A Visual Guide to ECG Interpretation
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A VISUAL GUIDE TO ECG
INTERPRETATION
SECOND EDITION
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A VISUAL GUIDE TO ECG
INTERPRETATION
SECOND EDITION
Jennifer L. Martindale, MD
Clinical Assistant Professor
Department of Emergency Medicine
SUNY Downstate/Kings County Hospital
Brooklyn, New York
David F. M. Brown, MD
Chair
Department of Emergency Medicine
Massachusetts General Hospital
MGH Trustees Professor of Emergency Medicine
Harvard Medical School
Boston, Massachusetts
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Second Edition
Copyright © 2017 Wolters Kluwer
Copyright © 2012 by LIPPINCOTT WILLIAMS & WILKINS, a WOLTERS KLUWER business. All
rights reserved. This book is protected by copyright. No part of this book may be reproduced or transmitted in
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Printed in China
Library of Congress Cataloging-in-Publication Data
Names: Martindale, Jennifer L., author. | Brown, David F. M., author.
Title: A visual guide to ECG interpretation / Jennifer L. Martindale, David F. M. Brown.
Other titles: Rapid interpretation of ECGs in emergency medicine
Description: Second edition. | Philadelphia : Wolters Kluwer, [2017] | Preceded by Rapid interpretation of
ECGs in emergency medicine / Jennifer L. Martindale, David F.M. Brown. 2012. | Includes bibliographical
references and index.
Identifiers: LCCN 2016008759 | ISBN 9781496321534
Subjects: | MESH: Electrocardiography | Emergencies
Classification: LCC RC683.5.E5 | NLM WG 140 | DDC 616.1/207547—dc23 LC record available at
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any warranties as to accuracy, comprehensiveness, or currency of the content of this work.
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of each patient and consideration of, among other things, age, weight, gender, current or prior medical
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TO THE EMERGENCY MEDICINE RESIDENTS AND FACULTY AT SUNY
DOWNSTATE/KINGS COUNTY HOSPITAL.
– JLM
TO THE RESIDENTS AND GRADUATES OF THE HARVARD AFFILIATED EMERGENCY
MEDICINE RESIDENCY WHO CONTINUE TO AMAZE AND INSPIRE ME EVERY DAY.
– DFMB
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PREFACE
The main objective of this book is to provide a visual tool that will help physicians and other emergency care
providers quickly recognize important ECG patterns. By the end of the book, the reader will have developed a
mental repertoire of ECGs that represent medically significant conditions, including some that are potentially
fatal. We hope that our illustrations and easy-to-follow explanations help to demystify ECG interpretation.
This book is intentionally graphic and nontechnical. It is designed to help clinicians make visual diagnoses by
pointing out abnormalities in a colorful and pictorial fashion.
The second edition of this book maintains the same format of the book. An ECG is first shown in its
native state to give the reader a chance to recognize and interpret salient features. Abnormal patterns are
enlarged, highlighted in color, and described in brief text on the following page. We have added ECGs that
we have collected over recent years and chosen to include those that emphasized critical pathologies including
hyperkalemia, coronary occlusion, and massive pulmonary embolism. In the ischemia chapter, we decided to
include ECGs with more subtle signs of coronary occlusion. The second edition is accompanied by access to
an online appendix that presents ECG abnormalities in random order. We hope this will allow our readers to
practice and consolidate their learning.
We would like to thank everyone who contributed electrocardiograms to this collection.
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CONTENTS
Preface
1 Concept Review
2 Sinus Dysfunction
3 Bundle Branch and Fascicular Blocks
4 AV Conduction Blocks
5 Premature Beats
6 Abnormal QRS Morphology
7 Abnormal T Waves
8 QT Abnormalities and Electrolyte Disturbances
9 Voltage Abnormalities
10 Fast and Narrow
11 Fast and Wide
12 Ischemic Patterns
13 Paced Rhythms
Online Appendix
Index
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CHAPTER 1
Concept Review
Action Potential—Myocardial Cell
The different phases of the action potential relate directly to the waveforms, intervals, and segments that
constitute a cardiac cycle on the ECG. Each phase is distinguished by an alteration in cell membrane
permeability to sodium, potassium, and calcium ions. A basic understanding of these phases and their major
ion currents will help in learning the ECG features associated with conduction abnormalities, drug toxicities,
and electrolyte disturbances.
The action potential of the myocardial cell is divided into five phases (phases 0–4). The first phase, phase 0,
represents ventricular depolarization. Rapid depolarization depends on initial sodium entry that triggers the
explosive influx of more sodium through fast-gated sodium channels. This phase takes the myocardial cell
from its resting potential of −90 mV to a positive potential of 20 mV. The summation of this phase across the
ventricular myocardium is represented on the ECG as the QRS wave.
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FIGURE 1.1 Action potential of a myocardial cell and phases of the action potential as they relate to ECG waves and segments.1 The action
potential also represents the cell membrane in this figure, with the area under the action potential representing intracellular space and the area
above the action potential representing extracellular space.
Ventricular repolarization occurs during phases 1, 2, and 3. By phase 1, the fast sodium channels are closed
(and inactivated), and the cell returns to a neutral potential by the opening of potassium channels that allow
for the outward movement of potassium.
During phase 2, the neutral potential is maintained by balancing potassium efflux with the sustained entry of
calcium ions. Calcium entry during this phase initiates the release of intracellular calcium stores necessary for
sarcomere shortening and ventricular contraction. The ST segment corresponds to phase 2.
Phase 3 represents rapid repolarization to the negative resting potential by potassium ion efflux and the
closure of calcium channels on the cell membrane. This phase corresponds to the T wave.
After the membrane returns to the resting potential, this potential is maintained during phase 4 by continued
potassium efflux and the Na+;/K+; ATPase pump (red oval). The ventricular myocardium is at its resting
potential (phase 4) between the end of the T wave and the beginning of the next QRS wave (T-Q segment).
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Action Potential—Pacemaker Cell
Cardiac pacemaker cells are specialized to spontaneously depolarize and initiate action potentials. The action
potential of pacemaker cells is divided into three phases (phases 0, 3, and 4). Spontaneous phase 4
depolarization (represented by an upsloping phase 4 in the action potential) distinguishes pacemaker cells
from myocardial cells. During this phase, slow inward sodium current results in the gradual rise of the
membrane potential toward its threshold potential. The current responsible for phase 4 depolarization is also
known as the pacemaker current or funny current ( I f ).
FIGURE 1.2 Action potential of a pacemaker cell. Lines of the action potential also represent the cell membrane of the pacemaker cell.
Once threshold potential is attained, calcium channels open to depolarize the cell during phase 0.
Repolarization occurs in phase 3 with the opening of potassium channels and closure of calcium channels.
When the membrane potential returns to its resting potential, sodium channels immediately open again.
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FIGURE 1.3 Effect of sympathetic and parasympathetic stimulation on phase 4 of the pacemaker action potential.
The slope of phase 4 is directly affected by sympathetic and parasympathetic tone. Sympathetic stimulation
results in a steeper phase 4 and consequently a faster heart rate. Norepinephrine (NE) released from
sympathetic nerves increases the membrane’s permeability to sodium. Vagal tone decreases the slope of phase
4 and, consequently, the heart rate. Acetylcholine (ACh) released by the vagus nerve increases the cell
membrane’s permeability to potassium while decreasing its permeability to sodium.2
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Refractory Periods
Once myocardial cells have entered phase 0 depolarization, the cells become refractory to the conduction of
incoming impulses. This allows cells to recover from depolarization. The relative differences in refractory
states depend on the state of the fast sodium channels. Refractory states are defined by the strength of impulse
required for a myocardial cell to generate and propagate an action potential. Figure 1.4 shows how these
different refractory periods relate to phases of the action potential.2 Refractory periods are especially relevant
to ECG rhythms resulting from a reentry circuit and to antiarrhythmic drugs that prolong the duration of the
action potential.
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Effective Refractory Period
During phases 0 to 2 and part of phase 3, the myocardial cell is unable to propagate an action potential in
response to a stimulus, regardless of the strength of that stimulus.
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Relative Refractory Period
Before the cell has returned to its resting membrane potential of −90 mV, it may respond to a stronger than
normal stimulus. This can occur during phase 3 of repolarization. The response to this stimulus is slower than
normal.
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Supranormal Period
A smaller than normal impulse can elicit a normal action potential.
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FIGURE 1.4 Refractory periods during different phases of the action potential and cardiac cycle on ECG.
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Reentry Circuits
A reentrant circuit consists of two separate pathways that differ in refractory period duration. An impulse may
simultaneously encounter a group of refractory cells and a group of cells ready to conduct. Conduction
preferentially occurs down the pathway out of its refractory period.
FIGURE 1.5 Variable refractory periods play a key role in reentry.
Drugs that prolong the action potential and effective refractory period are used to terminate reentrant circuits.
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Class IA Antiarrhythmics
Quinidine, procainamide, and disopyramide prolong the effective refractory period by blocking the sodium
channels responsible for rapid depolarization, thereby prolonging phase 0. This is represented on the ECG by
QRS widening.
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Class III Antiarrhythmics
Amiodarone, dofetilide, and ibutilide prolong the action potential duration by blocking the outward flow of
potassium during phase 3. This increases the effective refractory period of cardiac myocytes. On the ECG,
this is represented by QT prolongation.
FIGURE 1.6 Effect of Na+; channel blockade and K+; channel blockade on action potential duration.
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Conduction Anatomy
Normal conduction is essential to coordinated and efficient ventricular contraction. Impulses from the sinus
node activate the atrial myocardium and travel down internodal tracts to the AV node. After a brief delay at
the AV node, simultaneous conduction down the right and left bundle branches allows for synchronous
contraction of the right and left ventricles. Simultaneous conduction down the left anterior and posterior
fascicles of the left bundle branch allows for coordinated contraction of the left ventricular free wall.
FIGURE 1.7 Anatomy of the conduction system.
FIGURE 1.8 Properties of the AV node.
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Retrograde Conduction Patterns
Basic teaching of conduction anatomy addresses anterograde conduction down normal pathways from the
sinus node to the His-Purkinje system. Conduction can also occur in retrograde fashion (in a ventricular to
atrial direction) through normal and bypass conduction pathways.
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