior right atrium. When atrial depolarization originates from the SA node, we call it a sinus rhythm. Because of the SA node’s location and the typical path of depolarization through the atria that follows, the P wave produces a predictable pattern on the EKG. When the rhythm is sinus, the

P wave will ALWAYS be upright in leads I and II and inverted in aVR. The direction of atrial depolarization is also called the axis. The electrical axis can be determined for all waves of depolarization and repolarization. The inherent rate of the SA node at rest is generally between 50 and 90 beats/minute. However, sympathetic and parasympathetic activity cause variations in the rate. As we age, the inherent rate of the SA node decreases. This is usually due to an increase in fibrous tissue within the node. If enough fibrous tissue develops, the SA node may cease to transmit its impulse to the surrounding myocardium, leading to an SA block.

Note the upright P waves in leads I and II and the inverted P waves in aVR. You may also notice that the P waves are “notched.” The first half of the P wave is the right atrium depolarizing, the second half is the left atrium.

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Notched P waves.

NORMAL SINUS RHYTHM Normal sinus rhythm (NSR) is the basic rhythm of our existence. By definition, NSR begins in the SA node and has a regular atrial and ventricular rate of 60 to 100 beats/minute. Although called “normal” sinus rhythm, slightly faster or slower rates may be completely normal for an individual. Children have much faster rates at rest than adults, with infant rates typically 110 to 150 beats/minute. The rate will gradually slow over the first 6 years of life. Endurance athletes and the elderly may have much slower rates than the rest of the adult population. However, to be called NSR, it must meet the following criteria.

Characteristics of Sinus Rhythm 1. Rate of 60 to 100 beats/minute 2. Regular rhythm 3. QRS complexes are typically narrow (0.12 second) if there is a complete block of one of the bundle branches.

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Normal sinus rhythm. Note the upright P waves in leads I and II and the inverted P wave in aVR. The rhythm is regular. The rate is 77 beats per minute and falls in the range for NSR (60-100 bpm).

6: SINUS RHYTHMS

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Treatment Why is there a section about treatment under NSR? You’re right, the overwhelming majority of the time there is absolutely no evaluation or treatment needed. However, you should always consider what the normal rhythm is for your patient. If the patient has a baseline heart rate of 45 and presents with a resting heart rate of 95, something may be wrong. Consider dehydration, anemia, or other causes of this “tachycardia.” Always evaluate the EKG in the context of what is normal for the patient.

ARE P WAVES PRESENT? You have learned that the rate, regularity, and width of the QRS complex are important factors when interpreting the rhythm. The next important step is recognizing the presence or absence of P waves. If the rhythm is sinus, P waves should be present and upright in leads I and II and inverted in aVR. In the following chapters you will see that P waves may be pointing the wrong direction or missing altogether. Noting the presence and axis of P waves is an important clue that will help you to make an accurate interpretation. Add this step to your systematic approach. 1. What’s the rate? 2. Is the rhythm regular or irregular? 3. Is the QRS narrow or wide? 4. Are P waves present? Are they upright in I and II and inverted in aVR?

ARRHYTHMIAS Every rhythm we discuss from this point forward can be classified as an arrhythmia. That doesn’t always mean that the rhythm is dangerous or even truly abnormal. Before we dive into the following rhythms, let’s talk about what an arrhythmia is. The definition of arrhythmia is

“a problem with the rate or rhythm of the heartbeat. During an arrhythmia, the heart can beat too fast, too slow, or with an irregular rhythm.”—National Heart, Lung, and Blood Institute (n.d.). In other words, if it isn’t NSR with normal atrioventricular (AV) conduction, it’s an arrhythmia. It can be anything from a single abnormal beat to a rhythm that continues indefinitely. The causes are numerous and as we discuss each arrhythmia we will review the most common possibilities.

SINUS BRADYCARDIA A sinus rhythm with a rate less than 60 beats/minute is called sinus bradycardia (SB). Slower rates are seen in patients such as the elderly and athletes who have an increase in vagal tone, especially during rest or during sleep. Slower rates can also be seen in patients who take medications that decrease the sympathetic response (e.g., beta-blockers). Often the slower rate is of little or no concern unless it is less than 50 beats/minute. That said, there are healthy people who have rates as slow as 35 to 40 beats/minute at rest or during sleep who are asymptomatic. SB has the same diagnostic criteria as NSR, except for the slower rate.

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Characteristics of Sinus Bradycardia 1. Rate less than 60 beats/minute 2. Regular rhythm 3. QRS complexes are typically narrow (100 beats/minute

The Fibrillatory Waves In AF, coordinated atrial depolarization is lost. Instead of a P wave, we see fibrillary (f) waves that demonstrate the constant bedlam taking place in the atria.

Fibrillatory waves vary from fine, almost imperceptible waves (when present for a long time) to coarse impulses that can be confused with P waves. The fibrillary waves indicate the constant flux in amplitude, polarity, and frequency of the impulses taking place in the atria. Because blood is not being pumped efficiently from the atria, it begins to pool. This can lead to clot formation that most commonly occurs within the left atrial appendage. Eventually these thrombi may be ejected from the heart and set loose to roam throughout the body. Unfortunately, this leads to significant complications such as ischemic stroke and limb or bowel ischemia.

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Atrial fibrillation. The fibrillatory (f) waves are fine, which can occur with long-standing atrial fibrillation. The diagnosis can be made based on the absence of P waves and the irregularity of the ventricular response.

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The Ventricular Response AF is a rhythm with an irregularly irregular ventricular response. The R-R intervals have no discernible pattern. Just try and tap your foot to it. You can’t do it. As mentioned above, the ventricles can only depolarize when the atrial impulse overcomes time- and voltage-dependent refractoriness at the AV node. Even though the ventricles don’t approach the outrageous rate of the atria, they can still conduct quite rapidly. Ventricular rates can exceed 200 beats/minute in special circumstances (e.g., catecholamine excess, Wolff–Parkinson–White syndrome). However, rates are most commonly between 90 and 170 beats/minute. When the ventricular rate in Afib is greater than 100 beats/minute, it is called a rapid ventricular response (RVR). This is incredibly common. Without treatment, the rate is often 110 to 140 beats/minute. The faster the ventricular response, the more difficult it can be to detect the irregularity of the R-R interval. This requires close inspection with calipers or other means so that the diagnosis is not missed. Fast ventricular rates can cause a decrease in cardiac output. Because the atria are shaking like a 50-cent ladder in a windstorm, the ventricles are completely reliant on passive filling. When there is an RVR, the ventricles do not have time to fill adequately before contracting. This decrease in cardiac output can cause significant problems such as myocardial ischemia, pulmonary edema, and hypotension.

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Atrial fibrillation with a rapid ventricular response (RVR). There are no true P waves. The ventricular response is irregularly irregular. Because of the fast ventricular rate, the irregularity may not be clear without close inspection.

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Ashman’s Phenomenon Because AF originates above the ventricles, depolarization typically moves normally through the His-Purkinje system. This results in a narrow QRS complex. However, there are times when conduction through the ventricles is aberrant, leading to an abnormally wide QRS complex. This is called Ashman’s phenomenon. Ashman’s phenomenon is a result of the varied R-R intervals that occur in AF. The sporadic R-R intervals occur because of the irregularly irregular ventricular response. As the heart rate speeds up (short R-R), the refractory period of the His-Purkinje system decreases. And as the heart rate slows down (long RR), the refractory period lengthens. If there is a long-short R-R cycle, only one of the bundle branches may be ready to conduct an impulse. Typically the right bundle has a longer refractory period and may be unable to conduct. Therefore, the path through the ventricles is aberrant. This leads to an abnormally wide complex that resembles a right bundle branch block or premature ventricular complex.

Atrial fibrillation. The 7th complex in the rhythm strip is an example of Ashman’s phenomenon. Note the varied appearance of the QRS complex.

Risk Factors There are multiple risk factors for AF, an arrhythmia whose incidence continues to rise. Increasing age is a major risk factor for AF. Seventy percent of patients with AF are at least 65 years old. Almost 10% of the population over the age of 80 is in AF (Spragg & Kumar, 2019). Afib is usually associated with underlying heart disease. The two most common chronic health problems that place a patient at risk are hypertensive heart disease and coronary artery disease that leads to acute myocardial infarction (MI). Studies have shown that 6% to 10% of patients after acute MI have transient AF, possibly due to atrial ischemia or stretch of the atria caused by heart failure. Valvular disease such as mitral stenosis, mitral regurgitation, and tricuspid regurgitation has also been associated with increased prevalence of Afib (Ganz & Spragg, 2018). Obesity is also a significant risk factor. The Framingham Heart Study showed that with every unit of increase in body mass index (BMI), the risk for AF went up 5% (Vyas & Lambiase, 2019). Obesity is common in patients with obstructive sleep apnea (OSA), which also increases the risk for Afib. Both obesity and OSA can lead to an increased workload for the left atrium and ventricle. If left untreated, this can cause hypertrophy of the left ventricle and fibrosis of the left atrium, leading to the development of ectopic foci. Sixty percent of binge drinkers will experience AF, even with no underlying cardiac disease. This is often called “holiday heart syndrome.” Afib is incredibly common after cardiac surgery, affecting 30% to 60% of patients in the early postoperative period (Maisel, Rawn, & Stevenson, 2001). Other risk factors include hyperthyroidism, family history of Afib, heart failure, and metabolic syndrome.

Symptoms Symptoms can range from none to myocardial ischemia and heart failure. The severity of symptoms is dependent upon the presence of underlying cardiovascular disease, age, and the speed of the ventricular rate. Common symptoms include palpitations, shortness of breath, lightheadedness, dyspnea on exertion, fatigue, and malaise.

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Treatment Precise treatment strategies are beyond the scope of this text (January et al., 2014). Treatment of AF is complex and is dependent on multiple factors. However, there are three clearly defined categories of treatment worth discussing here. 1. Rate control Most symptoms and complications of AF are due to an excessive ventricular rate. Rather than attempt to restore a normal sinus rhythm, the clinician may opt to leave the patient in AF and simply manage the ventricular response. This treatment option is often a good solution for the patient with recurrent episodes of AF. Patients who can tolerate chronic AF do better when the ventricular response is under control. Some advocate for ventricular rates to mimic those of patients in sinus rhythm with resting rates 80 or less at rest and 110 or less with moderate exercise, but no consensus exists. Patients with chronically higher ventricular rates are prone to developing a left ventricular cardiomyopathy (Ganz, 2018). Patients who are symptomatic, but stable, because of an RVR need to have the rate reduced urgently. This is typically done with the use of intravenous (IV) medications that slow AV node conduction. Common medications include calcium channel blockers such as verapamil and diltiazem. Beta-blockers such as metoprolol, propranolol, and esmolol are also commonly used. Occasionally the rate needs to be controlled emergently. Patients not only may have symptoms but can become hemodynamically unstable. Symptoms of decreased cardiac output include hypotension, signs of myocardial ischemia or heart failure, and impaired mental status. Rate control in these patients must happen immediately. Synchronized DC cardioversion is recommended with 100 to 200 joules, although occasionally more is required. 2. Rhythm restoration Sometimes it is the preference of the clinician to restore the patient to a normal sinus rhythm. If there is difficulty keeping the ventricular rate bridled despite use of medications, it may be worth considering this option. Other considerations would include patients under the age of 65 who are not tolerating AF despite rate control or patients who have just recently developed AF. Restoring sinus rhythm can be accomplished by elective synchronized cardioversion or use of antiarrhythmic medications. However, this should only take place after adequate anticoagulation and careful evaluation to rule out an atrial appendage thrombus with transesophageal echocardiography (TEE). Cardioverting a patient with a thrombus can lead to thromboembolic complications such as stroke. And that leads us to our last treatment strategy. 3. Prevention of thromboembolic events As the atria quivers, blood pools, particularly in the left atrial appendage. As clot forms, the patient is at increased risk for thromboembolic events such as stroke. By placing the patients on appropriate anticoagulant therapy, the risk of embolic events can be significantly reduced, but an anticoagulant can also increase the risk for unwanted bleeding. Medications such as warfarin, dabigatran, rivaroxaban, apixaban, or edoxaban can be utilized. A risk-benefit analysis must be completed to determine the best strategy.

Tips and Pitfalls AF is incredibly common. You will, without a doubt, encounter it in your practice on a regular basis. Keep these tips and pitfalls in mind.

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1. When the fibrillatory waves are fine, the baseline may appear isoelectric. In these situations, remember that AF is missing P waves and the ventricular response will always be irregular. Take time to march out the R-R intervals. 2. When the fibrillatory waves are coarse, they can mimic P waves. If the rhythm is irregular, the baseline is in constant motion, and you are struggling to determine if something could possibly be a P wave, it’s probably NOT a P wave. It’s AF. 3. Tremors from a patient with Parkinson’s disease or who is cold can mimic fibrillation waves. This can be cleared up by taking a look at your patient or attempting to replace poorly connected electrodes. Also, if the R-R interval is regular, it is NOT AF. 4. One more. As the ventricular rate speeds up, the irregularity of AF can be difficult to eyeball. Take a moment with closer inspection using calipers to march out the R-R interval. Again, if there are no clearly identifiable P waves, the baseline is constantly quivering, and the rhythm is irregular, it’s AF.

ATRIAL FLUTTER Atrial flutter is a supraventricular arrhythmia typically seen in patients with underlying heart disease. It is the result of a single stable macro reentrant circuit within the right atrium that travels through the cavo-tricuspid isthmus (CTI), a part of the right atrium that lies between the opening of the inferior vena cava and the tricuspid valve. It is less common than AF. In the United States, approximately 200,000 new cases are diagnosed each year (Phang, Prutkin, & Ganz, 2019). The most common type, “typical” or CTI-dependent atrial flutter, has a reentry circuit that usually moves counterclockwise around the tricuspid valve (90%). On occasion, the typical reentry circuit may move in a “reverse” or clockwise direction (10%).

The rotational movement of the reentry circuit causes the hallmark sawtooth waves that are classic for atrial flutter. “Atypical” cases of atrial flutter are not dependent upon the CTI to complete the circuit. It is not uncommon for patients with atrial flutter to also have episodes of AF.

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Atrial flutter with classic “sawtooth” waves. The flutter waves are at approximately 300/min, while the ventricular response (QRS complexes) are approximately 75 beats/min.

Characteristics of Atrial Flutter 1. Ventricular rate is variable. With the most common atrial to ventricular ratio, 2:1, the rate is typically 140 to 160 beats/minute. 2. May be regular or irregular. The regularity of the rhythm is dependent upon the ratio of the ventricular response to the rapid atrial depolarization. Sometimes this is regular; sometimes it is not. 3. Ventricular rate is a ratio of the atrial rate. The ventricular response may be regular or irregularly irregular. 4. Narrow QRS complex. Because it originates from above the ventricles. 5. Flutter or “sawtooth” waves replace P waves. Flutter waves are best seen in inferior leads (II, III, aVF) and may resemble P waves in V1. 6. No PR interval. No P waves, so no PR interval. 7. Absence of isoelectric baseline. The macro reentry circuit never stops, so the electrical movement is always present.

Flutter waves often mimic P waves in V1

Flutter Waves The most classic finding in atrial flutter is the flutter wave with a “sawtooth” appearance. The flutter waves replace normal P waves. Flutter waves occur because of the rotational circuit taking place within the right atrium. Because the circuit originates from a single stable source, all flutter waves will look identical. Flutter waves are best seen in the inferior leads (II, III, aVF). When the movement is counterclockwise, the flutter waves are inverted. Clockwise rotation causes upright flutter waves in the inferior leads. The flutter waves can mimic P waves in V1 and occasionally V2.

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The right atrium must be abnormally large to support the reentry circuit of atrial flutter. This is why it is almost always seen in the presence of organic cardiac disease. The necessary size of the enlarged atrium leads to a fairly predictable flutter rate, typically averaging 300 beats/minute (range 200–400/minute), or one large block apart on the EKG. Because of the necessary cycle length to complete the circuit, flutter waves cannot be closer together than four small blocks.

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Atrial flutter. Flutter waves are clearly seen in the inferior leads (II, III, aVF) and resemble P waves in V1.

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Ventricular Response The ventricular response in atrial flutter is usually an even ratio of the atrial rate (2:1, 4:1). The ratio describes the number of flutter waves to ventricular complexes. Occasionally the ventricular response may be irregularly irregular with no predictable ratio. In untreated atrial flutter, the most common atrial to ventricular ratio is 2:1. Rarely, the ratio may be 1:1. This causes an insanely fast ventricular rate that will lead to a hemodynamically unstable patient in a hurry. When a 2:1 ratio is present, flutter waves can be difficult to identify. One flutter wave is present before the QRS complex and the other is hidden within it. Vagal maneuvers and medications such as adenosine can be used to temporarily delay the ventricular response and help reveal flutter waves, hopefully making the diagnosis more clear. Because the atrial rate is somewhat predictable (average 300 beats/minute), the ventricular response is also fairly predictable. With a 2:1 ratio, the ventricular rate is approximately 150 beats/minute (300/2), a 4:1 ratio approximately 75 beats/minute (300/4). This can be a useful clue in a 2:1 flutter.

Any time there is a regular rhythm with a consistent rate between 140 and 160 beats/minute, you should consider atrial flutter.

Atrial flutter with a 2:1 atrial/ventricular ratio. Ventricular rate is approximately 150 beats/ minute. P waves are seen before the QRS complex while another is hidden within.

Risk Factors Any risk factor that can lead to AF can also cause atrial flutter. This includes hyperthyroidism, obesity, pulmonary disease, use of antiarrhythmics, and cardiac surgery. It almost always occurs in a patient with organic heart disease. Patients with a healthy heart are unlikely to experience atrial flutter.

Symptoms As with most arrhythmias, palpitations are not uncommon. The patient may also experience fatigue, lightheadedness, and shortness of breath. If the ventricular rate is very fast or the patient is very ill, the symptoms and complications will be more significant. Some patients may experience angina, near syncope, hypotension, or worsening of heart failure.

Treatment The treatment strategy is very similar to that for AF. 1. Rate control—Usually this involves use of non-dihydropyridine calcium channel blockers or beta-blockers. It is more difficult to gain control of the rate in atrial flutter. Often the patient can get stuck in a 2:1 conduction. 2. Rhythm restoration—Because it is difficult to stop the recurrence of atrial flutter and to control the rate, restoration of sinus rhythm is an excellent option. Because atrial flutter arises from a macro reentry circuit involving the CTI, these patients are highly amenable to radiofrequency (RF) catheter ablation. This procedure has a high success

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rate and is becoming the preferred treatment for most patients in atrial flutter. Patients who underwent RF ablation had improved outcomes compared to pharmacologic treatment. Many more remained in sinus rhythm, fewer were rehospitalized, and in general they felt better during their activities of daily living. 3. Prevention of thromboembolic events—The current recommendation by most cardiologists is that patients with lone atrial flutter receive anticoagulation in the same manner as patients with AF. Those with episodes of AF/atrial flutter or history of AF should be on anticoagulation. Anticoagulation before cardioversion or ablation is very important. The risk for thromboembolic events is greatly increased after restoration of sinus rhythm. Anticoagulants that may be used include warfarin, apixaban, dabigatran, edoxaban, and rivaroxaban.

Tips and Pitfalls Keep these things in mind: 1. The most common ratio in atrial flutter is 2:1. This results in a ventricular rate around 150 beats/minute. Any time there is a regular rhythm with a consistent rate between 140 and 160 beats/minute, you should consider atrial flutter. 2. When the ratio is 2:1, consider covering the tops of the QRS complexes with a piece of paper. This may help you see the flutter waves more clearly. Occasionally turning the paper upside down can make the flutter waves more apparent. 3. The inferior (II, III, aVF) leads are best at revealing flutter waves. Always look at these leads when considering atrial flutter. 4. Don’t forget that flutter waves look a lot like P waves in V1. Don’t accidentally call it sinus rhythm. 5. Flutter waves frequently fire at a rate near 300 beats/minute. This just happens to be equal to one large block on the EKG paper. If you are considering atrial flutter, look for waves that occur approximately one large block apart. This may help you to separate flutter waves that you are confusing with possible P/T waves.

Vagal Maneuvers

What they are useful for? Vagal maneuvers are a safe way to attempt to reduce the rate in patients with paroxysmal supraventricular tachycardia. The choice of which maneuver to use depends on the patient’s ability to cooperate and health condition. Valsalva—Place the patient in a supine or semirecumbent position and have her or him exhale forcefully against a closed glottis. If done properly, it should cause neck vein distention, a flushed face, and increased muscle tone of the abdominals. Encourage the patient to continue to strain for 10–15 seconds, after which time the patient can breathe normally. A modified technique has been shown to be more helpful in supraventricular tachycardia. The patient is placed in a semirecumbent position and strains as described above. After 15 seconds, the patient is placed flat and the legs are passively raised to 45 degrees. This technique has a 43% success rate compared with 17% with the standard technique in a the REVERT trial (Appelboam et al., 2014).

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Carotid Sinus Massage—The patient should be placed flat with the neck extended back. This allows easy access to the carotid artery. Steady pressure is then held to ONE carotid sinus for 5–10 seconds. If this proves unsuccessful, the other side can then be compressed after a 1- to 2-minute wait. Carotid sinus massage should not be performed in patients with a previous transient ischemic attack (TIA) or stroke within the past 3 months. You should also listen for a bruit, and if noted, carotid sinus massage should not be performed. Also, if there is concern about the patient having increased risk for a stroke, use a different vagal maneuver. Diving Reflex—Other than on an episode of the old TV show ER, I have never seen this technique used in practice. In this method, the patient is placed upright with a basin of cold water in front of him. The patient then submerges the face in the water for 20–30 seconds while holding the breath. You cross your fingers and pray that the patient returns to a sinus rhythm before he drowns.

CASE STUDY 8.1 James Truett, MD History of Present Illness: A 65-year-old man presents to the ED complaining of shortness of breath, vomiting, and fatigue for 1 week. He says that 4 hours prior to arrival, he began to have severe constant right upper quadrant pain. The pain seems out of proportion to findings on his physical exam. He also notes nausea with vomiting since the pain began. Although the abdominal pain is his primary reason for coming to the ED, he has been feeling progressively worse over the last several weeks. The patient admits to long-term alcohol use and tobacco smoking. EKG is performed and is as shown below. Vital Signs: BP 184/151, RR 26, Temp 35.9°C, Wt 101.2 kg, BMI 31

Past Medical History Hypertension, coronary artery disease, peripheral artery disease

Surgical History Coronary artery catheterization with balloon angioplasty, lower limb angiography

Physical Exam General: Alert, moderate distress Skin: Cool, pale Head: Normocephalic, atraumatic Neck: Supple without tenderness Eyes: Pupils equal round reactive to light and accommodating (PERRLA) Cardiovascular: Tachycardia, no murmur Respiratory: Tachypnea, crackles in bilateral bases Gastrointestinal: Severe right upper quadrant tenderness, with guarding and rebound Musculoskeletal: Normal range of motion (ROM), no gross abnormalities Psych: Anxious, cooperative Neuro: A&O × 4- alert and oriented × 4, no focal deficits

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Imaging/Labs

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Chest X-ray: Mild cardiomegaly with mild perihilar interstitial infiltrate CT Abdomen and Pelvis: Mild diffuse colonic wall thickening of unknown significance, mild colitis cannot be excluded; other non-acute findings are consistent with chronic vascular disease Significant Labs: Lactic acid 5.9 mmol/L, WBC count 18.6 × 103/μL

Thought Questions 1. What risk factors does this patient have for AF? What are the most common causes of AF? 2. What three treatment categories are there for AF? What would be the most appropriate treatment for this patient? Why? 3. In the setting of presumed sepsis, what are the risks and benefits of pharmacologic rate control? 4. This patient was later found to have ischemic colitis causing his abdominal pain. What association does AF have to the diagnosis?

CASE STUDY 8.2 History of Present Illness: A 51-year-old White woman presents to the ED because she feels like her heart is beating out of her chest. These symptoms have been occurring intermittently over the past 6 months. She says she thought originally her increase in heart rate was due to stress as she just experienced the death of an old high school friend, a change in jobs, and monetary stress, but now she isn’t so sure. She came into the ED because she is feeling symptomatic right now and her husband was very worried and encouraged getting her heart worked up by medical professionals. Past Medical/Social History: Patient has hypertension, has hyperlipidemia, and is prediabetic. She works as an elementary school teacher. She drinks a glass of red wine each night and drinks socially with friends every other weekend. Family Medical History: Mother: hypertension, type 2 diabetes mellitus (DM), and coronary artery disease. Father: coronary artery disease, myocardial infarction, peripheral vascular disease

ROS Cardiovascular: Positive for dizziness, lightheadedness Pulmonary: Shortness of breath Psych: Anxiety All other systems negative Medications: Lisinopril, daily multivitamin Vital Signs: BP 138/88, RR 16, Temp 97.6°F, O2 sat 96%, Ht 5′6″, Wt 194 lb

Physical Examination General: Appears moderately anxious and is slightly diaphoretic HEENT: Examination without findings, negative for nystagmus or vertigo upon movement of head Neck: Supple, no JVD, no carotid bruit Cardiovascular: Tachycardia, no murmurs, gallops, or rubs; capillary refill less than 2 seconds Pulmonary: Lung examination is clear on auscultation without wheezing, rales, or rhonchi Musculoskeletal: Normal strength, range of motion, and gait Neuro: Cranial nerves II–XII intact; oriented to person, place

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EKG:

Labs/Imaging

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Thought Questions 1. What risk factors does this patient have for the arrhythmia? 2. What is the treatment plan for this patient? Include pharmacologic and nonpharmacologic interventions. 3. Why is the heart rate an important clue in making this diagnosis?

Systematic Approach

1. 2. 3. 4. 5.

What’s the rate? Is the rhythm regular or irregular? Is the QRS narrow or wide? Are P waves present? Are they upright in I and II and inverted in aVR? What’s the duration of the PR interval?

TABLE 8.1 Rhythm Review Rhythm

Rate (beats/ minute)

Regular/Irregular

QRS Wide or Narrow

P Waves/PR Interval

Atrial fibrillation

90–170, but can be slower or faster

Irregularly irregular

Narrow

No P waves, fibrillatory waves

Atrial flutter

140–160, but can be faster or slower

Regular, irregular

Narrow

Flutter, “sawtooth” waves

TAKE-HOME POINTS • Both AF and atrial flutter are the result of reentry circuits that keep the abnormal rhythm going. • AF is the most common sustained arrhythmia in the United States. ▪ The hallmark of AF is the irregularly irregular ventricular response. ▪ Instead of P waves, AF has fibrillatory waves that can vary from fine to coarse. • Atrial flutter is seen in patients with underlying heart disease. ▪ Flutter, “sawtooth” waves are a hallmark of atrial flutter. ▪ The ventricular rate is a ratio based on the atrial rate. • Treatment options for both AF and atrial flutter include ▪ Rate control ▪ Rhythm restoration ▪ Thromboembolic prevention

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EXERCISES 1. Define the following terms: Paroxysmal, permanent, rapid ventricular response, Ashman’s phenomenon

2. Name seven risk factors of atrial fibrillation. 1. 2. 3. 4. 5. 6. 7. 3. Which lead often mimics P waves in atrial flutter? _______________ 4. It is not uncommon for a coarse fibrillation wave to mimic ______________ waves. 5. Flutter waves are best identified in the ___________________ leads. 6. The most common AV ratio in atrial flutter is ______________. 7. Any time there is a regular rhythm with a consistent rate of _______________, you should consider atrial flutter. On each of the following EKGs: Interpret the rate and determine if it is regular or irregular; note if the QRS is narrow or wide; determine if P waves are present, and if they are present, are they upright or inverted; and diagnose what type of supraventricular rhythm is present.

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1.

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Rhythm: Regular or irregular _______________________

PR duration: _______________________

Final interpretation: _______________________

P waves: Present, not present, upright, or inverted _______________________

QRS: Narrow or wide _______________________

Rate: _______________________

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2.

Rate: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

3.

Rate: _______________________

Final interpretation: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

4.

Rate: _______________________

Final interpretation: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

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Final interpretation: _______________________

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5.

Rate: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

6.

Rate: _______________________

Final interpretation: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

7.

Rate: _______________________

Final interpretation: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

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Final interpretation: _______________________

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8.

Rate: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

9.

Rate: _______________________

Final interpretation: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

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Final interpretation: _______________________

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10.

Rate: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

11.

Rate: _______________________

Final interpretation: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

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Final interpretation: _______________________

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12.

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Final interpretation: _______________________

QRS: Narrow or wide _______________________ PR duration: _______________________

Rhythm: Regular or irregular _______________________

P waves: Present, not present, upright, or inverted _______________________

Rate: _______________________

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13.

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PR duration: _______________________

Final interpretation: _______________________

P waves: Present, not present, upright, or inverted _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide ______________________

Rate: _______________________

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14.

Rate: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

15.

Rate: _______________________

Final interpretation: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

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Final interpretation: _______________________

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16.

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PR duration: _______________________

Final interpretation: _______________________

P waves: Present, not present, upright, or inverted _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide ______________________

Rate: _______________________

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17.

Rate: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

18.

Rate: _______________________

Final interpretation: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

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Final interpretation: _______________________

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19.

Rate: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

20.

Rate: _______________________

Final interpretation: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

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Final interpretation: _______________________

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21.

Rate: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

22.

Rate: _______________________

Final interpretation: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

23.

Rate: _______________________

Final interpretation: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

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Final interpretation: _______________________

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24.

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PR duration: _______________________

Final interpretation: _______________________

P waves: Present, not present, upright, or inverted _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide ______________________

Rate: _______________________

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25.

Rate: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

26.

Rate: _______________________

Final interpretation: _______________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide _______________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: _______________________

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Final interpretation: _______________________

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REFERENCES/RESOURCES Appelboam, A., Reuben, A., Mann, C., Gagg, J., Ewings, P., Barton, A., . . . Benger, J., on behalf of the REVERT trial collaborators. (2014). Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. The Lancet, 386(10005), 1747–1753. doi:10.1016/S0140-6736(15)61485-4 Centers for Disease Control and Prevention. (n.d.). Atrial fibrillation fact sheet. Retrieved from https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_atrial_fibrillation.htm Ganz, L. I. (2018, May 15). Control of ventricular rate in atrial fibrillation: pharmacologic therapy. In G. M. Saperia (Ed.), UpToDate. Retrieved from https://www.uptodate.com/contents/ control-of-ventricular-rate-in-atrial-fibrillation-pharmacologic-therapy Ganz, L. I., & Spragg, D. (2018, March 12). Epidemiology of and risk factors for atrial fibrillation. In P. J. Zimetbaum (Ed.), UpToDate. Retrieved from https://www.uptodate.com/contents/ epidemiology-of-and-risk-factors-for-atrial-fibrillation/abstract/24-27 Heart Rhythm Society. Retrieved from http://resources.hrsonline.org/practical-management.html January, C. T., Wann, L. S., Alpert, J. S., Calkins, H., Cigarroa, J. E., Cleveland, J. C., Jr., . . . Yancy, C. W. (2014). 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation. Journal of the American College of Cardiology, 64(21):e1–e76. doi:10.1016/j.jacc.2014.03.022 Maisel, W. H., Rawn, J. D., & Stevenson, W. G. (2001). Atrial fibrillation after cardiac surgery. Annals of Internal Medicine, 135(12), 1061–1073. doi:10.7326/0003-4819-135-12-200112180-00010 Phang, R., Prutkin, J. M., & Ganz, L. I. (2019, May 27). Overview of atrial flutter. In P. J. Zimetbaum (Ed.), UpToDate. Retrieved from https://www.uptodate.com/contents/overview-of-atrial-flutter Spragg, D., & Kumar, K. (2019, July 23). Paroxysmal atrial fibrillation. In G. M. Saperia (Ed.), UpToDate. Retrieved from https://www.uptodate.com/contents/paroxysmal-atrial-fibrillation Vyas, V., & Lambiase, P. D. (2019). Obesity and atrial fibrillation: Epidemiology, pathophysiology and novel therapeutic opportunities. Arrhythmia & Electrophysiology Review, 8(1), 28–36. doi:10.15420/aer.2018.76.2  

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Chapter

9

Wolff–Parkinson– White Syndrome Wolff–Parkinson–White syndrome (WPW) is the presence of an accessory atrioventricular (AV) pathway that can cause tachyarrhythmias and, potentially, sudden death. Normally, impulses from the atria can only reach the ventricles via the AV node. In a patient with WPW, depolarization can also travel from the atria to the ventricles by using an accessory path called the bundle of Kent. The extranodal accessory tract can be found anywhere along the AV ring on the septum. Not only does it allow premature impulses to travel from the atria to the ventricles (antegrade), but depolarization may also travel up the path from the ventricles to the atria (retrograde).

The condition was first described in 1930 by Louis Wolff, John Parkinson, and Paul Dudley White. They discovered that the presence of the additional path can lead to tachyarrhythmias, such as AV reentry tachycardia (AVRT) and atrial fibrillation (AF), and even cause sudden death as a result of

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ventricular fibrillation. Since that time, the WPW pattern has been found in approximately 0.25% of the population. Not all those with WPW pattern will have a documented arrhythmia. The incidence of tachyarrhythmias varies widely among studies, from 13% to 80% (Di Biase & Walsh, 2018). EKG findings may occur intermittently or, eventually, disappear forever.

WPW pattern + tachyarrhythmia = WPW syndrome

The classic EKG findings in WPW syndrome are a result of early ventricular depolarization by way of the bypass tract. You may remember, the AV node has the ability to slow down conduction, allowing the ventricles to fill before they contract (decremental conduction). This time period is seen on the EKG as the PR interval. However, the accessory path does not have the ability to put on the brakes. Therefore, the ventricles depolarize prematurely, resulting in a short PR interval. This is called ventricular preexcitation. Ventricular depolarization gets a head start through the bundle of Kent. Because depolarization from the accessory tract is premature and inefficient (outside the His-Purkinje system), there is a unique slurring at the beginning of the QRS complex called a delta wave. The slurring is created by the collision of inefficient depolarization from the bypass tract and the efficient depolarization from the AV node that follows. Soon after depolarization moves through the accessory tract, the AV node fires and quickly completes the job of ventricular depolarization using the His-Purkinje system. The remainder of the QRS complex appears normal. The overall time to complete ventricular depolarization is prolonged, resulting in a wide QRS. These changes in conduction lead to the classic WPW triad: short PR interval, delta wave, and a wide QRS complex that may be seen during normal sinus rhythm.

WPW Triad: 1. Short PR interval 2. Delta wave 3. Wide QRS complex

Characteristics of WPW Pattern 1. Short PR interval. Less than 0.12 second. This is often the most helpful clue. Make sure to measure intervals. Don’t skip steps in your interpretation. Other causes of a short PR include junctional escape rhythm. 2. Delta wave. Slurred upstroke at beginning of QRS. This is the result of preexcitation of the ventricles by the bundle of Kent. Sometimes this is hard to detect. It can even be absent if the AV node conducts faster than the accessory tract.

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3. Prolonged QRS. Greater than 0.11 second. Although ventricular depolarization gets a head start through the accessory pathway, it takes longer because it starts outside the His-Purkinje system. Soon after, the SA node fires and completes depolarization in a more timely manner. 4. ST-T wave discordance. ST segment and T waves point in the opposite direction of the primary wave of the QRS complex. In other words, if the QRS complex is mainly positive, the ST segment may be depressed, and the T waves will be inverted. Or if the QRS complex is mainly negative, the ST segment may be elevated and the T waves will be upright. 5. Pseudo-infarction pattern. Abnormally wide or deep Q waves can be a sign of myocardial infarction (MI). Because of negatively deflected delta waves that can occur in the inferior and anterior leads, WPW may take on the appearance of an MI (70%). These deflections are called “pseudo-Q waves.” WPW can also cause abnormally tall R waves in the right-sided chest leads (V1–V3) mimicking posterior MI.

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WPW pattern. Note the short PR interval, slurred delta wave at the beginning of the slightly widened QRS complex best seen in the chest leads and leads I, aVL, and II. An abnormally large Q wave is present in lead III and inappropriately tall R waves in V1 to V2 that can mimic a posterior myocardial infarction.

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AV REENTRANT TACHYCARDIA AV reentrant tachycardia (AVRT) is the second most common cause of supraventricular tachycardia (SVT) following AV nodal reentry tachycardia (AVNRT). It is a tachyarrhythmia that occurs in patients with an abnormal accessory pathway. It is frequently seen in young women and children. Orthodromic AVRT makes up the majority of tachyarrhythmias seen in patients with WPW (90%–95%). Orthodromic means that the nerve impulse is traveling forward through the AV node and backward through the bundle of Kent. Ventricular rates can reach breakneck speeds, potentially causing hemodynamic instability. Orthodromic AVRT is initiated by a premature atrial complex (PAC). When a PAC occurs, the impulse is unable to cross the bundle of Kent, which is still refractory. Instead it travels down the AV node and the His-Purkinje system. As the ventricles depolarize, the impulse reaches the accessory pathway, now ready for depolarization. This allows the impulse to reach the atria in a retrograde fashion. The first reentry loop has occurred and the cycle will continue.

Characteristics of Orthodromic AVRT 1. Rate 150 to 250 beats/minute. Can be as fast as 300 beats/minute. 2. Regular rhythm. 3. Narrow QRS complex. The QRS will be narrow because depolarization is traveling in antegrade fashion through the AV node. 4. Inverted or missing P waves. P waves may be difficult to spot because they are often hidden within the QRS complex. P waves may also be upside down because the atria are depolarized in retrograde fashion from the impulse arising out of the bundle of Kent. 5. ST segment depression and T wave inversion may occur. This is similar to the ST depression that can occur with AVNRT. It does not indicate myocardial ischemia. This description may sound familiar. It is often indistinguishable from AVNRT and only suspected when the patient has WPW. Fortunately, it is treated in the same way.

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Orthodromic AVRT. Regular rhythm with rate of 225 beats/minute. No P waves are seen. Narrow QRS complex. Patient has known WPW syndrome. Source: Reproduced with permission from Dr. Edward Burns, www.lifeinthefastlane.com

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Symptoms Depending on rate and underlying health condition, symptoms may be mild or severe. Palpitations, shortness of breath, fatigue, and chest pain are common. Syncope, although rare, may be a sign that the patient is at increased risk for sudden death.

Treatment Vagal maneuvers such as carotid sinus massage and Valsalva maneuver are usually attempted first. This is successful approximately 75% of the time. If conservative measures fail, intravenous (IV) adenosine is given rapid IV push. This converts 80% to 90% of patients in AVRT. If IV adenosine fails, IV verapamil may be used in adults, as long as there is no contraindication (e.g., hypotension). And if all else fails, synchronized cardioversion can be employed to halt the rhythm.

ATRIAL FIBRILLATION IN WPW AF occurs in 10% to 30% of patients with WPW. Because the accessory pathway has a shorter refractory period than the AV node, ventricular rates can get extremely fast. Patients often become symptomatic and can suffer hemodynamic compromise. Rate control or rhythm restoration should occur without delay.

Characteristics of AF in WPW 1. Irregularly irregular rhythm. With very fast rates, the irregularity may be difficult to spot. The rhythm may look regular and give the appearance of ventricular tachycardia. 2. Ventricular rates up to 300 beats/minute. If the ventricular rate is greater than 220 beats/minute, an accessory pathway must be considered. 3. Wide QRS. Could be mistaken for AF with bundle branch block. 4. Bizarre QRS morphologies that vary in appearance. The QRS width can change along with the shape.

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Atrial fibrillation in a patient with WPW. Rhythm is irregular. Rate is fast. No identifiable P waves. Source: Reproduced with permission from Dr. Edward Burns, https://litfl.com/pre-excitation-syndromes-ecg-library

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Treatment of AF in WPW WPW can often be misdiagnosed as AVNRT, AF with a bundle branch block, or ventricular tachycardia. The error can lead to inappropriate and potentially deadly management of the rhythm. If the patient is unstable, urgent synchronized electrical cardioversion should be performed. If the patient is hemodynamically stable, IV medications should be used.

AV nodal blockers (e.g., beta-blockers, calcium channel blockers, amiodarone, adenosine) typically used for AF should NOT be used to treat AF in WPW. These medications block the AV node and promote conduction through the bypass tract, potentially making ventricular rates faster. This can cause the patient to decompensate and potentially lead to death. Verapamil, a non-dihydropyridine calcium channel blocker, is extremely dangerous. Not only does it encourage depolarization down the bypass tract, it decreases myocardial contractility and systemic vascular resistance. This can lead to a rebound in sympathetic activity, increasing ventricular rates further. Patients have experienced cardiac arrest due to ventricular fibrillation after verapamil administration. If medication is needed, antiarrhythmics, such as ibutilide or procainamide, are recommended to treat AF in WPW. They can help to reduce the ventricular rate and potentially restore sinus rhythm.

TREATMENT OF WPW Symptomatic patients with WPW typically undergo ablation. The 2015 American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS) guidelines recommend it as a first-line therapy (Page et al., 2015). Asymptomatic patients with a WPW pattern are at low risk of sudden cardiac death. The chance of developing symptoms is highest in children and lowers with age. The 2015 ACC/AHA/HRS guidelines say that observation in patients with WPW pattern is reasonable. However, they also believe that catheter ablation is a reasonable option (Page et al., 2015). It may be best to refer all patients with WPW pattern, with or without symptoms, to an electrophysiologist for consultation.

LOWN–GANONG–LEVINE SYNDROME Lown–Ganong–Levine syndrome (LGL) was brought to light in 1952 by physicians of the same names. Its proposed pathophysiology and EKG findings have some similarities to WPW (Lown, Ganong, & Levine, 1952). Although discussed in EKG literature, LGL’s significance and existence have been debated by some. It is characterized by a short PR interval and tachyarrhythmias. Approximately 0.5% of the population is thought to have a PR interval less than or equal to 0.12 second. Abnormalities in AV conduction, either through an accessory pathway (e.g., James fibers or Mahaim fibers) or faster AV conduction (enhanced AV node conduction [EAVNC]), result in a short PR interval. According to Lown et al. (1952), 17% of patients with the short PR interval had tachyarrhythmias that led to symptoms of palpitations, lightheadedness, and/or shortness of breath. Because depolarization is still traveling through the His-Purkinje system, the QRS remains narrow and is absent of the delta wave seen in WPW. There is concern that medications such as sympathomimetic agents, which increase the heart rate, could lead to an arrhythmia. But no data have yet demonstrated this to be the case.

Characteristics of LGL 1. Short PR interval. Less than 0.12 second. LGL is called short PR syndrome by some. 2. Narrow QRS complex. Normal depolarization through the His-Purkinje system.

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TAKE-HOME POINTS • Preexcitation of the ventricles from the bundle of Kent is responsible for the EKG findings associated with WPW. ▪ Short PR interval ▪ Delta wave ▪ Prolonged QRS complex • Orthodromic AVRT is the most common arrhythmia seen in WPW. • AF in patients with an accessory bypass tract can reach ventricular rates up to 300 beats/minute.

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EXERCISES 1. Define antegrade and retrograde.

2. In your own words, describe the reason for the classic WPW triad.

3. Define orthodromic.

4. QRS complexes in WPW patients with AF can vary in _____________ and ________________. On each of the following EKGs: Calculate the rate; determine if it is regular or irregular; note if the QRS is narrow or wide; determine if P waves are present, and if they are present, are they upright or inverted; and diagnose what type of supraventricular rhythm is present.

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1.

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Rhythm: Regular or irregular ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

PR duration: _______________

Final interpretation: _______________

QRS: Narrow or wide: ______________

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2.

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Rhythm: Regular or irregular ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

PR duration: ______________

Final interpretation: _______________

QRS: Narrow or wide: ______________

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3.

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Rhythm: Regular or irregular ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

PR duration: _______________

Final interpretation: _______________

QRS: Narrow or wide: ______________

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4.

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Rhythm: Regular or irregular ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

PR duration: _______________

Final interpretation: _______________

QRS: Narrow or wide: ______________

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5.

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Rhythm: Regular or irregular ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

PR duration: _______________

Final interpretation: _______________

QRS: Narrow or wide: ______________

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REFERENCES/RESOURCES Di Biase, L., & Walsh, E. P. (2018). Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis. In S. Lévy & B. P. Knight (Eds.), UpToDate. Retrieved from https:// www.uptodate.com/contents/wolff-parkinson-white-syndrome-anatomy-epidemiology-clinical -manifestations-and-diagnosis Lown, B., Ganong, W. F., & Levine, S. A. (1952). The syndrome of short P-R interval normal QRS complex and paroxysmal rapid heart action. Circulation, 5(5), 693–706. doi:10.1161/01.CIR.5.5.693 Page, R. L., Joglar, J. A., Caldwell, M. A., Calkins, H., Conti, J. B., Deal, B. J. . . . Al-Khatib, S. M. (2015). 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia. Circulation, 133(14), e506–e574. doi:10.1161/CIR.0000000000000311 Wolff, L., Parkinson, J., & White, P. D. (2006). Bundle-branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia. Annals of Noninvasive Electrocardiology, 11(4), 340–353. doi:10.1111/j.1542-474X.2006.00127.x. (Originally published in 1930, The American Heart Journal, 5(6), 686–704)

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Chapter

10

Ventricular Arrhythmias Rhythms that begin in the ventricles have a wide QRS complex.

INTRODUCTION In this chapter, we discuss rhythms that originate in the ventricles. The abnormal depolarization begins below the atrioventricular (AV) junction. Because ventricular arrhythmias do not completely utilize the His-Purkinje system,

rhythms that begin in the ventricles have a wide QRS complex (>0.12 second). Normal ventricular depolarization travels down a central route through the interventricular septum. By proceeding through the electrical wiring that lies between and within the ventricles, an efficient and simultaneous conduction/contraction of the ventricles is produced. However, when depolarization begins outside the electrical system, conduction slows down. Instead of traveling through the heart’s efficient wiring, it travels solely through the myocardium. And because the impulse often begins in the right or left ventricle, it must travel inefficiently from one side of the heart to the other. This makes ventricular depolarization take longer than usual and results in a wide QRS complex (>0.12 second). Because of the delay in depolarization, contraction of the right and left ventricles is not simultaneous. Thus, ventricular arrhythmias often have a decrease in stroke volume. When the weaker contraction is combined with fast ventricular rates the patient can quickly decompensate.

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PREMATURE VENTRICULAR COMPLEXES Premature ventricular complexes (PVCs) are common. PVCs often arise from an irritable ectopic focus somewhere within the ventricles. They cause premature ventricular depolarization that may or may not retrogradely depolarize the atria. Although they occur more frequently in patients with organic heart disease, studies have shown that almost half of all healthy individuals have at least one PVC during a 24-hour period. Fortunately, PVCs are benign when they occur in relative isolation and do not cause significant symptoms (Manolis, 2019).

Characteristics of PVCs 1. No apparent P wave. When a PVC occurs, the atria usually remain unaware of the activity that lies beneath. The sinoatrial (SA) node will continue to pace at its normal rate and scheduled interval; however, the P wave will frequently be hidden within the wide QRS complex. Sometimes the atria may be reset by retrograde depolarization traveling up through the AV node from the ventricles. If not hidden within the QRS complex, it may be seen as an inverted P wave immediately after the QRS. 2. Premature QRS complex. The QRS complex is happening sooner than the next expected sinus beat. March out the R-R intervals and you will see an irregularity in the rhythm. 3. Wide QRS (>0.12 second). When a PVC is present, ventricular depolarization usually begins outside the normal conductive system. The wave of depolarization travels slower through the myocardium and takes longer to complete. The QRS duration is also dependent upon the site of origin of the ectopic focus. The ectopic focus is often in the left or right ventricle. The further the origin from the interventricular septum, the longer it will take depolarization to complete. On a rare occasion, the PVC may originate from the interventricular septum and result in a relatively narrow QRS complex. On a surface EKG this is indistinguishable from a premature junctional contraction. Don’t lose sleep over it. 4. Bizarre. PVCs often stick out like a sore thumb. They are wide and unusual looking. Often they begin in the right or left ventricle and take on the appearance of a bundle branch block (Chapter 14, EKG Axis Interpretation). When they originate in the right ventricle, they have the appearance of a left bundle branch block. When the ectopic focus is in the left ventricle, they look similar to a right bundle branch block. 5. ST-T wave discordance. Ventricular repolarization may also occur abnormally. This results in an ST segment and T wave that point in the opposite direction of the QRS complex. If the QRS complex is positive, the ST segment will be depressed and the T wave will be inverted. If the QRS complex is negative, the ST segment will be elevated and the T wave will be upright. ST-T wave discordance can be seen with any ventricular ectopic beat or rhythm, except ventricular fibrillation (VF).

Discordant: QRS points in the opposite direction of the ST-T wave. Concordant: QRS points in the same direction as the ST-T wave.

6. Compensatory pause is often present. PVCs do not typically depolarize the atria and reset the SA node. This causes the next sinus beat to occur “on time” at an interval equal to twice the preceding R-R interval.

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Sinus rhythm with two PVCs.

Polymorphic Versus Monomorphic The terms polymorphic and monomorphic are used to describe the appearance of the PVC when evaluated in a single lead. As the name implies, monomorphic PVCs will have the same appearance each time they occur. This is because they come from the same ectopic focus. When PVCs have different shapes in a single lead, we call them polymorphic. This often means they are arising from multiple ectopic foci. However, the different shapes can also be due to a single focus with different paths of depolarization.

PVC Terminology

Bigeminy: PVC every other beat. Trigeminy: PVC every third beat. Couplet/Pair: Two PVCs in a row. Ventricular Tachycardia: Three PVCs in a row.

Sinus rhythm with polymorphic PVCs.

Causes PVCs can occur in patients with no structural heart disease. However, certain conditions are known to cause more frequent PVCs. These include hypertension with left ventricular hypertrophy, acute myocardial infarction (MI), chronic obstructive pulmonary disease (COPD), and sleep apnea. PVCs are seen in nearly one third of routine EKGs in patients with mitral valve prolapse. Drugs such as nicotine, cocaine, amphetamines, and alcohol can increase the frequency of PVCs. Digitalis toxicity can cause multifocal and bigeminal PVCs. Believe it or not, there

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is no clear evidence that caffeine increases ventricular ectopy. However, stimulant medications such as beta-agonists, decongestants, and antihistamines are related to an increased number of PVCs (Manolis, 2019).

Symptoms Depending on the frequency of PVCs and the patient’s underlying condition, patients may have no symptoms or a few minor complaints. Some experience palpitations, which are often more apparent if the patient lies on the left side because the heart is up against the chest wall. Others may note a feeling that their heart stopped for a moment because of the presence of a compensatory pause. Patients may also complain of a pounding sensation in the neck due to cannon A waves. These waves can be seen in the jugular vein and are the result of the atria and ventricles contracting simultaneously. In rare circumstances the patient may become lightheaded or even complain of near syncope.

Treatment PVCs are seen on a daily basis in clinical practice and are usually benign. In the healthy individual with infrequent PVCs, treatment is rarely indicated. If the patient experiences disturbing symptoms, look for stimulants that may be reduced or stopped. If this fails to make the patient feel better, beta-blockers may be considered to reduce the frequency and symptoms related to the premature contractions. If PVCs are frequent, evaluation for an underlying disorder should take place. If discovered, treatment of the condition is usually all that is required. If symptoms persist despite treatment of the condition, avoid stimulants and consider use of beta-blockers, particularly in patients with impaired ventricular systolic function and/or heart failure. Antiarrhythmic drugs have not been shown to improve outcomes and may actually increase risk of death.

Sinus rhythm with bigeminal PVCs.

Note the two PVC couplets and run of ventricular tachycardia.

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Don’t Forget the Systematic Approach 1. What’s the rate? 2. Is the rhythm regular or irregular? 3. Is the QRS narrow or wide? 4. Are P waves present? Are they upright in I and II and inverted in aVR? 5. What’s the duration of the PR interval?

MONOMORPHIC VENTRICULAR TACHYCARDIA Monomorphic ventricular tachycardia, often just called ventricular tachycardia or V-tach (VT), is a life-threatening regular wide complex tachycardia that is usually initiated by a PVC. If persistent, it can lead to cardiac arrest. It is most frequently seen in patients with an underlying cardiac abnormality such as ischemic heart disease. If untreated, the combination of decreased cardiac output and increased oxygen demand can lead to an even more troublesome rhythm, VF.

Characteristics of Ventricular Tachycardia 1. Three or more consecutive PVCs with the same morphology. 2. Rate >120 beats/minute. Rate is usually 140 to 200 beats/minute. If patients are on antiarrhythmics, VT can be as slow as 120 beats/minute. When the rate is greater than 200 beats/minute and looks like a sine wave, it is given the name ventricular flutter. 3. Regular rhythm. Although some irregularity may be seen early in the transition as the rate is speeding up, VT has regular R-R intervals. 4. Wide QRS (>0.12 second). 5. Atrioventricular dissociation. There is no conduction through the AV node. The atria and ventricles are a disgruntled couple and failing to communicate with each other. Each is acting independently, doing their own thing at their own pace. This is considered a hallmark of VT.

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Ventricular tachycardia. Regular rhythm with a rate near 150 beats/minute. The QRS is wide (approximately 0.20 second). Source: Reproduced with permission from Dr. Edward Burns, https://litfl.com/ ventricular-tachycardia-monomorphic-ecg-library

AV Dissociation Because there is no conduction through the AV node, the atria and ventricles function independently of each other. This is known as AV dissociation. This is a hallmark of VT and other ventricular arrhythmias; however, it is often difficult to identify. Because of the wide QRS complex and fast rate of VT, atrial depolarization is frequently hidden. Occasionally AV dissociation may be identified by subtle differences in the ST-T morphology caused by superimposed P waves.

Fusion and Capture Beats Other indicators of AV dissociation that help to make the diagnosis of VT are fusion and capture beats. A fusion beat is an unusual hybrid complex that is created when atrial depolarization collides with a late PVC. The shape and duration are usually a combination of the two competing pacemakers. A capture beat (Dressler beat) is a normal-appearing complex that occurs when atrial depolarization “captures” the ventricles. If atrial depolarization reaches the AV node after the refractory period and before ventricular depolarization, it can capture and depolarize the atria. It looks like a sinus beat sitting among the run of VT.

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Ventricular tachycardia followed by a fusion beat and two capture beats (Dressler beats).

Other Helpful Identifying Features of VT Although VT is often easy to identify, supraventricular tachycardia with aberrant ventricular conduction (uncommon) can mimic it. There are other EKG features that are highly suggestive of VT. Here are a few: • Concordant QRS complexes in all chest leads—all QRS complexes point in the same direction. This has a 90% or greater specificity for VT. • If an RS wave is present, the distance from the onset of the R wave to the lowest part of the S wave is greater than 100 ms in one precordial lead. • If an Rsr′ is present and the initial R is taller than r′. • QRS greater than 160 ms. • QRS is positive in aVR, negative in I and aVF • If it’s a wide complex tachycardia and the patient has a history of coronary artery disease or MI,

or if there is any doubt, treat it as VT until proved otherwise.

Causes Although VT can occur in patients with normal hearts, most have underlying cardiac disease. Risk factors include ischemic heart disease, heart failure, dilated cardiomyopathy, and hypertrophic cardiomyopathy. Previous MI causes a scar. Reentry circuits can develop around the scar causing persisting ventricular depolarization. Acute MI may also cause the myocardium to become irritable and develop increased automaticity leading to VT. Although antiarrhythmics are used to treat and prevent arrhythmias, they are also a well-known cause of them. Other medications that can cause VT include methamphetamines and cocaine. Medications that prolong the QT interval can also result in dangerous arrhythmias. Consider electrolyte abnormalities, especially hypokalemia. Low magnesium and calcium can also result in episodes of VT. Other causes include hypoxia that could be the result of conditions such as COPD or sleep apnea. Ventricular tachycardia is usually initiated by PVC that occurs after a short-long cycle. Sinus beat/PVC (short), compensatory pause/sinus beat (long)—>VT.

Symptoms The symptoms depend on a few factors—the patient’s underlying cardiac function and the rate and duration of VT. Some healthy patients with non-sustained VT may not experience any symptoms at all. Others note palpitations, chest pain, or shortness of breath. If a patient

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has existing structural heart disease or the VT lasts more than 20 to 30 seconds, the patient may begin to have hemodynamic compromise. The fast ventricular rate does not allow for the ventricles to fill adequately before contracting. This causes cardiac output to drop. The patient may experience syncope and hemodynamic collapse. As VT persists, the myocardium fails to receive the blood supply required. It becomes ischemic and acidotic and the patient can deteriorate into VF.

Treatment When possible, look for the underlying cause of VT. This is not always clear or possible. Consider ischemia, medications, heart failure, and electrolyte abnormalities. Symptomatic yet stable patients who experience episodes of non-sustained VT are usually treated with beta-blockers such as metoprolol or carvedilol. Not only do beta-blockers reduce the risk of recurrence, but they are often beneficial in the treatment of the underlying cardiac disease (coronary artery disease, heart failure) that led to the ectopic rhythm. Calcium channel blockers may be considered if the patient cannot tolerate the beta-blocker or fails to improve with beta-blockers alone. The patient should be evaluated by a cardiologist for medical treatment, possible radiofrequency catheter ablation, or implantation of a cardioverter-defibrillator. Stable patients who have sustained VT can decompensate quickly and without warning. Intravenous medications such as amiodarone, procainamide, or lidocaine are often utilized first in an attempt to pharmacologically cardiovert the patient. However, if those attempts fail, or the patient becomes unstable, electrical cardioversion is used. If the patient is stable, procedural sedation can be considered before the synchronized cardioversion. But caution must be used as these medications have the potential to drop the patient’s blood pressure. If the patient is unstable, intravenous (IV) medication is not indicated as the initial treatment. Instead, do not pass go, go directly to joules. Synchronized electrical cardioversion with 100 joules is indicated. If the patient is having significant symptoms or becomes hypotensive, sedation can be considered if it does not delay treatment or seem to pose an unnecessary risk.

Ventricular tachycardia.

Sustained VT

VT that lasts >30 seconds or hemodynamic collapse that occurs in 0.12 second). 4. No P waves. No atrial activity. 5. ST-T wave discordance may be present. A negative QRS complex may be followed by ST elevation and an upright T wave. A positive QRS complex may be followed by ST depression and an inverted T wave.

Ventricular escape rhythm. Regular rhythm with rate around 30 beats/minute. It can be distinguished from junctional escape rhythm by measuring the width of the QRS complex. (Junctional 0.12 second.)

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Symptoms Symptoms depend upon the rate of the escape rhythm. If the rate is fast enough, patients may be asymptomatic. Slow rates or comorbid conditions make it more likely the patient will develop hemodynamic compromise and become unstable. Dizziness, hypotension, shortness of breath, and chest pain are a few examples.

Treatment If the patient is symptomatic and unstable, the patient may be treated with IV atropine. Transcutaneous or transvenous pacing may also be considered if the patient fails to respond. The rate may also be increased by using dopamine or epinephrine drips. Never use antiarrhythmic drugs to treat an escape rhythm.

ACCELERATED IDIOVENTRICULAR RHYTHM Occasionally the ventricles pace at a rate faster than an escape rhythm (>50 beats/minute) but slower than the definition of VT (0.12 second) 4. Absence of P waves 5. Self-limiting

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AIVR with sinus capture beats. Source: Reproduced with permission from Dr. Edward Burns, https://litfl.com/accelerated-idioventricular-rhythm-aivr

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Causes/Treatment Up to 90% of patients will develop AIVR after reperfusion of the coronary artery following an MI. It is usually seen in the first few hours and decreases in frequency after 12 hours. It can remain present for as long as 24 hours after reperfusion. The rhythm is also seen in patients with hypertensive, congenital, and rheumatic heart disease and digoxin toxicity. Because of the reasonable rate, the patients rarely have symptoms and treatment is usually not required.

CASE STUDY 10.1 Elizabeth Capelle, PA-S History of Present Illness: A 41-year-old Caucasian man presents to the clinic for follow-up on blood pressure, medications, and lab results. The patient reports a constant middle anterior chest pain which he describes as tight. He says it wakes him from his sleep and worsens with exercise. He is also complaining of constant dizziness, headache, shortness of breath, and diaphoresis with hot flashes. The patient reports a constant fluttering feeling in his chest. He reports blurry vision and numbness and tingling, which are new complaints after his chest pain started. He also reports regular syncopal episodes; the last episode occurred approximately 1 week ago.

Past Medical/Social History Bipolar disorder Schizophrenia Chest pain Type 2 diabetes mellitus Pure hyperglyceridemia Essential (primary) hypertension Syncope and collapse Appendectomy Admits to tobacco smoking: 1 pack/day

ROS Pulmonary: Positive for shortness of breath, no cough Cardiovascular: Positive for palpitations, chest pain, syncope Neurologic: Positive for numbness and tingling All other systems negative VS: BP 129/68, RR 17, Temp 97.8°F, O2 sat 97%, Wt 255 lb

Current Medications Gabapentin Gemfibrozil Atorvastatin Hydroxyzine Metformin Paroxetine Risperidone Trazodone

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Physical Examination General: Ill-appearing patient in no acute distress Skin: Normal, no rashes, no lesions noted HEENT: Normocephalic, no lesions, PERRLA Neck: Supple, no masses, no bruits Pulmonary: Lungs clear, no rales, no rhonchi, no wheezes Cardiovascular: Irregular rhythm, no murmurs, no rubs, no gallops Extremities: Full range of motion (FROM), no deformities, no edema, no erythema Neuro: CN II–XII intact

Imaging/Labs Lipid panel, CMP, CBC, TSH, and EKG obtained; abnormal values listed below

Lipid Panel Total cholesterol 261 (HIGH)

normal 40 mg/dL

Triglycerides

normal 200

Regular

Wide

No obvious P waves

Ventricular fibrillation

150–550

Irregular

Varies

No P waves

Torsades de pointes

150–250

Irregular

Wide, varies

No P waves

Ventricular escape rhythm

20–50

Regular

Wide

No P waves

Regular

Wide

No P waves

Accelerated idioventricular 60–100 rhythm

TAKE-HOME POINTS • Rhythms that originate in the ventricles have a wide QRS complex (>0.12 second). • Ventricular arrhythmias can lead to hemodynamic collapse and cardiac arrest. • Wide complex tachycardias should be treated as VT until proved otherwise. • VF is total chaos and lacks any organized rhythm. • Torsades de pointes is a polymorphic VT caused by a prolonged QT interval. • Ventricular escape rhythm is a backup when all other pacemakers fail, but it is often too slow to provide adequate cardiac output.

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EXERCISES 1. Define the following terms: polymorphic, monomorphic, bigeminy, couplet, fusion beat, capture beat

2. Fine fibrillatory waves may mimic _________________, the absence of all electrical activity. 3. Write the first five steps in the systematic approach to EKG interpretation. 1. 2. 3. 4. 5. 4. Describe ST-T wave discordance.

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On each of the following EKGs: Answer the first five questions in the systematic approach to EKG interpretation. Calculate the rate; determine if it is regular or irregular; note if the QRS is narrow or wide; determine if P waves are present, and if they are present, are they upright or inverted; and diagnose the type of sinus rhythm. Unless otherwise stated, all rhythm strips are lead II. List possible treatments for the rhythm.

1.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

2.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

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222 MASTERING THE 12-LEAD EKG

3.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

4.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

5.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

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6.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

7.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

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224 MASTERING THE 12-LEAD EKG

8.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

9.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

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10.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

11.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

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226 MASTERING THE 12-LEAD EKG

12.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

13.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

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14.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

15.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

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228 MASTERING THE 12-LEAD EKG

16.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

17.

Rate: ___________________________

Rhythm: Regular or irregular: _______________

QRS: Narrow or wide _____________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ___________

Final interpretation: _______________________

Possible treatments: _____________

REFERENCES/RESOURCES Manolis, A. S. (2019, March 14). Ventricular premature beats. In H. Calkins (Ed.), UpToDate. Retrieved from https://www.uptodate.com/contents/ventricular-premature-beats Podrid, P. J. (2018, April 18). Pathophysiology and etiology of sudden cardiac arrest. In B. Olshansky & S. Manaker (Eds.), UpToDate. Retrieved from https://www.uptodate.com/ contents/pathophysiology-and-etiology-of-sudden-cardiac-arrest Surawicz, B., & Knilans, T. K. (2008). Chou’s electrocardiography in clinical practice: Adult and pediatric (6th ed., pp. 405–439). Philadelphia, PA: Elsevier Saunders. doi:10.1016/B978 -141603774-3.10017-6

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11:: AT 11 ATRI ATRIOVENTRICULAR RIOV OVEN E TR EN RICU IC CULAR RB BLOCKS LOCK LO CKS S 22 2 9 229

Chapter

11

Atrioventricular Blocks Delays or interruptions of conduction between the atria and ventricles are called atrioventricular (AV) blocks.

INTRODUCTION Normal depolarization of the heart begins with the sinoatrial (SA) node. When the SA node fires, depolarization spreads out like a wave toward the left atrium and AV node. Upon reaching the AV node, conduction is slowed, allowing the ventricles to fill. The impulse then continues down the bundle branches and through the Purkinje fibers. As we have already learned, normal conduction does not always take place. Sometimes, the conduction through the AV node or His bundle is impaired. It may be delayed or fail to transmit an impulse altogether. These

delays or interruptions of conduction between the atria and ventricles are called AV blocks. Atrioventricular blocks (AVBs) are named based on their severity, as follows: First-degree AVB Second-degree AVB ▪ Type I (a.k.a. Wenkebach or Mobitz I) ▪

Type II (a.k.a. Mobitz II)

High-grade AVB Third-degree AVB (complete)

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230 MASTERING THE 12-LEAD EKG

The PR Interval The PR interval is the period from the beginning of the P wave to the beginning of the QRS complex. As you know, the P wave represents depolarization of the atria. The isoelectric portion following the P wave and before the QRS represents decremental conduction through the AV node and transmission to the ventricles before ventricular depolarization begins.

Therefore, to look for blocks or delays occurring between the atria and ventricles, we need to look at the PR interval.

Normal PR interval: 0.12–0.20 second

FIRST-DEGREE AVB Although called a “block,” first-degree AVB is really prolonged conduction through the AV node. After the increased delay, depolarization of the ventricles occurs without interruption. In other words, a QRS complex should follow the prolonged PR interval. Normal AV conduction should occur in 0.12 to 0.20 second. Therefore, a

PR interval greater than 0.20 second is called a first-degree AVB.

Characteristics of First-Degree AVB 1. PR interval > 0.20 second. This is the result of prolonged conduction through the AV node. Typically, the prolongation is 0.21 to 0.40 second, but can reach lengths of 0.60 second. If the PR interval is greater than 0.30 second, it may be called “marked” first-degree AVB. When PR intervals are extraordinarily long, the P wave may land on the preceding T wave. 2. No missing QRS complexes. As will be seen, other blocks can completely stop conduction from reaching the ventricles. When this happens, the QRS complexes are missing. Because a first-degree AVB is only a delay, no QRS complexes are dropped. Every P is followed by a QRS and every QRS is preceded by a P.

Sinus rhythm with first-degree AVB. PR interval is approximately 0.34 second (>0.20 second) followed by a QRS complex.

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Causes The most common cause of a first-degree AVB is an increase in vagal tone. It is not uncommon to see it in well-conditioned athletes. It may also be a normal variant. One study found PR intervals as long as 0.28 second among healthy aviators (1.6%). Other common causes include medications such as beta-blockers, non-dihydropyridine calcium channel blockers, and digoxin. Electrolyte abnormalities such as hyperkalemia can extend the PR interval. Myocarditis and inferior myocardial infarction (MI) may also cause a first-degree AVB.

Treatment Symptoms are rarely experienced, and treatment is almost never required. The patient with marked delay in AV conduction may experience a phenomenon called “pacemaker syndrome.” This occurs when there is loss of AV synchrony. The PR interval is so long that it actually seems to follow ventricular conduction rather than precede it. This can lead to fatigue, dyspnea, and even syncope. These patients may require a pacemaker.

Sinus rhythm with first-degree AVB. P wave is partially superimposed on the preceding T wave. This patient may suffer from pacemaker syndrome due to lack of AV synchrony.

SECOND-DEGREE AVB S There are two types of second-degree AVB: type I (a.k.a. Wenckebach/Mobitz I) and type II (a.k.a. Mobitz II). Both are characterized by intermittent failure of the AV node to depolarize the ventricles. This means QRS complexes are missing. Not every P is followed by a QRS. Often, they have a regular pattern of AVB (2:1, 3:2, 4:3) but it can vary. The difference between the two second-degree AVBs is found in the PR interval. Type I has gradually lengthening PR intervals. In type II, the PR intervals remain constant.

Second-Degree AVB Type I Second-degree AVB type I, or Wenckebach, occurs in repeated cycles in which conduction through the AV node is gradually prolonged. Each time depolarization reaches the AV node, the node becomes more refractory to the impulse. Each subsequent impulse takes longer to complete. Eventually the AV node tires out and says, “No more, I need a break.” Conduction through the AV node fails, and the ventricles will not depolarize. This is identified on the EKG as

cycles of progressive PR lengthening with intermittently dropped QRS complexes. Wenkebach can be present in healthy athletes but may also be the result of underlying heart disease. It rarely causes significant symptoms or requires treatment.

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232 MASTERING THE 12-LEAD EKG

Characteristics of Second-Degree AVB Type I 1. Progressive lengthening of the PR interval. The PR interval prolongs because of increasing fatigue of the AV node. Eventually the AV node fails to depolarize the ventricles. In the example below, the PR interval is noticeably longer with each beat in the cycle. There are times the interval may remain unchanged for several beats. However, when the cycle is evaluated over time, the PR interval will get longer. The lengthened PR interval may not occur until just before the dropped QRS. The PR interval is longest before the dropped beat. The PR interval is shortest after the dropped beat. 2. Dropped QRS complexes. The AV node eventually decides to take a break and is unable to transmit the wave of depolarization to the ventricles. This leads to a non-conducted P wave. The dropped QRS allows the AV node time to recover and the cycle can begin again. 3. More P waves than QRS complexes. When there are too many P waves, consider second-degree AVB. 4. Grouped beating. Because the block of ventricular depolarization occurs in cycles, groups of beats/QRS complexes can be seen. This finding is a possible clue to diagnosing a second-degree AVB.

Sinus rhythm with second-degree AVB type I. Note the three “grouped” beats in the center of the strip. Each PR interval gradually increases in duration until the non-conducted P wave occurs (4:3 ratio, 4 P waves:3 QRS complexes). The cycle begins again with a shorter PR interval.

A. K. A. You may have noticed there is more than one name for second-degree AVB: Wenckebach and Mobitz I. Karl Wenckebach first described the rhythm in 1899. Many people still love to call it by his name because it is fun to say [ven-ke˘-bak′]. It’s also helpful to think of the saying “Wenckebach takes a walk.” It may help you remember the QRS complex walks further and further from the P wave before it leaves. Later, in 1924, Woldemar Mobitz divided second-degree AVB into the two current subtypes. Therefore, he has also staked claim to the name (Mobitz I/II).

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Sinus rhythm with Wenckebach/Mobitz I. Close inspection of the PR intervals demonstrates increasing prolongation before the dropped QRS complex.

Causes Just like first-degree AVB, Wenckebach can be seen in healthy individuals owing to an increase in vagal tone (up to 10% of long-distance runners). Reversible causes include medications, inferior myocardial ischemia/infarction, myocarditis, mitral valve surgery, and hyperkalemia. Cardiac conduction disease can also be to blame.

Treatment Often no treatment is required. But rare situations can arise in which the patient is unable to tolerate the rhythm. If hemodynamically unstable, the patient can be given intravenous (IV) atropine 0.5 mg. If the patient fails to respond, temporary pacing can be utilized while potential reversible causes are evaluated. IV pressors such as dopamine or dobutamine may be utilized to improve symptoms of hypotension and shock. If symptomatic and no reversible cause is found, the patient may require a permanent pacemaker.

Second-Degree AVB Type II/Mobitz II Second-degree AV block type II is another rhythm with intermittently dropped QRS complexes. But unlike first-degree AVB,

the PR interval remains constant before the intermittently dropped QRS complexes. Patients in Mobitz II typically have some type of underlying cardiac problem. It is frequently related to MI, medications, or disease of the conduction system.

Characteristics of Second-Degree AVB Type II 1. Constant PR interval. The duration may be normal or prolonged (>0.20 second), but the PR interval does NOT gradually lengthen. 2. QRS is often wide but may be narrow. Mobitz II is more frequently caused by a block below the His bundle (75%). When this happens, the QRS will be wide. When the block is above or within the His bundle, the QRS will be narrow (25%). 3. Dropped QRS. There may be a pattern with a consistent AV ratio, but the dropped QRS can also be haphazard and without warning.

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234 MASTERING THE 12-LEAD EKG

4. The R-R of the dropped beat is an exact multiple of the preceding R-R interval. 5. P waves will “march out” at regular intervals. 6. More P waves than QRS complexes. When there are too many P waves, consider second-degree AVB.

Sinus rhythm with Mobitz II. Consistent PR interval with single non-conducted P wave. Note the wide QRS that occurs in about 75% of Mobitz II. P waves march out. The R-R of the dropped beat is double that of the preceding R-R interval.

Causes Causes of Mobitz II include anterior MI that leads to necrosis of the septum, which contains the bundle branches. Cardiac surgery, particularly mitral valve repair; inflammatory disease such as rheumatic fever or systemic lupus erythematosus; hyperkalemia; and medications (beta-blockers, calcium channel blockers, digoxin, amiodarone) can also precipitate the rhythm.

Symptoms Patients will usually present with symptoms, but severity can vary. If the rate is fast enough and there are few dropped beats, the symptoms may be minimal. But if the patient is in sinus bradycardia and has frequent non-conducted P waves, the patient can be hemodynamically unstable. Fatigue, shortness of breath, chest pain, presyncope/syncope, and even sudden cardiac arrest may result.

Treatment Treatment options are essentially the same as those with Mobitz I. If the patient is stable, no urgent treatment is required. However, the patients are at increased risk of complete heart block. Therefore, they should have pads in place, ready to temporarily pace if needed. If symptomatic and unstable, the patient should receive atropine 0.5 mg IV with temporary pacing ready to go if improvement is not seen. Look for reversible causes and correct. If none is found, the patient may require a permanent pacemaker.

2:1 AVB When a 2:1 AV conduction block is present, it is impossible to know for certain if the rhythm is second-degree type I or II. This is because there are no consecutive PR intervals to evaluate for gradual lengthening. Some findings may suggest one rhythm over the other. A wide QRS is more likely to be second-degree type II. Blocks that worsen with atropine or exercise are also more likely to be type II. A good strategy is to observe the patient and rhythm for a longer period of time in hopes that consecutive PR intervals develop.

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Sinus rhythm with 2:1 AVB. Non-conducted P waves sit on the tail end of the previous T wave. If you look very closely, you will see the 2:1 block does not begin until after the second QRS complex. By measuring the PR intervals of the first and second beats, you will see that the PR is getting longer before the block occurs. This is Mobitz I, followed by a 2:1 AVB.

HIGH-GRADE AVB If the AVB is 3:1 or greater, it is known as a high-grade or advanced AVB. This reveals itself by having more than one dropped QRS complex in a row. Patients who remain in the rhythm should be treated with a permanent pacemaker.

Characteristics 1. Atrial rate is faster than the ventricular rate. Because of block at the AV node, the atrial and ventricular rates can vary greatly. The ventricular rate is the most important in regard to your patient’s hemodynamic status. If the ventricular rate is very slow, your patient may be compromised. 2. Atrioventricular ratio of 3:1 or greater. This is seen on the EKG as three P waves for every QRS. 3. P waves and QRS complexes are related to each other. The atria and ventricles are still talking to each other, just not as often as they should for a happy marriage. As you will see, they can eventually go their separate ways.

High-grade AVB. 4:1. If you march out the P waves, you will see one is hidden within each T wave.

THIRD-DEGREE AVB (COMPLETE) In third-degree AVB, atrial impulses are unable to reach the ventricles. The atria and ventricles refuse to talk to each other anymore. Each is doing its own separate thing at its own rate of speed. It is often related to cardiac conduction disease but may also be the result of reversible causes. Many times, the patient requires placement of a permanent pacemaker.

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236 MASTERING THE 12-LEAD EKG

Characteristics of Third-Degree AVB 1. P waves are present. In third-degree AVB, atrial depolarization often still originates in the SA node. The pace will be consistent with its inherent rate (60–100 beats/minute). However, it is possible for the atria to be paced by an ectopic focus/foci. Atrial rhythms can include atrial flutter and atrial fibrillation. 2. QRS complexes are present, usually. The ventricles may be paced by a junctional or ventricular escape rhythm. Yes, it is considered an escape rhythm because it is escaping the influence of the atrial pacemaker. The ventricles pace at the inherent rate of the escape focus, which is most often slower than the atrial rate. The ventricular pacer can be identified by the width of the QRS and the rate of the rhythm (ventricles wide and 20–50 beats/minute, junctional narrow and 40–60 beats/minute). If there is no ectopic focus able to fire, no QRS complexes will be present. This is called ventricular standstill. 3. P waves and QRS complexes have no relationship to one another. Like a disgruntled couple, the atria and ventricles are not communicating with each another. Impulses are completely blocked. Because the atria and ventricles are firing at different rates, the P wave and QRS complexes will not match up. Everything is disorganized. P waves may be found before or after a QRS or hidden within the QRS or T wave. 4. Random PR intervals. Because the P waves and QRS complexes are unrelated, the “PR intervals” will appear random. Long, short, maybe even appear to be missing. Looking at the PR intervals is a great way to evaluate rhythms that have more P waves than QRS complexes.

Sinus rhythm with complete heart block. There are more P waves than QRS complexes, a clue that the atrial rate is faster than the ventricles. You can see that the QRS complexes and P waves have no relationship to one another and the “PR intervals” are completely random. Some P waves are completely hidden within the T waves (first T wave). The narrow QRS complex points to a junctional escape rhythm.

Complete heart block with ventricular standstill. A ventricular escape focus (wide QRS) is attempting to pace the ventricles but is failing. Note the multiple P waves without QRS complexes. This can be distinguished from high-grade AVB because of the lack of relationship between the atria and ventricles (random PR).

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Atrial fibrillation with complete heart block. The atria are quivering. The QRS complexes are wide and regular. This is because they are coming from a ventricular escape rhythm that is not hearing from the atria.

Causes More than 50% of the time, complete heart block is the result of degenerative conduction disease. However, it can be related to reversible conditions such as medications (beta-blockers, calcium channel blockers, and digoxin), myocardial ischemia, hyperkalemia, or cardiac surgery.

Symptoms Symptoms are variable dependent upon the patient’s health condition and rate of the escape rhythm pacing the ventricles. If the patient is otherwise healthy and the rate is reasonable (50–60 beats/minute), few symptoms may develop. However, if the rate is slow (0.20 second

Mobitz I

Variable

Irregular

Narrow

Too many P/ gradually longer

Mobitz II

Variable

Irregular

Wide (75%) Narrow (25%)

Too many P/ constant

High-grade AVB

Variable

Irregular

Narrow

Too many P

Third-degree AVB

Variable

Regular

Narrow/wide

Too many P/random

Asystole

Zero

—

—

—

AVB, atrioventricular block.

TAKE-HOME POINTS • AVBs are described as delays or interruptions in conduction between the atria and ventricles. • AVBs are named based on their severity. • The five types of AVBs ▪ First-degree AVB—Constant PR >0.20 second, no dropped QRS ▪ Mobitz I—Progressive lengthening of PR interval, intermittent dropped QRS ▪ Mobitz II—Constant PR interval, intermittent dropped QRS ▪ High-grade AVB—AVB of 3:1 or greater ▪ Third-degree AVB—Atrial and ventricles not working together, each with its own rate

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EXERCISES 1. When evaluating a patient for an AV heart block, which interval is most important to examine? __________ 2. The most common cause for a first-degree AVB is _______________. 3. Over 50% of the time, third-degree AVB is the result of ___________________ disease. 4. Define the following terms: pacemaker syndrome, grouped beating

5. Describe pulseless electrical activity.

On each of the following EKGs: Answer the first five questions in the systematic approach to EKG interpretation. Calculate the rate; determine if it is regular or irregular; note if the QRS is narrow or wide; determine if P waves are present, and if they are present, are they upright or inverted. Name the type of rhythm and AVB that is present.

1.

Rate: ____________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

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Final interpretation: __________________________

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244 MASTERING THE 12-LEAD EKG

2.

Rate: ____________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

3.

Rate: ____________________

Final interpretation: __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

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Final interpretation: __________________________

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4.

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PR duration: ______________________

Final interpretation: __________________________

P waves: Present, not present, upright, or inverted _______________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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246 MASTERING THE 12-LEAD EKG

5.

Rate: ____________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

6.

Rate: ____________________

Final interpretation: __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

7.

Rate: ____________________

Final interpretation: __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

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Final interpretation: __________________________

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8.

Rate: ____________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

9.

Rate: ____________________

Final interpretation: __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

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Final interpretation: __________________________

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248 MASTERING THE 12-LEAD EKG

10.

Rate: ____________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

11.

Rate: ____________________

Final interpretation: __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

12.

Rate: ____________________

Final interpretation: __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

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Final interpretation: __________________________

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13.

Rate: ____________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

14.

Rate: ____________________

Final interpretation: __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

15.

Rate: ____________________

Final interpretation: __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

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Final interpretation: __________________________

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250 MASTERING THE 12-LEAD EKG

16.

Rate: ____________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

17.

Rate: ____________________

Final interpretation: __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

18.

Rate: ____________________

Final interpretation: __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________ P waves: Present, not present, upright, or inverted _______________________ PR duration: ______________________

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Final interpretation: __________________________

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19.

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PR duration: ______________________

Final interpretation: __________________________

P waves: Present, not present, upright, or inverted _______________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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20.

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PR duration: ______________________

Final interpretation: __________________________

P waves: Present, not present, upright, or inverted _______________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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21.

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PR duration: ______________________

Final interpretation: __________________________

P waves: Present, not present, upright, or inverted _______________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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Chapter

12

EKGs and Pacemakers Pacemakers are electronic devices that can be used to kick-start depolarization of the atria and/or ventricles.

INTRODUCTION We discussed atrioventricular (AV) blocks in the last chapter. As you could see, there are times when conduction in the heart is delayed, is interrupted, or fails altogether. Fortunately, we have means at our disposal to help patients who suffer from cardiac conduction disturbances. Pacemakers are electronic devices that can be used to kick-start depolarization of the atria and/or ventricles. They can also be used to improve synchronization of the ventricles when left ventricular (LV) dysfunction and left bundle branch block (LBBB) are present. They may be a temporary solution while reversible problems are corrected or implanted permanently in the chest when the condition is irreversible.

INDICATIONS If the patient is symptomatic or unstable owing to a bradycardia or heart block, a pacemaker may be indicated. These complications may be the result of reversible conditions such as myocardial ischemia, electrolyte disturbances, or recent cardiac surgery. However, electrical disturbances can be chronic as the result of cardiac conduction disease. Depending on the source of the problem, temporary or permanent pacemakers may be used.

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256 MASTERING THE 12-LEAD EKG

TYPES OF PACEMAKERS Temporary Pacemakers A few different types of temporary pacemakers can be utilized when the condition is thought to be reversible or to buy time until a permanent pacemaker can be inserted. Transcutaneous. This type of pacemaker is placed on the chest using conductive pads. It can be applied in a hurry in an emergent situation with minimal training. Unfortunately, it requires a high level of energy to transmit the impulse through the chest. This can be very uncomfortable for an alert patient. Sedation could be used but may potentially worsen the hemodynamic status. Transvenous. This type of pacemaker is inserted through a vein such as the femoral or subclavian. The wire is threaded through the vein to the right ventricle. Placement of the pacemaker requires a higher level of training and preferably is performed under fluoroscopy. The patient may be prone to ventricular beats or arrhythmias during insertion. Once the pacemaker is in place, the patient can be safely paced without discomfort. This type of pacemaker can remain in place for days or weeks. Unfortunately, the patient must remain still while the leads are in place. Epicardial. The wires for an epicardial pacemaker are usually inserted during cardiac surgery. Before closing the chest, the wires are pulled through the chest wall and are available should the need arise. If the leads need to be used, an external pacemaker is attached to the wires and placed on the desired settings. The patients do not experience any pain while paced and remain mobile. These wires generally fail within 1 week and therefore will be removed.

Permanent Pacemakers Permanent pacemakers are extremely valuable to those with irreversible conduction defects that cause symptomatic bradycardia or heart blocks. They are made up of two primary parts: a generator and leads. The generator is implanted in the chest wall, usually in the left upper chest. It serves as both a battery and computer that senses and paces the heart. It can detect electrical conduction from the heart and turn off pacing when not needed. It can also detect when there is a delay or interruption and turn on when required. The leads or electrodes are placed in the atria, ventricles, or both. Usually the wires are in the right atrium and/or ventricle. But when used for LV dysfunction and LBBB, leads are typically placed in both the right and left ventricles. This allows for synchronization of the ventricles and improvement in coordinated ventricular contraction (cardiac resynchronization therapy). This type of pacemaker is called biventricular and often is combined with an implantable cardioverter defibrillator (ICD). The ICD can detect life-threatening arrhythmias and respond by defibrillating the patient and restoring normal rhythmicity.

EKG OF PACEMAKERS We can usually detect the presence of a pacemaker easily on the EKG.

Characteristics of a Paced Rhythm 1. “Pacing spike.” When the atria are paced, a sharp vertical deflection is seen before the P wave. If the ventricles are being paced, the sharp deflection will be seen before the QRS. If both the atria and ventricles are being paced, well, the spike will be in front of both the P and QRS. On occasion, the amplitude of the pacing spike is so small that it may be missed or unable to be seen.

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2. Wide QRS. Most of the time the ventricles are paced with a single wire placed in the right ventricle. Because depolarization is not beginning in the ventricular septum, the impulse must travel from one side of the heart all the way to the other. Because depolarization takes longer to complete, the QRS will be wide. Because the wire is placed in the right ventricle, the wide complex will resemble an LBBB. 3. ST-T discordance. The ST segment and T wave will point in the opposite polarity of the QRS complex. This is a sign of abnormal repolarization caused by abnormal depolarization of the ventricles.

AV paced rhythm. Pacing spikes are seen before the P wave and QRS complex. Therefore, we know it is pacing in both the atria and the ventricles. The QRS is wide. The T wave is discordant to the QRS complex.

Atrial paced rhythm. Pacing spikes are seen before the P wave. Only the atria are being paced. The QRS is narrow because of normal conduction though the His-Purkinje system.

Ventricular paced rhythm. Pacing spikes are seen after the intrinsic P wave and before the paced ventricular beat. The QRS is wide. T waves are discordant to the QRS complex.

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258 MASTERING THE 12-LEAD EKG

PACEMAKER MALFUNCTIONS Most of the time pacemakers are very reliable at their job. They pace beat after beat, year after year. Turn on when needed. Turn off when they aren’t. But sometimes issues come up that you need to be able to detect and correct.

Failure to Capture When the pacemaker fires, we see a pacing spike on the EKG. It’s showing us the pacemaker attempted to kick-start depolarization. This should lead to a P wave or QRS complex. However, there are times the pacemaker fires when it should, but the myocardium does not respond. The pacemaker “fails to capture” and depolarize the myocardium. This is demonstrated on the EKG by

correctly timed pacing spikes without subsequent depolarization of the myocardium. 1. Correctly timed pacing spikes. The pacemaker is kicking in when needed. There was a pause or block and the pacemaker detected it. A spike is seen. 2. No P wave/QRS after the pacing spike. The pacemaker attempted to depolarize the atria/ventricles but no complex followed the appropriately timed pacing spike. It failed to capture.

Cause Failure to capture may be caused by a dislodged lead or leaking around the pacing circuit. It may also be an issue with the output of the generator. The setting may not be providing enough energy to depolarize the myocardium. The myocardium may also be requiring more energy to pace than usual. The increase in threshold could be caused by ischemia, fibrosis, or electrolyte imbalances such as hyperkalemia.

Pacing spikes are occurring when they should. The pause is the result of the pacemaker failing to capture the myocardium.

Failure to Sense The pacemaker has the ability to sense intrinsic electrical activity coming from the atria and ventricles. When properly detected, the pacemaker knows it is not needed and will not fire. However, there are times when the pacemaker “fails to sense” the native electrical activity of the myocardium. This is demonstrated on the EKG by

extra and inappropriately timed pacing spikes.

Causes The computer may be failing to sense the intrinsic rhythm because of a low amplitude signal. This could be from myocardial scar or poor contact of the lead. The pacemaker also may need to be reprogrammed to a more appropriate setting.

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Pacing spikes are occurring in places they shouldn’t. They are not sensing the underlying cardiac rhythm and are trying to pace when their help is not needed.

Failure to Pace There are times the pacemaker needs to kick into gear, but for some reason it thinks it isn’t needed. The rhythm is slow and we are waiting on the pacemaker to do its job. The pacemaker “fails to pace” when it should. It is seen on the EKG as

slow intrinsic rhythm without evidence of pacing spikes where they are expected.

The patient’s atria are paced by the sinoatrial (SA) node, but the ventricles require the assistance of a pacemaker. This is evident by the pacing spike before the QRS complex. Unfortunately, the ventricular pacemaker failed to fire after the third P wave above and the ventricles were not paced.

Causes The pacemaker may be detecting activity that simulates an intrinsic rhythm. This could be caused by skeletal muscle or diaphragmatic contraction. It can also be the result of external electrical equipment such as an MRI or electrocautery.

TREATMENT Problems with pacemaker settings, generators, or leads are typically out of the provider’s control. However, the medical device representative may be contacted to interrogate the pacemaker and may be able to adjust settings that can correct the problem. If needed, contact the cardiologist or electrophysiologist for further evaluation and treatment.

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260 MASTERING THE 12-LEAD EKG

Systematic Approach

1. 2. 3. 4.

What’s the rate? Is the rhythm regular or irregular? Is the QRS narrow or wide? Are P waves present? Are they upright in I and II and inverted in aVR? Are there too many P waves? 5. What’s the duration of the PR interval? Does it remain the same, increase, or randomly change?

TAKE-HOME POINTS • Pacemakers are indicated for ▪ Symptomatic bradycardia ▪ Symptomatic heart blocks ▪ LV dysfunction/asynchrony • Pacemakers can be ▪ Temporary or permanent ▪ Atrial, ventricular, or both • Pacemaker activity can often be identified by a pacing spike before the P wave or QRS complex. • Pacemakers can malfunction.

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EXERCISES 1. Explain why ventricular paced rhythms have a wide QRS complex.

Match the following types of pacemakers to their description below: Transcutaneous

Transvenous

Epicardia

Biventricular/ICD

2. What type of pacemaker is often used after a cardiac surgery? _______________ 3. Which pacemaker utilizes conductive pads placed on the chest and can be painful for the patient? _______________ 4. What pacemaker is indicated when the patient has LV dysfunction and is at risk for life-threatening arrhythmias? _______________ 5. Which type of temporary pacemaker requires a higher level of training to insert and can be used for days or weeks? _______________ Match the following types of pacemaker malfunctions to their description below: Failure to capture

Failure to sense

Failure to pace

6. Slow intrinsic rhythm without evidence of pacing spikes where they are expected. _______________ 7. Correctly timed pacing spikes without subsequent depolarization of the myocardium. _______________ 8. Extra and inappropriately timed pacing spikes. _______________

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262 MASTERING THE 12-LEAD EKG

On each of the following EKGs: Answer the first five questions of a systematic approach to EKG interpretation. Calculate the rate; determine if it is regular or irregular; note if the QRS is narrow or wide; determine if P waves are present, and if they are present, are they upright or inverted. Interpret the rhythm and pacemaker malfunction if present.

1.

Rate: ________________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

2.

Rate: ________________________

Final interpretation: _____________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

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Final interpretation: _____________________

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3.

Rate: ________________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

4.

Rate: ________________________

Final interpretation: _____________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

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Final interpretation: _____________________

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264 MASTERING THE 12-LEAD EKG

5.

Rate: ________________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

6.

Rate: ________________________

Final interpretation: _____________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

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Final interpretation: _____________________

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7.

Rate: ________________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

8.

Rate: ________________________

Final interpretation: _____________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

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Final interpretation: _____________________

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266 MASTERING THE 12-LEAD EKG

9.

Rate: ________________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

10.

Rate: _______________________

Final interpretation: _____________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

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Final interpretation: _____________________

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11.

Rate: _______________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

12.

Rate: _______________________

Final interpretation: _____________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

13.

Rate: _______________________

Final interpretation: _____________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

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Final interpretation: _____________________

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14.

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Final interpretation: _____________________

QRS: Narrow or wide ______________ PR duration: ___________________

Rhythm: Regular or irregular ________________________

P waves: Present, not present, upright, or inverted _____________________

Rate: _______________________

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15.

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Final interpretation: ____________________

QRS: Narrow or wide ______________ PR duration: ___________________

Rhythm: Regular or irregular ________________________

P waves: Present, not present, upright, or inverted _____________________

Rate: _______________________

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270 MASTERING THE 12-LEAD EKG

16.

Rate: _______________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

17.

Rate: _______________________

Final interpretation: _____________________

Rhythm: Regular or irregular ________________________

QRS: Narrow or wide ______________ P waves: Present, not present, upright, or inverted _____________________ PR duration: ___________________

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Final interpretation: _____________________

02-Dec-19 5:02:20 PM

18.

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Final interpretation: ____________________

QRS: Narrow or wide ______________ PR duration: ___________________

Rhythm: Regular or irregular ________________________

P waves: Present, not present, upright, or inverted _____________________

Rate: _______________________

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Chapter

13

EKG Artifacts Artifact is movement on the EKG tracing that is not made by the heart’s electrical activity. It can make it difficult or even impossible to make an accurate interpretation.

INTRODUCTION Now that you have learned all the important rhythms, let me throw a curve ball your way. Unfortunately, not all EKG tracings are nice and neat. There will be many times that you have to deal with artifact. Artifact is movement on the EKG tracing that is not made by the heart’s electrical activity. It can make it difficult or even impossible to make an accurate interpretation. You need to become familiar with the various types of artifact so that you can determine the problem and improve the situation should it arise, and it will.

LOOSE LEAD ARTIFACT Loose electrodes can be a frequent source of frustration. Applying electrodes to a hairy patient or a patient who is diaphoretic can be troublesome. Hair and sweat make it difficult for electrodes to stick to your patient. And without proper skin contact, you will experience artifact. The constant motion of the baseline that can occur with loose lead artifact may mimic atrial fibrillation, as in the example on the next page. Measure out the R-R intervals and you will see the ventricular response is regular. This rules out atrial fibrillation. With close inspection, you can also make out P waves before each QRS complex. Moving the limb electrodes to a less hairy position or shaving hair from the chest/legs may be required for adequate adherence to the skin. Dry the skin as best as possible before applying the electrodes. You can consider using a skin adhesive such as benzoin but use caution because it is flammable. Benzoin and defibrillation pads may not play nice together. Some manufacturers have developed electrodes specifically for the diaphoretic patient and those may be helpful. Electrodes that are from a freshly opened package will also have an improved sticking ability.

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274 MASTERING THE 12-LEAD EKG

Loose lead artifact. No, it is not atrial fibrillation. The R-R intervals are regular and P waves can be seen before each QRS complex.

WANDERING BASELINE Patient movement or breathing can cause a wandering baseline. This displays as a slow constant up and down of the baseline. Try comparing your ST segment to an “isoelectric” baseline that is flopping in the wind. Where is the baseline? It’s here! No, it’s there! Not all patients like to sit still. Some are just being ornery, but others may be in too much pain to sit quietly while you do an EKG. Even seemingly normal movement and breathing can cause some fluctuation in the baseline. Try replacing the electrodes. They may be dry and making poor contact. Make sure electrodes are being stored in a sealed package so they don’t dry out prior to use. You can encourage your patients to hold as still as possible. It’s unlikely you can ask them to stop breathing. “Sorry, sir, I know you are having crushing chest pain, but could you try holding your breath for the next 15 seconds?”

MUSCLE TREMOR ARTIFACT Muscle tremors are another frequent source of artifact. Patients who are cold and shivering, nervous, or suffer from Parkinson’s disease can all have tremors that mimic atrial fibrillation or other arrhythmias. Warm your patients. Make sure they are not propping themselves up on the side rails with their arms. And if you think it could be atrial fibrillation, make sure to evaluate the R-R intervals to see if they are regular. Atrial fibrillation will always be irregular.

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Muscle tremor artifact. Looks a lot like ventricular tachycardia. Don’t shock this patient. If you look closely, you can see narrow QRS complexes within the artifact (leads III, V1–V5).

ELECTROMAGNETIC INTERFERENCE Sometimes electromagnetic interference can cause a 60-cycle “hum” to be present on the EKG. It’s not always easy to find the source, but it could be due to electrical power lines, faulty equipment, or a mobile phone. Some monitors allow you to adjust settings that may minimize the noise. Electromagnetic interference appears as a thick black line made up of 60 up and down lines/waves per second.

This EKG is suffering from a 60-cycle hum and a wandering baseline.

CPR COMPRESSION ARTIFACT/SHOCK Chest compressions during CPR make the EKG impossible to read. The motion of the chest with each compression causes a distinct artifact. This is why rhythm and pulse checks must be performed at intervals during advanced cardiac life support. The rate of compressions can be counted by looking at the artifact on the EKG.

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276 MASTERING THE 12-LEAD EKG

The first four “beats” are chest compressions followed by ventricular fibrillation. Compressions were stopped to assess the rhythm. Looks like it’s time for defibrillation.

When the patient is cardioverted/defibrillated it causes an artifact. You can evaluate a rhythm strip and see when patients received the defibrillation and if they converted to a normal sinus rhythm. But you can’t tell if they screamed or not.

The center of this EKG strip shows an attempt to defibrillate a patient in ventricular fibrillation. Unfortunately, the patient remained in ventricular fibrillation after the shock.

NEUROMODULATION ARTIFACT Neuromodulators are being implanted more often to treat many patient complaints and illnesses. They may be used to treat seizures, tremors, chronic pain, and gastroparesis. These devices may cause artifact that creates multiple spikes among the QRS complexes, similar to pacing spikes. Many cannot be turned off in order to remove the artifact.

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ARTERIAL PULSE TAPPING EFFECT Arterial pulse tapping was first reported in 2005. A limb electrode was accidentally placed over the radial artery. A large T wave was noted that corresponded with the pulse in the radial artery. As the artery pulsated, it moved the electrode that was placed on the right wrist causing the artifact. If you see this rare phenomenon, move the electrode to a new position on the arm.

Systematic Approach

1. 2. 3. 4.

What’s the rate? Is the rhythm regular or irregular? Is the QRS narrow or wide? Are P waves present? Are they upright in I and II and inverted in aVR? Are there too many P waves? 5. What’s the duration of the PR interval? Does it remain the same, increase, or randomly change?

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278 MASTERING THE 12-LEAD EKG

EXERCISES On each of the following EKGs: Calculate the rate; determine if the rhythm is regular or irregular; note if the QRS is narrow or wide; determine if P waves are present, and if they are present, are they upright or inverted; and measure the PR interval. Diagnose the rhythm and name the type of artifact.

1.

Rate: ________________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide __________________ P waves: Present, not present, upright, or inverted ________________________ PR duration: ___________________

2.

Rate: ________________________

Final interpretation: ________________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide __________________ P waves: Present, not present, upright, or inverted ________________________ PR duration: ___________________

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Final interpretation: ________________________

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3.

Rate: ________________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide __________________ P waves: Present, not present, upright, or inverted ________________________ PR duration: ___________________

4.

Rate: ________________________

Final interpretation: ________________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide __________________ P waves: Present, not present, upright, or inverted ________________________ PR duration: ___________________

5.

Rate: ________________________

Final interpretation: ________________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide __________________ P waves: Present, not present, upright, or inverted ________________________ PR duration: ___________________

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Final interpretation: ________________________

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280 MASTERING THE 12-LEAD EKG

6.

Rate: ________________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide __________________ P waves: Present, not present, upright, or inverted ________________________ PR duration: ___________________

7.

Rate: ________________________

Final interpretation: ________________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide __________________ P waves: Present, not present, upright, or inverted ________________________ PR duration: ___________________

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Final interpretation: ________________________

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8.

Rate: ________________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide __________________ P waves: Present, not present, upright, or inverted ________________________ PR duration: ___________________

9.

Rate: ________________________

Final interpretation: ________________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide __________________ P waves: Present, not present, upright, or inverted ________________________ PR duration: ___________________

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Final interpretation: ________________________

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282 MASTERING THE 12-LEAD EKG

10.

Rate: ________________________

Rhythm: Regular or irregular _______________________

QRS: Narrow or wide __________________ P waves: Present, not present, upright, or inverted ________________________ PR duration: ___________________

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Final interpretation: ________________________

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14:: EK 14 EKG G AX AXIS XIS IINTERPRETATION NTER NTER NT E PR RET ETAT ATIO ION N 28 2 3 283

Chapter

14

EKG Axis Interpretation The primary direction of depolarization in the ventricles is called the electrical axis of the heart.

INTRODUCTION Five major categories need to be interpreted on every EKG: 1. Rate 2. Rhythm 3. Axis 4. Hypertrophy 5. Ischemia/infarction So far we have learned how to calculate the rate and interpret lots of different rhythms. Now it’s time to kick some axis.

TIME TO KICK SOME AXIS During depolarization of the myocardium, electrical current flows in many different directions. The EKG machine doesn’t show us each of the individual currents taking place. Instead, it is designed to record the average or mean of the electrical activity occurring in the myocardium at a given time. The main direction of electrical flow is known as the axis. We can evaluate the axis of any part of electrical conduction. This includes atrial and ventricular depolarization and repolarization. But the axis we are most interested in is the wave of depolarization through the ventricles in the frontal plane.

The primary direction of depolarization in the ventricles is called the heart’s electrical axis.

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284 MASTERING THE 12-LEAD EKG

The electrical axis is a basic element that should be interpreted on every 12-lead EKG. Noting abnormalities in the axis can provide evidence for conditions such as ventricular hypertrophy, myocardial infarction (MI), and pulmonary embolism. Therefore, it is a critical part of every 12-lead EKG interpretation. Because the heart’s electrical axis is determined by the direction of ventricular depolarization in the frontal plane,

the QRS is evaluated in the limb leads to determine the electrical axis.

THE HEXAXIAL DIAGRAM The heart’s electrical axis is read in the frontal plane. Therefore, to determine the electrical axis, we evaluate the QRS in the limb leads (I, II, III, aVR, aVL, aVF). Unlike the precordial leads where QRS complexes tend to have a predictable pattern (R wave progression), the limb leads can have considerable diversity. This is due to the variability of the electrical position of the heart because of anatomic variations or pathologic conditions. The hexaxial diagram tells us how each of the limb leads takes a picture of the heart’s electrical activity in the frontal plane. Understanding the hexaxial diagram is critical to understanding and calculation of the heart’s electrical axis. You may remember that each of the leads is assigned a number called the angle of orientation. This number is used when calculating and describing the axis. If you haven’t learned it already, now is the time to put these numbers to memory.

NORMAL DEPOLARIZATION OF THE ATRIA AND VENTRICLES Lead I: 0° Lead II: +60° aVF: +90° Lead III: +120° aVR: −150° aVL: −30°

Normal depolarization begins in the sinoatrial (SA) node, which sits in the upper right atrium. The wave goes out simultaneously in all directions. The impulse will travel from right to left across the atria as well as down toward the atrioventricular (AV) node. Once the impulse reaches the AV node, decremental conduction causes a slight delay before it continues down both bundle branches. The wave then proceeds quickly and simultaneously throughout the ventricular myocardium by way of the Purkinje fibers. Because the left ventricle has a larger mass, there is more electrical activity occurring in the left ventricle. Therefore,

the normal electrical axis should point down and toward the left ventricle.

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NORMAL AXIS In the absence of disease, the electrical axis will typically fall in the normal range. However, there are many different opinions on what constitutes a normal range. The most conservative estimates place the normal axis from 0° to +90° (between lead I and aVF) to more liberal parameters of −30° to +120° (between aVL and lead III). One reason there is confusion is because the axis can vary on serial EKGs by as much as 30° in a healthy patient with no pathology.

ABNORMAL AXIS There are essentially four types of conditions that can cause the axis to shift. 1. If the heart changes position, the electrical axis will also change. Body habitus can cause the heart to change position and thus the axis to shift. In obese patients, the diaphragm pushes up on the heart, causing it to tilt on its side. However, in tall thin patients the heart sits more upright in the chest. 2. Ventricular hypertrophy can cause the axis to shift. In long-standing systemic hypertension, the left ventricle has to work hard to overcome the elevated pressures. Eventually the left ventricle enlarges from the persistent workout. Because the ventricle is larger, there is more electrical current flowing through it. In this circumstance, the electrical axis will shift toward the hypertrophied left ventricle.

The axis points toward hypertrophy. 3. A myocardial infarction can cause a shift in the electrical axis. Infarcted myocardium is dead. Dead heart muscle does not produce any electrical current. This means that the average electrical current is shifted toward the healthy heart muscle and

the axis points away from the MI. 4. Electrical conduction problems can cause the axis to deviate. The anterior fascicle of the left bundle is responsible for depolarization of the anterior and upper portion of the left ventricle. When a left anterior fascicular block occurs, depolarization of this portion of the myocardium is delayed. This leads to a left axis deviation.

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Causes of Abnormal Axis

1. 2. 3. 4.

Physical change in the position of the heart Ventricular hypertrophy Myocardial infarction Electrical conduction problems

Left Axis Deviation When the axis is between −30° and −90°, it is considered left axis deviation (LAD). This may be a sign of pathology or a normal variant that can be seen with age. Physical shifts in the heart that can cause LAD include a high diaphragm caused by obesity or pregnancy. Left ventricular hypertrophy due to hypertension or an atrial septal defect may also result in LAD. An inferior MI may cause necrosis of the right ventricle. This can result in a shift to the left. A left anterior fascicular block and left bundle branch block can also cause LAD.

Right Axis Deviation When the axis is between +90° and +180°, it is called a right axis deviation (RAD). If the patient is tall and slender, the heart may physically shift to the right and the electrical axis may shift with it. Right ventricular hypertrophy can cause an RAD toward the enlarged ventricle. A lateral MI that damages the left ventricle can cause the axis to shift away from the necrotic tissue. A left posterior fascicular block can be the cause of RAD. On rare occasion, the axis may be between +180° and −90°. This is called severe or extreme right axis deviation (ERAD).

Causes of Axis Deviation

Right Axis Deviation

Left Axis Deviation

Extreme Right Axis Deviation

• Right ventricular hypertrophy • Pulmonary embolism • Lateral MI • Chronic obstructive pulmonary disease • Hyperkalemia • Wolff–Parkinson–White syndrome • Left posterior fascicular block • Normal pediatric EKG • Tall thin patient • Ventricular ectopy • Sodium channel blocker toxicity

• Normal variant due to age • Left ventricular hypertrophy • Atrial septal defect • Left bundle branch block • Inferior MI • Ventricular pacing • Ventricular ectopy • Wolff–Parkinson– White syndrome • Left anterior fascicular block • Pregnancy • Obesity

• Ventricular rhythms • Hyperkalemia • Severe right ventricular hypertrophy

MI, myocardial infarction.

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CALCULATING THE AXIS Several different methods can be used to determine the axis, each with pros and cons. It is not necessary to be a master at all of them, but it is important to understand the concepts that each of them teach you about calculating the axis. In the end, find one you are most comfortable with and stick to it. Calculating the axis requires a solid understanding of the hexaxial diagram and the four laws of EKG. Before we begin, take a moment to refresh your memory.

Four Laws of EKG 1. A wave of depolarization flowing toward a positive electrode will record a positive wave. 2. A wave of depolarization flowing away from a positive electrode will record a negative wave. 3. A wave of depolarization moving perpendicular to a positive electrode will record a biphasic wave.

– – –

+ + +

4. All the effects caused by repolarization have the reverse effect on the waves. For example, a wave of repolarization moving away from a positive electrode will result in a positive wave.

The Quadrant Method The first system we will discuss is called the quadrant method. It is described by Dr. Dale Dubin in his text Rapid Interpretation of EKGs (2000). The quadrant method does not provide the interpreter with a specific degree of axis but gets it in the ballpark. The normal axis in this method is a more conservative 0° to +90°. Anything less than 0° is classified as LAD, more than +90°, RAD.

By looking at the QRS complex in leads I and aVF, we can place the axis in one of four quadrants. Remember: • Lead I’s positive electrode is placed on the left arm. It has an angle of orientation of 0°. • aVF’s positive electrode is placed on the left foot and sits at the bottom of the hexaxial diagram. It has an angle of orientation of +90°. Each quadrant represents an axis (Table 14.1): • Normal (0° to +90°) • LAD (0° to −90°) • RAD (+90° to ±180°) • ERAD (±180° to −90°) In the following EKG, start by evaluating the QRS complex in lead I. Determine if the QRS complex is positive (R > S), equiphasic (R = S), or negative (R < S).

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288 MASTERING THE 12-LEAD EKG

• If the QRS is upright/positive (R > S), the axis points to the side of the diagram toward lead I. This would place it in either the left axis or normal axis quadrant. • If the QRS is negative (R < S), then the axis points away from lead I into one of the RAD quadrants. • If equiphasic (R = S), well, that is where we will need to learn an alternative technique. In this example, lead I is positive. Next, look at lead aVF.

• If the QRS is positive in aVF, the axis points down into either the right axis or normal axis quadrant. • If the QRS is negative, the axis points up, away from aVF to the extreme right or left axis quadrant. In this example, lead aVF is also positive.

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Now put the information you gained from leads I and aVF together. The quadrant where the two meet is the general location of the axis. This patient has a normal axis.

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290 MASTERING THE 12-LEAD EKG

TABLE 14.1 Parameters of the Quadrant Method Lead I

Lead aVF

Quadrant

Axis

Positive

Positive

Normal axis (0° to +90°)

Positive

Negative

Possible LAD (0° to −90°)

Negative

Positive

RAD (+90° to 180°)

Negative

Negative

Extreme right axis (−90° to 180°)

LAD, left axis deviation; RAD, right axis deviation.

The Three-Lead Method The quadrant method is incredibly simple once you understand it. But it has a conservative range for a normal axis. If we want to expand the normal range to −30° to +90°, we need to add one more lead to this evaluation method. The three-lead method utilizes leads I, II, and aVF.

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By adding lead II, we can widen the normal range to −30°.

Lead II sits at +60° on the hexaxial diagram. When lead II is positive, the axis must be between −30° and +120°. When combined with a positive complex in lead I, the axis cannot exceed +90° (if it did, lead I would no longer be positive), so it remains in the expanded normal range (−30° to +90°).

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292 MASTERING THE 12-LEAD EKG

TABLE 14.2 Parameters of the Three-Lead Method Expanded Normal Axis (0° to −30°)

LAD (−30° to −90°)

RAD (90° to 180°)

ERAD (−90° to −180°)

Lead

Normal Axis (−30° to +90°)

Lead I

Positive

Positive

Positive

Negative

Negative

Lead II

Positive

Equiphasic

Negative

Positive

Negative

aVF

Positive

Negative

Negative

Positive

Negative

ERAD, extreme right axis deviation; LAD, left axis deviation; RAD, right axis deviation.

Equiphasic Lead Method The last technique is called the equiphasic method. It can give us a much more precise estimate of the electrical axis. In fact, it will get us within 30° of the actual axis. This technique also utilizes the hexaxial diagram with the four laws of EKG. Remember: A wave of depolarization moving perpendicular to a positive electrode will record a biphasic wave. When a biphasic wave is equiphasic (R = S), the wave of depolarization is 90° from that lead. To use this method, first find the limb lead with the most equiphasic QRS complex. This type of complex is not always present. In the following example, the most equiphasic lead is lead aVL. Using the hexaxial diagram, we know that lead aVL sits on the left side of the chest at –30. Because aVL is nearly equiphasic, our axis is approximately 90 degrees away from aVL (+60 or –120).

Next, find the lead(s) with the tallest R wave or R/S ratio. A wave of depolarization traveling toward a positive electrode will create a positive wave. Those with the tallest R waves are in the most direct line of site. On this EKG, lead II has the tallest R wave. Finally, calculate the axis. The axis will be approximately 90° from the most equiphasic lead and pointing in the direction of the positive leads. In this example, leads II, III, and aVF are upright. This tells us that the axis is pointing toward the bottom of the hexaxial diagram, not the top. Therefore, our axis is +60°.

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294 MASTERING THE 12-LEAD EKG

We can confirm the accuracy of our axis by looking at the computer calculation of the axis in the upper left-hand corner. It tells us the axis is +87°. Oh, did I forget to tell you that the computer calculates the axis? Oops.

The Computer The 12-lead EKG computer usually calculates the axis of atrial depolarization (P), ventricular depolarization (QRS), and ventricular repolarization (T). It tends to be accurate, but it can make mistakes. A master EKG interpreter will be familiar with at least one method of manually calculating the axis.

Systematic Approach

1. 2. 3. 4.

What’s the rate? Is the rhythm regular or irregular? Is the QRS narrow or wide? Are P waves present? Are they upright in I and II and inverted in aVR? Are there too many P waves? 5. What’s the duration of the PR interval? Does it remain the same, increase, or randomly change? 6. What’s the axis?

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TAKE-HOME POINTS • Heart’s electrical axis ▪ Primary direction of depolarization of the ventricles in the frontal plane • Calculating the axis requires understanding of the hexaxial diagram and the four laws of EKG • Axis ▪ Normal: −30° to +90° ▪ LAD: −30° to −90° ▪ RAD: +90° to ±180° ▪ ERAD: ±180° to −90°

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296 MASTERING THE 12-LEAD EKG

EXERCISES 1. List the four types of conditions that can cause a shift in the axis. 1. 2. 3. 4. 2. Name four potential causes for left axis deviation. List four potential causes for right axis deviation. 1. 2. 3. 4. 3. Axis points ______________________ hypertrophy. 4. Axis points ________________________ from myocardial infarction. 5. Draw the hexaxial diagram with angles of orientation.

On each of the following EKGs: Calculate the rate; determine if the rhythm is regular or irregular; note if the QRS is narrow or wide; determine if P waves are present, and if they are present, are they upright or inverted; measure the PR interval, and interpret the axis. If the axis is abnormal, list three potential causes.

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1.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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2.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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3.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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4.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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5.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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6.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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7.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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8.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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9.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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10.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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11.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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12.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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13.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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14.

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PR duration: ___________________

Axis: ___________________

Final interpretation: ___________________

P waves: Present, not present, upright, or inverted __________________________

Rhythm: Regular or irregular __________________________

QRS: Narrow or wide __________________________

Rate: ____________________

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REFERENCE/RESOURCE Dubin, D. (2000). Rapid interpretation of EKGs (6th ed.). Tampa, FL: Cover Publications.

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Chapter

15

Bundle Branch Blocks One or multiple fascicles of the right or left bundle branches can fail to depolarize the ventricles. This halt in conduction is called a fascicular or bundle branch block. These blocks are named after the fascicle or bundle that is affected.

IS THE QRS NARROW OR WIDE? Throughout the book we have talked about the importance of measuring the QRS complex and noting if it is narrow or wide. This important step helps us to determine the most likely origin of the rhythm. By now you know that a narrow QRS complex means that the rhythm originated above the ventricles. I hope you also remember that all rhythms that begin in the ventricles have a wide QRS complex. But not all rhythms with a wide QRS are ventricular in origin. In this chapter we discuss supraventricular rhythms that have a wide QRS due to aberrant/abnormal conduction through the His-Purkinje system. This aberrant conduction is due to failure of one or more fascicles of the bundle branches to transmit the impulse to the ventricles. We call this type of abnormality a bundle branch block (BBB). They are named after the fascicle or bundle that is affected. There are two main bundles branches, right and left, which develop off the bundle of His. Both follow along the septal surface of each respective ventricle. After separating from the bundle of His, the left branch quickly separates into two distinct fascicles, one anterior and the other posterior. The right branch, however, remains a single fascicle until reaching the end of the distal interventricular septum.

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NORMAL CONDUCTION After a wave of depolarization reaches the atrioventricular (AV) node, the impulse travels down the bundle of His. It then spreads out through the bundle branches. The left bundle fires ever so slightly before the right, causing the left side of the interventricular septum to depolarize first (phase 1). Depolarization continues down the bundle branches and into the Purkinje fibers, depolarizing the right and left ventricles simultaneously (phase 2). Normal depolarization of the ventricles is completed in 0.10 second or less. When depolarization fails to move normally through the His-Purkinje system because of a BBB, ventricular depolarization takes longer. This results in a

QRS complex that is greater than 0.12 second.

THE QRS COMPLEX There are two distinct phases of ventricular depolarization that form the QRS complex: Phase 1: Left to right depolarization of the interventricular septum

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Phase 2: Right to left vector during ventricular depolarization, with the vector going toward the larger left ventricle

Although this activity is represented in every lead, the direction of depolarization is most easily noted by looking at leads V1 and V6. V1 is the farthest right-sided chest lead. Depolarization moving to the right should cause a positive deflection in V1. When the impulse is moving to the left, it will be negative. The opposite is true for V6, the lead farthest to the left on the chest. When depolarization is moving to the left, V6 will create a positive deflection. When moving to the right, V6 will be negative. Using these two leads, we can easily gather valuable information about the direction of depolarization occurring in the ventricles.

Normal ventricular depolarization causes a predictable pattern of the R wave height in the chest leads. V1 starts with a small r wave that gradually increases in size as the perspective of the leads changes across the precordium. Somewhere around V3 or V4, the R wave should be nearly as tall as the S wave is deep (transition zone). From there, the height continues to grow until it maxes out at V5 or V6. This is known as R wave progression. When ventricular depolarization is abnormal, as in a BBB, the R waves and QRS patterns will change from their typical appearance. To make the diagnosis of a BBB we need to not only note the width of the QRS but also note the morphology of the QRS complex.

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Bundle branch blocks will have a predictable QRS morphology that is often easiest to see in V1 and V6.

BUNDLE BRANCH BLOCKS Right Bundle Branch Block Right bundle branch block (RBBB) is a fairly common finding on the EKG (0.2%–0.8%). It can be seen in healthy individuals as well as in those with organic heart disease. Its incidence increases with age. It is caused by failure of the right bundle to transmit an impulse to the ventricles. It may be permanent or transient. It can come and go based on variations in the heart rate (rate dependent). Remember, the right bundle has a longer refractory period than the left bundle. If the rate is fast, the right bundle may not be ready to depolarize and this will result in an intermittent RBBB. As you consider RBBB, remember the two phases that create the QRS complex. The first phase is a left to right depolarization of the interventricular septum. This is created by the early firing of the left bundle branch. A block of the right bundle will not impact phase 1. This deflection on the EKG remains undisturbed. V1 shows an initial positive wave, V6 negative. In phase 2, the vector shifts back toward the left ventricle. In normal conduction, both ventricles depolarize simultaneously, with the vector shifting laterally owing to the larger mass of the left ventricle. When an RBBB occurs, right ventricular depolarization is delayed. The left ventricle depolarizes first and the wave points to the left. Phase 2 of the QRS complex will not be affected by the RBBB. V1 will be negative, V6 positive. So far things are looking pretty good. However, the right ventricle still needs to complete depolarization. It is waiting on the impulse to come from the left bundle/Purkinje fibers. This creates a third phase in which the vector shoots back to the right to complete depolarization of the right ventricle.

The final portion of the QRS complex is shifted toward the final portion of the ventricles being depolarized. This is usually the dominant/largest deflection. The abnormal depolarization leads to a diagnostic QRS morphology (rsr′), sometimes referred to as “rabbit ears” in V1/V2. The second rabbit ear will always be taller than the first. The delayed activation of the right ventricle also creates a QRS that is wider than normal.

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Characteristics of Right Bundle Branch Block 1. Wide QRS complex (>0.12 second). This is caused by delayed depolarization of the right ventricle. 2. QRS morphology: rsr′, rsR′, or rSR′ in V1 or V2. Some people refer to this as “rabbit/ bunny ears.” It may also appear as a wide notched R wave if phase 2 does not cross the baseline. QRS may have a slurred S in the lateral leads (I, aVL, V5, V6).

Notched R in V2 consistent with RBBB.

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318 MASTERING THE 12-LEAD EKG

3. ST-T wave discordance. The ST-T changes are often minimal, but discordant when present. T waves are frequently inverted in the right chest leads (V1–V2) as a result of the conduction delay.

A right bundle branch block has a wide QRS with an rsr’ morphology in V1 or V2.

Source: A. Rad. (2006, January 2). Right bundle branch block ECG characteristics [Image file]. Retrieved from https://en.wikipedia.org/wiki/File:Right_bundle_branch_block_ECG _characteristics.png

Right bundle branch block. Wide QRS. sR’ in V1, notched R in V2.

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Sinus bradycardia with right bundle branch block. rSR’ in V1 and V2.

Causes/Treatment Many patients have no underlying heart disease or disorder. The cause of RBBB in these situations is unclear. Conditions that affect the right side of the heart can result in an RBBB. Examples include atrial septal defect, chronic obstructive pulmonary disease (COPD), pulmonary artery hypertension, and pulmonary embolism. Patients with acute myocardial infarction (MI) may develop an RBBB, usually related to occlusion of the left anterior descending artery. The block itself requires no treatment. Just make sure it isn’t the result of something you need to treat.

Causes of Right Bundle Branch Block

Degenerative change/age, cor pulmonale, right ventricular hypertrophy, pulmonary embolism, myocardial ischemia/infarction, myocarditis, hypertension

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Incomplete Bundle Branch Block

If the QRS morphology is consistent with a bundle branch block, but the duration is 0.10 to 0.12 second, it is called incomplete. This is usually related to slowing of conduction through the affected bundle.

Left Bundle Branch Block Left bundle branch block (LBBB) is less common than RBBB; however, it is almost always the result of heart disease or other pathology. It affects between 0.06% and 0.1% of the general population. It is usually caused by a proximal block of the left bundle, affecting both the anterior and posterior fascicles. LBBB may be permanent, transient, or rate dependent. When considering LBBB, it is helpful to remember the normal phases of ventricular conduction. Phase 1 is created by early depolarization of the left bundle. This causes a left to right depolarization of the interventricular septum. Because the left bundle is blocked, the initial phase is unable to be completed. The septal wave is lost. V1 and V6 lose their initial QRS deflection. A normal phase 2 is created by simultaneous depolarization of the right and left ventricles. Because of the larger mass of the left ventricle, the vector points toward the left. This creates a negative deflection in V1 and positive deflection in V2. Although depolarization is not simultaneous in an LBBB, this phase is undisturbed. The impulse that began in the right ventricle is traveling leftward. The left ventricle must wait on the impulse to travel from the right side of the heart. Therefore the length of depolarization of the left ventricle is prolonged. This results in a wide QRS complex. Remember, the final portion of the QRS shifts toward the final portion of myocardium that is being depolarized.

Characteristics of Left Bundle Branch Block 1. Wide QRS complex (>0.12 second). Because the left bundle has failed, it takes longer for ventricular depolarization to be completed. 2. V1 has a QS complex. On rare occasion, a small r wave may still be seen (rS). The QS can also be notched and resemble “W.” 3. V6 has tall wide R waves. The R wave may be notched and resemble an “M” in V6. The tall R waves are also seen in the other lateral leads (I, aVL, V5–V6). 4. Lateral leads will not have Q waves. Phase 1 is missing in an LBBB and so are the q waves that represent it. 5. Appropriate ST-T wave discordance. When the QRS is negative the ST segment may be elevated. This makes the diagnosis of MI more difficult when LBBB is present. In

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Chapter 19, Infarction Detection on the EKG, we discuss validated criteria for diagnosing an MI in the presence of an LBBB (Sgarbossa criteria). 6. Left axis deviation may be present. 7. Poor R wave progression. Normally, the R waves should gradually increase in height throughout the chest leads. By V3 to V4, the r and s waves should be near equal in size. When an LBBB is present, this progression is delayed.

An LBBB has a wide QS complex in V1 and tall R wave in V6.

Sinus tachycardia (rate about 125 beats/minute) with left bundle branch block. Note wide QRS (0.12 second) with entirely negative QS complex in V1. Tall R in V6 with no preceding q wave, similar in all lateral leads (I, aVL, V5–V6). Appropriate ST-T discordance.

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Sinus bradycardia (rate around 55 beats/minute) with left bundle branch block. Wide QRS (0.16 second). QS in lead V1. Tall wide R in V6. Appropriate ST-T discordance. Left axis deviation (lead I upright, aVF negative).

Sinus rhythm with left bundle branch block. Note wide QRS with entirely negative QS complex in V1.

Causes LBBB is usually the result of a pathologic condition. It has been associated with an increase in allcause mortality rate of older patients. Its presence may provide a clue to undiscovered advanced coronary artery disease, valvular heart disease, hypertensive heart disease, or other type of cardiomyopathy. If it is newly discovered, patients should undergo evaluation for potential causes.

Treatment If the QRS duration is greater than 0.15 second and the patient has heart failure due to a reduced ejection fraction, a biventricular pacemaker may be helpful. This device is used to synchronize ventricular depolarization and improve cardiac output. It is known as cardiac resynchronization therapy (CRT).

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Causes of Left Bundle Branch Block

Acute anterior myocardial infarction, dilated cardiomyopathy, degenerative disease of conduction system, hypertension, coronary artery disease, myocardial ischemia, digoxin toxicity, hyperkalemia

Tip You will soon be learning how to diagnose an MI on the EKG. One of the ways an MI can show up is by the presence of Q waves. LBBB and septal/anterior MIs with Q waves (V1–V3) can look very similar. Be careful not to confuse the two. Carefully measure the duration of the QRS complex and look closely at V6 for a tall R wave with no preceding q wave. Unfortunately, these two problems can occur together and make for a challenging diagnosis. This will require special criteria you will learn about in Chapter 19, Infarction Detection on the EKG.

FASCICULAR BLOCKS The left bundle branch is made up of two primary fascicles: The anterior depolarizes the anterior, superior, and lateral walls of the left ventricle. And the posterior depolarizes the inferior and posterior portions of the left ventricle. Fascicular blocks, also called hemiblocks by some, occur when one of the fascicles of the left bundle stops conducting, but the other remains functional. These blocks affect the direction of depolarization. Fascicular blocks do not significantly impact the duration. Because they affect the direction of depolarization,

you must be able to calculate the QRS axis to find fascicular blocks.

Left Anterior Fascicular Block Left anterior fascicular block (LAFB) is the most common type of hemiblock. It is seen in approximately 2.5% of individuals, and the incidence increases with age. The anterior fascicle can be damaged by high pressures that occur in the left ventricular outflow tract where the fascicle crosses. Among other things, disease in the left anterior descending coronary artery may be the cause.

Characteristics of Left Anterior Fascicular Block 1. Left axis deviation, −45 to −90 degrees. The anterior fascicle is responsible for the anterior/superior and lateral walls. When conduction is blocked, the initial impulse travels posteriorly and inferiorly. Once that portion of the myocardium is depolarized, the

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main vector then shifts toward the anterior/superior and lateral heart. This also shifts the axis in the same direction, creating a left axis deviation. 2. QRS morphology: qR or R in lateral leads (I, aVL). This too is the result of abnormal depolarization of the ventricles. The initial small deflection travels posteriorly and inferiorly, creating the small q, when present. The final large deflection back to the anterior/superior and lateral walls creates the large R. Remember, the final portion of the QRS complex is shifted toward the final portion of the ventricles to be depolarized. This is usually the dominant deflection. 3. QRS duration less than 0.12 second, often less than 0.10 second.

LAFB leads to left axis deviation and a mild prolongation of the QRS complex with a qR morphology in the lateral leads.

Sinus rhythm (rate about 75 beats/minute), premature atrial contraction (9th beat) with LAFB. Left axis deviation. qR in lateral leads (I, aVL). QRS is narrow.

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Sinus rhythm with LAFB. Left axis deviation. qR in lateral leads (I, aVL). QRS is narrow.

Causes LAFB can be a nonspecific finding. It may be the result of damage to the fascicle from high flow pressures that occur in the left ventricular outflow tract, where it sits. Severe disease to the left anterior descending coronary artery may also lead to an LAFB. Other causes include hypertension, neuromuscular disease, and aging (8% of patients over 90).

Treatment Patients are asymptomatic. If the LAFB is isolated and unrelated to a pathologic condition, no treatment or further investigation is necessary. If there is underlying neuromuscular disease, patients may receive a pacemaker. The pacemaker is not to correct the LAFB, but is prescribed because of the high risk for further deterioration of the conduction system.

Left Posterior Fascicular Block Isolated left posterior fascicular block (LPFB) is a rare occurrence. It usually occurs along with RBBB. Because fascicular blocks mainly affect the direction of current, the axis shifts significantly to the right when LPFB occurs.

Characteristics of Left Posterior Fascicular Block 1. Right axis deviation, usually greater than +120 degrees, but can be as little as +90 degrees. The block in the posterior fascicle causes the initial wave of depolarization to aim left, anteriorly, and superiorly. The final and main deflection of the QRS complex then completes depolarization of the right, posterior, and inferior portions of the myocardium. This also shifts the axis to the right. 2. QRS morphology: rS in the lateral leads (I, aVL), qR in the inferior leads (II, III, aVF). Initial depolarization is left toward the lateral leads and superior. The main and final vector then shifts away from the lateral leads and inferiorly. Q wave should always be seen in lead III. It might be small or absent in aVF.

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3. QRS duration less than 0.12 second. Although altered direction of current is the main effect of a fascicular block, a slight prolongation of interventricular conduction occurs.

LPFB causes right axis deviation and a mild prolongation of the QRS complex with a qR morphology in the inferior leads. The diagnosis of LPFB should only be made after other causes of right axis deviation are excluded. See Chapter 13, EKG Artifacts, for a complete list.

Sinus bradycardia with LPFB. Right axis deviation. qR in inferior leads (II, III, aVF). Narrow QRS complex.

Causes The rhythm disturbance does not cause symptoms. LPFB can be caused by severe cardiovascular disease, inferior MI, hyperkalemia, myocarditis, and neuromuscular disease. Treat the underlying condition. If neuromuscular disease is present, a permanent pacemaker may be considered because of the potential for further conduction system failure.

BIFASCICULAR BLOCKS The term bifascicular block refers to a combination of an RBBB and an LAFB or LPFB. Bifascicular blocks can be identified by recognizing the typical findings for RBBB and the abnormal axis associated with the fascicular block. Although conduction of the ventricles is dependent upon a single remaining fascicle, only 1% of asymptomatic individuals go on to develop complete (third-degree) heart block.

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Sinus tachycardia with bifascicular block. RBBB + LAFB. rsR’ in V1. qRS in lateral leads (I, aVL), left axis deviation. Terminal S is due to the presence of RBBB.

Causes Causes for bifascicular blocks are essentially the same as for every other AV block. They can be caused by myocardial ischemia, medications that slow AV conduction, and neuromuscular disease. MI, myocarditis, and hyperkalemia may also be to blame.

Treatment Patients with bifascicular blocks are usually asymptomatic. As always, look for reversible causes. If the patient has presyncope or syncope prior to arrival, he or she may be experiencing intermittent complete heart block. The patient should be admitted, and consideration given to placement of a permanent pacemaker.

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Systematic Approach

A wide QRS can be the result of a ventricular arrhythmia, but it can also be due to aberrant conduction through the His-Purkinje system. This abnormal conduction can be caused by a block in one or more of the fascicles of the bundle branches. Now that you know how to identify them, add the following question to step 3 in your systematic approach. When you see a wide QRS, ask yourself, does it have a bundle branch block morphology? 1. 2. 3. 4. 5.

What’s the rate? Is the rhythm regular or irregular? Is the QRS narrow or wide? If it’s wide, does it have a BBB morphology? Are P waves present? Are they upright in I and II and inverted in aVR? What’s the duration of the PR interval? Does it remain the same, increase, or randomly change? 6. What’s the axis?

TAKE-HOME POINTS • Bundle branch blocks ▪ Aberrant conduction due to failure of one or more fascicles of the bundle branches ▪ Named based on location of block ▪ QRS is wide (≥0.12 second) ▪ Have unique QRS morphology

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EXERCISES 1. Describe the two phases of normal ventricular depolarization.

2. When the QRS morphology is consistent with a bundle branch block, but the duration is 0.10 to 0.12 second, it is called an _____________________ bundle branch block. 3. The QRS morphology of an RBBB is _____________________ in V1. 4. The QRS morphology of an LBBB is _____________________ in V1 and _____________ in V6. On each of the following EKGs: Calculate the rate, determine if the rhythm is regular or irregular, note if the QRS is narrow or wide and if a BBB is present, evaluate the P waves, measure the PR interval, and interpret the axis.

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1.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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2.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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3.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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4.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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5.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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6.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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7.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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8.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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9.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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10.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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11.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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12.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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13.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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14.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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15.

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PR duration: _________________

QRS: Narrow or wide ________________

Axis: ______________

Final interpretation: ________________________

P waves: Present, not present, upright, or inverted ______________

Rhythm: Regular or irregular ________________________

BBB present?/type: ___________________

Rate: __________________

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REFERENCES/RESOURCES Eriksson, P., Hansson, P. O., Eriksson, H., & Dellborg, M. (1998). Bundle-branch block in a general male population. Circulation, 98(22), 2494–2500. doi:10.1161/01.cir.98.22.2494 Haataja, P., Nikus, K., Kähönen, M., Huhtala, H., Nieminen, T., Jula, A., . . . Eskola, M. (2013). Prevalence of ventricular conduction blocks in the resting electrocardiogram in a general population: The Health 2000 Survey. International Journal of Cardiology, 167(5), 1953–1960. doi:10.1016/j. ijcard.2012.05.024 Kelley, G. P., Stellingworth, M. A., Broyles, S., & Glancy, D. L. (2006). Electrocardiographic findings in 888 patients ≥90 years of age. American Journal of Cardiology, 98(11), 1512–1514. doi:10.1016/j.amjcard.2006.06.055 Kusumoto, F. M., Schoenfeld, M. H., Barrett, C., Edgerton, J. R., Ellenbogen, K. A.,  Gold, M. R., . . . Varosy, P. D. (2019). 2018 ACC/AHA/HRS guideline on the evaluation and management of patients with bradycardia and cardiac conduction delay. Circulation, 140, e382–e482. doi:10.1161/ CIR.0000000000000628 McAnulty, J. H., Rahimtoola, S. H., Murphy, E., DeMots, H., Ritzmann, L., Kanarek, P. E., & Kauffman, S. (1982). Natural history of “high risk” bundle branch block: Final report of a prospective study. New England Journal of Medicine, 307(3), 137–143. doi:10.1056/NEJM198207153070301 Scherbak, D., & Hicks, G. J. (2019, January). Left Bundle Branch Block (LBBB) [Updated 2019, April 7]. Treasure Island, FL: StatPearls Publishing. Retrieved from https://www.ncbi.nlm.nih.gov/ books/NBK482167

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Chapter

16

Ventricular Hypertrophy Hypertrophy or dilation of the atria and ventricles may cause abnormal findings to appear on the EKG. There are five major categories that should be evaluated on every EKG: 1. Rate 2. Rhythm 3. Axis 4. Hypertrophy 5. Ischemia/infarction We have made it through the first three, now it’s time for number four: hypertrophy. The electrical axis can be a helpful clue to several pathologic conditions of the heart. One of those is myocardial hypertrophy. You may remember that the electrical axis shifts toward the enlarged ventricle. A shift in axis is just one of the changes that can be seen to help us make the diagnosis of hypertrophy. In this chapter we discuss other important findings that can help you to detect this abnormality.

HYPERTROPHY AND DILATION Hypertrophy or dilation of the atria and ventricles may cause abnormal findings to appear on the EKG. Enlargement of the chambers is typically the result of increased pressure, volume overload, or genetic abnormalities. When the myocardium becomes hypertrophic, the muscle has increased in size in an attempt to compensate for the problem. However, the muscle growth that occurs is not normal. The myocytes remodel and become fibrotic tissue that does not stretch and contract normally. The stiff myocardium leads to a decrease in left ventricular function and increases the risk of arrhythmias.

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EKG findings for hypertrophy and dilation are not always very sensitive or specific, but in the right situation they can provide helpful clues to the diagnosis. The best test to detect hypertrophy is an echocardiogram. When EKG changes are present, enlargement is often detected by either an increase in voltage or prolonged depolarization. Here we discuss each chamber and how enlargement can be diagnosed.

Dilation: The heart muscle is stretched. Chamber becomes enlarged. Hypertrophy: Heart muscle increases in size.

ATRIAL ENLARGEMENT Atrial enlargement can be caused by chamber dilation or hypertrophy. Because atrial depolarization is represented by the P wave, the P wave is what we need to evaluate when looking for atrial abnormalities. You may remember from Chapter 2, Electrical Conduction System of the Heart, that the P wave has two parts, often best seen in lead V1’s biphasic wave. The first half of the P wave represents right atrial depolarization, the second, left atrial depolarization.

Right Atrial Abnormality Right atrial abnormality (RAA) is caused by simultaneous depolarization of the atria causing an increase in the voltage. This EKG finding can be the result of hypertrophy or chamber dilation, but can also be secondary to myocardial scarring or a conduction abnormality. Because the abnormal P wave can be related to conditions other than an enlarged right atrium, it is called an “abnormality” rather than hypertrophy. The tall P wave seen in RAA is usually the result of pulmonary disease or congenital heart disease. Because of its association with pulmonary disease, the abnormal P waves are called P pulmonale.

Normal P wave duration: less than 0.12 second Normal P wave height: less than 2.5 mm

Characteristics of Right Atrial Abnormality 1. P wave greater than 2.5 mm amplitude in lead II. The P waves are measured in lead II because of its direct line of sight of the atrial current. The tall narrow P waves are usually best seen throughout the inferior leads (II, III, aVF). The initial positive deflection of the P wave in V1 may be taller than 1.5 mm. The abnormally tall P waves occur because of the increased voltage associated with simultaneous depolarization of both atria. 2. P wave has normal duration: less than 0.12 second. RAA does not affect P wave duration. In fact, owing to the simultaneous depolarization of the right and left atrium, the P wave may be narrow.

To make the diagnosis of RAA, look for a P wave in lead II that is greater than 2.5 mm in height.

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Right atrial abnormality. Note the tall peaked P waves in V1.

Sinus rhythm (rate approx. 80 beats/minute). Tall P waves in multiple leads consistent with RAA. The patient also has a right axis deviation because of right ventricular hypertrophy (discussed later).

Causes Pulmonary disease is one of the most common causes of RAA. This includes acute problems like pulmonary embolism or a chronic condition such as emphysema. Congenital abnormalities such as pulmonary valve stenosis, atrial septal defect, and tetralogy of Fallot may also cause RAA. It can also be seen in healthy individuals with a tall slender frame as a result of the heart assuming a vertical position.

Left Atrial Abnormality Left atrial abnormality (LAA) is the result of delayed left atrial depolarization. The prolonged P wave may be caused by atrial hypertrophy, dilation, or intraatrial conduction defect due to myocardial scarring. It is often seen in the presence of aortic and mitral valve disease. In fact, because it was first associated with rheumatic mitral valve disease, the abnormally prolonged P wave is called P mitrale.

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Characteristics of Left Atrial Abnormality 1. P wave has a normal amplitude: less than 2. 5 mm in height. 2. Notched P wave greater than 0.12 second in lead II. Again, the P wave is evaluated in lead II because it has the best seat in the house for atrial depolarization. There is usually greater than 0.04 second between the two peaks of the bifid P wave. The abnormal P is the result of delayed activation of the left atrium. 3. Terminal negative deflection in V1 greater than or equal to 0.04 second and/or greater than 1 mm in depth. The terminal negative deflection of the P wave in V1 is created by the left atrium. The atrial abnormality can be seen as a prolonged depolarization or an increase in voltage.

The diagnosis of LAA is made by a P wave greater than 0.12 second in duration.

Left atrial abnormality. Note the wide bifid P wave. Duration is just over 0.12 second. The peaks of the P wave are just over 0.04 second apart.

Biphasic P waves are often seen in V1. The terminal/negative portion represents left atrial depolarization. The terminal portion measures over 0.04 second, consistent with left atrial abnormality.

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Biphasic P wave in V1 with terminal portion over 1 mm in depth. Consistent with LAA.

Causes LAA can be caused by valvular heart disease such as mitral valve regurgitation/stenosis and aortic regurgitation/stenosis. It may also be the result of coronary artery disease, hypertensive heart disease, or constrictive pericarditis.

VENTRICULAR ENLARGEMENT EKG changes associated with ventricular enlargement are related to hypertrophy and dilation. Findings of hypertrophy on the EKG include an

increase in voltage, shift in axis, and repolarization abnormalities. The increased voltage of the ventricles is the result of expanded muscle mass or surface size, increased blood volume, or the ventricle’s proximity to the chest wall. You already learned that the axis shifts toward hypertrophy because of increased electrical activity occurring in the enlarged ventricle. Multiple criteria can be used to evaluate the EKG for ventricular hypertrophy. No one method is significantly better than another. Each has varying specificity or sensitivity. Below we discuss some of the common methods used to determine ventricular hypertrophy. It can be easy to be overwhelmed by the amount of material here. Pick a method and become familiar with it. It may also be beneficial to have a pocket guide available as a resource to jog your memory for criteria such as these.

Right Ventricular Hypertrophy An enlarged right ventricle can occur with pulmonary hypertension, pulmonic stenosis, or with significant lung disease. These changes are the result of a prolonged increase in pressure or volume overload over months or years. Below are common criteria that can be used to evaluate the EKG for possible right ventricular hypertrophy (RVH). The more criteria the patient meets, the more likely RVH is present. The best test to evaluate the patient for RVH remains an echocardiogram.

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General Characteristics of Right Ventricular Hypertrophy 1. Tall R waves in right chest leads (V1–V3), R > S. Deep S waves in left chest leads (V4–V6), S > R. Because forces are shifted to the right, the right-sided chest leads have QRS complexes with tall positive R waves. Unfortunately, other conditions can cause similar EKG changes including posterior myocardial infarction (MI), right bundle branch block (RBBB), and Wolff–Parkinson–White syndrome (WPW). 2. Right axis deviation. An electrical axis of greater than or equal to 110 degrees. Remember, axis shifts toward hypertrophy. There are other potential causes for RAD including lateral MI, RBBB, WPW, and chronic obstructive pulmonary disease (COPD). 3. ST-T wave discordance in leads with tall R waves. The tall R waves occur in the right chest leads (V1–V2). ST depression and T-wave inversions may also be seen in the inferior leads (II, III, aVF).

Sinus rhythm (rate approx. 93 beats/minute). Right axis deviation. Right ventricular hypertrophy: Note the tall R waves in the right precordial leads (V1–V3), right axis deviation, and ST depression/T-wave inversions in the leads with tall R waves.

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Specific Criteria for Right Ventricular Hypertrophy The following criteria are specific, but they lack in sensitivity. The list is not all-inclusive. qR in V1 (most specific for severe RVH) Right axis deviation ≥ 110 degrees R/S ratio in V1 >1 R in V1 >7 mm S in V1 ≤2 mm R in V1 + S in V5 or V6 >10.5 mm S > R in leads I, II, and III (S1, S2, S3)

Supporting Evidence Supporting evidence for RVH may include the presence of P pulmonale, ST depression and T-wave inversions in the right chest leads, and deep S waves in the lateral leads.

Causes Causes of RVH include pulmonary hypertension, mitral stenosis, pulmonary embolism, chronic lung disease, and congenital heart disease.

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Left Ventricular Hypertrophy Left ventricular enlargement is due to pronged pressure or volume overload. Conditions such as systemic hypertension and aortic stenosis/regurgitation can be the cause. As with RVH, there are many suggested EKG criteria to evaluate the patient for left ventricular hypertrophy (LVH). Although many are specific (80%–90%), they are not very sensitive (30%–60%). The more criteria present, the more likely LVH is present.

General Characteristics of Left Ventricular Hypertrophy 1. Increased R wave amplitude in left-sided/lateral leads (I, aVL, V4–V6). S waves are deeper in right-sided leads (III, aVR, V1–V3). Increased voltage is due to increased mass of the left ventricle. 2. Left axis deviation. Axis shifts toward the hypertrophied left ventricle. 3. ST-T wave discordance. This is the result of delayed repolarization in the thickened left ventricle. It is more common in patients with coronary artery disease and larger ventricular mass.

Sinus rhythm (rate approx. 75 beats/minute). Slight left axis deviation. Left ventricular hypertrophy. Note the tall R waves in the left-sided chest leads and the deep S in the right-sided chest leads. ST-T-wave depression is seen in leads with tall R waves.

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Voltage Criteria for LVH When the myocardium increases in size, voltage often increases as well. This makes it the most sensitive way to detect LVH. However, it is also the cause of many false positives. To reduce the false-positive diagnoses, it should only be used in patients over the age of 40. It can also be combined with other findings suggestive of LVH such as left axis deviation, ST-T changes, and presence of LAA. Below is a sample of commonly used voltage criteria.

Sokolow–Lyon Criteria Among the most commonly used measurements are the Sokolow–Lyon criteria, published in the American Heart Journal (Sokolow & Lyon, 1949). The following criterion combines the voltage of the most left-sided and right-sided chest leads: S wave in V1 + R wave in V5 or V6 (use tallest) greater than or equal to 35 mm

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Other criteria created in the studies by Sokolow and Lyon are listed below. They can be utilized if the QRS is less than 0.12 second. The list is not exhaustive. R wave in aVL >11 mm (most specific for LVH) R wave in aVF >20 mm S wave in aVR >14 mm R wave in lead I + S wave in lead III greater than 25 mm

R wave in aVL >11.

Cornell Voltage Criteria A group of physicians from Cornell developed gender-specific voltage criteria and published the results in Circulation (Casale, Devereux, Alonso, Campo, & Kligfield, 1987). S in V3 + R in aVL >28 mm (men) S in V3 + R in aVL >20 mm (women)

Romhilt–Estes Point-Score System Romhilt and Estes (1968) developed a point-score system that combines voltage, QRS duration, R wave peak time, and axis. R wave peak time, or intrinsicoid deflection, is the time measured from the beginning of the QRS complex to the peak of the R wave. A score of 5 is considered “definite” LVH. A score of 4 is “probable” LVH. TABLE 16.1 Romhilt–Estes Point System Criterion

Points

Amplitude (any of the following): Largest R or S wave in any limb lead ≥20 mm S in V1 or V2 ≥30 mm R in V5 or V6 ≥30 mm

3

ST depressions or T-wave inversions in lateral precordial, I, and/or aVL

3

Left atrial enlargement

3

Left axis deviation

2

QRS duration ≥90 ms

1

Intrinsicoid deflection in V5 or V6 ≥50 ms

1

4 points, probable LVH; 5 points, definite LVH. LVH, left ventricular hypertrophy.

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Sinus rhythm (rate approx. 65). Left axis deviation. Left ventricular hypertrophy: Large R waves in left chest leads and deep S waves in right chest leads. ST-T-wave discordance. Sokolow–Lyon criteria met.

Voltage Stumbling Blocks Certain conditions can create false positives or a potential missed diagnosis of LVH on the EKG. Young healthy patients, particularly men, often have increased voltage and can mimic LVH voltage criteria. Because of this, voltage criteria should be used cautiously to make a diagnosis in patients under the age of 40. Look for other supportive findings such as repolarization abnormalities or a left axis deviation. Voltage can be increased in women with previous mastectomy, causing an incorrect diagnosis of LVH. Thin cachectic patients may also have an increase in voltage. African Americans can also have an increase in voltage unrelated to LVH. Voltage is decreased in obese patients or those with large breasts. This may cause LVH to be overlooked. Low hematocrit has also been known to decrease QRS voltage.

Causes/Outcomes LVH can be the result of volume overload and increased pressures caused by conditions such as systemic hypertension and aortic stenosis. Patients with LVH are at increased risk for cardiovascular complications such as heart failure and ventricular arrhythmias. They also have an increase in all-cause mortality and sudden cardiac death rates.

FINAL THOUGHTS The sensitivity and specificity of EKG changes related to chamber enlargement is not ideal. However, the EKG remains a useful tool for determining hypertrophy. It allows for a quick and inexpensive way to evaluate your patient for cardiac disease. If questions remain about chamber enlargement or abnormalities, an echocardiogram should be ordered and further evaluation completed.

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CASE STUDY 16.1 HPI: A 47-year-old man presents to the office for a routine checkup. Because of a lack of insurance, he has not been seen by a provider in several years. But after obtaining a policy through his new employer, he has decided to be evaluated. Other than an occasional complaint of sharp right shoulder pain when reaching over his head, he has no complaints. Past Medical/Social History: Tonsillectomy at age 8; denies smoking or alcohol use Family History: Hypertension Allergies: NKDA Medications: None Vital Signs: BP 176/88, RR 12, Temp 97.7°F, Wt 197 lb, Ht 5′11″

Physical Exam General: No acute distress Neuro: Awake, alert, and oriented HEENT: Head is normocephalic and atraumatic Neck: No carotid bruit; no JVD Pulmonary: Lungs are clear to auscultation bilaterally Cardiovascular: Heart rate is regular with no murmurs; extremities are non-edematous Abdomen: Abdomen is soft, non-distended, non-tender; bowel sounds are normal and active in all four quadrants Skin: No rashes are noted on the visible skin Routine labs and imaging were performed for wellness exam including an EKG.

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Thought Questions 1. What type of chamber enlargement do you suspect based on the EKG? 2. What does the EKG tell you is likely about the patient’s elevated blood pressure? 3. What test would provide the definitive diagnosis about the suspected chamber enlargement?

Systematic Approach

Time to add yet another step to your systematic approach to interpreting the 12-lead EKG. Look for evidence of atrial or ventricular hypertrophy. 1. 2. 3. 4.

What’s the rate? Is the rhythm regular or irregular? Is the QRS narrow or wide? Are P waves present? Are they upright in I and II and inverted in aVR? Are there too many P waves? 5. What’s the duration of the PR interval? Does it remain the same, increase, or randomly change? 6. What’s the axis? 7. Is there evidence of atrial/ventricular hypertrophy?

TAKE-HOME POINTS • The EKG can provide helpful clues about hypertrophy of the atria and ventricles. • Atrial enlargement ▪ Right atrial abnormality, a.k.a. P pulmonale ○ P wave greater than 2.5 mm amplitude in lead II ▪ Left atrial abnormality, a.k.a. P mitrale ○ Notched P wave greater than 0.12 second in lead II • Ventricular enlargement ▪ Based on several criteria that include evaluating the voltage, axis, and looking for repolarization abnormalities ▪ Criteria can be specific but not very sensitive. ○ Left ventricular hypertrophy ◽ R wave greater than 11 mm in aVL is most specific. ○ Right ventricular hypertrophy ◽ qR in V1 is most specific.

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EXERCISES 1. The normal P wave duration is ____________. The normal P wave height is __________. 2. List at least three specific criteria to diagnose right ventricular hypertrophy. Name three potential causes of RVH.

3. List at least three specific criteria to diagnose left ventricular hypertrophy. Name three potential causes of LVH.

4. When can using voltage criteria to diagnose ventricular hypertrophy cause a missed or incorrect diagnosis?

On each of the following EKGs: Calculate the rate; determine if the rhythm is regular or irregular; note if the QRS is narrow or wide; if a bundle branch block is present, evaluate the P waves; measure the PR interval; look for evidence of hypertrophy, and interpret the axis.

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1.

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Rhythm: Regular or irregular ______________

Evidence of hypertrophy: ______________

PR duration: _____________________

Axis: ______________

QRS: Narrow or wide ______________

Final interpretation: ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

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2.

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Rhythm: Regular or irregular ______________

Evidence of hypertrophy: ______________

PR duration: _____________________

Axis: ______________

QRS: Narrow or wide ______________

Final interpretation: ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

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3.

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Rhythm: Regular or irregular ______________

Evidence of hypertrophy: ______________

PR duration: _____________________

Axis: ______________

QRS: Narrow or wide ______________

Final interpretation: ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

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4.

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Rhythm: Regular or irregular ______________

Evidence of hypertrophy: ______________

PR duration: _____________________

Axis: ______________

QRS: Narrow or wide ______________

Final interpretation: ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

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5.

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Rhythm: Regular or irregular ______________

Evidence of hypertrophy: ______________

PR duration: _____________________

Axis: ______________

QRS: Narrow or wide ______________

Final interpretation: ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

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6.

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Rhythm: Regular or irregular ______________

Evidence of hypertrophy: ______________

PR duration: _____________________

Axis: ______________

QRS: Narrow or wide ______________

Final interpretation: ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

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7.

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Rhythm: Regular or irregular ______________

Evidence of hypertrophy: ______________

PR duration: _____________________

Axis: ______________

QRS: Narrow or wide ______________

Final interpretation: ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

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8.

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Rhythm: Regular or irregular ______________

Evidence of hypertrophy: ______________

PR duration: _____________________

Axis: ______________

QRS: Narrow or wide ______________

Final interpretation: ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

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9.

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Rhythm: Regular or irregular ______________

Evidence of hypertrophy: ______________

PR duration: _____________________

Axis: ______________

QRS: Narrow or wide ______________

Final interpretation: ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

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10.

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Rhythm: Regular or irregular ______________

Evidence of hypertrophy: ______________

PR duration: _____________________

Axis: ______________

QRS: Narrow or wide ______________

Final interpretation: ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

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11.

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Rhythm: Regular or irregular ______________

Evidence of hypertrophy: ______________

PR duration: _____________________

Axis: ______________

QRS: Narrow or wide ______________

Final interpretation: ______________

P waves: Present, not present, upright, or inverted ______________

Rate: ______________

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REFERENCES/RESOURCES Casale, P. N., Devereux, R. B., Alonso, D. R., Campo, E., & Kligfield, P. (1987). Improved sex-specific criteria of left ventricular hypertrophy for clinical and computer interpretation of electrocardiograms: Validation with autopsy findings. Circulation, 75(3), 565–572. doi:10.1161/01.cir.75.3.565 Mirvis, D. M., & Goldberger, A. L. (2019). Electrocardiography. In D. P. Zipes, P. Libby, R. O. Bonow, D. L. Mann, & G. F. Tomaselli (Eds.), Braunwald’s heart disease: A textbook of cardiovascular medicine (11th ed., pp. 117–153). Philadelphia, PA: Elsevier. Myers, G. B., Klein, H. A., & Stofer, B. E. (1948). The electrocardiographic diagnosis of right ventricular hypertrophy. American Heart Journal, 35(1), 1–40. doi:10.1016/0002-8703(48)90182-3 Oreto, G., Luzza, F., Donato, A., Satullo, G., Calabrò, M. P., Consolo, A., & Arrigo, F. (1992, May). Electrocardiographic changes associated with haematocrit variations. European Heart Journal, 13(5), 634–637. doi:10.1093/oxfordjournals.eurheartj.a060227 Romhilt, D. W., & Estes, E. H. (1968). Point-score system for the ECG diagnosis of left ventricular hypertrophy. American Heart Journal, 75, 752. doi:10.1016/0002-8703(68)90035-5 Sokolow, M., & Lyon, T. P. (1949). The ventricular complex in right ventricular hypertrophy as obtained by unipolar precordial and limb leads. American Heart Journal, 38(2), 273–294. doi:10.1016/0002-8703(49)91335-6

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Chapter

17

Causes of ST Elevation and Depression on the EKG ST-T changes can be caused by numerous things including ischemia and infarction. It is important to be familiar with the potential causes so you can make the right diagnosis. Evaluating the ST segment and T wave for abnormalities is crucial, as they are important in identifying the warning signs of ischemia and infarction. Unfortunately, the concerning diagnoses of ischemia and infarction are not the only conditions that can cause changes in the ST segment and T wave. We need to be familiar with all the potential possibilities so we can recognize what sets them apart and make the correct diagnosis. As you have already learned, discordance that causes ST elevation can be seen in conditions such as left ventricular hypertrophy (LVH) and left bundle branch block (LBBB). Normal variants, inflammation of the pericardium, pulmonary disease, and even intracranial bleeds can cause ST-T changes that can make our interpretation more difficult. Before diving into ST-T changes associated with ischemia and infarction, let’s review some common causes of ST-T abnormalities and introduce a few new important differentials to consider.

ST-T WAVE The ST segment and T wave represent ventricular repolarization. Under most normal circumstances the ST segment should be flat/isoelectric. T waves should be upright in all leads, except for aVR and V1, where they are inverted. An inverted T wave is occasionally a normal finding in

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lead III. The T-wave height is typically less than 10 mm in the limb leads and 5 mm in the precordial leads. It is asymmetric with a slow rise to the top and a quick descent.

ST ELEVATION Left Bundle Branch Block When the left bundle fails to transmit an impulse to the ventricles, the QRS becomes abnormally wide and takes on a recognizable morphology in the right (QS) and left chest leads (tall R). Not only is ventricular depolarization abnormal, ventricular repolarization also displays changes called appropriate discordance. The ST shifts in the opposite direction of the major deflection of the QRS. When the QRS is mainly positive, the ST will demonstrate depression. When the QRS is mainly negative, as in leads V1–V3, the ST can be elevated, mimicking an anteroseptal myocardial infarction (MI). Because LBBB typically occurs in patients with heart disease, it is no surprise that it can be seen at the same time as an MI. The Sgarbossa criteria have been developed to help make the right diagnosis in this circumstance.

Sinus bradycardia with left bundle branch block, rate 55, left axis deviation. Note the wide QRS (0.16 second), QS in V1 and tall R in V6. The ST elevation and depression is caused by the LBBB and resultant ST-T discordance.

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Left Ventricular Hypertrophy Conditions such as long-standing hypertension or aortic stenosis/regurgitation can cause the left ventricle to enlarge. This can be identified on the EKG by an increase in QRS voltage. Commonly used diagnostic criteria include Sokolow–Lyon (S in V1 + R in V5 or V6 ≥35 mm) and the height of the R wave in aVL (>11 mm). Appropriate discordance is a common finding associated with LVH. This produces ST elevation in leads with deep S waves and ST depression in leads with tall R waves. The ST elevation is most commonly seen in V2–V3.

Sinus rhythm, rate 65, left axis deviation, left ventricular hypertrophy. The ST elevation and depression is caused by left ventricular hypertrophy and the resultant ST-T discordance.”

Pericarditis Pericarditis is defined as inflammation of the pericardial sac. It may be caused by trauma, systemic inflammatory disease, or bacterial or viral infections. Some reports say that it makes up 5% of patients who present to the ED with nonischemic chest pain. The pain is often described as sharp or pleuritic and made more comfortable by sitting up and leaning forward. The patient may have a friction rub on physical exam. Pericarditis, particularly when caused by a virus such as coxsackie, is responsible for classic changes on the EKG.

Characteristics of Pericarditis 1. Widespread concave ST elevation is seen in multiple leads, both chest and limb. Although it is possible to have an MI affect several leads, it is uncommon. This “saddleback” ST morphology is very similar to that seen in benign early repolarization (BER; discussed next). Reciprocal ST depression can be seen in aVR and possibly V1. 2. ST/T ratio less than 0.25. This makes it more likely than BER. In order to calculate the ST/T ratio, start by measuring the height of the ST and T in V6. Divide the height of the ST segment by the height of the T wave. For example, if the ST is 1 mm and the T wave is 5 mm, the ratio would be 0.20.

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378 MASTERING THE 12-LEAD EKG

3. Widespread PR depression. PR depression is seen in most of the chest and limb leads. Reciprocal elevation may be seen in aVR and possibly V1. 4. Sinus tachycardia. This doesn’t have to be present, but because of pain or a concomitant pericardial effusion, sinus tachycardia is a frequent finding.

Sinus tachycardia, rate 115, normal axis, widespread ST concave ST elevation and PR depression. Reciprocal PR elevation and ST depression in aVR. Findings consistent with pericarditis.

Treatment Pericarditis is usually treated with a combination of a nonsteroidal anti-inflammatory drug (NSAID) and colchicine. The treatment duration is based on how long it takes for symptoms to disappear. Usually patients improve in 2 weeks or less. The medications can be tapered once the patient is symptom free for 24 hours.

Benign Early Repolarization BER is a term given to a normal EKG variant typically seen in young men. It is characterized by ST elevation at the J point with a slurred or notched morphology. It can be found in up to 13% of the general population and can often be misdiagnosed as an ST elevation MI (STEMI). As the patient ages, the ST elevation gradually disappears, making it less common after the age of 50 and rare by the age of 70. It was long thought to be a sign of excellent health; however, more recent studies show an increased risk of death from ventricular fibrillation, albeit this is very rare. The patient will have no symptoms related to this normal incidental finding and it should not cause concern.

Characteristics of Benign Early Repolarization 1. Widespread concave ST elevation. The ST, or J point, elevation is usually seen in several leads. It is most notable in the mid to left chest leads, V2–V5. The concave ST segment is often said to resemble a smiley face or saddleback. 2. Notching or slurring at the J point. Some refer to this as a “fishhook sign.” It is most often seen in the mid to left precordial leads (V4 most common).

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3. Tall asymmetric T waves. The T waves slope up in the shape of a smile and quickly come down from the peak. 4. No reciprocal ST depression. Remember that ST depression in some leads while others have ST elevation is most concerning for a STEMI. 5. ST changes remain constant. STEMIs evolve and the ST abnormalities will gradually change as the myocardium suffers damage. BER will remain unchanged from EKG to EKG. If in doubt about the diagnosis, don’t hesitate to repeat the EKG and see if the ST segments remain the same. Ordering serial EKGs is a great move by great clinicians.

Sinus rhythm, rate 75, normal axis, widespread concave ST elevation with tall asymmetric T waves. Note the “fishhook” in V4. Findings consistent with benign early repolarization.

Tip Be careful not to overdiagnose BER in patients with symptoms consistent with angina, especially in men over the age of 50. Think STEMI until you are certain it is not. Remember that ST elevation gradually disappears as the patients age. ST elevation in an older patient is much more likely to be something sinister.

Brugada Syndrome Brugada syndrome was first described in 1992 by the Brugada brothers. It is an autosomal dominant genetic disorder that can cause ventricular tachyarrhythmias and sudden cardiac death. Some reports say that it accounts for 40% to 60% of idiopathic ventricular fibrillation. It is also known as sudden unexplained nocturnal death syndrome (SUNDS), which is a major cause of death among Southeast Asian populations and may have some relationship to sudden infant death syndrome (SIDS). The pattern is also frequently seen in patients with schizophrenia (11.6%). Brugada syndrome is a sodium channelopathy that causes shortening of the cardiac action potential. This leads to a “pseudo” right bundle branch block (RBBB) with ST elevation

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in leads V1 and V2. To be diagnosed as Brugada syndrome, the pattern must occur in the presence of specific symptoms. The pattern may be intermittent and revealed by conditions such as fever, ischemia, medications, and hypokalemia.

Characteristics of Brugada Syndrome 1. Pseudo RBBB pattern. rsR′ or sR′ in right chest leads 2. Coved ST-segment elevation greater than 2 mm in right chest leads (V1–V3) 3. T-wave inversion in right chest leads (V1–V3)

Plus one of the following: • Documented ventricular fibrillation or polymorphic ventricular tachycardia (VT) • Family history of sudden cardiac death under the age of 45 years • Same coved ST morphology in family members • VT can be induced by electrical stimulation • Syncope • Nocturnal agonal respiration

Treatment If the pattern is discovered without symptoms, the patient may be referred to a cardiologist for further evaluation as deemed necessary. The patient who presents with the pattern and symptoms (Brugada syndrome) is at high risk for sudden cardiac death. The patient should be admitted to the hospital for monitoring and placement of an implantable cardioverter defibrillator (ICD).

Prinzmetal Angina Prinzmetal angina is also known as vasospastic angina. It is a condition that causes chest pain at rest due to coronary artery vasospasm that causes a high-grade occlusion. Often the symptoms occur between midnight and early morning and last from 5 to 15 minutes. The spasm may be related to an imbalance in the vagal and sympathetic tone;

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however, the jury is still out. Drugs such as alcohol, marijuana, cocaine, and amphetamines are possible triggers. Smoking and male gender are highly associated with coronary vasospasms.

Characteristics of Prinzmetal Angina 1. Widespread ST elevation during chest pain. This is caused by transmural ischemia. 2. Quick resolution of ST elevation upon relief of chest pain, although T waves may remain inverted for a short time afterward.

Treatment Patients may undergo coronary arteriography with provocative tests if there is doubt about the diagnosis. This is done by injecting substances such as acetylcholine or ergonovine into the coronary artery to see if it causes vasospasm. Patients respond well to nitrates and calcium channel blockers that help put a stop to the vasoconstriction. Smoking cessation is also very important.

Takotsubo Cardiomyopathy Takotsubo is the name of an octopus trap used by Japanese fishermen. This pot has been used to describe the ballooning shape of the left ventricle during this STEMI mimic. Because it is often brought on by emotional stress, it has been referred to as “broken-heart syndrome.” This cardiomyopathy causes temporary akinesis of the apex of the left ventricle. This can cause ST elevation, Q waves, QT prolongation, and/or inverted T waves to occur. Most of the EKG changes occur in the chest leads.

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Characteristics of Takotsubo 1. Widespread ST elevation. This may remain for a few days (1–3 days). There is no reciprocal depression. The ST elevation may extend beyond the range of leads typically seen with a single coronary artery. 2. Reversible Q waves. The Q waves are caused by Purkinje cell death, not myocardial necrosis. Thus, the Q waves typically disappear within 30 days. Q waves caused by MI are permanent. 3. T-wave inversion. The T-wave inversions will appear after the ST elevation has resolved. They can often become very deep and may remain for several months. 4. QT prolongation. Occurs along with T-wave inversions. However, it has not been connected with any significant life-threatening arrhythmias.

Treatment Although Takotsubo is not caused by a coronary artery occlusion, it is impossible to tell based on the EKG alone. Immediate cardiac consultation with a trip to the catheterization lab is indicated. Treat these patients just as if they were having an STEMI.

Electrical Cardioversion Electrical cardioversion may be utilized to convert a patient in an unwanted rhythm such as atrial fibrillation with a rapid ventricular response or atrial flutter. Following cardioversion, some patients may have ST elevation of 5 mm or more. This ST elevation usually last less than a few minutes and should not be a cause of concern.

Hyperkalemia Hyperkalemia is diagnosed as a potassium level above 5.5 mEq/L. EKG changes associated with hyperkalemia are discussed in more detail in Chapter 20, Electrolytes, Medications, and Disease on the EKG, but it is important to mention here among causes of ST elevation. Potassium in an important electrolyte involved in the electrical activity of the heart.

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When levels are too high, it can cause ST elevation to occur that mimics a STEMI. This ST elevation is usually found in the right chest leads (V1–V3) and can be associated with tall pointed T waves.

T-WAVE INVERSIONS Right Bundle Branch Block The right bundle branch can fail, causing abnormal depolarization of the ventricles. Just like an LBBB, an RBBB results in a wide QRS complex with a predictable morphology in the chest leads. V1 and/or V2 will show an rsR′ followed by ST-T-wave discordance. Although the ST-segment depression is often minimal, the T-wave inversion in the right chest leads is inevitable.

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Right Ventricular Hypertrophy Right ventricle enlargement can occur as the result of pulmonary hypertension and significant lung disease. The findings of inappropriately placed tall R waves in the right chest leads, a right axis deviation, and ST-T-wave discordance help to make the diagnosis. There is usually little ST elevation present on the EKG, but leads with tall R waves will have ST depression followed by T-wave inversion (V1–V3). This was formerly called a strain pattern but that term has fallen out of favor because it inaccurately describes the cause of the abnormality.

Arrhythmogenic Right Ventricular Cardiomyopathy In arrhythmogenic right ventricular cardiomyopathy (ARVC), the healthy myocardium is replaced by fibrous scar tissue. This can result in deadly ventricular arrhythmias such as VT. This life-threatening condition is usually the result of an autosomal dominant trait. It is three times more common in men than in women and often seen in those of Greek or Italian descent.

Characteristics of ARVC 1. Prolonged S-wave upstroke is seen in leads V1–V3. From the bottom (nadir) of the S wave to the end of the QRS complex takes greater than 0.55 second. This must be present in the absence of a complete RBBB. 2. Epsilon wave is a small positive deflection at the end of the QRS complex. It may have some similarities to the appearance of the “fishhook” seen in BER. It is not always present, but is the most specific finding for ARVC. 3. Inversion of T waves in right chest leads is an important finding in ARVC. T-wave inversion in V1–V3 or beyond is considered a major criterion for the diagnosis by the 2010 Task Force (when there is not a complete RBBB and in patients over the age of 14 years). Half of the patients with ARVC who present with VT have T-wave inversions in V1–V3.

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Symptoms Patients are frequently presenting and getting an EKG performed because of symptoms related to ARVC. This includes palpitations, syncope, chest pain, dyspnea, and even right ventricular heart failure. They often have ventricular arrhythmias such as frequent premature ventricular contractions (PVCs) or sustained VT. VT, when it occurs, usually originates in the right ventricle. This results in a QRS complex that has an LBBB appearance during the episode of VT.

Treatment Treatment includes avoiding strenuous exercise and competitive sports that increase the risk of arrhythmias and heart failure. Beta-blockers are frequently employed for prevention of arrhythmias. Implantation of an ICD is also considered.

Elevated Intracranial Pressure Elevated intracranial pressure (ICP) can occur with tumors, infections, or intracranial bleeds. Believe it or not, the EKG can provide evidence for raised ICP. The EKG can demonstrate the following characteristic changes.

Characteristics of Raised ICP 1. Widespread giant T-wave inversions. These are often called cerebral T waves. 2. Prolonged QT interval 3. Bradycardia. This is part of Cushing’s triad: bradycardia, respiratory depression, and hypertension.

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Cerebral T waves. If your patient’s mental status didn’t clue you in that something is wrong, this should.

Pulmonary Embolism Most pulmonary emboli (PE) arise from the lower extremity proximal veins, where a deep vein thrombus (blood clot) breaks loose and finds its way to the lung vasculature. This occludes arterial blood flow to the lungs and may cause an increase in pulmonary vascular resistance (PVR). PVR is the amount of pressure the heart must obtain to supply the lungs with oxygenated blood. The right ventricle is strained and may not be able to meet the demand. This may cause T-wave inversions in the right chest leads.

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ST DEPRESSION Digitalis Effect The use of digoxin can cause ST depression to occur. This is known as the digitalis effect and is seen as a slight sagging or swooping ST depression that some compare to Salvador Dali’s mustache. Because of the narrow therapeutic window, the use of digoxin has fallen off over the last several years.

Hypokalemia Low potassium, typically less than 2.7 mEq/L, may cause ST depression to occur along with flattened T waves. Hypokalemia can be the result of decreased intake or increased excretion from the urine or gastrointestinal (GI) tract. Patients with low potassium may complain of muscle weakness and cramps.

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Arrhythmias You may recall that ST depression can also be seen in supraventricular tachycardia and Wolff–Parkinson–White syndrome (WPW). Although you will soon learn that ST depression can be the result of ischemia, the ST depression in these rhythms is not the result of hypoxic myocardium. Once the rhythm is converted, the ST depression resolves.

Persistent Juvenile T-Wave Pattern T-wave inversions can be the result of persistent juvenile T-wave pattern. Children normally have asymmetric T-wave inversions that extend normally through the right precordial leads (V1–V3). This pattern may persist in young adults, particularly African American women under the age of 30. Cardiopulmonary disease should be ruled out before calling it a juvenile T-wave pattern.

TAKE-HOME POINTS • ST-T-wave changes can be caused by multiple conditions including ischemia and infarction. Conditions include ▪ Pericarditis ▪ Benign early repolarization ▪ Brugada syndrome ▪ Prinzmetal angina ▪ Takotsubo cardiomyopathy ▪ Arrhythmogenic right ventricular cardiomyopathy ▪ Elevated ICP ▪ Pulmonary embolism ▪ Persistent juvenile T-wave pattern

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EXERCISES 1. The ST segment should be _____________________________ in most normal conditions. 2. The T wave should be inverted in leads _____________________ and _______________________ and sometimes in lead ______________________. 3. Pericarditis leads to ________________________________ ST elevation and _______________________ PR ____________________. 4. Benign early repolarization becomes infrequent after the age of __________________ and caution should be used when making the diagnosis. 5. Brugada syndrome is an inherited sodium channelopathy that can cause sudden death. It is identified by a “pseudo” _________________________________ with ST elevation in leads ______ and _______. 6. Prinzmetal angina is caused by coronary ____________________________. 7. Takotsubo cardiomyopathy is caused by ________________________________________. 8. Arrhythmogenic right ventricular hypertrophy can be identified by looking in leads V1–V3 for a prolonged ________________ stroke, ____________________ wave, and _____________________ T waves. 9. Elevated ICP can be identified on the EKG by ___________________________ T waves. On each of the following EKGs: Provide a complete interpretation of the EKG including all five major categories.

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1.

Hypertrophy: ______________

Final interpretation: _______________________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Axis: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

A 67-year-old male found unresponsive on the floor in his home.

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2.

Hypertrophy: ______________

Final interpretation: _______________________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Axis: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

A 34-year-old male who presents to the ER after syncopal episode.

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3.

Hypertrophy: ______________

Final interpretation: _______________________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Axis: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

A 76-year-old female with history of coronary artery disease.

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4.

Hypertrophy: ______________

Final interpretation: _______________________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Axis: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

A 28-year-old male with complaints of chest pain for 1 hour.

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5.

Hypertrophy: ______________

Final interpretation: _______________________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Axis: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

A 52-year-old female with sharp chest pain.

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6.

Hypertrophy: ______________

Final interpretation: _______________________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Axis: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

A 69-year-old female with who presents with left shoulder pain.

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REFERENCE/RESOURCE Gordan, R., Gwathmey, J. K., & Xie, L. H. (2015). Autonomic and endocrine control of cardiovascular function. World Journal of Cardiology, 7(8), 466–475. doi:10.4330/wjc.v7.i8.466

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Chapter

18

Ischemia Detection on the EKG The EKG is an essential first-line diagnostic tool to diagnose ischemia. We have now covered four out of the five major categories of EKG interpretation. We are ready to move on to the last, but certainly not least: ischemia and infarction. Not knowing the difference between a premature atrial complex (PAC) or a premature ventricular complex (PVC) won’t hurt anyone, but miss signs of myocardial ischemia or infarction and things can go south in a hurry. What follows in the next two chapters is among the most important information in this text, and may be among the most important of your career. Diagnosing myocardial infarction (MI) or ischemic changes on the EKG will require you to use the knowledge you have gained throughout the text. A solid understanding of the anatomy and physiology of the heart, hexaxial diagram, axis, and other conditions that can mimic ischemia and infarction is invaluable in making the right diagnosis. In this chapter, we start with a brief introduction to acute coronary syndrome (ACS). Then we move on to signs of myocardial ischemia on the EKG. You are also introduced to a potential death-dealing dilemma called Wellens’ syndrome that predicts an imminent MI.

ACUTE CORONARY SYNDROME ACS is an umbrella term that includes three more specific diagnoses: unstable angina (UA), acute non-ST elevation myocardial infarction (NSTEMI), and acute ST elevation myocardial infarction (STEMI). Each of these conditions presents with similar symptoms and can only be distinguished by using an EKG and cardiac enzymes (troponin). Troponin, a protein released as a result of myocardial injury, can take as long as 3 hours to show up in the blood. Fortunately, worrisome EKG findings can show up within minutes. Therefore,

the EKG is an essential first-line diagnostic tool to diagnose ischemia and infarction.

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Unstable Angina: Absence of ST elevation; negative troponin Non-ST Elevation MI: Absence of ST elevation; positive troponin ST Elevation MI: ST elevation; positive troponin

Symptoms of ACS include angina at rest that lasts longer than 20 minutes, angina that is new and severely limits physical activity, and angina that is increasing in duration or with less activity than before. When these patients arrive at your clinic or ED, a 12-lead EKG should be completed without delay. Findings on the EKG will vary depending on the amount of time that has occurred since the event began, the amount of myocardium affected, and the location of the myocardium suffering from the coronary occlusion.

Symptoms Consistent With Angina • Often described as discomfort, not pain • May be described as squeezing, tightness, pressure, burning, knot, heaviness • Discomfort difficult to localize • Radiation to upper abdomen, shoulders, arms, wrist, neck and throat, lower jaw • Provoked by activity that increases myocardial oxygen demand, relieved when activity halted Symptoms Inconsistent With Angina • Sharp, knifelike pain • Localized with one finger • Pain reproduced with movement, palpation • Lasts for days • Lasts only a few seconds • Radiates to lower extremities or above lower jaw

NORMAL ST SEGMENT AND T WAVES The ST segment and T wave represent ventricular repolarization. This is where the first signs of ischemia and infarction can be found. Under most normal circumstances, the ST segment should be flat/isoelectric when compared to the baseline. However, several conditions can cause ST elevation or depression. T waves should be upright in all leads, except for aVR and V1, where they are inverted. An inverted T wave is occasionally a normal finding in lead III, but could be the sign of a problem. The T-wave height is typically less than 5 mm in the precordial leads and 10 mm in the limb leads. It should be asymmetric with a slow rise to the top and a quick drop on the back side.

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EKG CRITERIA FOR MYOCARDIAL ISCHEMIA Repolarization abnormalities, particularly T-wave changes, are the earliest EKG findings seen in myocardial ischemia or infarction. ST-segment depression or elevation, inverted or flattening T waves, and hyperacute T waves can be clues that something is amiss. As the myocardium becomes necrotic, abnormal Q waves may develop. Specific criteria have been developed that can help us make the diagnosis of ischemia and infarction on the EKG. We discuss those for UA and NSTEMI in this chapter. Changes associated with STEMI will be unpacked in the next. A group of experts from the European Society of Cardiology, American College of Cardiology, American Heart Association, and World Heart Federation began meeting in 2007 to create a universal definition for MI. In 2018, they released an updated Fourth Universal Definition for Myocardial Infarction (Thygesen et al., 2018). Over the years, they have refined our understanding of how to make the diagnosis of ischemia and MI based on EKG changes and lab results. This group of experts has developed the following EKG criteria for the diagnosis of

UNSTABLE ANGINA AND NON-ST ELEVATION MI New horizontal or down-sloping ST depression greater than or equal to 0.5 mm in two anatomically contiguous leads, or T-wave inversion greater than 1 mm in two anatomically contiguous leads with prominent R wave or R/S ratio greater than 1 The term “two anatomically contiguous leads” refers to the relative position of the leads on the hexaxial diagram or chest. Those that sit next to each other on the body/diagram, not the EKG paper, are considered contiguous. For example I and aVL are contiguous leads. II and aVF are another example of contiguous leads.

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EKG Changes in Acute Coronary Syndrome

ST depression or elevation Hyperacute (tall) T waves Inverted T waves Abnormal Q waves Normal EKG

HORIZONTAL OR DOWN-SLOPING ST DEPRESSION As mentioned above, the criteria for ischemia include new horizontal or down-sloping ST depression greater than or equal to 0.5 mm. To evaluate the EKG for ST depression, compare the voltage of the ST segment at the J point to that of the TP segment. Count the number of blocks that separate the voltage of the TP and the height/depth of the ST segment. If the ST depression is equal to or more than half a small block, ischemia needs to be in your differential.

The various morphologies of ST depression.

The next important step is evaluating the shape or morphology of the ST segment. Look at the direction the ST segment goes after leaving the J point. Does the depressed ST segment come straight out from the J point? This is horizontal and concerning for ischemia. Does the ST segment slope down from the J point? This is down-sloping, of course, and also a concerning morphology for ischemia. If the ST segment rises from the depressed J point, this is considered upsloping and it is less likely an ischemic change. Remember that these changes must be seen in two anatomically contiguous leads to be considered for ischemia.

T-WAVE INVERSIONS T waves that flip from their normal upright position are called inverted. For T-wave inversions to meet the criteria for ischemia, they must be more than one small block deep (>1 mm). T waves are normally upright in leads with tall R waves (e.g., I, aVL, V5, V6) and inverted where the S wave is dominant (e.g., V1, aVR). Look for T-wave inversions that have altered from their normal axis and occur in at least two anatomically contiguous leads.

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T-wave inversions in leads II, III, and aVF are the result of inferior ischemia.

LOCATION The location of the coronary stenosis can be postulated by looking at the leads involved and combining it with our basic knowledge of the anatomy of coronary arteries. For example, if ST depression is occurring in leads II, III, and aVF, it may be described as inferior ischemia. Because we know that the right coronary artery (RCA) supplies the posterior and inferior portions of the myocardium, we can suspect that it is the likely site of the problem. Predicting the exact vessel with the lesion isn’t a perfect science because people can be made a little different from each other. Some common descriptors for anatomical descriptions of the location of ischemia and infarction are as follows along with the common culprit: Inferior: II, III, aVF—RCA Anterioseptal: V1, V2—LAD Strictly anterior: V3, V4—LAD Anterolateral: V5, V6—LAD High lateral: I and aVL—LCX There will be times when the EKG changes do not fall neatly into any of these categories. The EKG changes may overlap more than one area. Don’t fret. When necessary, just document the findings and relay to your colleague the leads in which you see the abnormalities.

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T-wave inversion in V1–V6. The result of anterior myocardial ischemia.

SERIAL EKGs When evaluating a patient with suspected ACS, a troponin test should be ordered along with the EKG. Often other lab tests include a CBC, CMP, PT/INR, PTT, and chest x-ray as part of the chest pain evaluation. Keep in mind, the initial EKG may be normal. A study demonstrated that 15% to 20% of initial EKGs were NORMAL in patients presenting with an acute MI (Millard, Nagarajan, Kohan, Schutt, & Keeley, 2017).

If the patient continues to have signs and symptoms consistent with ischemia/ infarction, an EKG must be repeated at least every 15 to 30 minutes. This is called obtaining serial EKGs. Performing a series of EKGs can be extremely valuable and save your patient’s life. It is a great move by a great clinician. Be a great clinician. EKG changes associated with ischemia and infarction are considered dynamic. This means that as the injury progresses, the EKG will continue to change. This is an important clue in making the diagnosis. As time passes, more muscle is injured and the EKG changes may become more obvious. As they say, “time equals muscle.”

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Previous EKGs can also provide insight into the EKG abnormalities as well. Obtaining old EKGs can be invaluable. For example, noting the same T-wave inversions on an EKG from 6 months ago may decrease your suspicion for ischemia. However, if they were not there on the previous EKG, your spidey senses should be elevated and you may need to call in the Avengers™.

NONSPECIFIC ST-T CHANGES As mentioned above, T-wave inversions or flattening may be seen, or the ST depression may take on a different morphology or depth than those described by the Task Force. These are considered nonspecific changes. Although it is possible they are signs of ischemia, they may also be the result of things such as medications, hypertrophy, or electrolyte abnormalities. If the changes are related to ischemia, performing serial EKGs could help unObtaining old EKGs can be cover dynamic changes that will be present. invaluable. EKGs may remain completely unchanged with UA and NSTEMI. If only a small portion of the myocardium is affected or in an electrically silent portion of the heart, the EKG may remain normal. Only after the troponin has returned from the lab can the final diagnosis of UA or NSTEMI be made.

A normal EKG does not eliminate the possibility of an acute cardiac event. The abnormal signs of ischemia and infarction could be just around the corner or hiding from you.

OTHER FINDINGS ASSOCIATED WITH ISCHEMIA Hyperacute T Waves Hyperacute T waves can be described as symmetric, broad-based waves that are taller than normal. This T-wave change is often the earliest sign of acute ischemia. The T wave is large when compared to the QRS complex. It may be so large that the QRS complex could fit inside it. If hyperacute T waves are seen on the EKG in a patient with concerning symptoms or history, serial EKGs should be performed to watch for progression to ST elevation that often follows. It may be the first sign of an impending STEMI (Levis, 2015).

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Straightening of T Waves This finding can often be seen in association with the hyperacute/tall T waves mentioned above. The ST segment disappears and is replaced by a T wave that jumps right off the QRS complex. Some call this the “R-T sign” or “checkmark sign” because of its appearance. Even though there may not be ST elevation … yet, serial EKGs should be performed because the findings of a STEMI could be imminent. Checkmark T waves should be considered ischemia until proved otherwise.

Note the straight ST-T that follows the QRS complex in V2.

T-Wave Inversion in aVL Isolated T-wave inversion in aVL, according to one retrospective study, has been found to have high specificity for mid left anterior descending (LAD) occlusion (86.9%). It has also been connected to right ventricular involvement in an inferior MI. It is not a sensitive finding, showing up in only 9.8% of patients, but when present, it is a valuable clue to your patient’s diagnosis. Because the abnormal T-wave inversion is only seen in one lead, it can often be overlooked (Hassen et al., 2014; Nakanishi, Goto, Ikeda, & Kasai, 2016). When your patient presents with angina, make sure to evaluate the EKG for this isolated abnormality. Consider repeating the EKG to see if other concerning findings develop.

New Upright T Waves in V1 As mentioned above, the T wave is normally inverted in V1 owing to its position on the right side of the chest. A new upright T wave in V1 (NUTV1) has a significant association with coronary artery disease. To determine if this is a new finding, you must obtain an old EKG for comparison. When NUTV1 is a new finding in a patient with angina, it should be considered a sign of ischemia. A study demonstrated that 84% of patients with an NUTV1 had significant coronary artery disease. The EKG abnormality is most frequently associated with a left circumflex (LCX) and/or RCA stenosis greater than 75% (Manno, Hakki, Iskandrian, & Hare, 1983).

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If a previous EKG is not available, look for a T wave that is taller in V1 than in V6. This is called a loss of precordial T-wave balance. If present on the old EKG, the finding may or may not be of concern and a decision should be made based on other findings.

Wellens’ Syndrome An important cause of T-wave inversions is Wellens’ syndrome. This syndrome was first described by Dutch cardiologist Hein J.J. Wellens in 1982 (de Zwaan, Bär, & Wellens, 1982). He discovered that deep symmetric T waves in V2–V3 were incredibly specific for a dangerous and critical stenosis of the LAD. In his first study he sent home his patients with the T-wave abnormality. Within just a few weeks 75% had returned with a large anterior MI. In a second study of 180 patients with the EKG abnormality, all 180 underwent cardiac catheterization and had stenosis of the LAD. The stenosis ranged from 50% to 100%, with an average of an 89% occlusion. There are two patterns of Wellens’ waves: Type A: Biphasic T waves in leads V2 and V3 (25%) or Type B: Deeply inverted T wave in V2 and V3, and may spread to other precordial leads (75%) Plus one of the following: • Isoelectric or minimally elevated ST segment ( 1. On each of the following EKGs: Address all five categories of a complete EKG interpretation.

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1.

Ischemia: ______________

Final interpretation: ______________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Hypertrophy: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

An 81-year-old female who presenting with chest pressure that radiates to lower left jaw.

Axis: ______________

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2.

Ischemia: ______________

Final interpretation: ______________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Hypertrophy: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

A 53-year-old male with complaint of midsternal chest tightness.

Axis: ______________

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3.

Ischemia: ______________

Final interpretation: ______________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Hypertrophy: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

A 62-year-old male with history of hypertension presenting with chest pain.

Axis: ______________

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4.

Ischemia: ______________

Final interpretation: ______________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Hypertrophy: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

A 36-year-old male type one diabetic with complaint of increasing shortness of breath on exertion.

Axis: ______________

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5.

Ischemia: ______________

Final interpretation: ______________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Hypertrophy: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

A 49-year-old female with chest pain described as “someone sitting on my chest”.

Axis: ______________

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6.

Ischemia: ______________

Final interpretation: ______________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Hypertrophy: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

A 75-year-old female with complaint of intermittent chest pain.

Axis: ______________

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7.

Ischemia: ______________

Final interpretation: ______________

PR duration: _____________________

P waves: Present, not present, upright, or inverted __________________

Hypertrophy: ______________

QRS: Narrow or wide ______________

Rhythm: Regular or irregular ______________

Rate: ______________

A 38-year-old smoker with complaint of chest pain with activity.

Axis: ______________

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REFERENCES/RESOURCES Abulaiti, A., Aini, R., Xu, H., & Song, Z. (2013). A special case of Wellens’ syndrome. Journal of Cardiovascular Disease Research, 4(1), 51–54. doi:10.1016/j.jcdr.2013.02.016 de Zwaan, C., Bär, F. W., & Wellens, H. J. (1982). Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. American Heart Journal, 103(4, Pt. 2), 730–736. doi:10.1016/ 0002-8703(82)90480-x Hassen, G. W., Costea, A., Smith, T., Carrazco, C., Hussein, H., Soroori-Rad, B., … Fernaine, G. (2014). The neglected lead on electrocardiogram: T wave inversion in lead aVL, nonspecific finding or a sign for left anterior descending artery lesion? The Journal of Emergency Medicine, 46(2), 165–170. doi:10.1016/j.jemermed.2013.08.079 Levis, J. T. (2015). ECG diagnosis: hyperacute T waves. The Permanente Journal, 19(3), 79. doi:10.7812/TPP/14-243 Manno, B., Hakki, A., Iskandrian, A., & Hare, T. (1983). Significance of the upright T wave in precordial lead V1 in adults with coronary artery disease. Journal of the American College of Cardiology, 1(5), 1213–1215. doi:10.1016/s0735-1097(83)80132-6 Millard, M. A., Nagarajan, V., Kohan, L. C., Schutt, R. C., & Keeley, E. C. (2017). Initial electrocardiogram as determinant of hospital course in ST elevation myocardial infarction. Annals of Noninvasive Electrocardiology, 22(4). doi:10.1111/anec.12429 Nakanishi, N., Goto, T., Ikeda, T., & Kasai, A. (2016). Does T wave inversion in lead aVL predict mid-segment left anterior descending lesions in acute coronary syndrome? A retrospective study. BMJ Open, 6(2), e010268. Retrieved from https://bmjopen.bmj.com/content/6/2/e010268 Rashduni, D. L., & Tannenbaum, A. K. (2003). Utility of ST segment depression in lead AVL in the diagnosis of right ventricular infarction. New Jersey Medicine, 100(11), 35–37. Smith, S. W., Zvosec, D. L., Sharkey, S. W., & Henry, T. D. (2002). The ECG in acute MI: An evidence-based manual of reperfusion therapy (p. 358). Philadelphia, PA: Lippincott Williams & Wilkins. Thygesen, K., Alpert, J. S., Jaffe, A. S., Chaitman, B. R., Baz, J. J., Morrow, D. A.., & White, H. D. (2018). Fourth universal definition of myocardial infarction (2018). Journal of the American College of Cardiology, 72(18), 2231–2264. Retrieved from http://www.onlinejacc.org/content/accj/ early/2018/08/22/j.jacc.2018.08.1038.full.pdf Turhan, H., Yilmaz, M. B., Yetkin, E., Atak, R., Biyikoglu, S. F., Senen, K., … Kutuk, E. (2003). Diagnostic value of aVL derivation for right ventricular involvement in patients with acute inferior myocardial infarction. Annals of Noninvasive Electrocardiology, 8(3), 185–188. doi:10.1046/j.1542-474X.2003.08303.x

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Chapter

19

Infarction Detection on the EKG The EKG is an essential first-line diagnostic tool to diagnose infarction.

ST ELEVATION MYOCARDIAL INFARCTION Every year, nearly 800,000 Americans suffer from a myocardial infarction (MI). This is equivalent to one every 40 seconds. More people survive MIs now than in previous decades owing to improved recognition and treatment options, but those who do can be left with permanent complications such as heart failure from impaired ventricular function. MI is more prevalent in men than in women. Those who have a family history of coronary artery disease, smoke tobacco, have hypertension, and/or dyslipidemia are at increased risk. Obesity and diabetes are on the incline. These conditions, which often occur together, place patients at higher risk for MI. Acute ST elevation MIs (STEMIs) are usually due to the rupture of vulnerable atherosclerotic plaque. This initiates a clotting cascade that occludes the artery with thrombus. The thrombus halts the blood supply to the affected myocardium. Within seconds the tissue becomes ischemic and can progress to permanent cell death within 20 minutes. The injured myocardium does not function normally, and cardiac output suffers. Ischemic tissue surrounding the infarcted area is irritable and can be prone to life-threatening ectopic activity such as ventricular fibrillation.

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Usually these patients experience chest discomfort or angina. They may describe it as tightness, heaviness, pressure, squeezing, or even sharp. Usually the pain will persist for 30 to 60 minutes and may radiate into the neck, lower jaw, shoulder, and/or left arm. The chest pain can be accompanied by shortness of breath and diaphoresis. Women and diabetics tend to have symptoms that are less “typical.” A study performed in 2003 revealed that 43% of females did not have chest pain, but instead only complained of shortness of breath, weakness, and fatigue (McSweeney et al., 2003).

EKGs are an invaluable tool used to make the urgent diagnosis of a STEMI. When a patient arrives with symptoms concerning for angina, an EKG should be completed as soon as possible (within 10 minutes or less). If the EKG is normal and concern remains for acute coronary syndrome (ACS), the EKG should be repeated in 15 to 30 minutes. When the EKG demonstrates a STEMI, there is no need to wait around on troponin results. Its presence should prompt swift action to alleviate the coronary occlusion causing necrosis of the myocardium.

Failure to recognize a STEMI in a timely manner can lead to permanent left ventricular (LV) dysfunction, dangerous arrhythmias, and death. So let’s learn how to recognize a STEMI, shall we?

ST Segment The ST segment and T wave represent ventricular repolarization.

And ventricular repolarization is where the first signs of ischemia and infarction can be found. The ST segment starts at the J point, or “junction,” at the end of the QRS complex. The J point is an important area to locate to make the diagnosis of STEMI. It is the elevation or depression of the J point that determines where the ST segment will begin. Under most normal circumstances, the ST segment should take off from the J point at the same height/voltage as the isoelectric baseline. Any deviation from the baseline should make you stop and take notice. Unfortunately, a STEMI is just one of several conditions that can cause the ST segment to become abnormal. Being able to separate other causes from this medical emergency is important. Obtaining old EKGs can help you to consider if the ST changes are from an acute or chronic condition. Review Chapter 17, ST Elevation and Depression Causes on the EKG, if you need a refresher on topics that can cause ST elevation and depression.

STEMI Evolution Findings associated with ischemic injury depend on a few factors: duration, size, and location. If the patient arrives early in the process or only a small portion of the myocardium hidden from EKG leads is being injured, changes on the EKG may not be present. It is important to remember

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that a STEMI is an active and dynamic process. As time passes, more muscle is injured and the EKG will evolve. Therefore, performing serial EKGs can be extremely valuable. The following is a typical EKG evolution during a STEMI. 1. Normal EKG. Yes!

The initial EKG can be normal. Studies have shown that 45% of initial EKGs are nondiagnostic and another 20% may be completely normal early in STEMI. Do not assume that if the first EKG is normal the patient is not having a serious problem. If concern for ACS remains, repeat the EKG every 15 to 30 minutes looking for evolving changes. The importance of serial EKGs cannot be stressed enough. EKGs are cheap, easy, and painless to obtain. Don’t hesitate to repeat the test if there is any doubt in your diagnosis. 2a. Hyperacute (tall) T waves. As the injury progresses, hyperacute T waves can develop. T waves that are unusually tall compared to the height of the QRS complex are concerning and should make you pay close attention. The T wave may be so tall that the QRS could easily fit underneath it. This EKG finding could be your first clue that a STEMI is on the way. An EKG master will be on the lookout for these changes. Hyperacute T waves also may have some T-wave straightening, which is discussed next.

2b. T-wave straightening. T waves may take on a “checkmark” appearance and look as if they come straight off the QRS complex. Even in the absence of an elevated J point, this should make you raise an eyebrow. Watch things closely. Repeat the EKG to look for dynamic changes. The checkmark could be a sign that your patient is trying to check out.

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3. ST elevation. This is the hallmark of acute myocardial injury. A sign that things are going very badly and the myocardium is under full force attack. The ST-segment elevation will remain until the affected tissue completely necroses or the blood flow is restored. According to Miracle Max, when there is ST elevation, the myocardium is mostly dead, which is different from all dead. Mostly dead is slightly alive. But if we don’t act soon, people will start looking for loose change. 4. Q-wave development. Pathologic Q waves appear once the affected portion of the myocardium is all dead. They usually develop within 6 to 14 hours after the onset but can occur sooner. Abnormal Q waves can persist indefinitely. 5. T-wave inversion. As the ST-segment elevation begins to fall, T waves become inverted. This change can remain long after the ST has normalized and can persist for months.

STEMI Criteria According to the 2018 task force comprising the European Society of Cardiology, the American College of Cardiology, American Heart Association, and World Health Federation (O’Gara et al., 2018),

the following criteria are required to diagnose STEMI on the EKG: New ST elevation at the J point that is greater than or equal to 1 mm in two anatomically contiguous leads except for V2 and V3 ≥2 mm in men ≥40 years of age V2 and V3 ≥2.5 mm in men V2 • ST elevation in V1 + ST depression in V2 (highly specific) • ST elevation in V3R–V6R

Inferior STEMI with right ventricular involvement. ST elevation in II, III, and aVF. Reciprocal depression in I, aVL, and V6. ST elevation in lead III greater than in lead II.

Right-Sided Chest Leads Standard 12-lead EKGs provide a wealth of information; however, at times they fail to reveal all the areas of the myocardium that we need to see. Additional leads can be placed to get a more complete picture of the heart’s activity. These include posterior and right-sided chest leads. Some experts recommend the use of these supplemental leads in patients with angina and an initial nondiagnostic EKG. The right side of the heart is an area that is poorly visualized with the standard 12 leads. Therefore, it can be helpful to place additional electrodes to obtain an EKG tracing of the right side of the heart. Electrodes and corresponding wires can be moved to the right side

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of the chest in a mirror image to those normally placed on the left. V1 becomes V1R, V2 becomes V2R, and so on. The most useful lead is V4R, which sits at the right midclavicular line in the fifth intercostal space.

Greater than 1 mm of ST elevation in V4R is 88% sensitive and 78% specific for a right ventricular MI.

Posterior Infarct Up to 15% to 20% of STEMIs will involve the posterior myocardium. It is usually an extension of an inferior or lateral MI; however, on rare occasions it may occur in isolation (3%). When it occurs by itself,

a posterior MI can easily be missed because it does not have ST elevation typically seen in STEMI. Instead, it is diagnosed when there is ST depression in V1 and V2. This can lead to a misdiagnosis of ischemia and delay urgently needed reperfusion. Make sure you are aware of this, but of course now you are. When a posterior MI extends from an inferior or lateral MI, there is an increased risk of LV dysfunction and death. Because none of the standard 12 leads look directly at the posterior myocardium, the anterior leads help us to identify a posterior MI. They will demonstrate a mirror image of the back of the heart. Therefore, instead of ST elevation, we see ST depression in the anterior leads. And instead of the development of abnormal Q waves, we see tall dominant R waves in leads. Tall R waves in V1 and V2 can be seen in other conditions such as right ventricular hypertrophy (RVH), right bundle branch block (RBBB), Wolff–Parkinson–White syndrome (WPW), and an uncommon normal variant in women. These conditions should be excluded prior to making the diagnosis of posterior MI. To differentiate from other conditions, electrodes can be placed on the back just under the left scapula creating leads V7, V8, and V9. Wires, most often from V4–V6, are removed and placed on the back in sequential order. As little as

0.5 mm of ST elevation is required in the posterior leads to make the diagnosis of posterior MI.

Characteristics of Posterior MI Horizontal ST-segment depression and upright T waves in V1 and V2 Dominant R wave in V2 (R/S ratio >1) ST-segment elevation in V7–V9 (≥0.5 mm)

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Inferolateral STEMI with posterior involvement. ST elevation in II, aVF, V6, I. Horizontal ST depression as a result of posterior extension in V1–V3 with upright T waves following. Dominant R waves in V2.

Posterior leads placed below left scapula, V7–V9. ST elevation greater than 0.5 mm consistent with posterior STEMI.

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ST DEPRESSION IN V1–V3 The Fourth Universal Definition of Myocardial Infarction was released in 2018 (Thygesen et al., 2018). This panel of experts recommends the use of supplemental posterior or rightsided chest leads in patients with angina and an initial nondiagnostic EKG. An occlusion of the LCX can cause isolated ST depression in V1–V3 that is less than 0.5 mm. Use of posterior leads can help uncover the acute occlusion that should be managed as a STEMI. Look for ST depression greater than or equal to 0.5 mm in leads V1–V3 ST elevation greater than or equal to 0.5 mm in leads V7–V9 (≥1 mm if V1 Widespread ST elevation in all except the inferior leads

DE WINTER’S T WAVES Robbert J. de Winter and colleagues first described this STEMI equivalent in 2008. It presents as tall symmetric T waves in the precordial leads with upsloped ST depression.

Although there is no ST elevation, de Winter’s T waves are considered a sign of an acute occlusion of the LAD, and the patient should have emergent reperfusion. This EKG abnormality has been said to occur in up to 2% of LAD occlusions. It is typically seen in younger males with a history of hypercholesterolemia. Typical STEMI patterns may occur before or after de Winter’s T waves appear.

Characteristics of de Winter’s T Waves Tall symmetric T waves in the precordial leads Upsloped ST-segment depression greater than 1 mm at the J point in precordial leads Absence of ST elevation ST-segment elevation (0.5–1 mm) in aVR

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de Winter’s T waves, a STEMI equivalent. Tall symmetric T waves in the precordial leads with upsloped ST-segment depression greater than 1 mm. No ST elevation is seen. aVR with slight ST elevation.

TREATMENT OF STEMI Reperfusion The primary goal is to restore the blood flow to the myocardium (reperfusion) and do it as quickly as possible. You have probably heard the saying “time is muscle.” Restoring blood flow halts the injury of the myocardium and can prevent permanent death of the tissue. Reperfusion can happen in a couple different ways. Percutaneous coronary intervention (PCI) is most ideal. This involves opening up the occluded artery by using a balloon that inflates in the artery, pushing the plaque out of the way. PCI has demonstrated better survival and less potential for harm than clot-busting drugs called fibrinolytics. The goal is to have the patient reperfused with PCI within 90 minutes (no more than 120 minutes) from their presentation. Some call this a door to balloon time. If this cannot be accomplished, consideration must be given to fibrinolytics. If the facility does not have the ability to perform PCI within the recommended time frame, fibrinolytics should be administered after consultation with a cardiologist. Ideally they are given within the first 4 hours of symptoms. Fibrinolytics have the potential to cause bleeding that can sometimes be severe.

Is MONA Dead? A popular mnemonic, MONA, was created some years ago to help providers remember treatment options for ACS. It stands for morphine, oxygen, nitrates, and aspirin. However, some recent studies have raised some questions about a few of the letters in this memory tool. Morphine: Morphine has been used as an analgesic for unrelenting chest pain in ACS. Despite its place in the mnemonic, some experts urge caution with its use. A large retrospective study shows it could create worse outcomes for our patients. It has demonstrated a drug-to-drug interaction with aspirin and other antiplatelet drugs, possibly making them less effective as anticoagulants. Consider using morphine only when patients remain in significant discomfort after other measures have been taken (Bellandi et al., 2016; Puymirat et al., 2016). Oxygen: A study was released in September 2017 that reported on the use of supplemental oxygen in patients with acute MI and normal oxygen saturation (>94%). It confirmed that adding oxygen under these circumstances wasn’t helpful and failed to improve outcomes. Although the myocardium is suffering from hypoxia during an MI, giving oxygen to a well-oxygenated patient doesn’t mean the oxygen will get where it needs to go. The highway to the heart is blocked, and no amount of oxygen is going to get through. The heart wants what it can’t have. So, additional oxygen is as useless

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as a banana Now and Later candy. However, if your patient has an O2 saturation less than 94%, adding supplemental oxygen is a good idea. Nitroglycerin: Sublingual or IV nitrates are beneficial for patients with STEMI. Nitrates dilate large coronary arteries and increase perfusion to the ischemic tissue. However, use caution because it may cause hypotension from decreasing preload, especially in patients with a right ventricular infarct or those taking a phosphodiesterase inhibitor for erectile dysfunction. Aspirin: Use of antiplatelet drugs such as aspirin has demonstrated improved outcomes. A dose of 162 to 325 mg aspirin should be chewed or crushed and given as soon as possible after the diagnosis has been made.

STEMI AND LEFT BUNDLE BRANCH BLOCK Left bundle branch block (LBBB) makes the diagnosis of STEMI more challenging. As you may remember, an LBBB is often accompanied by appropriate discordance of the ST segment. If the QRS complex is mainly negative, the ST segment demonstrates an expected ST elevation. Identifying a STEMI under these circumstances poses unique challenges. As recently as 2013, the American College of Cardiology Foundation/American Heart Association STEMI guidelines recommended emergent reperfusion in all patients with a newly discovered LBBB accompanied by symptoms of angina (O’Gara et al., 2013). In other words, if the LBBB could not be confirmed on an old EKG, and the patient was complaining of chest pain, it was considered a STEMI equivalent. This caused many patients to undergo unnecessary intervention. However, in 2013, the guidelines were updated and now

a newly diagnosed LBBB with angina is no longer considered a STEMI equivalent. Many providers still remain unaware of this update. Now, instead of assuming the patient is having a STEMI, relatively new criteria have been established to make the diagnosis in the presence of an LBBB. These rules are called the Sgarbossa criteria.

Sgarbossa Criteria The Sgarbossa criteria were first published in February 1996 by Elena B. Sgarbossa et al. They are currently the

most validated tool to make the diagnosis of STEMI in the presence of an LBBB. They are highly specific, but lack in sensitivity. The changes mentioned here only have to be present in one lead. Rule A: Concordant ST elevation greater than or equal to 1 mm in a lead with a positive QRS complex—5 points Rule B: Concordant ST depression greater than or equal to 1 mm in leads V1, V2, or V3—3 points Rule C: Excessively discordant ST elevation greater than or equal to 5 mm in leads with a negative QRS complex—2 points

Greater than or equal to 5 points has 100% specificity for STEMI, but only 14% sensitivity.

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Greater than or equal to 3 points has 98% specificity for diagnosing STEMI, with a sensitivity of 20% to 79%.

Smith-Modified Sgarbossa Criteria The Smith-modified criteria were first published in 2012 in the Annals of Emergency Medicine (Smith, Dodd, Henry, Dvorak, & Pearce, 2012). Smith modified Sgarbossa’s rule C and made it much more sensitive in making the diagnosis of STEMI (91%). Instead of evaluating the EKG for ST discordance greater than 5 mm, it looked for ST elevation with a ST/T ratio of 25% or more. This became a validated tool in 2015. Smith-modified rule C: Discordant ST elevation with amplitude greater than 25% of the depth of the preceding S wave (ST/S ratio >0.25)

As in any situation, if the diagnosis is uncertain but concern for ischemia/infarction remains, serial EKGs and troponin should be obtained, looking for dynamic changes. A bedside echocardiogram may also be considered to look for an acute wall motion abnormality.

FINAL THOUGHTS There you have it. Another chapter in the book. Take some time to soak it all in. Just reading about how to diagnose a STEMI won’t make you an expert, but time and practice will help. Now, get to work on the practice.

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CASE STUDY 19.1 ATYPICAL ACUTE MYOCARDIAL INFARCTIO N Thomas Alleva, PA-C Patient Chief Complaint: “I just can’t get a good breath.” History of Present Illness: This patient is a 70+-year-old Caucasian man, who presented to the ED with a complaint of dyspnea at rest and on exertion, not amenable to increasing his basal 2 L nasal cannula oxygen level. He reports that he usually requires anywhere from 2 to 3 L nasal cannula, depending on his level of activity, but today, since getting ready for the day this morning before breakfast, he has increased to the maximum recommended by his pulmonologist, which was 4 L, with no relief and feels it is getting progressively worse. The patient also reports two episodes of severe, central to left chest pain that happened this morning. One episode woke him up before his alarm went off and lasted about 45 minutes. The other episode hit him right after breakfast, approximately 1 hour after the other one relented, and it lasted about 30 minutes, but was so severe he vomited up a small bit of breakfast. Since then, he has not had any more chest pain episodes. No relieving factors. The exacerbating factor is physical exertion. Denies any other complaints at this time but patient and patient family at bedside voiced their concerns over pneumonia because he had similar symptoms last year and was diagnosed with an almost fatal bout of pneumonia. Review of Systems: All systems besides those listed in HPI are negative. Past Medical History: Hypertension, hyperlipidemia, NSTEMI (approximately 8–10 years prior), advanced COPD (chronic bronchitis type), lung cancer (bronchogenic carcinoma recently diagnosed), osteoarthritis of both knee joints Physical Examination • Blood pressure: 162/97 • Pulse: 107 • Respiratory rate: 26 • Oxygen saturation: 94% (6 L via simple face mask) • Temperature: 98.9°F Patient lying on bed in a reclined position, obvious increased work of breathing, mild to moderate distress, and understandably anxious disposition overall.

Pertinent Exam Findings Skin: Pale with diffuse distribution of faint mottling appreciated more toward distal extremities; patient forehead seems to have the presence of a light perspiration Heart: Tachycardia, mild S3 gallop, 1+ pitting edema noted in bilateral lower extremities Lungs: Tachypnea, noted moderate use of accessory muscles for inspiration, loud coarse crackles are diffusely present and diminish toward the lung bases bilaterally DDx: Pulmonary embolism, acute myocardial infarction, congestive heart failure, respiratory failure secondary to acute exacerbation of COPD, pneumonia

Laboratory and Diagnostic Findings ProBNP: 872, troponin I: >100.0, venous pH (patient refused ABG): 7.36 EKGs (comparisons) First: 2 months prior Second: on initial presentation Third: approximately 1 hour following initial presentation

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(1)

(2)

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(3)

Imaging CXR: Hyperexpansion consistent with COPD with no evidence of acute pulmonary congestion; median sternotomy wires present; little change from comparison 2 months prior CTA PE Protocol: Negative for pulmonary embolism Diagnosis: Acute myocardial infarction Pertinent Diagnostic LHC findings: 100% occlusion of LAD; 70% occlusion of RCA

Thought Questions 1. What are your working diagnoses initially with this patient presentation? 2. Based on your analysis of the EKGs, if the patient were having an acute MI, what coronary vasculature would be involved? 3. Comparing the EKGs in this case, what ominous changes are present that would represent a significant infarction as well as signs indicative of a near-complete infarction? 4. If a clear acute coronary event is not discernible in the first EKG taken on a patient in whom you have high clinical suspicion for such pathology, what is the best option moving forward in the evaluation of the patient?

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Systematic Approach 1. What’s the rate? 2. Is the rhythm regular or irregular? 3. Is the QRS narrow or wide? If wide, does it have a bundle branch block morphology? 4. Are P waves present? Are they upright in leads I and II and inverted in aVR? 5. What’s the duration of the PR interval? 6. What is the axis? 7. Is there evidence of atrial/ventricular hypertrophy? 8. Are there findings consistent with ischemia or infarction?

TAKE-HOME POINTS • The initial EKG in a patient with ACS is normal or nondiagnostic 65% of the time. • Use of serial and old EKGs can be extremely valuable in making the right diagnosis. • The coronary artery affected can be postulated by the location of the leads demonstrating ST elevation. • STEMI criteria ▪ New ST elevation at the J point in two anatomically contiguous leads greater than or equal to 1 mm in all leads except ○ V2 and V3 ≥2 mm in men ≥40 years of age ○ V2 and V3 ≥2.5 mm in men 2.6 mmol/L) are hyperparathyroidism and malignancy. Symptoms vary based on acuity and level of calcium. They include constipation, fatigue, anorexia, nausea, and muscle weakness.

Abnormal calcium levels affect the ST segment and thus the QT duration. Calcium usually does not influence the morphology of P or T waves. Cardiac arrhythmias are also uncommon.

Characteristics of Hypercalcemia 1. Short ST segment. It may even be missing. 2. Short QTc interval. Inversely proportional to the serum calcium level. QTc stands for corrected QT. See Measuring the QT Interval below.

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Hypercalcemia. Very short ST/QT. The T wave occurs almost immediately after the QRS complex.

Hypocalcemia Hypocalcemia (