Goldberger's Clinical Electrocardiography, Tenth Edition PDF

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Copyrighted Material GOLDBERGER'S Enh need DIGITAL VERSION Cl in ica I 1ndu d El ectroca rd iogra p hy A Simplified Approach ELSEVIER Any scree1 Any time. Anywhere Activate the eBook version of this title at no additional charg( Elsevier eBo oks+ gives you the power to br owse, search, and cus to mize your content, make note s and highligh ts, and have content read aloud. Unlock your eBook today. 1. Visi t http://ebooks.health.elsevier.com/ 2. Log in or Sign up 3. S crat ch box below to reveal your code 4. Type your access code into t he "Redeem A ccess Code" box 5. Click "Redeem" Place Peel Off It's that easy! Sticker Here For technical assistance: em ail textbookscom.suppor [email protected] call 1-800-545-2522 (inside the US) call +44 1 865 844 640 (outside the US) Use of the current edition of the electronic version of this book (eBook) is subject to the terms of the nontransferable, limited license granted on http://ebooks.health.elsevier.com/. Access to the eBook is limited to the first individual who redeems the PIN, located on the inside cover of this book, at http://ebooks.health.elsevier.com/ and may not be transferred to another party by resale, lending, or other means. Elsevier 1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899 GOLDBERGER'S CLINICAL ELECT ROCARDIOGRAPHY, TENTH EDITION ISBN: 978-0-323-82475-0 Copyright© 2024 by Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, induding photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher's permissions policies and our arrangements with organizations such as the Co171right Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein). Notice Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds or experiments described herein. Because of rapid advances in the medical sciences, in particular, independent verification of diagnoses and drug dosages should be made. To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors or contributors for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Previous editions copyrighted 2018, 2013, 2006, 1999, and 1994. Senior Content Strategist: Melanie Tucker Content Development Manager: Ranjana Sharma Content Development Specialist: Ranjana Sharma Publishing Services Manager: Shereen Jameel Project Manager: Haritha Dharmarajan Design Direction: Brian Salisbury Working together to grow libraries in Printed in India developing countries www.elsevier.com www.booka1d.org Last digit is the print number: 9 8 7 6 S 4 3 2 1 Make everything as simple as possible, but not simpler. Albert Einstein INTRODUCTORY REMARKS OVERVIEW with tachycardias and bradycardias. Part III presents more specialized material, including sudden cardiac death, This book is an introduction to electrocardiography pacemakers, and implantable cardioverter-defibrillators written especially for medical students, house offi- (ICDs), and it also reviews selected “marquee” topics cers, and nurses. The text, which assumes no previous presented from different perspectives (e.g., digitalis tox- instruction in reading electrocardiograms (ECGs), icity, sudden cardiac arrest) to add dimensionality to the has been widely used in entry-level courses. Frontline earlier presentations. We make additional materials for clinicians, including emergency medicine physicians, review and further exploration available in online sup- hospitalists, emergency medical technicians, physician plements (ExpertConsult.com). assistants, and cardiology trainees wishing to review the essentials have consulted previous editions. A high degree of ECG “literacy” is increasingly ECG SKILL DEVELOPMENT AND important for those involved in acute clinical care at INCREASING DEMANDS FOR ECG all levels, requiring knowledge that far exceeds simple LITERACY pattern recognition and mnemonic aids. ECG inter- pretation is important not only as a focal point of clin- Throughout, we seek to stress the clinical applications ical medicine but as an exemplar of critical thinking. and implications of ECG interpretation. Each time The rigor demanded by competency in ECG analysis we mention an abnormal pattern, a clinical correlate requires attention both to the subtlest of details and to is introduced. Although the book is not intended as a the subtending arcs of integrative reasoning: of “seeing manual of therapeutics, we briefly discuss general prin- the trees and the forest.” ciples of treatment and clinical management where rel- Furthermore, ECG analysis is one of those unique evant. Whenever possible, we have tried to put ourselves areas in clinical medicine where you literally observe in the position of the clinician who has to look at ECGs physiologic and pathophysiologic dynamics “play out” without immediate specialist backup and make critical over seconds down to milliseconds. Not infrequently, decisions—sometimes at 3 a.m.! bedside rapid-fire decisions are based on real-time ECG In this spirit, we have tried to approach ECGs in data. The alphabetic P-QRS-T-U sequence, much more terms of a rational, simple differential diagnosis based than a flat graph, represents a dynamic mapping of mul- on pathophysiology, rather than through the tedium tidimensional electrical signals literally exploding into of rote memorization. It is reassuring to discover that existence (automaticity) and spreading throughout the the number of possible arrhythmias that can produce heart (conduction) as part of the fundamental processes a resting heart rate of more than 150 beats or more per of activation and recovery. The ECG provides some minute is limited to just a handful of choices. Only three of the most compelling and fascinating connections basic ECG patterns are observed during most cardiac between basic “preclinical” sciences and the recognition arrests. Similarly, only a limited number of conditions and treatment of potentially life-threatening problems cause low-voltage patterns, abnormally wide QRS com- in outpatient and inpatient settings. plexes, ST segment elevations, and so forth. This new, tenth edition follows the general format of the previous one. The material is divided into three ADDRESSING “THREE AND A HALF” KEY sections. Part I covers the basic principles of 12-lead electrocardiography, normal ECG patterns, and the CLINICAL QUESTIONS major abnormal depolarization (QRS) and repolariza- In approaching any ECG, readers should get in the tion (ST-T-U) patterns. Part II describes the mechanism habit of posing “three and a half ” essential queries: of sinus rhythms, followed by a discussion of the major What does the ECG show and what else could it be? arrhythmias and conduction abnormalities associated What are the possible causes of the waveform pattern vi  INTRODUCTORY REMARKS vii or patterns? What, if anything, should be done about interactions where recognition of normal and abnormal the finding(s)? patterns is only the starting point in patient care. Most basic and intermediate-level ECG books focus The tenth edition contains updated discussions of mul- on the first question (“What is it?”), emphasizing pattern tiple topics, including intraventricular and atrioventricu- recognition. However, waveform analysis is only a first lar (AV) conduction disturbances, electronic pacemakers step, for example, in the clinical diagnosis of atrial fibril- and implantable cardioverter–defibrillators (ICDs), sud- lation. The following issues must always be addressed den cardiac arrest, myocardial ischemia and infarction, as part of answering the initial diagnostic question: takotsubo cardiomyopathy, atrial fibrillation and flutter, What is the differential diagnosis? (“What else could it drug toxicities, amyloid cardiomyopathy, and COVID-19 be?”) Are you sure that the ECG actually shows atrial infection, we highlight differential diagnoses, along with fibrillation and not another “look-alike pattern,” such as “pearls and pitfalls” in ECG interpretation. Familiarity multifocal atrial tachycardia (MAT), sinus rhythm with with the limitations as well as the uses of the ECG is essen- atrial premature beats, atrial flutter with variable block, tial for novices and give special attention more seasoned or even an artifact resulting, for example, from parkin- clinicians. Reducing medical errors related to ECGs and sonian tremor or a noisy baseline? maximizing the information content of these recordings, “What could have caused the arrhythmia?” is the therefore, continue to be major themes. question framing the next set of considerations. Is the We also continue to give special emphasis to com- atrial fibrillation associated with valvular or nonval- mon points of confusion. Medical terminology (jargon) vular disease? If nonvalvular, is it related to hyper- is rife with ambiguities that cause confusion and some- tension, cardiomyopathy, coronary disease, advanced times promote miscommunication. Students of electro- age, hyperthyroidism, or other factors, singly or in cardiography face a barrage of challenges. Why do we combination? On a deeper level are issues concerning call the “P-QRS interval” the “PR interval”? What is the the most basic electrophysiologic mechanisms. With difference between ischemia and injury? What is meant atrial fibrillation, these mechanisms are still being by the term “paroxysmal supraventricular tachycardia worked out and involve a complex interplay of factors (PSVT)” and how does it differ (if it actually does) from including abnormal pulmonary vein automaticity, “supraventricular tachycardia”? Is “complete AV heart micro-reentrant loops (wavelets) in the atria, inflam- block” synonymous with “AV dissociation”? mation and fibrosis (“atriopathy”), and autonomic I am delighted that the two coauthors on the pre- perturbations. vious two editions, Zachary D. Goldberger, MD, and Finally, deciding on treatment and follow-up (“What Alexei Shvilkin, MD, PhD, continue in this role on the are the therapeutic options and what is the best course new tenth edition. We again thank our trainees and to do choose in this case?”) depends in an essential way colleagues for their probing and challenging questions. on answers to the questions posed above, with the ulti- Finally, we wish to express special gratitude to our fami- mate goal of delivering the highest level of scientifically lies for their inspiration and encouragement. informed, compassionate care. This edition again honors the memory of two remarkable individuals: the late Emanuel Goldberger, MD, a pioneer in the development of electrocardiogra- TENTH EDITION: ADDITIONAL NOTES phy and the inventor of the aVR, aVL, and aVF leads, With these clinical motivations in mind, the continuing who was coauthor of the first five editions of this text- aim of this introductory text is to present the contempo- book (with ALG), and the late Blanche Goldberger, an rary ECG as it is used in hospital wards, office settings, exceptionally gifted artist and woman of valor. outpatient clinics, emergency departments, intensive/ cardiac (cardiovascular) care units, and telemedicine, Ary L. Goldberger, MD  1 Essential Concepts: What Is an ECG? The electrocardiogram (ECG or EKG) is a special type of The device used to obtain and display the conven- graph that represents changes in cardiac electrical activ- tional (12-lead) ECG is called the electrocardiograph, or ity from one instant to the next. Specifically, the ECG more informally, the ECG machine or device. It records provides a time-voltage chart of the heartbeat. cardiac electrical currents (voltages or potentials) by 10 seconds of ECG data (lead II) from healthy young adult. Note variation in rate due to breathing. The ECG is a key component of clinical diagnosis means of sensors, called electrodes, selectively positioned and management of inpatients and outpatients because on the surface of the body.a Students and clinicians are it often provides critical information. Therefore, a major often understandably confused by the basic terminology focus of this book is on recognizing and understanding that labels the graphical recording as the electrocardio- the “signature” ECG findings in life-threatening condi- gram and the recording device as the electrocardio- tions such as acute myocardial ischemia and infarction, graph! We will point out other potentially confusing hypertension, severe hyperkalemia or hypokalemia, hypo- ECG semantics as we go along. thermia, certain types of drug toxicity that may induce Contemporary ECGs used in day-to-day clinical cardiac arrest, pericardial (cardiac) tamponade, abnormal medicine are usually recorded with disposable paste-on heart rhythms (arrhythmias) among many others. (adhesive) silver–silver chloride electrodes. For the stan- The general study of ECGs, including its clinical dard ECG recording, electrodes are placed on the lower applications, technologic aspects, and basic science arms, lower legs, and across the chest wall (precordium). underpinnings, comprises the field of electrocardiogra- In settings such as emergency departments, cardiac and phy, or more generally, electrocardiology. The broader intensive care units (CCUs and ICUs), and ambulatory field of cardiac electrophysiology includes electrocardiog- (e.g., Holter and long-term) monitoring, only one or raphy (recordings from the surface of the body), intra- two “rhythm strip” leads may be recorded, usually by cardiac recordings and cardiac implantable electronic means of a few chest and abdominal electrodes. devices (pacemakers and defibrillators; Chapter 22), We are also well into a burgeoning era of ECG ablation therapy, as well as basic studies of the electrical recorders being directly marketed to consumers. These properties of cardiac cells and tissues. a As discussed in Chapter 3, stated more precisely, ECG “leads” Please go to expertconsult.inkling.com for additional online record the time-varying differences in electrical potential material for this chapter. between pairs or configurations of electrodes.  CHAPTER 1 Essential Concepts: What Is an ECG? 3 Fig. 1.1 Normally, the cardiac stimulus (electrical signal) is generated in an automatic way by pacemaker cells in the sinoatrial (SA) node, located in the high right atrium (RA). The stimulus then spreads through the RA and left atrium (LA). Next, it traverses the atrioventricular (AV) node and the bundle of His, which comprise the AV junction. The stimulus then sweeps into the left and right ventricles (LV and RV) by way of the left and right bundle branches, which are contin­ uations of the bundle of His. The cardiac stimulus spreads rapidly and simultaneously to the left and right ventricular muscle cells through the Purkinje fibers. Electrical activation of the atria and ventricles, respectively, leads to sequential contraction of these chambers (electromechanical coupling). Not shown are Bachmann’s bundle, a muscular structure connecting the right and left atria, and internodal fibers between the SA and AV nodes. products include hand-held devices that record single auto-regulatory adjustments is accomplished by changes lead or multi-lead ECGs. Users can then transmit the in heart rate, which, as described below, are primarily recordings to personal laptop or desktop computers and under the control of the parasympathetic and sympathetic send them electronically to medical caregivers. Comple- branches of the autonomic (involuntary) nervous system. mentary “medical wearable” products include “smart- The signal for cardiac contraction is the spread of watches” that record and transmit single lead ECGs synchronized electrical currents through the heart mus- (typically 30 seconds). Discussion of the uses and lim- cle. These currents are generated both by pacemaker cells itations of these devices, as well as of their underlying and by specialized conduction tissue within the heart and technologies, goes beyond the scope of this introductory by the working heart muscle itself. Pacemaker cells are book. like tiny clocks (technically called oscillators) that auto- matically generate electrical stimuli in a repetitive fash- ABCs OF CARDIAC ELECTROPHYSIOLOGY ion. The other heart cells, both specialized conduction tissue and working heart muscle, function like cables Before the basic ECG patterns are described, we review that transmit these electrical signals.b a few simple-to-grasp but fundamental principles of the heart’s electrical properties. Electrical Signaling in the Heart The central function of the heart is to contract In simplest terms, therefore, the heart is an electrically- rhythmically and pump blood to the lungs (pulmonary timed pump. The electrical “wiring” of this remarkable circulation) for oxygenation and then to pump this oxy- organ is schematized in Fig. 1.1. gen-enriched blood into the general (systemic) circu- lation. Furthermore, the amount of blood pumped has b Heart muscle cells of all types possess another important elec- to be matched precisely to meet the body’s constantly trical property called refractoriness. This term refers to the fact varying metabolic needs. The heart muscle and other that for a short term after they emit a stimulus or are stim- tissues require more oxygen and nutrients when we are ulated (depolarize), the cells cannot immediately discharge active compared to when we rest. A key facet of these again because they need to repolarize. 4 PART I Basic Principles and Patterns Normally, the signal for heartbeat initiation starts in bundle branch,e which distributes the stimulus to the the pacemaker cells of the sinus or sinoatrial (SA) node. left ventricle (see Fig. 1.1). This node is located in the right atrium near the opening The electrical signal spreads rapidly and simultane- of the superior vena cava. The SA node is a small, oval ously down the left and right bundle branches into the collection (about 2 × 1 cm) of specialized cells capa- ventricular myocardium (ventricular muscle) by way ble of automatically generating an electrical stimulus of specialized conducting cells called Purkinje fibers (spark-like signal) and functions as the normal pace- located in the subendocardial layer (roughly the inside maker of the heart. From the sinus node, this stimulus half or rim) of the ventricles. From the final branches spreads first through the right atrium and then into of the Purkinje fibers, the electrical signal spreads the left atrium. Interatrial electrical communication is through myocardial muscle toward the epicardium facilitated by a horizontal muscular band called Bach- (outer rim). mann’s bundle (not shown on the figure). Disruption of The bundle of His, its branches and their subdivi- Bachmann’s bundle by fibrosis or other pathologies may sions collectively constitute the His–Purkinje system. be associated with increased risk atrial fibrillation (see Normally, the AV node and His–Purkinje system provide Chapters 7 and 15). the only electrical connection between the atria and the Electrical stimulation of the right and left atria sig- ventricles, unless an abnormal structure called a bypass nals the atria to contract and pump blood simultane- tract is present. This abnormality and its consequences ously through the tricuspid and mitral valves into the are described in Chapter 18 on Wolff–Parkinson–White right and left ventricles, respectively. The electrical stim- (WPW) preexcitation patterns. ulus as it spreads through the atria reaches specialized In contrast, impairment of conduction over these conduction tissues in the atrioventricular (AV) junction.c bridging structures underlies various types of AV heart The AV junction, which acts as an electrical “relay” block (Chapter 17). In its most severe form, electrical connecting the atria and ventricles, is located near the conduction (signaling) between atria and ventricles is lower part of the interatrial septum and extends into the completely severed, leading to third-degree (complete) interventricular septum (see Fig. 1.1).d AV heart block. The result is usually a very slow escape The upper (proximal) part of the AV junction is the rhythm and a reduced cardiac output, causing weakness, AV node. (In some texts, the terms AV node and AV junc- lightheadedness or fainting, and even sudden cardiac tion are used synonymously.) arrest and sudden death (Chapter 21). The lower (distal) part of the AV junction is called Just as the spread of electrical stimuli through the the bundle of His. The bundle of His then divides into atria leads to atrial contraction, so the spread of stimuli two main branches: the right bundle branch, which dis- through the ventricles leads to ventricular contraction, tributes the stimulus to the right ventricle, and the left with pumping of blood to the lungs and into the general circulation. The initiation of cardiac contraction by electrical c Atrial stimulation is usually modeled as an advancing (radial) wave of excitation originating in the SA node, like the ripples stimulation is referred to as electromechanical coupling. induced by a stone dropped in a pond. The spread of activation A key part of the contractile mechanism involves the waves between the SA and AV nodes may also be facilitated by release of calcium ions inside the atrial and ventricu- so-called internodal “tracts.” However, the anatomy and elec- lar heart muscle cells, which is triggered by the spread trophysiology of these preferential internodal pathways, which of electrical activation. The calcium ion release and can be analogized as functioning a bit like “fast lanes” on the reuptake processes link electrical and mechanical func- atrial conduction highways, remain subjects of investigation tion (see Bibliography). and controversy among experts, and do not directly impact The ECG is capable of recording only relatively large clinical assessment. currents produced by the mass of working (pumping) d Note the potential confusion in terms. The muscular wall sep- arating the ventricles is the interventricular septum, while a similar term—intraventricular conduction delays (IVCDs)— e The left bundle branch has two major subdivisions called is used to describe bundle branch blocks and related distur- fascicles. (These conduction tracts are also discussed in bances in electrical signaling in the ventricles, as introduced Chapter 8, along with abnormalities called fascicular blocks or in Chapter 8. hemiblocks.)  CHAPTER 1 Essential Concepts: What Is an ECG? 5 heart muscle. The much smaller amplitude signals gen- conductivity and refractoriness. The rates with which erated by the sinus node and AV node are not detectable electrical impulses are conducted through different from the surface ECG recordings. Depolarization of the parts of the heart varies. Conduction velocity is fast- His bundle area can only be recorded from inside the est through the Purkinje fibers and slowest through heart during specialized cardiac electrophysiologic (EP) the AV node. The relatively slow conduction speed studies. through the AV node allows the ventricles time to fill with blood before the signal for cardiac contraction CARDIAC AUTOMATICITY AND arrives. Rapid conduction through the His–Purkinje system ensures synchronous contraction of both left CONDUCTIVITY: “CLOCKS AND CABLES” and right ventricles. Automaticity refers to the capacity of certain cardiac Refractoriness is an inherent electrophysiologic cells to function as pacemakers by spontaneously gener- property of normal cardiac cells and fibers that prevents ating electrical impulses, like tiny clocks. As mentioned them from initiating or conducting successive impulses. earlier, the sinus node normally is the primary (dom- This protective property applies both to the sinus node, inant) pacemaker of the heart because of its inherent to working (contractile) myocytes in the atria and ven- automaticity. tricles, and to the specialized (AV nodal-His Purkinje) Under special conditions, however, other cells conduction system. outside the sinus node (in the atria, AV junction, or The more you understand about normal physio- ventricles) can also act as independent (secondary/ logic stimulation of the heart, the stronger your basis subsidiary) pacemakers. For example, if sinus node for comprehending the abnormalities of heart rhythm automaticity is depressed, the AV junction can act as and conduction and their distinctive ECG patterns. a backup (escape) pacemaker. Escape rhythms gen- For example, incapacity of the sinus node to effectively erated by subsidiary pacemakers provide important stimulate the atria can occur because of a failure of physiologic redundancy (safety mechanisms) in the SA automaticity or because of local conduction block vital function of heartbeat generation, as described in that prevents the stimulus from exiting the sinus node Chapter 13. (Chapter 13). Either pathophysiologic mechanism can Normally, the more rapid intrinsic rate of SA node result in apparent sinus node dysfunction and sometimes firing suppresses the automaticity of these secondary symptomatic sick sinus syndrome (Chapter 19). Patients (ectopic) pacemakers outside the sinus node. However, may experience lightheadedness or even syncope sometimes their automaticity becomes abnormally (fainting) because of marked bradycardia (slow heart- increased in association with one or more factors, beat), requiring placement of an electronic pacemaker including drug effects, autonomic activation, met- (Chapter 22). abolic perturbations, heart failure, and so forth. As a In contrast, abnormal conduction within the heart result, pacemakers may compete with and even usurp can lead to various types of tachycardia due to reentry, a the sinus node’s normally dominant control of the mechanism in which an impulse “chases its tail,” short- heartbeat. (In addition, abnormally decreased auto- circuiting the normal activation pathways. Reentry plays maticity of the SA node may promote this disruption an important role in the genesis of certain paroxysmal of cardiac electrical regulation.) A rapid run of ectopic supraventricular tachycardias (PSVTs), including those atrial beats results in atrial tachycardia (Chapter 14). involving AV nodal dual pathways or an AV bypass tract, Abnormal atrial automaticity is also of central impor- as well as in many variants of ventricular tachycardia tance in the initiation of atrial fibrillation and atrial (VT), as described in Part II. flutter (Chapter 15). A rapid run of ectopic ventricular As noted, blockage of the spread of stimuli through beats results in ventricular tachycardia (Chapter 16), the AV node or infranodal pathways can produce vari- a potentially life-threatening arrhythmia, which may ous degrees of AV heart block (Chapter 17), sometimes lead to ventricular fibrillation and cardiac arrest with severe, symptomatic ventricular bradycardia or (Chapter 21). increased risk of these life-threatening complications, In addition to automaticity, the two other major, necessitating placement of a permanent electronic pace- inter-related electrical properties of the heart are maker (Chapter 22).  PART I Basic Principles and Patterns Fibrosis or factors impairing conduction in the bun­ SOME REASONS FOR ECG "LITERACY" dle branches themselves can produce right or left bundle Frontline medical caregivers are often required to branch block. The latter especially is a cause of electrical make on-the-spot, critical decisions based on their dyssynchrony, an important contributing mechanism in own ECG readings. many cases of heart failure (see Chapters 8 and 22). Computer (electronic) readings are often incomplete or incorrect and require expert over-read. CONCLUDING NOTES: WHY IS THE ECG Accurate readings are essential to early diagnosis and therapy of acute coronary syndromes, including SO USEFUL? ST segment (STEMI) and non-ST segment elevation The ECG is one of the most versatile and inexpensive myocardial infarction. clinical tests. Its utility derives from careful clinical and Insightful readings may also avert medical catastro­ phes and sudden cardiac arrest, such as those asso­ e:>..'J'erimental studies over more than a century showing ciated with the hereditary or acquired Jong OT syn­ its essential role in: drome, thereby preventing torsades de pointes. Diagnosing dangerous cardiac electrical disturbances Mistaken readings (false negatives and false posi­ causing brady- and tachyarrhythmias. Examples in­ tives) can have major consequences, both clinical and clude high-grade AV heart block, atrial fibrillation or medico-legal (e.g., missed or mistaken diagnosis of flutter, and ventricular tachyarrhythmias. atrial fibrillation). Providing immediate information about clinically The requisite combination of attention to details and important problems, including myocardial ischemia/ integration of these into the larger picture ("trees infarction, electrolyte disorders, and drug toxicity, and forest" approach) provides a template for critical as well as hypertrophy and other types of chamber thinking essential to all of clinical practice. overload. Affording clues ("tells") that allow canny clinicians to forecast preventable catastrophes. A major exam­ ple is a very long QT(U) pattern, usually caused by The second part deals with abnormalities of car­ a drug effect or by hypokalemia, which may herald diac rhythm generation and conduction that produce sudden cardiac arrest due to torsades de pointes. excessively fast or slow heart rates (tachycardias and bradycardias). The third part provides both a review and further PREVIEW: LOOKING AHEAD e:>..1.ension of material covered in earlier chapters, includ­ The first part of this book is devoted to e:>..'J'laining the ing an important focus on avoiding ECG errors. basis of the normal ECG and then examining the major Selected publications are cited in the Bibliography, conditions that cause abnormal depolarization (P and including freely available online resources. In addition, QRS) and repolarization (ST-T and U) patterns. This the online supplement to this book provides additional basic alphabet of ECG terms is defined in Chapters 2 material, with additional case studies and practice ques­ and 3. tions with answers.  2 Electrocardiogram Basics: Waves, Intervals, and Segments The first purpose of this chapter is to present two funda- negatively charged and the inside of the cell becomes mental electrical properties of heart muscle cells: (1) positive. This produces a difference in electrical voltage depolarization (activation) and (2) repolarization on the outside surface of the cell between the stimulated (recovery). Second, in this chapter, and the next, we depolarized area and the unstimulated polarized area define and show how to measure the basic waveforms, (Fig. 2.1B). Consequently, a small electrical current is segments, and intervals essential to electrocardiogram formed that spreads along the length of the cell as stim- (ECG) interpretation. ulation and depolarization occur until the entire cell is depolarized (Fig. 2.1C). The path of depolarization can DEPOLARIZATION AND REPOLARIZATION be represented by an arrow, as shown in Fig. 2.1B. Note: For individual myocardial cells (fibers), depo- In Chapter 1, the term electrical activation (stimulation) larization and repolarization proceed in the same was applied to the spread of electrical signals through direction. However, for the entire myocardium, depo- the atria and ventricles. The more technical term for the larization normally proceeds from innermost layer cardiac activation process is depolarization. The return (endocardium) to outermost layer (epicardium), of heart muscle cells to their resting state after depolar- whereas repolarization proceeds in the opposite direc- ization is termed repolarization. tion. The exact mechanisms of this well-established These key designations derive from the basic elec- asymmetry are not fully understood. trophysiologic finding that normal “resting” myocardial The depolarizing electrical current is recorded on the cells are polarized; that is, they carry electrical charges ECG as a P wave (when the atria are stimulated) and as a on their surface. Fig. 2.1A shows the resting polarized QRS complex (when the ventricles are stimulated). state of a normal atrial or ventricular heart muscle cell. Repolarization starts when the fully stimulated, Notice that the outside of the resting cell is positive and depolarized cell begins to return to the resting state. A the inside is negative (about −90 mV [millivolt] gradi- small area on the outside of the cell becomes positive ent between them).a again (Fig. 2.1D), and the repolarization spreads along When a heart muscle cell (or group of cells) is stim- the length of the cell until the entire cell is once again ulated, it depolarizes. As a result, the outside of the cell, fully repolarized. Ventricular repolarization is sequen- in the area where the stimulation has occurred, becomes tially recorded on the ECG as the ST segment, T wave, and U wave. Visit eBooks.Health.Elsevier.com for additional online ma- In summary, whether the ECG is normal or abnor- terial for this chapter. mal, it records just two basic events: (1) depolarization, a Membrane polarization is due to differences in the concen- tration of ions inside and outside the cell. A brief review of the spread of a stimulus (stimuli) through the heart this important topic is presented in the online material, and muscle, and (2) repolarization, the return of the stim- also see the Bibliography for references that present the basic ulated heart muscle to the resting state. The basic cel- electrophysiology of the resting membrane potential and cel- lular processes of depolarization and repolarization are lular depolarization and repolarization (the action potential) responsible for the waveforms, segments, and intervals underlying the ECG waves recorded on the body surface. seen on the body surface (standard) ECG.  PART I Basic Principles and Patterns --.- ·.··'-'-'"· · ·.a.: ·..a....* + (:_ +.::,,. s ·...- \ +..,_ _____________) + + + + "€ + ) ------------" A B + C D Fig. 2.1 Depolarization and repolarization. (A) The resting heart muscle cell is polarized; that is, it carries an electrical charge, with the outside of the cell positively charged and the inside nega­ tively charged. !Bl When the cell is stimulated (5). it begins to depolarize (stippled areal. (Cl The fully depolarized cell is positively charged on the inside and negatively charged on the outside. (D) Repolarization occurs when the stimulated cell returns to the resting state. The directions of depolarization and repolarization are represented by arrows. Depolarization (stimulation) of the atria produces the P wave on the ECG, whereas depolarization of the ventricles produces the ORS complex. Repolarization of the ventricles produces the ST-T complex. FIVE BASIC ECG WAVEFORMS: P, ORS, The five basic ECG waveforms, labeled alphabetically, are the: ST, T, AND U P wave - atrial depolarization The ECG records the electrical activity of a myriad of QRS complex - ventricular depolarization atrial and ventricular cells, not just tha t of single fibers. ST segment The sequential and organized spread of stimuli through T wave } ve ntricular repolariza tion the atria and ventricles followed by their return to the U wave resting state produces the electrical currents recorded on the ECG. Furthermore, each phase of cardiac elec­ ECG WAVEFORMS trical activity produces a specific wave or deflection. 1. P wave, representing the spread of a stimulus QRS waveforms are referred to as complexes (Fig. 2.2). through the atria (atrial depolarization); 2. ORS waveform, or complex, representing stimulus spread through the ventricles (ventricular depolariza­ tion). As the name implies, the ORS set of deflec­ tions (complex) includes one or more specific waves, labeled as 0, R. and S; 3. ST (considered both a waveform and, more specifi­ cally, a segment); 4. T wave (often grouped with the preceding ST compo­ nent as the "ST-T" waveform) representing the return of sti mulated ventricular muscle to the resting state (ventricular repolarization). Furthermore, the very begin­ ning of the ST segment (where it joins the ORS com­ Fig. 2.2 The P wave represents atrial depolarization. plex) is called the J point (see also Chapter 3); and The PR interval is the time from initial stimulation of the 5. U wave, a usually small deflection sometimes seen atria to initial stimulation of the ventricles. The ORS com­ just after the T wave. It represents the final phase plex represents ventricular depolarization. The ST seg­ of ventr icular repolarization, although its exact ment, T wave, and U wave are produced by ventricular mechanism is not known. repolarization.  CHAPTER 2 Electrocardiogram Basics: Waves, Intervals, and Segments 9 Fig. 2.3 Summary of major components of the ECG graph. These can be grouped into 5 wave- forms (P, QRS, ST, T, and U), 4 intervals (RR, PR, QRS, and QT), and 3 segments (PR, ST, and TP). Note that the ST can be considered as both a waveform and a segment. The RR interval is the same as the QRS–QRS interval. The TP segment is used as the isoelectric baseline, against which deviations in the PR segment (e.g., in acute pericarditis) and ST segment (e.g., in ischemia) are measured. You may be wondering why none of the listed waves occur during major cardiac arrhythmias and conduction or complexes represents the return of the stimulated disturbances, the subjects of future chapters. (depolarized) atria to their resting state. The answer is that the atrial ST segment (STa) and atrial T wave (Ta) are generally not observed on the routine ECG because ECG SEGMENTS VS. ECG INTERVALS of their low amplitudes. An important exception is ECG interpretation also requires careful assessment described in Chapter 12 with reference to acute peri- of the time within and between various waveforms. carditis, which often causes subtle but important devia- Segments constitute the portions of the ECG brack- tions of the PR segment. eted by the end of one waveform and the beginning Similarly, the routine body surface ECG is not sen- of another. Intervals are the portions of the ECG that sitive enough to record any electrical activity during include at least one entire waveform. the spread of stimuli through the atrioventricular There are three basic segments: (AV) junction (AV node and bundle of His) en route 1. PR segment: end of the P wave to beginning of the to the ventricular myocardium. This key series of QRS complex. Atrial repolarization begins in this events, which appears on the surface ECG as a straight segment. (Atrial repolarization continues during the line, is actually not electrically “silent” but reflects the QRS and ends during the ST segment.) spread of electrical stimuli through the AV junction 2. ST segment: end of the QRS complex to beginning of and the His–Purkinje system, just preceding the QRS the following T wave. As noted in the previous section, complex. the ST-T complex represents ventricular repolarization. In summary, the P/QRS/ST-T/U sequence represents The segment is also considered as a separate waveform, the cycle of the electrical activity of the normal heart- as noted. ST elevation and/or depression are major beat. This physiologic signaling process begins with the signs of ischemia, as discussed in Chapters 9 and 10. spread of a stimulus through the atria (P wave), initiated 3. TP segment: end of the T wave to beginning of the by sinus node depolarization, and ends with the return P wave. This segment, which represents the electrical of stimulated ventricular muscle to its resting state resting state, is important because it is traditionally (ST-T and U waves). As shown in Fig. 2.3, the basic car- used as the baseline reference from which to assess PR diac cycle normally repeats itself maintaining the rhyth- and ST deviations in conditions such as acute peri- mic pulse of life. Disruptions of this life-sustaining cycle carditis and acute myocardial ischemia, respectively. 10 PART I Basic Principles and Patterns Fig. 2.4 The basic cardiac cycle (P–QRS–T) normally repeats itself again and again. In addition to these segments, four sets of intervals 5–4–3 Rule for ECG Components are routinely measured: PR, QRS, QT/QTc, and PP/RR.b To summarize, the clinical ECG graph comprises wave- The latter set (PP/RR) represents the inverse of the ven- forms, intervals, and segments designated as follows: tricular/atrial heart rate(s), as discussed in Chapter 3. 5 waveforms (P, QRS, ST, T, and U) 1. The PR interval is measured from the beginning of 4 intervals (PR, QRS, QT/QTc, and RR/PP) the P wave to the beginning of the QRS complex. 3 segments (PR, ST, and TP) 2. The QRS interval (duration) is measured from the We make two brief notes to avoid possible semantic beginning to the end of the same QRS. confusion: (1) The ST is considered both a waveform 3. The QT interval is measured from the beginning of and a segment. (2) Technically, the duration of the P the QRS to the end of the T wave. When this interval wave is also an interval. is corrected (adjusted for the heart rate), the designa- However, to avoid confusion with the PR, the inter- tion QTc is used, as described in Chapter 3. val subtending the P wave is usually referred to clini- 4. The RR (QRS–QRS) interval is measured from one cally as the P wave width or duration, rather than the point (sometimes called the R-point) on a given QRS P wave interval. The P duration (interval) is also mea- complex to the corresponding point on the next. The sured in units of milliseconds or seconds and is most instantaneous heart rate (beats per minute) = 60/RR important in the diagnosis of left atrial abnormality interval when the RR is measured in seconds (sec). and interatrial conduction delays (Chapter 7). Normally, the PP interval is the same as the RR in- The major components of the ECG are summarized terval, especially in “normal sinus rhythm.” We will in Fig. 2.3. discuss major arrhythmias where the PP is different from the RR, for example, sinus rhythm with com- plete heart block (Chapter 17).c ECG GRAPH PAPER The P–QRS–T sequence is recorded on special ECG b The peak of the R wave is often selected. But students should graph paper that is divided into grid-like boxes (Figs. 2.4 be aware that any consistent points on sequential QRS com- and 2.5). Each of the small boxes is 1 millimeter square plexes may be used to obtain the “RR” interval, even S waves or (1 mm2). The standard recording rate is equivalent to QS waves. Similarly, the PP interval is also measured from the 25 mm/sec (unless otherwise specified). Therefore same location on one P wave to that on the next. This interval horizontally, each unit represents 40 msec = 0.04 sec gives the atrial rate. Normally, the PP interval is the same as the (25 mm/sec × 0.04 sec = 1 mm). Notice that the lines RR interval (see below), especially in “normal sinus rhythm.” between every five boxes are thicker, so that each 5-mm Strictly speaking, the PP interval is actually the atrial--to--atrial (AA) interval, since in two major arrhythmias—atrial flutter unit horizontally corresponds to 2000 msec = 0.2 sec and atrial fibrillation (Chapter 15)—continuous atrial activity, (5 × 0.04 sec = 0.2 sec). All of the ECGs in this book rather than discrete P waves, are seen. have been calibrated using these specifications, unless otherwise indicated. c You may be wondering why the QRS–QRS interval is not A remarkable (and sometimes taken for granted) measured from the very beginning of one QRS complex to the beginning of the next. For convenience, the peak of the R wave aspect of ECG analysis is that these recordings allow you (or nadir of an S or QS wave) is usually used. The results are to measure events occurring over time spans as short equivalent and the term RR interval is most widely used to as 40 msec or less in order to make decisions critical to designate this interbeat interval, which the inverse of instanta- patient care. A good example is an ECG showing a QRS neous heart rate. interval of 100 msec, which is normal, versus one with a  CHAPTER 2 Electrocardiogram Basics: Waves, Intervals, and Segments 11 Fig. 2.5 The ECG is recorded on graph paper divided into millimeter squares, with darker lines marking 5-mm squares. Time is measured on the horizontal (X) axis. With a paper speed of 25 mm/sec, each small (1-mm) box side equals 0.04 sec (40 msec) and each larger (5-mm) box side equals 0.2 sec (200 msec or one-fifth of a second). A 3-sec interval is denoted. The amplitude of a deflection or wave is measured in millimeters on the vertical (Y) axis. QRS interval of 140 msec, which is markedly prolonged We continue our discussion of ECG basics in the fol- and might be a major clue to bundle branch block lowing chapter, focusing on how to make key measure- (Chapter 8), hyperkalemia (Chapter 11), or ventricular ments based on ECG intervals and their normal ranges tachycardia (Chapter 16). in adults. How to Make Basic ECG Measurements This chapter continues the discussion of electrocardio­ have high QRS voltage caused by hypertrophy), there gram (ECG) basics introduced in Chapters 1 and 2. Here may be considerable overlap between the deflections on we focus on recognizing key components of the ECG in one lead with those one above or below it. When this order to make clinically important measurements from occurs, it may be advisable to repeat the ECG at one-half these time-voltage graphs. standardization to get the entire tracing on the paper. If the ECG complexes are very small, it may be advisable to STANDARDIZATION (CALIBRATION) double the standardization (e.g., to study a small Q wave OF THE ECG more thoroughly or augment a subtle pacing stimulus). Some electronic electrocardiographs do not display the The standard ECG recording is generally calibrated such calibration pulse. Instead, they print the effective paper that a signal of 1-mV amplitude produces a 10-mm de­ ("sweep") speed and standardization at the bottom of flection. Modern ECG units are electronically calibrated; the ECG paper ("25 mm/sec, 10 mm/mV"). older ones may have a manual calibration setting. Because the ECG is calibrated, any part of the P, QRS, and T deflections can be precisely described in two ECG as a Dynamic Heart Graph ways; that is, both the amplitude (voltage) and the width (duration) of a deflection can be measured. For clinical The electrocardiogram (ECG) is a real-time graph of the purposes, if the standardization is set at 1 mV = 10 mm, heartbeat. The small ticks on the horizontal axis corre­ the height of a wave is usually recorded in millimeters, spond to intervals of 40 msec (0.04 sec). The vertical not millivolts. In Fig. 3.2, for example, the P wave is axis corresponds to the magnitude (voltage) of the 1 mm in amplitude, the QRS complex is 8 mm, and the waves/deflections (10 mm= 1 mV) T wave is about 3.5 mm. The ECG recoding also includes other nonphysio­ As shown in Fig. 3.1, the standardization mark pro­ logic deflections. Notably, as described next, electronic duced when the machine is routinely calibrated is a 12-lead recorders inscribe vertical lines to separate square (or rectangular) wave 10 mm tall, usually dis­ leads on typical 12-lead displays. Artifacts, for example played at the left side of each row of the ECG. If the because of electrical interference, poor electrode con­ machine is not standardized in the e:>..l'ected way, the tact, and tremor, are described in Chapter 23. 1-mV signal produces a deflection either more or less than 10 mm, and the amplitudes of the P, QRS, and T deflections will be larger or smaller than they should be. PHYSIOLOGIC COMPONENTS OF THE The standardization deflection is also important ECG: WAVEFORMS, INTERVALS, AND because it can be varied in most electrocardiographs (see SEGMENTS Fig. 3.1). When very large deflections are present (e.g., We now describe in more detail the ECG alphabet of P, as occurs in some patients who have an electronic pace­ QRS, ST, T, and U waves. The measurements of PR in­ maker that produces very large stimuli ["spikes"] or who terval, QRS interval (width or duration), and QT/QTc Visit eBooks.Health.Elsevier.com for additional online ma­ intervals and RR/PP intervals are also described, along terial for this chapter. with their physiologic (normative) values in adults.  CHAPTER 3 How to Make Basic ECG Measurements 13 Fig. 3.1 Before taking an ECG, the operator must check to see that the machine is properly cal- ibrated so that the 1-mV standardization mark is 10 mm tall. (A) Electrocardiograph set at normal standardization. (B) One-half standardization. (C) Two times normal standardization. Fig. 3.3 Measurement of the PR interval (see text). Fig. 3.2 The P wave is positive (upward), and the T spread through the atria and pass through the atrioven- wave is negative (downward). The QRS complex is bi- tricular (AV) junction. (This physiologic delay allows the phasic (partly positive, partly negative), and the ST seg- ventricles to fill fully with blood before ventricular depo- ment is isoelectric (neither positive nor negative). larization occurs, to optimize cardiac output.) In adults the normal PR interval is between 0.12 and 0.2 sec (three to Note: The ECG waves described in the next section five small box sides). When conduction through the AV are usefully designated as positive or negative. By con- junction is impaired, the PR interval may become pro- vention, an upward deflection or wave is called positive. longed. As noted, prolongation of the PR interval above A downward deflection or wave is called negative. A 0.2 sec (200 msec) is called first-degree heart block (delay) deflection or wave that rests on the baseline is said to be (see Chapter 17). With sinus tachycardia, AV conduction isoelectric. A deflection that is partly positive and partly may be facilitated by increased sympathetic and decreased negative is called biphasic. For example, in Fig. 3.2 the vagal tone modulation. Accordingly, the PR may be rela- P wave is positive, the QRS complex is biphasic (initially tively short (e.g., about 0.10-0.12 sec [100-120 msec]), as positive, then negative), the ST segment is isoelectric a physiologic finding, in the absence of Wolff–Parkinson– (flat on the baseline), and the T wave is negative. White (WPW) preexcitation (see Chapter 18). P Wave and PR Interval QRS Complex The P wave, which represents atrial depolarization, is a The QRS complex represents the spread of a stimulus small positive (or negative) deflection before the QRS through the ventricles. However, not every QRS com- complex. The normal values for P wave axis, amplitude, plex contains a Q wave, an R wave, and an S wave— and width are described in Chapter 7. The PR interval is hence the possibility of confusion. The slightly awkward measured from the beginning of the P wave to the be- (and arbitrary) nomenclature becomes understandable ginning of the QRS complex (Fig. 3.3). The PR interval if you remember three basic naming rules for the com- may vary slightly in different leads, and the shortest PR ponents of the QRS complex in any lead (Fig. 3.4): interval should be noted when measured by hand. The 1. When the initial deflection of the QRS complex is PR interval represents the time it takes for the stimulus to negative (below the baseline), it is called a Q wave. 14 PART I Basic Principles and Patterns capital letters (QRS) are used to designate waves of rel- atively large amplitude and small letters (qrs) label rel- atively small waves. However, no exact thresholds have been developed to say when an s wave qualifies as an S wave, for example. The QRS naming system does seem confusing at first, but it allows you to describe any QRS complex and evoke in the mind of the trained listener an exact mental picture of the complex named. For example, in describ- ing an ECG you might say that lead V1 showed an rS complex (“small r, capital S”): or a QS (“capital Q, capital S”): Fig. 3.4 QRS nomenclature (see text). 2. The first positive deflection in the QRS complex is called an R wave. QRS Interval (Width or Duration) 3. A negative deflection after the R wave is called an S The QRS interval represents the time required for a stim- wave. ulus to spread through the ventricles (ventricular depo- Thus the following QRS complex contains a Q wave, larization). Normally, in adults this interval is ≤0.10 sec an R wave, and an S wave. In contrast, the following (100 msec) as measured by the eye, or ≤0.11 sec (110 complex does not contain three waves: msec) when electronically measured by computer algo- rithms (Fig. 3.5).a If the spread of a stimulus through a You may have already noted that the QRS amplitude (height or depth) often varies slightly from one beat to the next. This variation may be caused by a number of factors. One is related to breathing mechanics: as you inspire, your heart rate speeds up because of decreased cardiac vagal tone (Chapter 13), and it decreases with expiration because of increased vagal tone. Breathing may also change the QRS axis because changes in heart position and chest impedance change QRS amplitude If, as shown earlier, the entire QRS complex is posi- slightly. If the rhythm strip is long enough, you may even be tive, it is simply called an R wave. However, if the entire able to estimate the patient’s breathing rate. QRS changes may complex is negative, it is termed a QS wave (not just a Q also occur to slight alterations in ventricular activation, as with atrial flutter and fibrillation with a rapid ventricular response wave as you might expect). (Chapter 15). Beat-to-beat QRS alternans with sinus tachycar- Occasionally the QRS complex contains more than dia is a specific but not sensitive marker of pericardial effusion two or three deflections. In such cases the extra waves with tamponade pathophysiology because of the swinging heart are called R′ (R prime) waves if they are positive and S′ phenomenon (see Chapter 12). Beat-to-beat alternation of the (S prime) waves if they are negative. QRS is also seen with certain types of paroxysmal supraven- Fig. 3.4 shows the major possible QRS complexes and tricular tachycardias (PSVTs; see Chapter 14) and occasionally the nomenclature of the respective waves. Notice that with monomorphic ventricular tachycardia (Chapter 16).  CHAPTER 3 How to Make Basic ECG Measurements 15 Fig. 3.5 Measurement of the QRS width (interval) (see text). Fig. 3.7 ST segments. (A) Normal. (B) Abnormal eleva- tion. (C) Abnormal depression. Fig. 3.6 Characteristics of the normal ST segment and T wave. The junction (J) is the beginning of the ST segment. ventricular repolarization. The normal ST segment is usually isoelectric (i.e., flat on the baseline, neither pos- the ventricles is slowed, for example by a block in one of itive nor negative), but it may be slightly elevated or the bundle branches, the QRS width will be prolonged. depressed normally (usually by less than 1 mm). Patho- The differential diagnosis of a wide QRS complex is dis- logic conditions, such as myocardial infarction (MI), cussed in Chapters 18, 19, and 25.b that produce characteristic abnormal deviations of the ST segment (see Chapters 9 and 10) are a major focus of ST Segment clinical ECG diagnosis. The ST segment is that portion of the ECG cycle from The very beginning of the ST segment (actually the the end of the QRS complex to the beginning of the junction between the end of the QRS complex and T wave (Fig. 3.6). It represents the earliest phase of the beginning of the ST segment) is called the J point. Fig. 3.6 shows the J point and the normal shapes of b A subinterval of the QRS, termed the intrinsicoid deflection, the ST segment. Fig. 3.7 compares a normal isoelectric is defined as the time between the onset of the QRS (usually ST segment with abnormal ST segment elevation and measured in a left lateral chest lead) to the peak of the R wave depression. in that lead. A preferred term is R wave peak time. This inter- The terms J point elevation and J point depression are val is interpreted as an estimate of the time for the impulse to descriptive. They do not denote specific conditions (e.g., travel from the endocardium of the left ventricle to the epi- pericarditis, ischemia, etc.). For example, isolated J point cardium. The upper limit of normal is usually given as 0.04 elevation may occur as a normal variant with the early sec (40 msec), with increased values seen with left ventricular repolarization pattern (see Chapter 10) or as a marker of hypertrophy (>0.05 sec or 50 msec) and left bundle branch block (>0.06 sec or 60 msec). However, this microinterval is systemic hypothermia (where they are termed Osborn or hard to measure reliably (especially with notched QRS com- J waves; see Chapter 11). J point elevation may also be plexes) and reproducibly at conventional paper speeds used in part of ST elevations with acute pericarditis, acute myo- clinical electrocardiography. Therefore, the R wave peak time cardial ischemia, left bundle branch block or left ventric- has very limited utility in contemporary practice. ular hypertrophy (leads V1 to V3 usually), and so forth.  PART I Basic Principles and Patterns Similarly, J point depression may occur in a variety of As a result, you may be measuring the QU interval rather contexts, both physiologic and pathologic, as discussed than the QT interval. When reporting the QT (or related in subsequent chapters and summarized in Chapter 25. QTc) it might be helpful to cite the lead(s) you used. In clinical practice, the QT should be reported with a TWave "correction" or normalization for the heart rate. A variety The T wave represents the mid-latter part of ventricu­ of methods for correcting the QT for rate, termed QTc lar repolarization. A normal T wave has an asymmetric intervals, have been proposed. None is ideal and no for­ shape; that is, its peak is closer to the end of the wave than mal consensus has been reached on which one to use. Fur­ to the beginning (see Fig. 3.6). When the T wave is pos­ thermore, commonly invoked clinical "rules of thumb" (see itive, it normally rises slowly and then abruptly returns QT Cautions box) are often mistakenly cited on the wards. to the baseline. When it is negative, it descends slowly and abruptly rises to the baseline. The asymmetry of the normal T wave contrasts with the symmetry of abnor­ QT CAU TIONS: COMMON MISUNDERSTANDINGS A QT interval less than one-half the RR interval is mal T waves in certain conditions, such as MI (see Chap­ NOT necessarily normal (especially at slower rates). ters 9 and 10) and hyperkalemia (see Chapter 11). The A QT interval more than one-half the RR interval is exact point at which the ST segment ends and the T wave NOT necessarily long (especially at very fast rates). begins is somewhat arbitrary and usually impossible to pinpoint precisely. However, for clinical purposes, accu­ racy within 40 msec (0.04 sec) is usually acceptable. QT Correction (QTc) Methods 1: The Square Root Method QT/QTc Intervals The first, and still one of the most widely used QTc in­ The QT interval is measured from the beginning of dices, is derived from the original formula proposed by the QRS complex to the end of the T wave (Fig. 3.8). It Bazett. This algorithm divides the actual QT interval (in primarily represents the return of stimulated ventricles units of seconds) by the square root of the immediately to their resting state (ventricular repolarization). The preceding RR interval (also measured in seconds). Thus normal values for the QT interval depend on the heart using the "square root method," one applies the simple rate. As the heart rate increases (RR interval shortens), equation: the QT interval normally shortens; as the heart rate de­ creases (RR interval lengthens), the QT interval length­ OTc = QT/-../RR ens. The RR interval, as described later, is the interval Normally the QTc in adults is between about 0.33 between consecutive QRS complexes. (The rate-related and 0.35 sec (330-350 msec) and about 0.44 to 46 sec shortening of the QT, itself, is a complex process involv­ (440-460 msec). ing direct effects of heart rate on action potential dura­ tion and on neuroautonomic factors.) The use of this classic "square root" formula is You should measure the QT in the ECG lead (or leads) increasingly discouraged based on findings that showing the longest intervals. A common mistake is to it makes the QT at faster heart rates appear too limit this measurement to lead II. You can measure several long whereas making the QT at slower heart rates intervals and use the average value. When the QT interval appear too short.' is long, it is often difficult to measure because the end of the T wave may merge imperceptibly with the U wave. ·A technical point that often escapes attention is that imple­ menting the square root method requires that both the QT and RR be measured in seconds. The square root of the RR (sec) yields a value in units of sec½. However, the QTc itself is always reported by clinicians in units of seconds (not awk­ wardly as sec/sec½ = sec½). To make the units consistent, you can measure the RR interval in seconds but record it as a unit­ Fig. 3.8 Measurement of the QT interval. The RR inter­ less number (i.e., QT in sec/✓RR unitless). Then, tl1e QTc, like val is the interval between two consecutive ORS com­ the QT, will be expressed in units of sec. Multiplying by 1000 plexes (see text). will convert to units of milliseconds.  CHAPTER 3 How to Make Basic ECG Measurements 17 2: Two “Linear” Methods Given the major limitations of the square root method, a number of other formulas have been proposed for cal- culating a rate-corrected QT interval. We present two alternatives that are computationally easy to implement as they use linear equations: a. Hodges method: QTc (msec ) = QT (msec ) +1.75 (heart rate in beats/min − 60 ) To convert to seconds, simply divide the output in seconds by 1000 (e.g., 462 msec = 0.462 sec) Fig. 3.9 Abnormal QT interval prolongation in a patient b. Framingham method: taking the drug quinidine. The QT interval (0.6 sec) is QTc = QT + 0.154 (1− RR) , markedly prolonged for the heart rate (65 beats/min). The rate-corrected QT interval (normally about 0.44- where the QT/QTc and (the preceding RR are measured 0.45 sec or less) is also prolonged.* Prolonged repo- larization may predispose patients to develop torsades in units of seconds. To convert to milliseconds, multiply de pointes, a life-threatening ventricular arrhythmia (see the output by 1000. Chapter 16).* Use the three methods described in this Note also that with all of these methods, the QT chapter to calculate the QTc. (Assume here that the RR and the QTc (0.400 sec or 400 msec) are identical at of the preceding beats is same as RR subtending the.) heart rate of 60 beats/min (since the denominator is Answers: RR = 1 sec). 1. By the “square root” (Bazett) method: QTc = Several other formulas and approaches have been QT/√RR = 0.60 sec/√0.92 = 0.63 sec (630 msec). proposed for correcting or normalizing the QT to a QTc. 2. By Hodges method: QTc = QT + 1.75 (HR None has received “official endorsement.” The reason is in beats/min − 60) = 600 msec + 1.75 that no method is ideal for individual patient manage- (65 − 60) = 600 + 8.75 = 609 msec = 0.609 sec. ment. Furthermore, an inherent error/uncertainty is 3. By the Framingham method: QTc= QT + 0.154 (1-RR) = 0.60 + 0.154 (1-0.92) = 0.612 sec =612 unavoidably present in trying to localize the beginning msec. With all three methods, the QTc is mark- of the QRS complex and, especially, the end of the T edly prolonged, indicating a high risk of sudden wave. (Trainees can informally test the hypothesis that cardiac arrest caused by torsades de pointes (see substantial interobserver and intraobserver variability Chapters 16 and 21). Note that the Bazett formula of the measured QT interval exists by showing some under-corrects the rate here making it appear lon- de-identified ECGs to your colleagues and recording ger than other methods. their QT measurements.)d The upper and lower limits of normal for the QTc, assuming a normal duration QRS, are not precisely agreed upon. For women, a range of 360 to 460 msec has been proposed; for men, 350 to 450 msec. More sub- tly, a substantial change in the QTc interval within the d Some authors advocate drawing a tangent to the downslope normal range (e.g., from 0.34 to 0.43 sec) may be a very of the T wave and taking the end of the T wave as the point early warning of progressive QT prolongation resulting where this tangent line and the TQ baseline intersect. How- from one of the factors in the next paragraph. ever, this method is arbitrary since the slope may not be linear Many factors can abnormally prolong the QT interval and the end of the T wave may not be exactly along the isoelec- tric baseline. The U wave may also interrupt the T wave. With (Fig. 3.9) including multiple drugs used to treat cardiac atrial fibrillation, an average of multiple QT and associated arrhythmias (e.g., amiodarone, dronedarone, ibutilide, RR intervals values can be used. Clinicians should be aware of quinidine, procainamide, disopyramide, dofetilide, which method is being employed when electronic calculations and sotalol), as well as a large number of other types of are used and always double-check the reported QT and QTc. “noncardiac” agents (fluoroquinolones, phenothiazines, 18 PART I Basic Principles and Patterns pentamidine, macrolide antibiotics, haloperidol, meth- adone, certain selective serotonin reuptake inhibitors, etc.). Specific electrolyte disturbances (low potassium, magnesium, or calcium levels) are important causes of QT interval prolongation. Hypothermia prolongs the Fig. 3.10 Heart rate (beats per minute) can be mea- QT interval by slowing the repolarization of myocardial sured by counting the number of large (0.2-sec) time cells. The QT interval may be prolonged with myocardial boxes between two successive QRS complexes and di- viding 300 by this number. In this example the heart rate ischemia and infarction (especially during the evolving is calculated as 300 ÷ 4 = 75 beats/min. Alternatively phase with T wave inversions) and with subarachnoid (and more accurately), the number of small (0.04-sec) hemorrhage. QT prolongation is important in practice time boxes between successive QRS complexes can be because it may indicate predisposition to potentially counted (about 20 small boxes here) and divided into lethal ventricular arrhythmias. (See the discussion of 1500, also yielding a rate of 75 beats/min. torsades de pointes in Chapter 16.) Chapter 25 sum- marizes the differential diagnosis of a long QT/QTc (reported as number of heartbeats or cycles per minute) interval. from the ECG (Figs. 3.10 and 3.11). As noted, a short QT may be evidence of hypercalce- mia, or of the fact that the patient is taking digoxin (in 1: Box Counting Methods therapeutic or toxic doses). Finally, a very rare heredi- The simplest way, when the (ventricular) heart rate is tary “channelopathy” has been reported associated with regular, is to count the number (N) of large (0.2-sec) short QT intervals and increased risk of sudden cardiac boxes between two successive QRS complexes and di- arrest (see Chapter 21). vide a constant (300) by N. (The numerator is 300 be- cause 300 × 0.2 = 60 and the heart rate is calculated in U Wave beats per minute (i.e., per 60 seconds.) The U wave is a small, rounded deflection sometimes For example, in Fig. 3.10 the heart rate is 75 beats/ seen after the T wave (see Fig. 2.2). As noted previ- min, because four large time boxes are counted between ously, its exact significance is not known. Functionally, successive R waves (300 ÷ 4 = 75). Similarly, if two large U waves represent the last phase of ventricular repolar- time boxes are counted between successive R waves, the ization. Prominent U waves are characteristic of hypo- heart rate is 150 beats/min. With five intervening large kalemia (see Chapter 11). Very prominent U waves may time boxes, the heart rate will be 60 beats/min. also be seen in other settings, for example, in patients When the heart rate is fast or must be measured taking drugs such as sotalol, quinidine, or one of the very accurately from the ECG, you can modify the box phenothiazines or sometimes after patients have had a counting approach as follows: Count the number of cerebrovascular accident. The appearance of very prom- small (0.04-sec) boxes between successive R (or S waves) inent U waves in such settings, with or without actual waves and divide the constant (1500) by this number. QT prolongation, may also predispose patients to ven- In Fig. 3.10, 20 small time boxes are counted between tricular arrhythmias (see Chapter 16). QRS complexes. Therefore the heart rate is 1500 ÷ Normally the direction of the U wave is the same as 20 = 75 beats/min. (The constant 1500 is used because that of the T wave. Negative U waves sometimes appear 1500 × 0.04 = 60 and the heart rate is being calculated with positive T waves. This abnormal finding has been in beats per 60 sec [beats/min].) noted in left ventricular hypertrophy and in myocardial Note: some trainees and attending physicians have ischemia. adopted a “countdown” mnemonic by which they incant: 300, 150, 100, 75, 60, and so forth based on ticking off RR Intervals and Calculation of Heart Rate the number of large (0.2-sec box sides) between QRS We conclude this section on ECG intervals by discussing complexes. However, there is no need to memorize extra the RR interval and its inverse, namely the (ventricular) numbers: this countdown is simply based on dividing the heart rate. Two simple classes of methods can be used number of large (0.2-sec) intervals between consecutive R to manually measure the ventricular or atrial heart rate (or S waves) into 300. If the rate is 30, you will be counting  CHAPTER 3 How to Make Basic ECG Measurements 19 Fig. 3.11 Quick methods to measure heart rate. Shown is a standard 12-lead ECG with a con- tinuous rhythm strip (lead II, in this case). Method 1A: Large box counting method (see Fig. 3.10) shows between four and five boxes between R waves, yielding rate between 75 and 60 beats/ min, where rate is 300 divided by number of large (0.2-sec) boxes. Method 1B: Small box count- ing method more accurately shows about 23 boxes between R waves, where the rate is com- puted 1500 divided by number of small (0.04 sec) boxes = 65 beats/min. Method 2: QRS counting method shows 11 QRS complexes in 10 sec = 66 beats/60 sec or 1 min. Note: the short vertical lines here indicate a lead change and may cause an artifactual interruption of the waveform in the preceding beat (e.g., T waves in the third beat before switch to lead aVR, aVL, and aVF). down for quite a while! But 300/10 = 30 beats/min will 60 beats/min is called a bradycardia. (In ancient Greek, allow you to calculate the rate and move on with the key tachys means “swift,” whereas bradys means “slow.”) decisions regarding patient care. Thus, during brisk exercise you probably develop a sinus tachycardia, but during sleep or relaxation your pulse 2: QRS Counting Methods rate may drop into the 50s or even lower, indicating a If the heart rate is irregular, the first method described physiologic sinus bradycardia. (See Parts II and III for in the preceding section will not be accurate because an extensive discussion of the major bradyarrhythmias the intervals between QRS complexes vary from beat to and tachyarrhythmias.) beat. You can easily determine an average (mean) rate, whether the latter is regular or not, simply by count- HOW ARE HEART RATE AND RR ing the number of QRS complexes in some convenient time interval (e.g., every 10 sec, the recording length of INTERVALS RELATED? most 12-lead clinical ECG records). Next, multiply this The heart rate is inversely related to another interval, number by the appropriate factor (6 if you are using a described earlier, the RR interval (or QRS-to-QRS inter- standard 10-sec recording) to obtain the rate in beats val), which, as noted previously, is simply the temporal per 60 sec (see Fig. 3.11). This method is most usefully distance between consecutive, equivalent points on the applied in cases of arrhythmias with grossly irregular preceding or following QRS. (Conveniently, the R wave heart rates (e.g., atrial fibrillation or multifocal atrial peak is chosen, but this is arbitrary.) These measure- tachycardia). ments, when made using digital computer programs By definition, a heart rate exceeding 100 beats/min on large numbers of intervals, form the basis of heart is termed a tachycardia, and a heart rate slower than rate variability (HRV) studies, an important topic that is  PART I Basic Principles and Patterns outside our scope here (see Bibliography and the online BOX 3.1 Beware: Confusing ECG material). Terminology! Students should know that consecutive RR inter­ The RR interval is really the ORS-ORS interval. vals can be converted to the instantaneous heart rate The PR interval is really P onset to ORS onset. (Rarely, (IHR) by the following two simple, equivalent formulas, the term PO is used, but PR is favored even if the depending on whether you measure the RR interval in l ead does not show an R wave.) seconds (sec) or milliseconds (msec): The QT interval is really ORS (onset) to T (end) inter­ val. Instantaneous HR in beats/min= 60/RR(in sec) Not every ORS complex has a 0, R, and S wave. An entirely negative ORS is called a OS wave Instantaneous HR in beats/min= 60,000/RR(in msec) PP AND RR INTERVALS: ARE THEY ECG TERMS ARE CONFUSING! EQUIVALENT? Students and practitioners are often understandably confused by the standard ECG terms, which are arbi­ We stated in Chapter 2 that there were four basic sets trary and do not always seem logical. Because this ter­ of ECG intervals: PR, QRS, QT/QTc, and PP/RR. Here minology is indelibly ingrained in clinical usage, change we refine that description by adding mention of the in­ is unlikely. Nevertheless, it is still worth a pause to terval between atrial depolarizations (PP interval). The acknowledge these semantic confusions (Box 3.1). atrial rate is calculated by the same formula as the ven­ tricular, based on the RR interval; namely, the atrial rate (per min)= 60/PP interval (in sec). The PP interval and THE ECG: IMPORTANT CLINICAL RR intervals are obviously the same when sinus rhythm PERSPECTIVES is present with 1:1 AV conduction (referred to as normal Up to this point, we have discussed only the basic com­ sinus rhythm). The ratio 1:1 in this conte:>..1. indicates that ponents of the ECG. A number of general items deserve each P wave is successfully conducted through the AV consideration before proceeding. nodal/His-Purkinje system into the ventricles. In other 1. The ECG is a recording of cardiac electrical activity. It words, each atrial depolarization signals the ventricles does not directly measure the mechanical function of to depolarize. the heart (i.e., how well the heart is contracting and However, as we will discuss in Parts II and III of this performing as a pump). Thus a patient with acute book, the atrial rate is not always equal to the ventricular pulmonary edema may have a normal ECG. Con­ rate. Sometimes the atrial (P wave) rate is much faster versely, a patient with an abnormal ECG may have (especially with second- or third-degree AV block) and normal cardiac function. sometimes it is slower (e.g., with ventricular tachycardia 2. The ECG does not directly depict abnormalities in and AV dissociation).' cardiac structure such as ventricular septal defects and abnormalities of the heart valves. It only records the electrical changes produced by structural defects. The same rule can be used to calculate the atrial rate when However, in a number of major conditions, a specific non-sinus (e.g., an ectopic atrial) rhythm is present. Similarly, structural diagnosis such as mitral stenosis, acute the atrial rate with atrial flutter can be calculated by using the pulmonary embolism, or myocardial infarction/ flutter-flutter (FF) interval (see Chapter 15). Typically, in this ischemia can be inferred from the ECG because arrhythmia the atrial rate is about 300 cycles/min (about 220- 350 cycles/sec). In atrial fibrillation (AF), the atrial depolar­ a constellation of typical electrical abnormalities ization rate is variable and too fast to count accurately from develops. the surface ECG. The typical depolarization (electrical) rate 3. The ECG does not record all of the heart's electrical of 350-600/min rate in AF can be estimated from the ECG activity. Notably, the SA node and the AV node are the peak-to-peak fibrillatory oscillations. More accurate as­ completely silent. Furthermore, the electrodes placed sessments of atrial rate would require intracardiac recordings. on the surface of the body record only the currents  CHAPTER 3 How to Make Basic ECG Measurements 21 that are transmitted to the area of electrode place- Thus the presence of a normal ECG does not neces- ment. The clinical ECG records the summation of sarily mean that all these heart muscle cells are depo- electrical potentials produced by innumerable car- larizing and repolarizing in a normal way. Furthermore, diac muscle cells. Therefore there are “silent” electri- some abnormalities, including life-threatening condi- cal areas of the heart that