ecg interpretation for everyone -...

ECG Interpretation for Everyone

Kusumoto_ffirs.indd iKusumoto_ffirs.indd i 11/19/2011 7:17:31 PM11/19/2011 7:17:31 PM

ECG Interpretation for EveryoneAn On-The-Spot Guide

Fred Kusumoto MDAssociate Professor of MedicineDirector of Electrophysiology and PacingDivision of Cardiovascular DiseasesDepartment of MedicineMayo ClinicJacksonville, FL, USA

Pam Bernath RN, RN-CDivision of Cardiovascular DiseasesDepartment of MedicineMayo ClinicJacksonville, FL, USA

A John Wiley & Sons, Ltd., Publication

Kusumoto_ffirs.indd iiiKusumoto_ffirs.indd iii 11/19/2011 7:17:31 PM11/19/2011 7:17:31 PM

This edition first published 2012 © 2012 by John Wiley & Sons, Ltd.

Wiley-Blackwell is an imprint of John Wiley & Sons, formed by the merger of Wiley’s global Scientific, Technical and Medical business with Blackwell Publishing.

Registered OfficeJohn Wiley & Sons, Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK

Editorial Offices9600 Garsington Road, Oxford, OX4 2DQ, UKThe Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK111 River Street, Hoboken, NJ 07030-5774, USA

For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com/wiley-blackwell

The right of the author to be identified as the author of this work has been asserted in accordance with the UK Copyright, Designs and Patents Act 1988.

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, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher.

Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought.

The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by physicians for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of fitness for a particular purpose. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the author shall be liable for any damages arising herefrom.

Library of Congress Cataloging-in-Publication Data

Kusumoto, Fred.ECG interpretation for everyone : an on-the-spot guide / Fred Kusumoto and Pam Bernath. p. ; cm. Includes bibliographical references and index. ISBN-13: 978-0-470-65556-6 (pbk. : alk. paper) ISBN-10: 0-470-65556-9I. Bernath, Pam. II. Title. [DNLM: 1. Electrocardiography–Atlases. 2. Electrocardiography–Handbooks. WG 39] LC classification not assigned 616.1′207547–dc23

2011030261

A catalogue record for this book is available from the British Library.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Set in 8/11pt Frutiger by SPi Publisher Services, Pondicherry, India

1 2012

Kusumoto_ffirs.indd viKusumoto_ffirs.indd vi 11/19/2011 7:17:31 PM11/19/2011 7:17:31 PM

To Dr. Edward H. Wymanand to Laura, Miya, Hana, and Aya

Kusumoto_ffirs.indd ivKusumoto_ffirs.indd iv 11/19/2011 7:17:31 PM11/19/2011 7:17:31 PM

Kusumoto_ffirs.indd ivKusumoto_ffirs.indd iv 11/19/2011 7:17:31 PM11/19/2011 7:17:31 PM

vii

Master Algorithm, viiiPreface, ix

Chapter 1: Technical Issues, 1

Chapter 2: The Normal ECG, 13

Chapter 3: ECG Interpretation Basics, 32

Chapter 4: Abnormal Repolarization: ST Segment Elevation, 37

Chapter 5: Abnormal Repolarization: ST Segment Depression, 98

Chapter 6: Abnormal Repolarization: T Wave Changes and the QT Interval, 117

Chapter 7: Abnormal Depolarization: A Prominent R Wave in V1, 148

Chapter 8: Abnormal Depolarization: Wide QRS Complexes and Other Depolarization Abnormalities, 184

Chapter 9: Arrhythmias: Normal Rates and Skips, 214

Chapter 10: Arrhythmias: Bradycardia, 241

Chapter 11: Arrhythmias: Tachycardia, 272

Chapter 12: Arrhythmias: Pacing, 334

Chapter 13: Clinical Use of the ECG: Stress Testing, 347

Chapter 14: Clinical Use of the ECG: Clinical Problems, 366

Appendices, 380

Index, 387

Contents

Kusumoto_ftoc.indd viiKusumoto_ftoc.indd vii 11/19/2011 7:12:21 PM11/19/2011 7:12:21 PM

viii

Master Algorithm

Evaluate

the Rhythm

ST Segment Elevation ST Segment Depression

Heart Rate < 40 Heart Rate > 110

• Myocardial Infarction• Pericarditis• Bundle Branch Block• Hyperkalemia• Coronary Artery Spasm• Early Repolarization• LV Aneurysm• Normal Variant

• Sinus Node Dysfunction• AV block

Narrow QRS • SVT

Wide QRS • Ventricular Tachycardia • SVT with aberrancy

• Ischemia• LV Hypertrophy• Myocardial Infarction• Bundle Branch Block• Digoxin

Chapter 10

Chapter 4 Chapter 5

Chapter 11

Evaluate

the ST segment

Evaluate

the T wave

Evaluate the QRS

• T wave inversion• QT interval

Chapter 6

“On-the-Spot”

Positive in V1

• Right Bundle Branch Block• RV Hypertrophy• Dextrocardia• Accessory Pathway• Posterior MI• Duchenne• Normal Variant

Wide• Left Bundle Branch Block• Accessory Pathway• RV pacing

Q Waves and Axis

QRS Size

Chapter 7 Chapter 8

Negative in V1

Kusumoto_fbetw.indd viiiKusumoto_fbetw.indd viii 11/30/2011 6:39:26 PM11/30/2011 6:39:26 PM

ix

I have always been fascinated with learning more about the ECG, and over the last eight years, I have felt a growing desire to learn more about ECG interpretation. I feel that it is an essential tool that should be used on a regular basis by medical personnel who care for patients. After countless hours of study and the awareness that most people do not have this much time to spend on this subject, I realized the need for a “quick reference ECG recognition guide.” ECG changes can happen quickly and decisions will need to be made “on the spot”. This book is intended for this purpose because it can help the interpreter recognize key elements on the ECG that are pertinent to different arrhythmias or conditions. The book covers multiple ECGs with short descriptions of the arrhythmias or conditions, the ECG changes that can occur, and the clinical importance of each ECG change. The medical staff and physicians that work in any monitored unit, especially the emergency rooms and ICUs, should become more familiar with arrhythmias or changes that could represent ischemia, infarction, or dangerous cardiac arrhythmias. Hopefully, this handy pocket ECG guide will help make ECG identifica-tion more commonplace.

I would like to thank the nurses in the stress testing department and the ECG technicians at the Mayo Clinic. My two daughters, Alisa and Haley, and other family members have been with me through the long hours of being isolated in my office and they have supported and encouraged me during this busy time. Without the loving support of my husband, Mike, I would never have been able to start or complete this project. I would also like to thank my stepfather and mother, Dr. and Mrs. Edward H. Wyman, for encouraging me when they realized that I had a passion for ECG interpretation in my early years of nursing.

Pam Bernath, RN, RN-C

Preface

Kusumoto_fpref.indd ixKusumoto_fpref.indd ix 11/19/2011 7:12:41 PM11/19/2011 7:12:41 PM

x Preface

Pam Bernath is the major force behind this project that is designed to provide an introduction to ECG interpretation. She identified an unmet need for a simple text that would provide the basics of ECG interpreta-tion for the many different healthcare providers that use the ECG on a frequent basis. In thinking about the format of this book we were drawn to the idea of providing an illustration oriented “field guide” for rapid evaluation of ECGs. As a child I still remember pouring over Zim’s Guide to Butterflies and Moths (Golden Books, New York). I still have my well-worn friend that accompanied me on afternoon and weekend day trips to the country fields behind my house. After a short introduction, the book covered each of the major butterfly families using drawings, maps, and short paragraphs. This book is designed in a similar manner with a short introduction followed by ECG examples and important “keys” that help identify the critical diagnostic points. I hope that this small pocket book will help you identify ECGs as you are “out in the field,” just as Herbert Zim taught me the basics about butterflies and moths.

I too would like to thank my family for putting up with lost weekends and a somewhat distracted husband and dad. Finally, thank you to Sumiko and Howard Kusumoto who encouraged a naturally inquisitive son to look even more closely at the world around him.

Fred Kusumoto, MD

Kusumoto_fpref.indd xKusumoto_fpref.indd x 11/19/2011 7:12:41 PM11/19/2011 7:12:41 PM

1

ECG Interpretation for Everyone: An On-The-Spot Guide, First Edition. Fred Kusumoto and Pam Bernath.© 2012 John Wiley & Sons, Ltd. Published 2012 by John Wiley & Sons, Ltd.

It is always a bit worrisome when the first chapter has such a dry and uninspiring title, but it is extremely important to understand the fundamentals of the electrocardiogram (ECG) before using the ECG as a clinical tool. The ECG was originally developed over a century ago by Willem Einthoven and has become one of the most important diagnostic tools used for evaluating the heart. Very simply, the heart can be compared to a pump with a primary function of transporting blood to different parts of the body. “Control” of the pump requires an electrical system and, in the heart, contraction of the chambers begins and is controlled by electrical currents generated by cells with spontaneous electrical activity (also called pacemaker activity). The electrical activity produced by the heart causes small electrical changes on the skin that can be measured using skin electrodes. Don’t worry; with an average voltage of 1 mV or less, your body won’t power a flashlight. The electrodes are connected to a recording machine with special electronics that amplify and enhance the signal. In one subspecialty field of cardiology called electrophysiology, instead of measuring electrical activity from the body surface, electrical activity is measured directly from the inside of the heart chambers using specialized catheters, that are essentially wires coated with insulation and a metal electrode at the tip, inserted into one of the vessels of the body and threaded to the heart itself.

Before we can talk about the ECG and the heart, we have to discuss some extremely dry concepts that describe some of the technical issues on how the ECG is obtained. Although this portion of the book can be extremely mundane, details about electrodes, leads, and the ECG display are important and form the basis for understanding the ECG. Perhaps suffer through this first chapter with only a cursory read and come back to this chapter after you have read some of the other portions of the book.

CHAPTER 1

Technical Issues

Kusumoto_c01.indd 1Kusumoto_c01.indd 1 11/30/2011 6:32:04 PM11/30/2011 6:32:04 PM

2 ECG Interpretation for Everyone: An On-The-Spot Guide

Electrode placementThe ECG uses electrodes placed on the skin to measure the cardiac electrical activity. Obtaining good quality images is essential for proper interpretation and requires good and stable contact between the electrode and the skin. As an interesting aside, one of the seminal figures of cardiology, Augustus Waller (who provided the first comprehensive discussion of electrical activity of the heart), used a mouth electrode as a standard position, probably because this surface allowed better conductivity of electrical signals. In the past, to improve electrical conductivity, specialized gel was used between the skin and the metal electrodes. Now almost universally in industrialized nations, the electrodes are small specially designed disposable patches that have a light adhesive that also acts as a conductor to optimize transmission of the electrical signal from the skin to the ECG machine. Generally, the ECG is recorded while the patient is lying on his or her back (supine position) to avoid artifact introduced from body movement. Sometimes patient conditions such as tremors (Parkinson’s disease) or interference from other electrical equipment may make recording an ECG difficult. Within the ECG machine itself are special electronics that amplify the electrical signal and filter the electrical signal to “clean-up” the recording. As will be described later, sometimes the ECG is recorded while the patient is exercising on a treadmill. In order to reduce the artifact, these specialized machines use additional electronic circuitry to remove the excess noise introduced by body motion.

To obtain a 12 lead ECG, 10 electrodes are placed on the extremities and the chest (Figure 1.1). One electrode is placed on each of the four extremities: left and right arms and left and right legs. The extremities can be compared to “extension cords” and the ECG signal will not be affected by the exact position of the electrode on the extremity. In contrast, placing a limb electrode on the trunk will lead to some changes in the signals recorded by the ECG. The remaining six electrodes are placed on the anterior chest in specific positions. Collectively the chest electrodes are often called the precordial (the word comes from Latin – prae, “front of,” and cor, “heart”) leads and usually referred to as V1 through V6 moving from right to left on the chest. The V1 electrode is placed in the fourth intercostal space just to the right of the sternum and the V2 electrode is placed in the fourth intercostal space just to the left of the sternum. The V4 electrode is placed in the fifth intercostal space in


Technical Issues 3

line with the middle of the clavicle (collar bone). The V3 electrode is placed half way between V2 and V4. The V5 electrode is also placed in the fifth intercostal space at the same level as the V4 electrode but is located on the left anterior axillary line. The left anterior axillary line is an imaginary vertical line that extends from the front crease of the armpit (axilla is the Latin word for “armpit” or “side”). The V6 electrode is placed at the same level as the V4 and V5 electrodes, but in the mid axillary line which is an imaginary vertical line drawn from the middle of the armpit. Electrodes should be placed in regions with no or minimal hair as hair might prevent good contact between the skin and the electrode. Electrodes are not placed on bones because bony tissue does not conduct electrical activity as well as muscular issue. In women, the electrodes should generally be placed below the breast (closer to the heart) but if necessary can be placed on top of the breast if this position is closest to the standard electrode position. Misplacement of the chest electrodes will lead to significant changes in the ECG recordings.

Left arm

electrode

Right arm

electrode

Left leg

electrodeRight leg

electrode

Chest

electrodes

V4V3

V2

V1

V5

V6

(a) (b)

Figure 1.1:

(a): The location for the standard 10 electrodes used to record a 12 lead ECG.

(b): A close-up for the exact posi-tions of the six chest electrodes.

See the text for specific des cription. (Reproduced with permission from FM Kusumoto, Cardio-vascular Pathophysiology, Hayes Barton Press, Raleigh, NC, 2004.)



Some experts have advocated additional chest leads that extend around the back of the torso (V7–V9) or to the right chest (V4R, V5R, and V6R) to provide a more complete measurement of cardiac electrical activity. Although these additional lead positions may be extremely useful in certain specific situations, for the purposes of this discussion the reader should simply be aware that these additional electrode positions have been described and might be encountered in the hospital.

Often continuous ECG recordings are obtained while the patient is in the hospital to allow for rapid identification of cardiac problems. In this case, the 10 electrodes required for the standard ECG (4 on the limbs and 6 on the anterior chest) can be cumbersome for a patient to have on at all times so that depending on the system, 3 to 6 electrodes are placed on the torso. Specialized algorithms are then used to “derive” a full 12 lead ECG in some systems. Although these recording systems are useful for rapid evaluation of abnormal rhythms or marked changes on the ECG, the full 12 lead ECG using 10 separate electrodes is generally required for final interpretation of many abnormalities. For example, if a person in the hospital develops chest pain or a sustained abnormal heart rhythm, if possible, a standard 12 lead ECG should be obtained even if their cardiac rhythm is being monitored.

Electrodes and leadsIn order to measure any kind of electrical activity, two electrodes are required so that the measuring device can measure the voltage difference between the two locations. The ECG has traditionally used 12 electrode pairs or leads to measure the cardiac activity of the heart.

The ECG leads are generally divided into the frontal leads that use the extremity electrodes and measure electrical activity in a vertical plane, and the precordial leads that use the six chest electrodes and measure electrical activity in a roughly horizontal plane. Historically, the first leads that were used are referred to by Roman numerals I, II, and III (Figure 1.2): Lead I measures the voltage difference between the left arm and the right arm electrodes (with the right arm the “negative” electrode), lead II measures the difference between the right arm and the left leg electrodes (with the right arm as the “negative” electrode), and lead III measures the difference between the left leg and the left arm (with the left arm as the “negative” electrode). The right leg electrode is used as a ground. The ground is important for defining the zero voltage since ECG leads measure voltage differences rather than absolute values. From a practical


Technical Issues 5

standpoint, the ECG machine uses the signal from the ground to help filter extraneous electrical noise. The other three frontal leads are referred to by the shorthand aVR, aVL, and aVF and one electrode (the positive electrode) at the right arm, left arm, and left leg respectively compared to a composite electrode that is the averaged voltage from the remaining two electrodes. The small letter “a” is for “augmented” since the signal obtained is augmented or larger because the second electrode used is an averaged voltage from the other two limb leads.

Since leads I, II, III, aVR, aVL, and aVF measure activity in the same plane they are always considered together and traditionally represented by a large circle with the negative electrodes for each of the leads aligned in the middle of the chest (Figure 1.3). The positive electrodes extend outward in

aVR aVF aVL

(+) (+)

(+)

(–)

(+)

(–)

(+)

IIIII

(+)(–)

I

Unipolar limb leads

Bipolar limb leads

Figure 1.2: The electrodes used for obtaining the frontal leads of the ECG: I, II, III, aVR, aVL, and aVF. Leads aVR, aVL, and aVF are often called the unipo-lar limb leads because they record the voltage change in one of the

extremities relative to an averaged value of the other electrodes. (Reproduced with permission from FM Kusumoto, Cardiovascular Patho physiology, Hayes Barton Press, Raleigh, NC, 2004.)



Horizontal plane formed

by chest leads V1

I0°

90°

60°

–30°

120°

–150°

aVF

aVR aVL

IIIII

Frontal plane formed by

leads I, II, and III and the

three unipolar leads

(a) Frontal plane leads

(b) Horizontal plane leads

V2 V3V4

V5

V6

Figure 1.3:

(a): the limb leads with the nega-tive terminals aligned in the center of the torso fan out in a single plane called the frontal plane.

(b): The precordial leads with the negative terminal aligned in the

center fan out in a horizontal plane that is perpendicular to the frontal plane. (Reproduced with permission from FM Kusumoto, Cardiovascular Pathophysiology, Hayes Barton Press, Raleigh, NC, 2004).


Technical Issues 7

a circle in a single plane called the frontal plane. Specific orientations in the frontal plane are defined by the degrees of a circle with the horizontal axis toward the left is defined as 0° with positive values in the clockwise direction and negative values in the counter clockwise direction. In this way each of the extremity leads can be defined by a specific orientation: I, II, and III are 0°, 60°, and 120° respectively and aVR, aVL, and aVF are −150°, −30°, and 90° respectively. One way that can help you visualize this is a compass with North, East, South, and West equal to −90°, 0°, 90°, and 180°.

For the precordial leads electrical activity is measured between one of the six chest electrodes and the sum of the left arm, right arm, and left leg signals which is generally close to zero since the signals tend to cancel out (Figure 1.2). The composite electrode is considered the negative electrode and the electrode on the anterior chest as the positive electrode. With the negative electrode placed in the middle of the torso, the positive electrodes of the precordial leads fan out in a horizontal plane that is roughly perpendicular to the frontal plane (Figure 1.3).

Although truthfully voltage differences are measured between two electrodes, by convention the positive electrode of any electrode pair is used to indicate the general orientation of a specific lead. Don’t get too wrapped up into positive and negative electrodes (as it does not help the clinician very much), it is easier to think of the positive electrode as the location of the “sensor” for a particular lead receiving input from the heart. Thinking in this fashion the 12 leads of the ECG in the frontal and horizontal planes provide a relatively comprehensive 3 dimensional “sensor net” for evaluating the electrical activity of the heart. One useful analogy is to compare the positive electrodes of an ECG to windows located on different walls of a building. By looking through all of the windows at the same time, the viewer (“peeping Tom?!”) can get a fairly good idea of what is going on inside.

Clinically, the 12 leads can be grouped or divided based on the general orientation of the positive electrode relative to the heart (Figure 1.4). Leads II, III, and aVF are collectively called the “inferior leads” since they are oriented with the positive electrode “pointing upwards” and are in the best position measure electrical changes occurring on the bottom of the heart. Leads I, aVL, V5, and V6 are called the “lateral leads” since they best measure electrical activity on the left side of the heart, and leads V1, V2, V3, and V4 are called the “anterior leads.” Sometimes leads V1 and V2 are further subclassified as “anteroseptal.” Lead aVR is the only lead that is oriented on the right and best measures activity from the right side



(perhaps with a little contribution from leads III and V1). Grouping the leads in this way is very helpful for identifying myocardial (heart muscle) injury and localizing the region of damage.

Since the positive electrodes of the leads are oriented in different positions around the heart, the shape of the deflections recorded on a lead will give the clinician some clue of the direction of depolarization. The electrical activity of cardiac cells is generally divided into two periods. When the cell is excited it is depolarized and this leads to contraction in heart cells. After a short period of time (about 0.4 seconds) the cell repolarizes and the heart cell relaxes. The terms depolarization and repolarization can sometimes be confusing but they come from the fact that at rest cells have a negative charge and when the cell is excited the charge is approximately zero (the cell has lost charge or has been depolarized).

Horizontal plane

formed by

chest leads

I0°

60°

–30°

120°

–150°

aVF 90°

aVR aVL

IIIII

Frontal plane formed by

leads I, II, and III and the

three unipolar leads

V1 V4V2 V3V5

V6

Inferior leads: II, III, aVFAnterior leads: V1-V4

Lateral leads:

aVL, I, V5 ,V6

Figure 1.4:Combining Figure 1.3A and 1.3B and showing the positive elec-trodes as “sensors.” Notice that certain leads can be grouped together based on their general orientation relative to the heart:

anterior, inferior, and lateral. (Adapted with permission from FM Kusumoto, Cardiovascular Pathophysiology, Hayes Barton Press, Raleigh, NC, 2004.)


Technical Issues 9

Progressive activation of the heart cells leads to a wave of depolarization that is measured by the ECG. By convention, when depolarization travels toward the positive electrode a positive deflection is recorded and if the wave of depolarization is travelling away from the positive electrode a negative deflection will be recorded. Conversely if the direction of repolarization is oriented toward the positive electrode of an ECG lead a negative deflection will be recorded. To continue our earlier “window and building” analogy, we can think of the electrical activity of the heart as a person walking inside the building. As the person walks toward a window in the front of the building, he appears larger (and the electrical signal is positive), but from a window in the back, he is walking away so he looks smaller (and the electrical signal is negative). In the next chapter we will discuss the specific shapes of waves due to atrial and ventricular depolarization and ventricular repolarization (we will also explain why we cannot evaluate atrial repolarization).

Displaying the ECGECG recording paper is divided into “small boxes” that are I mm by 1 mm and “large boxes” that are 5 mm by 5 mm (Figure 1.5). Usually the ECG machine is set so that a 1 mV signal will lead to a 10 mm deflection in the

“Large” box:

5 mm´5 mm

“Small” box:

1 mm´1 mm

5 “Large” boxes = 1 second

2 “Large” boxes = 1 mV

Figure 1.5:ECG paper is divided into 1 mm × 1 mm “small” boxes that are grouped together in 5 × 5 mm “large” boxes. At standard set-tings, in the horizontal direction,

5 large boxes (25 mm) is equal to one second and, in the vertical direction 2 large boxes (10 mm) is equal to 1 mV.



Frontal leads

aVR

aVR

I

I

II

III

II aVL

aVL

aVF

aVF

V3

V3

V2

V2

V1

V1

V6

V6

V5

V5

V4

V4

III

Precordial leads

*

*

Figure 1.6:

Top: The most common standard display of the ECG shows the 12 leads as four columns and three rows. The first column displays leads I, II, and III. The second column displays aVR, aVL, and aVF. The third column displays V1, V2, and V3. The fourth column displays V4, V5, and V6. In this way the frontal leads are grouped as the first two columns and the pre cordial leads are grouped as the second two columns. A standar dization mark (*) is always shown on the far left.

Bottom: A second standard display shows all of the leads one on top of another usually in the following order: I, II, III, aVR, aVL, aVF, V1, V2, V3, V4, V5, and V6. Both the top and the bottom ECGs are from the same person. Notice that the bottom ECG has smaller signals because it was recorded at “half standard.” (Look at the standardization mark (*), a 1 mV signal made only a 5 mm signal.)


Technical Issues 11

ECG in the vertical direction. In the horizontal direction, the usual paper speed is 25 mm per second so that each large box (5 mm) represents 0.20 seconds and each little box (1 mm) represents 0.04 seconds. The settings of an ECG machine can generally be determined by looking for a standard mark usually at the far left of an ECG, where a 1 mV signal for 0.2 seconds is delivered. If the ECG machine is set to its usual settings this leads to a standardization mark signal that is 10 mm tall and 5 mm wide (Figure 1.6). If the paper speed is decreased to 12.5 mm per second, the signals become more compressed on the horizontal axis because each large box represents 0.40 seconds and if the paper speed is increased to 50 mm per second (10 large boxes equals one second), each large box is 0.10 seconds. In the same way if the voltage standard is halved then a 1 mV deflection leads to a 0.5 mm deflection and the size of the signal will be “squished” (Figure 1.6). In general these other settings are not used for the 12 lead ECG.

Although monitors still use specially designed paper that produces long “strips” of signals, for the sake of convenience and easier evaluation

Lateral leads

I, aVL, V5, V6

Inferior leads

(II, III, aVF)

Anterior leads

(V1 - V4)

I

II

III aVF

aVL

aVR

V3

V2

V1

V6

V5

V4

Figure 1.7:Using the standard format combining Figure 1.4 and 1.6 that emphasizes and groups the ECG leads that look at similar areas of the heart: The inferior leads, the anterior leads, and the lateral leads.



of all 12 leads, 12 lead ECGs are generally printed on standard letter size paper. Most commonly, the 12 lead ECG is displayed in four columns and three rows (Figure 1.6). The first column shows I, II, and III, the second column shows aVR, aVL, and aVF, the third column shows V1, V2, and V3, and the fourth column shows V4, V5, and V6. Just remember that the first two columns are frontal leads and the second two columns show the precordial leads. If the ECG is set at the standard paper speed, on standard letter paper, the full ECG records 10 seconds of electrical activity and each lead has 2.5 seconds of recording. A standard piece of paper is 279 mm long or about 55 “large” boxes. Another format usually called a rhythm strip shows a single lead for 10 seconds. Three to twelve leads are shown one on top of another (Figure 1.6).

Using the standard format, the inferior leads (II, III, and aVF) take up the “bottom left corner” of the ECG, the anterior leads (V1–V4) are in the “upper right corner”, and the lateral leads (V5,V6, I, and aVL) are scattered all over (Figure 1.7).


13


Before we can discuss the normal ECG, a quick review of the anatomy and the function of the heart is essential to provide a framework for our discussion. Unoxygenated blood from the body returns to the heart via the large superior and inferior vena cavae. Blood from these large veins enters into the right atrium and if the tricuspid valve is open the right atrium is a large passive “passage way.” Atrial contraction causes a final surge of blood to fill the right ventricle and as the ventricles contract the tricuspid valve closes and the pulmonic valve opens and blood is expelled from the heart and is pumped to the lungs (Figure 2.1). Once oxygenated by the lungs the blood returns to the heart via the left atrium, and in a process similar to the right, blood flows fills the left ventricle both passively and actively when the left atrium contracts. When the left ventricle contracts, the mitral valve closes and the aortic valve opens and blood is expelled from the heart to the body. This process seems extremely complex but is actually fairly simple if we think about cardiac activity from two different vantage points. From the perspective of a single blood cell, blood travels sequentially through the vena cavae, right atrium, right ventricle, and pulmonary arteries to the lungs. Once oxygenated the blood cell travels through the pulmonary veins back to the left atrium, left ventricle, and finally is propelled into the aorta. From the perspective of heart cells, there is near simultaneous activation of the right and left atria and after a slight delay almost simultaneous activation of the right and left ventricles. This sequential pumping process is controlled by electrical signals generated by the heart that can be measured by the ECG.

CHAPTER 2

The Normal ECG


The Normal ECG 15

Normal electrical activity of the heartAtrial depolarizationCertain specialized cells exhibit spontaneous depolarization and are called “pacemaker” cells. Although cells in the AV node, His Purkinje system, and sometimes atrial and ventricular tissue exhibit spontaneous activity, since the rate of spontaneous depolarization is highest in a region called the sinus node, the sinus node generally serves as the prin-cipal pacemaker of the heart.

The sinus node is a small spindle shaped structure located at the junction of the superior vena cava and the right atrium. The sinus node has spontaneous pacemaker activity between 60–100 beats per minute. The sinus node receives nerve input from both the sympathetic and parasympathetic autonomic system and this is why the heart rate varies. With exercise, increased sympathetic input leads to an increase in the rate of spontaneous pacemaker activity that in turn will lead to faster depolarization of the atria and ventricles (and faster heart rates when you measure the peripheral pulse). At night, increased parasympathetic input leads to a slowing of the pacemaker rate. Sometimes this dynamic interplay can be observed during breathing. As a general rule, with slow inspiration the heart rate slows (check your own pulse) and with expiration the heart rate increases (particularly if you do not immediately take another breath). Although it initiates electrical activation, the sinus node is so small that the current it generates cannot be seen on the surface ECG (Figure 2.2).

Figure 2.1: Basic diagram of blood circulation in the body. Deoxygenated blood returns to the heart from the body via the inferior and superior vena cavae. Blood enters the right atrium and sequential right atrial and right ventricular contraction pumps blood to the lungs via the pulmonary arteries. Blood is

oxygenated in the lung and returns to the left atrium via the pul monary veins. Sequential con-traction of the left atrium and left ventricle pumps the oxygenated blood into the aorta. Blood is then distributed to the body and the cycle repeats. (Illustration by David Factor.)



Atrial depolarization 2 Ventricular repolarization

Ventricular depolarization 6

Sinus node

AV node 3,4,5

Ventricles at plateau phase

PR QT

P wave T wave

QRS

(a)

(b)

1

2

3

4

1

23

4

5 5

6

Sinoatrial node

Atrialmuscle

Atrioventricularnode

5

Hisbundle

Purkinjefibers

6 Ventricularmuscle


The Normal ECG 17

Figure 2.2:

(a). The ECG deflections of the different portions of the heart and commonly measured intervals.

(b). The specific points where different portions of the heart are depolarized in relation to the surface ECG.

The pacemaker activity produced by the sinus node is propagated through the atria, and since the sinus node is located “high and to the right,” the right atrium is activated before the left atrium and the general direction of atrial depolarization is “high to low” and “right to left.” Depolarization of the atrial tissue leads to release of Ca2+ ions from the sarcoplasmic recticulum in the cells of the atrium that in turn causes the heart cells to contract. On a larger scale, contraction of all of the atrial cells leads to contraction of the atrial chamber and provides the final filling of the right ventricle. It should be apparent that this is a fairly complex process and that there is a small but measurable delay between atrial depolarization and actual movement of blood (1. atrial cell is excited; 2. Ca2+ ions are released; 3. atrial cells (chambers) contract; and 4. blood moves). Electrical activity generated by atrial depolarization produces the P wave on the ECG.

Although depolarization of the sinus node cannot be seen on the ECG, evidence that the sinus node is generating the electrical impulse can be obtained by inspecting the shape of the P wave. If the sinus node is “driving” the heart, the P wave is negative in aVR and positive in lead II (“high to low” and “right to left”). Generally right atrial and left atrial depolarization proceed in the same direction so that in a given lead the P wave is positive or negative. Relook at Figure 1.6 from Chapter 1, and notice that the small P wave is generally either all negative (lead aVR) or predominantly positive (the rest of the leads). The common exception is lead V1 (Figure 2.3). In this case, right atrial depolarization travels “toward” V1 leading to an initial positive deflection, but sometimes a later negative deflection can be observed because of left atrial depolarization. In fact if you refer to Chapter 8, Figure 8.14 on left ventricular hypertrophy, you will see that a large negative deflection in lead V1 is an important indicator of left atrial enlargement.

Right and left atrial depolarization is usually complete within 0.10 seconds so the normal P wave is 2–3 little boxes wide. The atria have a



very small mass compared to the ventricles so the normal P wave is usually less than 2.5 mm (two and a half little boxes) tall. Atrial repolarization generates voltages so small it is not seen on the ECG.

Atrioventricular conduction(AV node, His bundle, bundle branches, and Purkinje system)Once the atria are depolarized and the atria contract, blood is pumped into the right and left ventricles. As has been mentioned, the speed of electrical activity is much faster than the speed of blood, so to better improve the timing of atrial and ventricular contraction, the electrical impulse of atrial depolarization encounters the AV node where the con-duction velocity is slowed. At this point, the atria are completely depolar-ized and the ventricles are about to be depolarized. Since there is no electrical activity that can be measured by the ECG (the electrical impulse traveling through the very small AV node cannot be measured from the body surface), an isoelectric period can be observed on the ECG (Figure 2.2). The duration of the isoelectric period will depend at least in part on the speed of the electrical impulse through the AV node. For example, if the electrical impulse is abnormally slow through the AV node, a long isoelectric period will be observed.

After slow depolarization of the AV node, the velocity of activation speeds up as the impulse travels through the His Purkinje system. The

Rightventricle

Leftventricle

V6

V1

Rightatrium

Leftatrium

Sinusnode *

Figure 2.3: Atrial depolarization relative to leads V1 and V6. Notice that since the sinus node is located in the right atrium, the right atrium is depolarized before the left atrium.


The Normal ECG 19

His Purkinje has several components (His bundle, right and left bundles, Purkinje tissue) but all have similar electrical properties and are able to rapidly conduct electrical impulses. The electrical impulse first travels through the common bundle or bundle of His (named for its discoverer Wilhelm His) and divides into a large left bundle that activates the left ventricle and a thinner right bundle that activates the right ventricle. The left bundle further divides into two major components: the left anterior fascicle and the left posterior fascicle. The terminal portions of these branching bundles and fascicles are a network of Purkinje tissues that spread out as a net in the interior surface of both the right and left ventricles. Although the His Purkinje system allows rapid conduction and is extensive, its overall mass is relatively small so activation of these tissues cannot be observed on the surface ECG. In fact, abnormalities of components of these systems are deduced because different portions of the ventricle are activated abnormally. In general, the normal His Purkinje system allows the electrical impulse to be ”delivered” to large portions of the ventricle at nearly the same time so that right and left ventricular depolarization can start simulta-neously and blood can be efficiently and forcefully expelled from the heart. If the His Purkinje system were not present or functioned abnormally some regions would contract before others and blood would not be pumped as efficiently.

Ventricular depolarizationVentricular depolarization leads to a large deflection called the QRS complex. Ventricular depolarization has historically been called the QRS because it is made up of multiple components that are called Q waves, R waves, and S waves. Since describing the shape and the components of ventricular depolarization is very important, a common “language” for describing the QRS complex has been developed and is important to learn. Although the nomenclature can seem daunting, arbitrary, and confusing at first, it is actually easily learned and applied. The first negative deflection is called a Q wave, the first positive deflection an R wave, and any negative deflection after the R wave is called an S wave. Capital let-ters are used for large deflections and lower case letters for smaller deflec-tions. In general larger deflections are produced because of larger mass or a more uniform direction of depolarization. If the ventricles are depolar-ized in several directions, the sum of their voltage as measured by the ECG will be smaller due to canceling out of activity. The decision on



Q-Negative deflection before a positive deflection

R-first positive deflection

S-Negative deflectionafter a postive deflection

qR

R

RS

QS

Figure 2.4: Nomenclature for ventricular depolarization (QRS complex) and some examples. (Reproduced with permission from FM Kusumoto,

ECG Interpretation: From Patho-physiology to Clinical Application, Springer, New York, NY, 2009.)

whether to use a capital letter or a lower case letter is often made by the clinician. A completely positive deflection is called an R wave and a com-pletely negative complex is called a QS complex. Additional positive and negative deflections are described using a prime symbol: r’ or s’ depend-ing on whether an additional positive or negative deflection is observed. Figure 2.4 shows some common complexes and their descriptors.

Normally the left ventricle has a larger mass than the right ventricle, so that even though the right and left ventricles are activated simultaneously the shape of the QRS complex is dominated by the left ventricle. For this reason, the general direction of ventricular depolarization in the frontal plane recorded by the limb leads is right to left and “high to low” (Figure 2.5).


The Normal ECG 21

Figure 2.5:The general direction of cardiac activation in the frontal plane is called the cardiac axis. The largest positive deflection will be recorded in the lead that is oriented most directly in the path of ventricular

depolarization (in this case, lead II). (Adapted with permission from FM Kusumoto, Cardiovascular Pathophysiology, Hayes Barton Press, Raleigh, NC, 2004.)

The cardiac axis is used to more precisely calculate the direction of ventricular depolarization. The value of the axis is given in degrees using the lead alignment shown in Figures 1.3 and 1.4 in Chapter 1. A normal cardiac axis can have a wide range between −35° and 110° but is usually about 60°. The easiest way to calculate the cardiac axis is to remember that the ECG lead that is “looking” most directly at the wave of depolarization will have the largest positive deflection with smaller positive deflections recorded as the recording lead “looks” at the wave of depolarization from larger and larger angles. When the lead is perpendicular to the wave of depolarization a biphasic signal that is first positive and then negative is recorded (Figure 2.6). For most people, the



Figure 2.6:The shape of the QRS complex will depend on the relationship between the wave of cardiac depolarization and the orientation of the lead. If the lead is directly in front of the depolarization wave a large positive signal will be recorded. As leads are oriented away from the wave of depolariza-tion, the size of the positive wave

will decrease and a terminal nega-tive wave will be recorded as the wave of depolarization is traveling away from the lead. When a lead is perpendicular to the depolariza-tion wave an equally biphasic wave will be recorded. When the wave of depolarization is directed away from the lead a negative deflection will be recorded.


The Normal ECG 23

largest QRS complex is observed in lead II and a completely negative QRS complex is often recorded in aVR (Figure 1.6 in Chapter 1).

If the axis is abnormally shifted to the right > 110° the largest positive wave will be recorded in lead III and if the axis is shifted to the left the largest R wave will be in aVL. Traditionally large sections of texts have been devoted to calculating the exact value of the QRS axis. Although useful for making sure someone knows the basis of ECGs, from a clinical standpoint estimating the general direction of ventricular depolarization is all that is required. The general direction of ventricular depolarization can be calculated by at least three different methods:

Find the lead with the largest QRS, and the mean electrical activation travels in the direction of the lead. If 2 leads are about the same height, the axis will be between these 2 leads.

Find the most isoelectric lead (most biphasic) and the largest QRS should be perpendicular to this lead. The lead with the largest QRS represents the general direction of the axis. Each limb lead has a corresponding perpendicular limb lead to form a pair: lead I and lead aVF; lead II and lead aVL; lead III and lead aVR.

The mean QRS axis can be calculated by the limb leads I and aVF. Keep in mind the four quadrants that are divided by 90 degrees.

● If lead I is positive and lead aVF is positive, the axis is normal because it falls between −30 to +110, which is the normal axis (normal quadrant).

● If lead I is positive, lead aVF is negative, and lead II is also negative, it falls between −30 and −90 which is left axis deviation (left quadrant).

● If lead I is negative and lead aVF is positive, this is a right axis deviation (right quadrant).

● If lead I is negative and lead aVF is negative, then this is extreme right axis deviation (northwest quadrant (using our compass analogy in the last chapter) or “no man’s land”).

Of these three methods, simply looking for the limb lead with the largest R wave is generally sufficient and the easiest method to remember. Although the QRS axis can be abnormal due to abnormalities of the heart, it is also important to remember that the cardiac axis reflects the



position of the heart relative to the body so will also be affected by conditions that change the position of the heart within the thorax. For example, in chronic obstructive lung disease the heart may hang more vertically in the chest and this leads to a more rightward axis even in the absence of any abnormalities of the heart itself.

The shape of the QRS complex in the precordial leads can also vary with the relative orientation of the ventricles in the chest cavity. Generally the QRS complex in lead V1 has an rS morphology. Initial septal activation occurs from left to right (because the left bundle branches off “first” compared to the right bundle) and since the left ventricle is usually positioned behind the right ventricle a large negative deflection is observed (Figure 2.7). In lead V6, the QRS complex will often have a small

V6

V5

V4

V3V2

V1

Figure 2.7:In the horizontal plane, the precordial leads generally record two components of ventricular depolarization. First septal activa-tion proceeds from left to tight and then a larger right to left wave of depolarization is observed since the left ventricle has much

more mass than the right ventri-cle. This second component of ventricular activation is usually much larger than septal activa-tion simply on the basis of mass (mass of the septum is small relative to the rest of the left ventricle).


The Normal ECG 25

q wave due to “left−to−right” septal activation followed by a large R wave due to left ventricular activation. Often the term R wave progression is used to describe the relative sizes of the R waves in the precordial leads. In lead V1 and lead V2 small r waves are present because they represent septal activation, but the R wave becomes larger laterally as it now represents left ventricular depolarization. The precordial leads where the R wave and S wave are approximately equal is called the transitional zone and usually occurs between leads V2 and V4, with lead V3 being the most common site.

As has been mentioned, the His Purkinje system is important for allow-ing simultaneous left ventricular and right ventricular activation. This phe-nomenon can be seen in the ECG, despite the ventricle being significantly larger than the atria and thus the QRS has a larger amplitude than the P wave, the duration of the P wave and the QRS complex are normally fairly similar – generally a little less than three little boxes or ≤ 0.12 seconds.

ST segmentOnce depolarized, the ventricles continue to contract for about 0.4 to 0.45 seconds to allow blood to be expelled from the heart to the lungs or body. During this period, the ventricular cells are in their plateau phase (they remain depolarized) so there are usually no electrical gradients that can be measured by the ECG so that after the QRS complex there is an isoelectric period often called the ST segment. As we will see later, changes in the ST segment are important for identifying myocardial injury and ischemia.

Ventricular repolarizationAs ventricular contraction is completed, the ventricles begin to repolarize and return to their baseline state to prepare for another depolarization/contraction sequence. Ventricular repolarization pro-duces the T wave. Ventricular repolarization is much more hetero-geneous when compared to ventricular depolarization (which is mediated by the His Purkinje system) and this leads to a T wave that is more broad based and generally of lower amplitude (think “squashed”) when compared to the QRS complex. It is an interesting paradox that the normal T wave generally is in “the same direction” as the direction of the QRS complex because depolarization proceeds from endocardium to epicardium (“inside−out”) and repolarization proceeds in the opposite direction from epicardium to endocardium (“outside−in”) (Figure 2.8). Part of the basis for this apparent



aVR aVL

II

aVR aVL

II

Figure 2.8:Depolarization (Top) and repolari-zation (Bottom) of the ventricles as observed in the frontal plane. Depolarization occurs almost simultaneously because of the His Purkinje system. Depolarization occurs from endocardium to epicardium and since the left ventricle has a larger mass than the right ventricle the overall direction of depolarization is from right to left and from the superior

portion of the ventricles to the lower portion of the ventricles. In general this leads to an axis of approximately 60° so that a large R wave is noted in lead II, an RS complex is observed in aVL (depolarization travels toward and then away from this lead), and a QS complex is noted in lead aVR. Depolarization occurs from epicardium to endocardium in a more gradual fashion. This leads


The Normal ECG 27

paradox is that the epicardial cells have a shorter action potential duration than endocardial cells.

Timing of normal cardiac activityIn the first section of this chapter we focused on the shape of the various waveforms but one of the important uses for the ECG is measuring the timing relationship of different cardiac events.

Heart rate (R−R interval)The most basic timing measurement of the ECG is the heart rate. Since the pulse is generated by ventricular contraction, the distance between two QRS complexes (the R−R interval) will provide an estimate of the heart rate. Remember that each large box represents 0.20 seconds so slower heart rates will be associated with larger distances between QRS complexes. For example if the heart rate is 60 beats per minute, QRS complexes will occur once every second and the QRS complexes will be separated by 5 large boxes at the standard paper speed. If the heart rate is 100 beats per minute only 3 large boxes or 0.60 seconds will separate each QRS complex. One can do the math and calculate the exact heart rate by using the formula:

Heart rate (beats per minute) = 60 / (the R−R interval in seconds)

This formula is accurate but can be rather cumbersome (and hard to remember) in clinical medicine. Since the importance of determining the exact heart rate is rarely clinically important, it is much easier to estimate the rate by the following formula (Figure 2.9):

Heart rate (beats per minute) = 300 / (the number of large boxes between two QRS complexes)

Figure 2.8: (Cont’d)to an upright T wave in II, a flat (slightly inverted in this example) in lead aVL, and an inverted T wave in aVR. Notice that since repolari-zation is generally in the opposite direction than depolarization, the

QRS and T wave orientation is usu-ally the same. (Reproduced with permission from FM Kusumoto, ECG Interpretation: From Patho-physiology to Clinical Appli cation, Springer, New York, NY, 2009.)



QRS interval

QT intervalPR interval

RR interval

1 2 3 4

“Two QT intervals are less

than the RR interval”

Figure 2.9:Calculation of rate and common intervals. In this case the QRS com-plexes are separated by 4 large boxes (R–R interval) so the rate is approximately 75 bpm (300/4). The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. The QRS interval is measured from the beginning of the QRS complex to the end of the QRS complex.

The QT interval is measured from the beginning of the QRS complex to the end of the T wave. In gen-eral the QT is normal if it less than half the R–R interval (“You can fit two QTs into one R–R”). (Reproduced with permission from FM Kusumoto, ECG Interpre tation: From Patho physiology to Clinical Appli cation, Springer, New York, NY, 2009.)

So that if the QRS complexes are separated by two large boxes the heart rate is 150 bpm, three large boxes yields a heart rate of 100 bpm, four large boxes 75 bpm, and five large boxes 60 bpm. Finally, another very simple way to estimate the rate is to remember that at a standard paper speed of 25 mm/s most 12 lead ECGs record 10 seconds of cardiac activ-ity. Simply count the number of beats and multiply by 6.

In most cases the rate of atrial activity will be the same as the rate calculated from ventricular depolarization (R−R interval) since the sinus node is normally the “driver” of the heart and the AV node/bundles conduct every atrial impulse to the ventricles. In some cases the atrial rate will be slower than the ventricular rate either due to more rapid ventricular depolarization or slower atrial activity due to abnormalities in sinus node function. In both of these conditions there will be more QRS


The Normal ECG 29

complexes than P waves. Conversely, sometimes the atrial rate will be more rapid than the ventricular rate because atrioventricular conduction does not maintain a 1:1 relationship between atrial depolarization and ventricular depolarization (more P waves than QRS complexes).

PR intervalThe PR interval is measured from the beginning of the P wave to the beginning of the QRS complex (Figure 2.2). The PR interval provides an estimate of atrioventricular conduction and represents right atrial depo-larization (remember AV node conduction usually begins near the end of right atrial depolarization and at the same time left atrial depolarization begins since the AV node is located in the interatrial septum between the right and left atria), AV node depolarization, and His Purkinje depolariza-tion. The normal PR interval gets longer with age, but for adults is ≤ 0.20 seconds and is most commonly about 0.16 s (4 little boxes).

UQTQT

Figure 2.10:Measurement of the QT interval. The end of the T wave is best calculated by drawing a tangent line along the steepest portion of

the T wave. In this case a prominent U wave is observed that should not be included in the measurement of the QT interval.



QRS intervalThe QRS interval is measured from the beginning of the QRS complex to the end of the QRS complex and provides a rough estimate of the time required for depolarization between the first portions of the ventricle to be activated to the last portion of the ventricle to be depolarized. The normal QRS interval is ≤ 0.12 seconds (3 little boxes). Generally, the pos-terior portion of the left ventricle closest to the spine is the last ventricular site to depolarize although this can change if there is blocked conduction in either the left or right bundle. In fact, the hallmark for identifying block in one of the bundles is a widened QRS interval > 0.12 seconds (Chapter 7, Figures 7.1 and 7.2; Chapter 8, Figures 8.1 and 8.2).

QT intervalThe last commonly measured interval is the QT interval. The QT interval is measured from the beginning of the QRS complex to the end of the T wave. The end of the T wave can sometimes be difficult to measure because the T wave has a much more gradual upslope and downslope but drawing a tangent line along the steepest part of the descending portion of the T wave has been advocated and accepted as the best way to measure the QT interval (Figure 2.10). Most commonly the QT inter-val is measured in lead II although recent guidelines recommend using the lead with the longest QT interval (usually lead V2 or V3). Measurement of the QT interval in leads V2 and V3 can be sometimes be more difficult to measure because of a U wave. A U wave is a very low amplitude signal that is probably due to rapid filling of the ventricles rather than another wave of repolarization. It is usually seen as a positive wave in leads V2 and V3 and is more commonly seen with slower heart rates. Although there has been some disagreement in the past, since the U wave does not appear to be due to ventricular repolarization most now agree that it should not be included in the measurement of the QT interval. The QT interval measures the time between the first ventricular cell to depolarize and the last ventricular cell to repolarize, and provides a rough estimate of the duration of the plateau phase of ventricular tis-sue. As described in Chapter 6, Figures 6.7–6.14, the QT interval is pro-longed in patients with electrolyte disorders, certain medications, and may be congenitally long due to abnormalities of K+ channels. The QT interval is longer in women and decreases with rate. For this reason the QT interval is usually corrected to rate by an algorithm and called the


The Normal ECG 31

QTc where “c” stands for “corrected.” The most common method for correcting the QT interval for rate is the Bazett’s formula:

QTc = QT (seconds) / (R−R)1/2

Where “R−R” is the R−R interval in seconds. Several other techniques for rate correction have been suggested but the Bazett’s correction is the most commonly used and the one provided by most automated ECG algorithms. A QTc > 450 s in men or > 460 s in women have been used as cut−off values for dividing normal and abnormal values but it should be remembered that in reality the QTc can vary from many causes and there is significant overlap in QTc intervals between patients with known genetic disorders that cause QTc prolongation and the normal popula-tion. An easy way to “get a feel” on whether the QT interval is prolonged is to remember that in general the QT interval should be less than half the R−R interval. Given the obvious difficulty in measuring the QT interval it is not surprising that even cardiologists, who are physicians that special-ize in heart diseases, often incorrectly measure the QT interval.


32


Now we come to the art of evaluating the ECG and using it in clinical context. Although computer analysis of the ECG has become far more accurate over the past two decades, the ability to carefully interpret an ECG remains an important skill in clinical medicine. However, although the ECG may be extremely useful, it is important to remember that, at best, the ECG provides supplementary information to a careful history and physical examination.

Traditionally ECG interpretation is taught by sequentially calculating the heart rate, measuring the cardiac axis, measuring cardiac intervals, evaluating the P wave, the QRS complex, the ST segment, and then the T wave. However, in clinical practice we appropriately focus on identify-ing potential life-threatening problems first. In fact, we believe that, in general, most of clinical training focuses on being able to distinguish “very, very” sick from “not-so” sick. In these emergent and urgent situ-ations the ECG is really useful for 1) evaluating abnormally fast and slow heart rates and 2) identifying myocardial injury.

With this in mind, use the algorithm in Figure 3.1 for your initial analysis of the ECG. First, make an initial assessment of the heart rhythm. Make sure that P waves are present and that every P wave results in a QRS complex, and, most important, that the overall heart rate is between 50 and 110 beats per minute. If these statements are true, then the heart rhythm is not life-threatening (although not necessarily normal). The point here is that any heart rhythm with these characteristics (P waves and QRS complexes with a 1:1 relationship at a normal rate) should be able to provide sufficient blood flow to the lungs, brain, and the rest of the peripheral circulation. Second, the ST segment after the QRS complex should be evaluated. The ST segment should be isoelectric – in other words, the segment separating the T wave and

CHAPTER 3

ECG Interpretation Basics


ECG Interpretation Basics 33

Fig

ure

3.1

:Ba

sic

algo

rithm

for

rap

id id

entif

icat

ion

of s

erio

us a

rrhy

thm

ias

or s

erio

us m

yoca

rdia

l inj

ury.

Ass

ess

th

e p

ati

en

t: s

ymp

tom

s a

nd

ph

ysic

al e

xam

ina

tio

n

Ap

pe

ara

nce

, vit

al s

ign

s, in

itia

l ph

ysic

al e

xam

ina

tio

n

Is t

he

re a

P w

av

e in

fro

nt

of

ev

ery

QR

S

an

d is

th

e r

ate

be

twe

en

50

–1

10

be

ats

pe

r m

inu

te?

Are

th

e S

T s

eg

me

nts

iso

ele

ctri

c?

Ye

s a

nd

Ye

sY

es

an

d N

oN

o a

nd

Ye

sN

o a

nd

No

Ta

ke a

de

ep

bre

ath

Go

to

Fig

ure

s 3

.3 a

nd

3.4

to c

on

firm

th

e p

rese

nce

of

a n

orm

al E

CG

Go

to

Fig

ure

4.1

for

Ev

alu

ati

on

of

ST

seg

me

nts

Go

to

Fig

ure

9.1

for

Ev

alu

ati

on

of

Arr

hyt

hm

ias

Loo

k a

t b

oth

Fig

ure

4.1

an

d 9

.1

an

d y

ou

ha

ve

a

ve

ry s

ick

pa

tie

nt

on

yo

ur

ha

nd

s

1.

2.



the P wave of the next beat (sometimes called the T–P interval and the period when the ventricle is filling “passively” without atrial contraction), the PR interval, and the ST segment should all be at the same level (Figure 3.2). If the ST segment is elevated or depressed, particularly if the patient is also complaining of chest pain or shortness of breath, myocardial injury may be present. No mystery, no voodoo, and no hocus pocus: probably 90–95% of emergent conditions in which the ECG provides rapid information that requires immediate clinical treatment is addressed by evaluating these two issues. If the rhythm is normal and the ST segments are isoelectric (“Yes and Yes”), interpretation of the ECG can take a more leisurely pace once the patient has been attended to.

It is important to remember that a comprehensive analysis of the ECG can have many components (Figure 3.3). In general, although all of these components fall into three major groups: Evaluation of the rhythm (Chapters 9–11), evaluation of ventricular depolarization (Chapters 7 and 8), and evaluation of ventricular repolarization (Chapters 4–6). The characteristics of a normal ECG are illustrated in Figure 3.4.

Figure 3.2:Evaluation of the ST segment. Use the T–P and PR segment (dotted line) to estimate the level of an isoelectric ST segment. ST segment elevation is an ST segment above this imaginary line, ST segment depression is an ST segment below this line, and an isoelectric ST interval will be level and near this line.

T-P/PR/ST line

T-P/PR/ST line

T-P/PR/ST line

ST segment elevation

ST segment depression

Isoelectric ST segment


ECG Interpretation Basics 35

Yes and Yes

Rhythm identification

(Chapter 9)

Evaluate ventricular

depolarization

(Chapter 7)

Upright P wave in II

PR interval <0.20 s

QRS narrow and negative in V1

Normal cardiac axis (–30° to 110°)

No abnormal Q waves

Normal QRS voltage

Evaluate ventricular

repolarization

(Chapter 4)

“Normal” T waves

Normal QT interval

(QTc < 0.45s M , < 0.47s W)

Components of ECG interpretation Normal findings

Figure 3.3:Once a life-threatening arrhythmia is ruled out and the presence of isoelectric ST segments is con-firmed, the ECG can be evaluated in a systematic fashion. Although there are many components to a comprehensive interpretation of the ECG that are beyond the scope of this introductory text, in general there are three essential parts to ECG analysis. First, the rhythm should be specifically iden-tified. We have already done some “triage” by identifying abnormally slow or fast heart rhythms. Second, ventricular depolarization

should be assessed. ECG findings suggestive of abnormal ventricular depolarization include a wide QRS complex (> 0.12 s), a QRS complex that is positive in lead V1, abnor-mal cardiac axis, and the presence of Q waves. Third, ventricular repolarization should be evalu-ated. Again, the reader has already done some triage by evaluating the ST segment but other abnor-malities of ventricular repolariza-tion include abnormal T waves (both inverted and peaked) and delayed ventricular repolarization (prolonged QT interval).



Figure 3.4:The characteristics of a normal ECG. First, the P wave is upright in lead II and negative in aVR suggest-ing that the atria are being depo-larized by the sinus node. Every P wave is followed by a QRS complex with a PR interval of < .20 s, these two findings confirm that the AV node is functioning normally. Second, ventricular depolarization is characterized by a narrow QRS complex (< 0.12 seconds), which suggests that the His Purkinje system is functioning normally with simultaneous activation of the right and left ventricles. The cardiac axis is approximately 60° with the

largest positive deflection in the limb leads identified in lead II. The precordial QRS complexes are nor-mal with a predominantly negative QRS complex in lead V1. A Q wave in lead aVR (and sometimes in III) is expected since ventricular depolari-zation is traveling away from this lead and small Q waves (< 0.04 ms) due to septal activation can be seen in the l ateral leads, particu-larly V6. Repolarization is normal with an isoelectric ST segment and T waves that are in the same gen-eral direction as the QRS in that lead. The QT interval is normal and less than half the R–R interval.

1. Rate should be between 50 and 110 bpm

2. A P before every QRS (Positive P in lead II)

3. The QRS in V1 (MCL 1) should be narrow and negative (rS)

4. The ST segment should be isoelectric

5. The T wave should be the same direction as the QRS

The normal ECG


37


You have come to this chapter in two ways. Either you identified ST segments that are not isoelectric or you have identified abnormal T waves (Figure 4.1). The ST segment and the T wave correlate with the plateau phase and repolarization of ventricular myocytes respectively and are particularly important for evaluation of the patient with chest pain or other symptoms suggestive of myocardial injury/ ischemia (ischemia means that an organ is not receiving adequate amounts of blood and comes from the Greek word iskhaimos: iskhein: “To hold back” and haima: “blood”). It is important to remember that all three of these repolarization changes (ST segment elevation, ST segment depression, and T wave changes) can sometimes be observed on a single ECG and are often related. Clinically ST segment elevation requires the most urgent treatment and should always be the primary focus of the evaluation. In other words, the leads that display ST segment elevation directs you to the location and type of problem (“Where the money is”). If the ECG has ST segment elevation, use the figures in this chapter to help you with the diagnosis. If the ECG has ST depression only, recheck to make sure there are no leads with ST elevation and go to Chapter 5, and if the ST seg-ments are isoelectric and only the T waves are inverted, go to Chapter 6. Very subtle ST segment elevation can be a normal finding in any lead, particularly in V2 and V3. However, any ST segment elevation > 2 mm in leads V2 or V3 or ST segment elevation > 1 mm in any of the other leads should be considered suspicious for a cardiac abnormality. Use Table 4.1 to decide whether: 1) The ST segment elevation is abnormal? and 2) Is the abnormal ST segment elevation due to myocardial injury?

CHAPTER 4

Abnormal Repolarization: ST Segment Elevation



ST segment Elevation (Figures 4.4–4.29)

ST segment Depression (Figures 5.1–5.8)

T wave changes

Precordial leads (anterior, lateral or both)

Inferior leads

Both inferior and precordial leads

Lead aVR

Location

Reciprocal ST segment depression other than aVR

T wave inversion (Chapter 5)

Prominent T waves (Chapter 5)

Prolonged QT interval (Chapter 6)

Accompanying Q waves

Figure 4.1:Evaluation of abnormal repolari-zation. If ST segment elevation is present the specific lead location(s) of the ST segment elevation should be identified. ST segment elevation associated with myocardial infarction is localized to one of the regions supplied by the major coronary arteries (see Figure 4.3). In addi-tion to the localization of the ST segment elevation to a particular

region supplied by a coronary artery, the presence of ST segment depression in other leads (so called reciprocal ST segment depression) or Q waves suggests myocardial injury as the cause of the ST segment elevation. Other repolarization abnormalities include ST segment depression (usually seen in the lateral leads), or abnormal T waves (See Chapters 5 and 6).


Abnormal Repolarization: ST Segment Elevation 39

Table 4.1: Factors determining whether abnormal ST segment is present and whether abnormal ST segment elevation is more likely due to ischemia

Is abnormal ST segment elevation present?(Yes to any questions means abnormal )● Is ST segment elevation > 2 mm in V2 and V3, or > 1 mm in the other leads?● Is the ST segment elevation present in two “adjacent” (contiguous) leads?

Is the abnormal ST segment elevation due to myocardial injury?(Yes to any questions means that myocardial injury is a likely cause)● Does the ST segment elevation correspond to a region supplied by a

coronary artery (anterior, lateral, inferior)?● Is reciprocal ST segment depression present?● Are the T waves also inverted?● Are Q waves present?

ST segment elevation is the hallmark ECG finding for patients who have total occlusion of one of the major coronary arteries that supply blood to the heart (Figure 4.2). In this case continued myocardial injury can lead to myocardial infarction (MI)-more commonly called a “heart attack.” (The word infarction comes from the Latin word “infarcire” which means to “plug up.”) The main reason for quickly identifying the presence of ST segment elevation is that several landmark studies have demonstrated the importance of reestablishing blood flow via either drugs to dissolve the clot (thrombolysis) or mechanically opening the artery (usually by taking the patient directly to the cardiac catheterization laboratory where cardiologists can restore blood flow with a variety of special techniques including balloons that dilate the narrowed area). In fact the data is so compelling for STEMI or “ST segment elevation myocardial infarction,” hospitals in the United States are now being “graded” on the timeliness and their response to this condition. Myocardial infarction can also occur in the setting of ST segment depression and T wave changes (usually T wave inversion), and the clinical term for these conditions is NSTEMI or “non ST segment elevation myocardial infarction.” The terms ischemia, injury, and infarction have traditionally been used to distinguish increasing degrees of severity based on ECG findings. “Ischemia” was characterized by ST segment depression



Lipid plaque

Plaque rupture

Thrombus

Formation

Figure 4.2:Schematic for the development of myocardial ischemia/injury/infarction. A lipid plaque ruptures and thrombus (blood clot) forms at the exposed tissue/lipid. If the thrombus completely occludes flow, the patient develops a myo-cardial infarction (usually charac-terized by ST segment elevation) in the downstream myocardium

(shaded area). Sometimes the clot does not completely occlude blood flow, but severe limitation of flow prevents sufficient blood to be supplied to the affected area (ischemia). (Adapted with permission from FM Kusumoto, Cardiovascular Pathophysiology, Hayes Barton Press, Raleigh, NC, 2004.)

or T wave changes, “Injury” was characterized by ST segment elevation without Q waves, and “Infarction” characterized by abnormal Q waves and ST segment elevation or depression. Now the diagnosis of myocardial damage is generally made by identifying abnormal amounts of cardiac proteins such as troponins in the blood. But the ECG is still used to distinguish myocardial infarctions associated with ST segment elevation (STEMI) and myocardial infarctions with any other ECG findings (NSTEMI).



One of the important hallmarks of ST segment elevation associated with a MI is localization of the ST segment elevation to a specific anatomic distribution. In most people there are three major coronary arteries that supply blood to the heart (Figure 4.3). The right coronary artery supplies blood to the inferior wall. The left main coronary artery almost immediately (usually within 1 or 2 cm) splits into a left anterior descend-ing coronary artery supplies blood to the anterior wall, and a circumflex coronary artery supplies blood to the lateral wall. Complete occlusion of a coronary artery will generally lead to ST segment elevation in the leads that “look” directly at these areas. In many cases “reciprocal” ST depres-sion will be observed in the other leads. The presence of a Q wave (initial negative deflection in the QRS complex) in a lead with ST segment elevation is very suggestive that a myocardial infarction is present.

As will be illustrated in the rest of the chapter, MI is associated with ST segment elevation in groups of leads (anterior: V1 to V4; inferior: II, III, and aVF; lateral: I, aVL, V5 and V6), depending on the site and extent of injury. As a corollary to this point, ST segment elevation due to myocardial infarction should be observed in several leads within a given lead group. Another commonly used way of emphasizing this important point is that significant ST segment elevation should be observed in two contiguous leads (leads that are roughly adjacent to each other). For further evalua-tion of ST segment elevation, it is easiest to consider the location (s) of the ST elevation: precordial (anterior and lateral), Inferior, both precordial and inferior, and only in aVR.

One specific point about anterior ST segment elevation requires special emphasis. Anterior ST segment elevation, particularly in leads V1 through V3, can be present in almost any condition that is associated with a wide negative QRS complex in lead V1. The most common example is left bundle branch block. The specific ECG characteristics of conditions associated with a wide QRS complex are covered more extensively in Chapter 7, but in general anything that causes abnormal ventricular depolarization will cause abnormal repolarization including changes in the ST segment that can make evaluation of ST segments extremely problematic and often useless. As always the clinician should make decisions based on the patient’s symptoms and “Hope for the best, but prepare for the worst.”



Obtuse marginal branch

lateral wall MI

Left anterior descending

anterior wall MI

Inferior wall

ST elevation: V1 - V4

Right coronary artery

inferior wall MI

ST elevation: V5 , V6 , I, aVL

ST elevation: II, III, aVF

Anterior Wall

Lateral wall



Figure 4.3:Localization of ST segment elevation in relationship to the affected coronary artery that is occluded. If the left anterior descending artery is occluded ST segment elevation is usually seen in the anterior leads V1–V4. In most people the circumflex artery often has one or two large obtuse marginal arteries and occlusion of one of these arteries leads to a

lateral wall myocardial infarction. ST segment elevation is usually seen in the lateral leads I, aVL, V5, and V6. The right coronary artery supplies the inferior wall in most people, so that occlusion leads to an inferior wall myocardial infarction. ST segment elevation is observed in the inferior leads II, III, and aVF.



V1

LBBB

QS

or

rS c

om

ple

x

QR

S >

0.1

2 s

ST

1–

4 m

m

Brug

ada

Synd

rome

rsR

’ co

mp

lex

QR

S >

0.1

2 s

ST

1–

4 m

m

Infarct

Ane

urysm

QS

co

mp

lex

QR

S <

0.1

2 s

ST

1–

4 m

m

Inve

rte

d T

wav

e

Injury

rS o

r Q

S c

om

ple

x

QR

S <

0.1

2 s

ST

1–

6 m

m

Normal

rS

co

mp

lex

QR

S <

0.1

2 s

ST

1

–2

mm

V3

-V6

Pericarditis

qR

or

R c

om

ple

x

QR

S >

0.1

2 s

ST

1–

4 m

m

“Sa

gg

ing

”

No

Q w

ave

PR

de

pre

ssio

n

Infarct

(Evo

lving)

qR

co

mp

lex

QR

S <

0.1

2 s

ST

1–

4 m

m

“Hu

mp

ed

”

Q w

ave

Inve

rte

d T

wav

e

Injury

rS o

r Q

S c

om

ple

x

QR

S <

0.1

2 s

ST

1–

6 m

m

“Hu

mp

ed

”

Q w

ave

?

Early

Repo

larization

R o

r q

R c

om

ple

x

QR

S <

0.1

2 s

ST

1

–2

mm

“Sa

gg

ing

”

No

Q w

ave

Pre

cord

ial S

T S

eg

me

nt

Ele

va

tio

n



Fig

ure

4.4

:W

hen

prec

ordi

al

ST

segm

ent

elev

atio

n is

ob

serv

ed

it is

ex

trem

ely

usef

ul t

o 1)

look

spe

cific

ally

at

V1

and

2) e

valu

ate

the

spec

ific

prec

ordi

al le

ads

that

hav

e ST

seg

men

t el

evat

ion.

If

the

QRS

in le

ad V

1 is

wid

e an

d pr

edom

inan

tly n

egat

ive

left

bu

ndle

bra

nch

bloc

k m

ay b

e pr

esen

t an

d ac

com

pany

ing

ST

segm

ent e

leva

tion

is v

ery

com

mon

. In

fact

EC

G id

entif

icat

ion

of m

yoca

rdia

l inf

arct

ion

in th

e pr

esen

ce o

f lef

t bun

dle

bran

ch

bloc

k ca

n be

ext

rem

ely

prob

lem

atic

(Fi

gure

4.2

7).

A m

uch

rare

r fin

ding

is

the

pres

ence

of

Brug

ada

Synd

rom

e th

at i

s ch

arac

teriz

ed b

y a

term

inal

pos

itive

def

lect

ion

(r’ w

ave)

and

ST

seg

men

t el

evat

ion

in V

1 (F

igur

es 4

.15

and

4.16

). In

situ

a-tio

ns w

here

the

ST

segm

ent

elev

atio

n is

onl

y pr

esen

t in

the

an

terio

r le

ads

(V1

thro

ugh

V4)

the

diff

eren

tial

diag

nosi

s is

ge

nera

lly f

airly

lim

ited.

Iso

late

d ST

seg

men

t el

evat

ion

in V

1 th

roug

h V

3 ca

n be

see

n as

a n

orm

al v

aria

nt,

part

icul

arly

in

youn

g m

en b

ut i

s us

ually

les

s th

an 2

mm

. Th

e ST

seg

men

t el

evat

ion

asso

ciat

ed

with

an

an

terio

r w

all

myo

card

ial

infa

rctio

n m

ay b

e ex

trem

ely

prom

inen

t, s

omet

imes

> 5

mm

an

d ha

s of

ten

been

des

crib

ed a

s ha

ving

a “

hum

ped”

sha

pe

and

may

obs

cure

eve

n la

rge

T w

aves

. Th

e pr

esen

ce o

f a

Q

wav

e (in

itial

neg

ativ

e de

flect

ion

or n

otch

) in

any

of t

he a

nte-

rior

lead

s V

1–V

4 is

abn

orm

al a

nd is

evi

denc

e fo

r a

myo

card

ial

infa

rctio

n. S

T se

gmen

t el

evat

ion

in t

he l

ater

al p

reco

rdia

l le

ads

V5

and

V6

are

asso

ciat

ed

with

so

me

addi

tiona

l po

ssib

ilitie

s. A

spe

cific

pat

tern

cal

led

early

rep

olar

izat

ion

(Fig

ure

4.6)

is

asso

ciat

ed w

ith l

ater

al S

T se

gmen

t el

evat

ion

and

prom

inen

t T w

aves

and

is p

artic

ular

ly c

omm

on in

Afr

ican

A

mer

ican

m

en.

In

addi

tion,

pe

ricar

ditis

(F

igur

e 4.

21)

a co

nditi

on w

here

the

re i

s ac

ute

infla

mm

atio

n of

the

sac

su

rrou

ndin

g th

e he

art

can

also

cau

se S

T se

gmen

t el

evat

ion.



Pre

cord

ial S

T S

eg

me

nt

Ele

vati

on

V1

, V2

,

V3

, or

V4

Mild

ST

se

gm

en

t e

lev

ati

on

(usu

ally

< 2

mm

)

Sm

all

sep

tal

R w

ave

(No

Q w

ave

)

II, II

I, a

VF

Iso

ele

ctri

c S

T s

eg

me

nt

No

re

cip

roca

l ch

an

ge

s

“No

rma

l” S

T s

eg

me

nt

ele

va

tio

n

No

t d

ue

to

myo

card

ial I

nju

ry



Fig

ure

4.5

:

Bac

kgro

un

d:

Prec

ordi

al

ST

segm

ent

elev

atio

n m

ay

be

obse

rved

, par

ticul

arly

in y

oung

men

.

ECG

: A

nter

ior

ST s

egm

ent

elev

atio

n <

2 m

m in

lead

s V

2 or

V

3 (<

2.5

mm

in m

en y

oung

er t

han

40 y

ears

old

) m

ay b

e a

norm

al f

indi

ng.

“Nor

mal

” ST

seg

men

t el

evat

ion

will

not

be

asso

ciat

ed

with

ab

norm

al

Q

wav

es

and

reci

proc

al

ST

segm

ent

depr

essi

on w

ill n

ot b

e ob

serv

ed.

Clin

ical

Iss

ues

: Th

e pr

esen

ce

of

“nor

mal

” ST

se

gmen

t el

evat

ion

does

not

cha

nge

clin

ical

pro

gnos

is.



V1

-V3

ST

se

gm

en

t e

lev

ati

on

(Mild

)

No

Q w

ave

V4

-V6

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Up

rig

ht

T w

ave

ST

se

gm

en

t e

lev

ati

on

(Mild

)Up

rig

ht

T w

ave

“Ho

ok

”

Pre

cord

ial S

T S

eg

me

nt

Ele

va

tio

n

“No

rma

l” S

T s

eg

me

nt

ele

va

tio

n

du

e t

o e

arl

y re

po

lari

zati

on



Fig

ure

4.6

:

Bac

kgro

un

d:

This

is

a

norm

al

varia

nt

in

youn

g m

en,

part

icul

arly

Afr

ican

Am

eric

ans.

ECG

: Th

e ST

ch

ange

s ar

e m

ost

prom

inen

t in

th

e an

terio

late

ral

lead

s. T

he J

poi

nt (

the

junc

tion

betw

een

the

QRS

and

the

ST

segm

ent)

will

be

elev

ated

> 1

mm

in a

t le

ast

2 of

the

rig

ht p

reco

rdia

l lea

ds in

90%

of

youn

g m

en. T

he S

T se

gmen

t w

ill

have

a

conc

ave

upw

ard,

sl

ight

ly

sagg

ing

appe

aran

ce b

etw

een

the

J po

int

and

the

T w

ave,

usu

ally

in

the

prec

ordi

al le

ads

V2

to V

6. It

is o

ften

gre

ates

t in

V4.

The

ST

seg

men

t el

evat

ion

rang

es f

rom

0.5

mm

to

5 m

m, b

ut it

is

usua

lly <

2 m

m in

the

pre

cord

ial l

eads

and

< 0

.5 m

m in

the

limb

lead

s. A

not

ch (o

r ho

ok) a

t th

e te

rmin

al p

ortio

n of

the

Q

RS c

ompl

ex i

s fr

eque

ntly

obs

erve

d an

d Q

wav

es a

re n

ot

pres

ent.

Clin

ical

Iss

ues

: Ea

rly r

epol

ariz

atio

n is

usu

ally

ben

ign,

but

th

ere

are

som

e sm

all

stud

ies

that

su

gges

t th

at

early

re

pola

rizat

ion

may

be

slig

htly

mor

e co

mm

on i

n pa

tient

s w

ith s

udde

n ca

rdia

c de

ath

due

to v

entr

icul

ar a

rrhy

thm

ias

whe

n co

mpa

red

to t

he g

ener

al p

opul

atio

n. C

urre

ntly

the

re

are

no te

sts

that

can

be

used

to id

entif

y th

e ve

ry s

mal

l gro

up

of

patie

nts

with

ea

rly

repo

lariz

atio

n w

ho

may

be

at

hi

gher

ris

k.



Pre

cord

ial S

T S

eg

me

nt

Ele

va

tio

n A

nte

rio

r Le

ad

s

Du

e t

o Q

RS

wid

en

ing

fro

m B

un

de

l Bra

nch

Blo

ck

No

t d

ue

to

myo

card

ial I

nju

ry

V2

, V3

, or

V4

Mild

ST

se

gm

en

t e

lev

ati

on

(usu

ally

< 2

mm

)

No

Q w

ave

Wid

e Q

RS



Fig

ure

4.7

:

Bac

kgro

un

d:

Alm

ost

any

cond

ition

tha

t is

ass

ocia

ted

with

ab

norm

al d

epol

ariz

atio

n ca

n be

ass

ocia

ted

with

min

or S

T se

gmen

t ch

ange

s.

ECG

: In

this

exa

mpl

e of

a p

atie

nt w

ith a

bnor

mal

con

duct

ion

in h

is b

undl

es (

right

bun

dle

bran

ch b

lock

and

lef

t an

terio

r fa

scic

ular

blo

ck) S

T se

gmen

t el

evat

ion

is o

bser

ved

in V

2 an

d V

3. W

hen

abno

rmal

dep

olar

izat

ion

due

to b

undl

e br

anch

bloc

k is

pre

sent

ST

segm

ent

elev

atio

n m

ay b

e ob

serv

ed i

n an

y le

ad w

here

the

QRS

is

entir

ely

nega

tive,

or

as i

n th

is

case

, whe

re t

he t

erm

inal

por

tion

of t

he Q

RS is

neg

ativ

e).

Clin

ical

Iss

ues

: N

o sp

ecifi

c tr

eatm

ent

for

the

ST s

egm

ent

chan

ges

is re

quire

d al

thou

gh th

e pr

esen

ce o

f bun

dle

bran

ch

bloc

k ca

n be

ass

ocia

ted

with

an

incr

ease

d ris

k of

fut

ure

prob

lem

s w

ith b

rady

card

ia.



V1

-V4

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

II, II

I, a

VF

ST

se

gm

en

t d

ep

ress

ion

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Pre

cord

ial S

T S

eg

me

nt

Ele

vati

on

An

teri

or

Wa

ll M

yoca

rdia

l In

farc

tio

n



Fig

ure

4.8

:

Bac

kgro

un

d:

Occ

lusi

on

of

the

left

an

terio

r de

scen

ding

co

rona

ry a

rter

y ca

n ca

use

a nu

mbe

r of

diff

eren

t pa

tter

ns o

f ST

seg

men

t el

evat

ion

depe

ndin

g on

the

site

of

occl

usio

n an

d th

e pa

tient

’s in

divi

dual

ana

tom

y. A

lthou

gh m

ost

peop

le

have

thr

ee m

ajor

art

erie

s, t

he b

ranc

hing

pat

tern

of

smal

ler

arte

ries

from

the

se m

ajor

bra

nche

s ca

n va

ry s

igni

fican

tly

from

per

son

to p

erso

n.

ECG

: A

n an

terio

r w

all

myo

card

ial

infa

rctio

n is

ass

ocia

ted

with

ST

segm

ent

elev

atio

n in

the

pre

cord

ial

lead

s, u

sual

ly

mos

t pr

omin

ent

in V

2 th

roug

h V

4. T

here

sho

uld

be S

T se

gmen

t el

evat

ion

in 2

adj

acen

t an

terio

r le

ads

in o

rder

to

mak

e th

e di

agno

sis

of A

nter

ior

MI.

In t

his

case

ST

segm

ent

elev

atio

n is

als

o se

en in

V5

and

subt

le S

T se

gmen

t el

evat

ion

is a

lso

pres

ent

in t

he la

tera

l lea

ds I

and

aVL.

In g

ener

al,

for

any

type

of

myo

card

ial i

nfar

ctio

n th

e ex

tent

of

ST s

egm

ent

elev

atio

n pr

ovid

es a

clu

e on

the

siz

e of

the

myo

card

ial

infa

rctio

n: M

ore

lead

s w

ith S

T se

gmen

t el

evat

ion

= L

arge

r m

yoca

rdia

l in

farc

tion.

The

pre

senc

e of

a Q

wav

e in

the

an

terio

r le

ads

is a

bnor

mal

and

is v

ery

stro

ng e

vide

nce

for

a m

yoca

rdia

l inf

arct

ion.

In s

ome

case

s, p

artic

ular

ly e

arly

in t

he

cour

se

of

a m

yoca

rdia

l in

farc

tion

Q

wav

es

will

no

t be

ob

serv

ed. I

n th

is e

xam

ple

abno

rmal

Q w

aves

in V

1 to

V5

and

aVL

are

pres

ent.

A s

lend

er Q

wav

e is

not

ed in

V6

but

sinc

e it

is le

ss t

han

1 m

m w

ide

it is

not

con

side

red

sign

ifica

nt. F

rom

a

clin

ical

sta

ndpo

int

thou

gh,

whe

ther

6 o

r 7

Q w

aves

are

pr

esen

t m

akes

litt

le d

iffer

ence

.

Clin

ical

Iss

ues

: Th

e an

terio

r w

all i

s th

e m

ost

impo

rtan

t of

th

e th

ree

regi

ons

(ant

erio

r, in

ferio

r, an

d la

tera

l) of

the

lef

t ve

ntric

le

and

ante

rior

wal

l m

yoca

rdia

l in

farc

tions

ar

e as

soci

ated

with

inc

reas

ed r

isk

of d

eath

and

hea

rt f

ailu

re

whe

n co

mpa

red

to in

ferio

r w

all a

nd la

tera

l wal

l myo

card

ial

infa

rctio

ns.



V2

-V4

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

II, II

I, a

VF

ST

se

gm

en

t d

ep

ress

ion

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Pre

cord

ial S

T S

eg

me

nt

Ele

va

tio

n

An

teri

or

Wa

ll M

yoca

rdia

l In

farc

tio

n

(wit

h R

igh

t B

un

dle

Bra

nch

Blo

ck)



Fig

ure

4.9

:

Bac

kgro

un

d:

Con

duct

ion

abno

rmal

ities

may

be

seen

in th

e se

ttin

g of

an

ante

rior

wal

l myo

card

ial i

nfar

ctio

n. O

ne o

f th

e ea

rlies

t br

anch

es o

f th

e le

ft a

nter

ior

desc

endi

ng a

rter

y is

the

“f

irst

sept

al p

erfo

rato

r” t

hat

“div

es”

into

the

sep

tum

and

pr

ovid

es b

lood

to

the

right

bun

dle

bran

ch a

nd t

he le

ft a

nte-

rior

fasc

icle

.

ECG

: Th

e EC

G f

or t

his

ante

rior

wal

l myo

card

ial i

nfar

ctio

n is

di

ffer

ent t

han

the

exam

ple

in F

igur

e 4.

7. B

oth

are

asso

ciat

ed

with

ST

segm

ent

elev

atio

n in

lea

ds V

2 th

roug

h V

4. I

n th

is

exam

ple

ST s

egm

ent

elev

atio

n is

not

pre

sent

in t

he la

tera

l pr

ecor

dium

in

lead

s V

5 an

d V

6 bu

t pr

omin

ent

ST s

egm

ent

elev

atio

n is

not

ed i

n I

and

aVL.

Pro

foun

d “r

ecip

roca

l” S

T se

gmen

t de

pres

sion

is n

oted

in t

he in

ferio

r le

ads

(II, I

II, a

nd

aVF)

. Th

e ex

act

mec

hani

sm f

or r

ecip

roca

l ST

dep

ress

ion

is

not

wel

l und

erst

ood,

but

fro

m a

n EC

G a

naly

sis

stan

dpoi

nt

the

pres

ence

of

“rec

ipro

cal”

cha

nges

in t

he in

ferio

r le

ads

is

very

str

ong

evid

ence

for

car

diac

inj

ury.

In

this

exa

mpl

e ab

norm

al Q

wav

es a

re p

rese

nt i

n V

1 an

d V

2. T

he f

inal

diff

eren

ce b

etw

een

Figu

res

4.7

and

4.8

is t

he Q

RS c

ompl

ex

in V

1. In

thi

s ex

ampl

e it

is w

ide

(0.1

6 s)

and

pre

dom

inan

tly

posi

tive.

Thi

s pa

tient

has

rig

ht b

undl

e br

anch

blo

ck a

nd le

ft

ante

rior

fasc

icul

ar b

lock

, pr

oble

ms

that

are

int

rodu

ced

in

Cha

pter

s 7

and

9. C

ompa

re t

his

ECG

and

the

EC

G i

n Fi

gure

4.7

. Myo

card

ial i

njur

y is

ass

ocia

ted

with

mor

e pr

om-

inen

t ST

seg

men

t el

evat

ion,

infe

rior

reci

proc

al S

T se

gmen

t de

pres

sion

and

Q w

aves

. In

fact

, of

all t

he E

CG

par

amet

ers,

ac

com

pany

ing

reci

proc

al S

T de

pres

sion

is t

he b

est

clue

for

de

cidi

ng t

hat

ST s

egm

ent

elev

atio

n is

due

to

myo

card

ial

inju

ry.

Clin

ical

Iss

ues

: A

s in

Fig

ure

4.7,

the

pre

senc

e of

an

acut

e an

terio

r w

all m

yoca

rdia

l inf

arct

ion

requ

ires

rapi

d id

entif

ica-

tion

and

an a

ttem

pt t

o re

stor

e bl

ood

flow

to

the

myo

car-

dium

at

risk.

In m

any

case

s th

is w

ill in

volv

e tr

ansp

ortin

g th

e pa

tient

to

the

cath

eter

izat

ion

labo

rato

ry f

or r

evas

cula

riza-

tion

(ang

iopl

asty

or

sten

t) b

ut c

ould

als

o re

quire

the

use

of

pow

erfu

l “cl

ot b

uste

r” m

edic

atio

ns if

nec

essa

ry.



V3

-V4

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

V5

-V6

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

Pre

cord

ial S

T S

eg

me

nt

Ele

va

tio

n

An

teri

or

Wa

ll M

yoca

rdia

l In

farc

tio

n

(wit

h la

tera

l ext

en

sio

n)



Fig

ure

4.1

0:

Bac

kgro

un

d:

An

ante

rola

tera

l myo

card

ial i

nfar

ctio

n ca

n be

du

e to

occ

lusi

on o

f th

e le

ft a

nter

ior

desc

endi

ng,

occl

usio

n of

a la

rge

diag

onal

bra

nch,

or

a co

rona

ry a

rter

y th

at a

rises

w

hen

the

left

ant

erio

r de

scen

ding

art

ery

and

the

circ

umfle

x co

rona

ry a

rter

y br

anch

. Thi

s ar

tery

is c

alle

d a

ram

us in

term

e-di

us a

nd i

n th

is c

ase

inst

ead

of b

ifurc

atin

g th

e le

ft m

ain

coro

nary

ar

tery

tr

ifurc

ates

w

ith

the

ram

us

inte

rmed

ius

form

ing

the

“mid

dle

tine

of t

he f

ork.

”

ECG

: In

an

ante

rola

tera

l m

yoca

rdia

l in

farc

tion

ST s

egm

ent

elev

atio

n is

usu

ally

not

obs

erve

d in

V1

and

V2

but

rath

er

exte

nds

mor

e la

tera

lly t

o V

5 an

d in

som

e ca

ses

V6.

In

this

ex

ampl

e ST

seg

men

t el

evat

ion

is o

bser

ved

in V

3 th

roug

h V

6 bu

t th

e “h

igh

late

ral”

lea

ds I

and

aV

L do

not

hav

e ST

se

gmen

t el

evat

ion.

No

reci

proc

al S

T se

gmen

t de

pres

sion

is

pres

ent

in t

his

exam

ple

and

ther

e ar

e no

Q w

aves

. How

ever

, no

tice

that

the

re i

s no

R w

ave

even

in

lead

V4.

Thi

s la

te

tran

sitio

n is

som

etim

es c

alle

d “p

oor

R w

ave

prog

ress

ion”

an

d is

con

side

red

by s

ome

to b

e eq

uiva

lent

to

a Q

wav

e.

Clin

ical

Iss

ues

: A

gain

as

in a

ny S

TEM

I, ur

gent

att

empt

s at

re

esta

blis

hing

blo

od fl

ow to

the

myo

card

ium

at r

isk

are

criti

cal.



V2

-V6

, I, a

VL

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

II, II

I, a

VF

ST

se

gm

en

t d

ep

ress

ion

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Pre

cord

ial S

T S

eg

me

nt

Ele

va

tio

n

An

teri

or

Wa

ll M

yoca

rdia

l In

farc

tio

n

(LA

RG

E w

ith

late

ral e

xte

nsi

on

)



Fig

ure

4.1

1:

Bac

kgro

un

d:

The

spec

ific

lead

s w

ith S

T se

gmen

t el

evat

ion

will

dep

end

on t

he e

xact

loca

tion

of t

he b

lock

age

and

the

bran

ches

fro

m t

he o

cclu

ded

arte

ry.

In g

ener

al t

he m

ore

wid

espr

ead

the

ST s

egm

ent

elev

atio

n, t

he m

ore

prox

imal

(“

upst

ream

”) t

he b

lock

age,

the

mor

e br

anch

es,

and

the

larg

er t

he a

rea

at r

isk.

ECG

: In

th

is

exam

ple

mar

ked

ST

segm

ent

elev

atio

n is

ob

serv

ed in

V2 t

hrou

gh V

5 and

I an

d aV

L. In

par

ticul

ar, t

he S

T se

gmen

t el

evat

ion

in V

4 is

ext

rem

ely

prom

inen

t: T

he S

T se

gmen

t is

23

mm

tal

l and

tal

ler

than

the

QRS

in t

hat

lead

. Ve

ry

prom

inen

t ST

se

gmen

t el

evat

ion

is

obse

rved

ea

rly

durin

g a

myo

card

ial i

nfar

ctio

n an

d ha

s be

en g

iven

the

nam

e

“tom

bsto

nes”

by

mor

bidl

y cr

eativ

e cl

inic

ians

to

emph

asiz

e th

e se

rious

ness

of

this

con

ditio

n. N

otic

e th

at s

ince

the

EC

G

is r

ecor

ded

early

in

the

myo

card

ial

infa

rctio

n pr

oces

s th

e on

ly a

bnor

mal

Q w

ave

is r

ecor

ded

in a

VL

and

no Q

wav

es

are

pres

ent

in

the

prec

ordi

al

lead

s.

Som

etim

es

the

ST

segm

ent

can

be h

ard

to s

epar

ate

from

the

QRS

com

plex

. In

this

cas

e th

e do

wns

lopi

ng S

T se

gmen

t el

evat

ion

in I

and

aVL

coul

d be

mis

take

n as

a w

iden

ed Q

RS c

ompl

ex.

Clin

ical

Issu

es:

Patie

nts

with

larg

er m

yoca

rdia

l inf

arct

ions

, if

left

unt

reat

ed,

have

a v

ery

high

fut

ure

risk

of s

udde

n ca

rdia

c de

ath

and

prog

ress

ive

hear

t fa

ilure

.



Pre

cord

ial S

T S

eg

me

nt

Ele

va

tati

on

V1

-V5

“do

me

d”

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(alm

ost

alw

ays

pre

sen

t)

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Loss

of

pre

cord

ial

R w

ave

s

Left

Ve

ntr

icu

lar

An

eu

rysm



Fig

ure

4.1

2:

Bac

kgro

un

d:

A le

ft v

entr

icul

ar a

neur

ysm

is a

def

ined

are

a of

the

lef

t ve

ntric

le t

hat,

ins

tead

of

cont

ract

ing,

mov

es

outw

ard

with

sys

tole

. Th

e m

ost

com

mon

cau

se o

f a

left

ve

ntric

ular

ane

urys

m i

s re

plac

emen

t of

nor

mal

con

trac

ting

myo

card

ium

with

sca

r tis

sue

due

to a

prio

r m

yoca

rdia

l in

farc

tion.

A

nter

ior

wal

l m

yoca

rdia

l in

farc

tions

du

e to

oc

clus

ion

of t

he le

ft a

nter

ior

desc

endi

ng c

oron

ary

arte

ry a

re

the

mos

t co

mm

on c

ause

of

left

ven

tric

ular

ane

urys

ms.

The

de

velo

pmen

t of

a le

ft v

entr

icul

ar a

neur

ysm

aft

er m

yoca

rdia

l in

farc

tion

is u

sual

ly r

ecog

nize

d 2–

6 w

eeks

aft

er t

he a

cute

ev

ent.

ECG

: Pe

rsis

tent

ST

segm

ent

elev

atio

n in

ant

erio

r le

ads

that

do

es n

ot r

esol

ve i

n 2

wee

ks a

fter

a m

yoca

rdia

l in

farc

tion

shou

ld r

aise

sus

pici

on o

f a

left

ven

tric

ular

ane

urys

m. T

he S

T se

gmen

t is

ele

vatio

n is

dom

e sh

aped

, ac

com

pani

ed b

y T

wav

e in

vers

ion

and

Q w

aves

and

is m

ost c

omm

only

obs

erve

d in

V3

and

V4.

Not

ice

that

unl

ike

som

e of

the

exa

mpl

es o

f m

yoca

rdia

l inj

ury

reci

proc

al S

T se

gmen

t ch

ange

s ar

e ab

sent

.

Clin

ical

Is

sues

: In

ge

nera

l, EC

G

chan

ges

due

to

left

ve

ntric

ular

ane

urys

m a

re id

entif

ied

by p

ersi

sten

t ST

segm

ent

chan

ges

and

Q w

aves

lon

g af

ter

(wee

ks)

any

sym

ptom

s fr

om t

he a

cute

myo

card

ial i

nfar

ctio

n ha

ve r

esol

ved.

Pat

ient

s w

ith a

left

ven

tric

ular

ane

urys

m a

re m

ore

susc

eptib

le t

o th

e de

velo

pmen

t of

co

nges

tive

hear

t fa

ilure

an

d ve

ntric

ular

ar

rhyt

hmia

s. T

o re

duce

the

lik

elih

ood

of l

eft

vent

ricul

ar

aneu

rysm

for

mat

ion

it is

im

port

ant

to t

reat

pat

ient

s w

ith

drug

s th

at l

ower

blo

od p

ress

ues

(ang

iote

nsin

con

vert

ing

enzy

me

inhi

bito

rs)

that

will

in

turn

red

uce

the

amou

nt o

f st

ress

on

the

left

ven

tric

le (

low

er r

esis

tanc

e th

at t

he h

eart

m

ust

“pum

p ag

ains

t”).



V1

-V4

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

II, II

I, a

VF

Iso

ele

ctri

c S

T s

eg

me

nt

or

min

ima

l de

pre

ssio

n

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Pre

cord

ial S

T S

eg

me

nt

Ele

va

tio

n

Ap

ica

l Ba

lloo

nin

g S

ynd

rom

e



Fig

ure

4.1

3:

Bac

kgro

un

d:

This

is a

syn

drom

e (a

syn

drom

e is

a c

olle

c-ti

on o

f cl

inic

al f

indi

ngs

that

doe

s no

t ha

ve a

def

ined

m

echa

nism

) of

tran

sien

t ba

lloon

ing

of t

he a

pica

l reg

ion

of

the

left

ven

tric

le t

hat

is n

ot a

ssoc

iate

d w

ith

coro

nary

ar

tery

occ

lusi

on.

The

apic

al b

allo

onin

g is

cha

ract

eriz

ed

by a

thi

n ne

ck w

ith

a la

rge

“out

pouc

hing

” of

the

dis

tal

vent

ricl

e. I

t is

mor

e co

mm

only

obs

erve

d in

wom

en w

ho

have

exp

erie

nced

a s

udde

n ad

rene

rgic

sur

ge.

The

nam

e “T

akot

subo

” is

de

rive

d fr

om

the

Japa

nese

w

ord

that

m

eans

“oc

topu

s po

t” t

hat

desc

ribe

s a

narr

ow-n

ecke

d ve

s-se

l th

at i

s us

ed t

o tr

ap o

ctop

i (o

ctop

i ca

n cr

awl

into

the

po

t bu

t ca

nnot

get

out

).

ECG

: A

nter

ior

ST s

egm

ent

elev

atio

n si

mila

r to

occ

lusi

on o

f th

e LA

D a

rter

y is

obs

erve

d. Q

wav

es c

an a

lso

be p

rese

nt.

Ove

r tim

e, t

he E

CG

will

ret

urn

to n

orm

al o

r ne

ar n

orm

al a

s th

e le

ft v

entr

icul

ar f

unct

ion

retu

rns

to n

orm

al.

In t

his

ECG

up

slop

ing

ST s

egm

ent

elev

atio

n is

obs

erve

d in

V3–

V5.

Clin

ical

Iss

ues

: Th

ere

may

be

larg

e ar

eas

of t

he a

pex

that

do

not

con

trac

t no

rmal

ly a

nd c

ardi

ac e

nzym

es m

ay b

e el

e-va

ted.

Ove

r tim

e, le

ft v

entr

icul

ar f

unct

ion

and

shap

e re

turn

s to

nor

mal

. Pat

ient

s th

at d

evel

op a

pica

l bal

loon

ing

synd

rom

e on

ce a

re p

roba

bly

at h

ighe

r ris

k of

dev

elop

ing

this

pro

blem

ag

ain

in s

ettin

gs a

ssoc

iate

d w

ith s

igni

fican

t st

ress

.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V1

-V3

ST

se

gm

en

t e

lev

ati

on

Larg

e s

ep

tal R

No

Q w

ave

II, II

I, a

VF

Iso

ele

ctri

c S

T s

eg

me

nt

Q w

ave

Pre

cord

ial S

T S

eg

me

nt

Ele

va

tio

n

Hyp

ert

rop

hic

Ca

rdio

myo

pa

thy



Fig

ure

4.1

4:

Bac

kgro

un

d:

Hyp

ertr

ophi

c ca

rdio

myo

path

y is

a h

ered

itary

di

seas

e ch

arac

teriz

ed b

y ab

norm

al t

hick

enin

g of

the

lef

t ve

ntric

le.

In

mos

t ca

ses

the

thic

keni

ng

is

gene

raliz

ed

thro

ugho

ut

the

entir

e ve

ntric

le

but

in

som

e ca

ses

the

thic

keni

ng is

mor

e pr

omin

ent

in s

peci

fic r

egio

ns s

uch

as t

he

inte

rven

tric

ular

sep

tum

or

the

apex

.

ECG

: Th

e EC

G i

n hy

pert

roph

ic c

ardi

omyo

path

y ca

n ha

ve

man

y di

ffer

ent

pres

enta

tions

bas

ed o

n th

e lo

catio

n, e

xten

t,

and

mag

nitu

de o

f th

e le

ft v

entr

icul

ar h

yper

trop

hy (

Cha

pter

5,

Fig

ure

5.7)

. Fo

r th

e pu

rpos

es o

f th

is d

iscu

ssio

n on

ST

segm

ent

chan

ges,

ab

norm

al

patt

erns

of

le

ft

vent

ricul

ar

depo

lariz

atio

n ca

n le

ad t

o an

terio

r ST

seg

men

t el

evat

ion.

The

ST s

egm

ent

elev

atio

n is

usu

ally

obs

erve

d in

lea

ds w

ith

larg

e Q

RS c

ompl

exes

and

ter

min

al S

wav

es a

nd i

s us

ually

as

soci

ated

with

pro

min

ent T

wav

es (V

2 and

V3 i

n th

is e

xam

ple)

.

Clin

ical

Iss

ues

: M

ost

of t

he g

enet

ic a

bnor

mal

ities

ass

oci-

ated

with

hyp

ertr

ophi

c ca

rdio

myo

path

y ar

e m

utat

ions

tha

t af

fect

pro

tein

s of

the

sar

com

ere

(the

con

trac

tile

unit

with

in

card

iac

cells

). Pa

tient

s w

ith h

yper

trop

hic

card

iom

yopa

thy

can

have

sho

rtne

ss o

f br

eath

due

to

inef

ficie

nt f

illin

g of

the

le

ft

vent

ricle

an

d pu

lmon

ary

cong

estio

n.

In

addi

tion,

pa

tient

s w

ith h

yper

trop

hic

card

iom

yopa

thy

are

susc

eptib

le

to v

entr

icul

ar a

rrhy

thm

ias

and

in s

ome

case

s an

impl

anta

ble

card

iac

defib

rilla

tor

(ICD

) is

requ

ired.



V1

, V2

“Sa

il”

ST

se

gm

en

t e

lev

ati

on

rSR

’I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Pre

cord

ial S

T S

eg

me

nt

Ele

va

tio

n

Bru

ga

da

Syn

dro

me

“S

ail”



Fig

ure

4.1

5:

Bac

kgro

un

d:

Ano

ther

her

edita

ry d

isea

se a

ssoc

iate

d w

ith

ante

rior

ST s

egm

ent

elev

atio

n is

the

Bru

gada

Syn

drom

e.

ECG

: Th

e EC

G in

the

Brug

ada

Synd

rom

e ha

s a

char

acte

ristic

ap

pear

ance

w

ith

a la

te

posi

tive

defle

ctio

n in

th

e rig

ht

prec

ordi

al l

eads

V1

and

V2.

In

addi

tion

to t

he l

ate

posi

tive

defle

ctio

n th

e ST

seg

men

t w

ill b

e el

evat

ed i

n th

ese

lead

s w

ith a

cha

ract

eris

tic “

sail”

or

“sha

rk f

in”

patt

ern.

Clin

ical

Iss

ues

: Pa

tient

s w

ith B

ruga

da S

yndr

ome

are

at

high

er r

isk

for

vent

ricul

ar a

rrhy

thm

ias

and

sudd

en d

eath

.


68

ECG

Inte

rpre

tati

on

fo

r Ev

eryo

ne:

An

On

-Th

e-Sp

ot

Gu

ide

V1,V2

Coved

ST segment elevation rSR’

Precordial ST Segment Elevation

Brugada Syndrome “Saddleback”

Kus

umot

o_c0

4.in

dd

68K

usum

oto_

c04.

indd

68

11/1

9/20

11

6:57

:16

PM

11/1

9/20

11

6:57

:16

PM


Fig

ure

4.1

6:

Bac

kgro

un

d:

Ano

ther

her

edita

ry d

isea

se a

ssoc

iate

d w

ith

ante

rior

ST s

egm

ent

elev

atio

n is

the

Bru

gada

Syn

drom

e.

ECG

: A

noth

er E

CG

pat

tern

ass

ocia

ted

with

the

Bru

gada

Sy

ndro

me

has

been

des

crib

ed.

The

late

ter

min

al p

ositi

ve

defle

ctio

n (lo

oks

like

right

bun

dle

bran

ch b

lock

– C

hapt

er 7

, Fi

gure

7.5

) is

pre

sent

but

the

ST

segm

ent

elev

atio

n ha

s a

sagg

ing

“sad

dleb

ack”

pat

tern

.

Clin

ical

Iss

ues

: Pa

tient

s w

ith B

ruga

da S

yndr

ome

are

at

high

er r

isk

for

vent

ricul

ar a

rrhy

thm

ias

and

sudd

en d

eath

. So

me

stud

ies

sugg

est

that

the

“sa

ddle

back

” fo

rm h

as a

be

tter

pro

gnos

is t

han

the

“sha

rk f

in”

form

.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V1

-V3

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

“Pe

ake

d”

or “

ten

ted

”

T w

ave

s

QR

S w

ide

nin

g

V4

-V6

QR

S w

ide

nin

g

Pre

cord

ial S

T S

eg

me

nt

Ele

va

tio

n

Hyp

erk

ale

mia



Fig

ure

4.1

7:

Bac

kgro

un

d:

Any

dis

ease

ass

ocia

ted

with

ren

al f

ailu

re c

an

be a

ssoc

iate

d w

ith h

yper

kale

mia

.

ECG

: Th

e cl

assi

c fin

ding

with

hyp

erka

lem

ia i

s pe

aked

T

wav

es (

Cha

pter

6,

Figu

re 6

.3).

How

ever

, hy

perk

alem

ia c

an

also

be

asso

ciat

ed w

ith S

T el

evat

ion

and

the

deve

lopm

ent o

f Q

wav

es a

nd c

an s

omet

imes

be

indi

stin

guis

habl

e fr

om a

n ac

ute

coro

nary

art

ery

occl

usio

n. T

he o

nly

clue

tha

t ca

n so

met

imes

ale

rt th

e cl

inic

ian

to h

yper

kale

mia

as

the

caus

e of

ST

seg

men

t el

evat

ion

is t

he p

rese

nce

of p

eake

d T

wav

es in

ad

ditio

n to

the

ST

segm

ent

elev

atio

n. I

n th

e ex

ampl

e ST

se

gmen

t el

evat

ion

(impo

ssib

le

to

dist

ingu

ish

from

an

an

tero

sept

al

myo

card

ial

infa

rctio

n)

but

narr

ow

base

d pe

aked

T w

aves

are

pre

sent

in

the

othe

r an

terio

r le

ads,

pa

rtic

ular

ly le

ad V

4. Im

port

antly

, hyp

erka

lem

ia s

houl

d no

t be

asso

ciat

ed w

ith c

hest

pai

n or

oth

er s

ympt

oms

of m

yoca

rdia

l is

chem

ia.

In p

atie

nts

with

sev

ere

hype

rkal

emia

pat

ient

s w

ill

deve

lop

QRS

wid

enin

g of

ten

with

out

a sp

ecifi

c le

ft o

r rig

ht

bund

le b

ranc

h bl

ock

patt

ern.

Clin

ical

Iss

ues

: H

yper

kale

mia

can

be

asso

ciat

ed w

ith l

ife

thre

aten

ing

arrh

ythm

ias

and

need

s to

be

rapi

dly

trea

ted

and

the

caus

e id

entif

ied

(usu

ally

ren

al f

ailu

re).

Hyp

erka

lem

ia i

s tr

eate

d w

ith i

nsul

in a

nd g

luco

se (

insu

lin 5

–10

units

and

gl

ucos

e 25

g (

1 am

p) i

ntra

veno

usly

), bi

carb

onat

e (4

4–88

m

Eq (1

–2 a

mps

) int

rave

nous

ly),

and

beta

ago

nist

s (n

ebul

ized

al

bute

rol

10–2

0 m

g) t

hat

quic

kly

shift

pot

assi

um t

o th

e in

trac

ellu

lar

spac

e.

In

rare

ca

ses,

in

trav

enou

s ca

lciu

m

gloc

onat

e (1

0%, 5

–30m

l) or

cal

cium

chl

orid

e (5

%, 5

–30

ml)

can

be a

dmin

iste

red.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

I, a

VL,

V5

,

an

d V

6

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

Oth

er

ST

se

gm

en

t ch

an

ge

s

de

pe

nd

en

t o

n e

xte

nt

of

infa

rct

II, II

I, a

VF

ST

se

gm

en

t d

ep

ress

ion

Pre

cord

ial S

T S

eg

me

nt

Ele

va

tio

n (

Late

ral)

Late

ral M

yoca

rdia

l In

farc

tio

n



Fig

ure

4.1

8:

Bac

kgro

un

d:

The

dist

inct

ion

betw

een

an

ante

rola

tera

l m

yoca

rdia

l in

farc

tion

and

true

la

tera

l w

all

myo

card

ial

infa

rctio

n m

ay v

ary

from

inte

rpre

ter

to in

terp

rete

r. G

ener

ally

a

late

ral w

all m

yoca

rdia

l inf

arct

ion

is d

ue t

o th

e oc

clus

ion

of

the

circ

umfle

x co

rona

ry a

rter

y or

one

of i

ts b

ranc

hes

but c

an

also

be

du

e to

oc

clus

ion

of

a ra

mus

int

erm

ediu

s or

a

diag

onal

bra

nch

from

the

left

ant

erio

r de

scen

ding

art

ery

if th

ese

arte

ries

supp

ly t

he la

tera

l wal

l in

an in

divi

dual

.

ECG

: In

a la

tera

l myo

card

ial w

all m

yoca

rdia

l inf

arct

ion

the

ST

segm

ents

w

ill

be

elev

ated

in

le

ads

I an

d aV

L.

Any

ac

com

pany

ing

ST s

egm

ent

elev

atio

n w

ill d

epen

d on

the

ve

ssel

tha

t is

aff

ecte

d. I

n th

is e

xam

ple

(com

pare

to

Figu

re

4.19

), ST

seg

men

t ele

vatio

n is

als

o ob

serv

ed in

the

prec

ordi

al

lead

s V

3 to

V6.

Sub

tle r

ecip

roca

l ST

depr

essi

on a

nd T

wav

e in

vers

ion

is o

bser

ved

in t

he in

ferio

r le

ads

(inve

rted

T w

aves

in

lead

s III

and

aV

F).

Clin

ical

Is

sues

: La

tera

l m

yoca

rdia

l in

farc

tions

ca

n be

as

soci

ated

with

sig

nific

ant

occl

usio

ns i

n an

y of

the

thr

ee

maj

or c

oron

ary

arte

ries

depe

ndin

g on

the

patie

nt’s

indi

vidu

al

anat

omy.

The

lef

t an

terio

r de

scen

ding

cor

onar

y ar

tery

has

br

anch

es

that

pl

unge

ve

rtic

ally

in

to

the

inte

rven

tric

ular

se

ptum

(ca

lled

sept

al p

erfo

rato

rs)

and

also

cou

rse

late

rally

to

war

d th

e la

tera

l ape

x (d

iago

nal b

ranc

hes)

. O

cclu

sion

of

a di

agon

al b

ranc

h ca

n ca

use

a la

tera

l m

yoca

rdia

l in

farc

tion.

Th

e ot

her m

ain

bran

ch o

f the

left

mai

n ar

tery

, the

circ

umfle

x co

urse

s la

tera

lly

betw

een

the

left

at

rium

an

d th

e le

ft

vent

ricle

an

d oc

clus

ion

of

eith

er

the

circ

umfle

x or

its

br

anch

es c

an c

ause

a l

ater

al m

yoca

rdia

l in

farc

tion.

As

has

been

men

tione

d, s

ome

patie

nts

have

a t

hird

bra

nch,

cal

led

a ra

mus

int

erm

ediu

s th

at c

an b

e as

soci

ated

with

a l

ater

al

wal

l myo

card

ial i

nfar

ctio

n. F

inal

ly, in

som

e pa

tient

s th

e rig

ht

coro

nary

art

ery,

aft

er t

he p

oste

rior

desc

endi

ng a

rter

y (w

hich

tr

avel

s al

ong

the

infe

rior

port

ion

of t

he i

nter

vent

ricul

ar

sept

um t

owar

d th

e ap

ex) b

ranc

hes

off,

will

ext

end

left

war

d an

d gi

ve r

ise

to l

arge

pos

tero

late

ral

bran

ches

tha

t su

pply

bl

ood

to t

he l

ater

al w

all.

Occ

lusi

on o

f on

e of

the

se d

ista

l po

ster

olat

eral

bra

nche

s ca

n le

ad t

o a

late

ral

myo

card

ial

infa

rctio

n.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

I, a

VL,

V5

,

an

d V

6F

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

Oth

er

ST

se

gm

en

t ch

an

ge

s

de

pe

nd

en

t o

n e

xte

nt

of

infa

rct

II, II

I, a

VF

ST

se

gm

en

t d

ep

ress

ion

“Pre

cord

ial”

ST

Se

gm

en

t E

lev

ati

on

(La

tera

l)

Late

ral M

yoca

rdia

l In

farc

tio

n (

On

ly in

I a

nd

aV

L)



Fig

ure

4.1

9:

Bac

kgro

un

d:

As

desc

ribed

in F

igur

e 4.

18, l

ater

al w

all m

yo-

card

ial i

nfar

ctio

n ca

n ha

ve m

any

man

ifest

atio

ns.

ECG

: G

iven

the

sig

nific

ant

patie

nt v

aria

bilit

y fo

r ca

uses

of

late

ral w

all m

yoca

rdia

l inf

arct

ions

it is

not

sur

pris

ing

that

the

ECG

man

ifest

atio

ns a

lso

vary

sig

nific

antly

. In

this

exa

mpl

e, in

ad

ditio

n to

ST

segm

ent

elev

atio

n is

onl

y pr

esen

t in

the

la

tera

l lea

ds I

and

aVL.

The

oth

er la

tera

l lea

ds V

5 an

d V

6 do

no

t ha

ve S

T se

gmen

t el

evat

ion.

Tru

e la

tera

l wal

l myo

card

ial

infa

rctio

ns w

ithou

t inv

olve

men

t of o

ther

wal

ls (a

nter

orla

tera

l or

infe

rola

tera

l) ar

e al

mos

t alw

ays

due

to a

n oc

clus

ion

in th

e ci

rcum

flex

coro

nary

art

ery

syst

em (

the

circ

umfle

x its

elf

or

one

of it

s br

anch

es, t

he o

btus

e m

argi

nals

). Th

e di

agno

sis

of

a ST

ele

vatio

n du

e to

a t

rue

late

ral m

yoca

rdia

l inf

arct

ion

can

som

etim

es

be

diff

icul

t to

m

ake,

bu

t th

e pr

esen

ce

of

reci

proc

al c

hang

es in

the

infe

rior

lead

s is

an

impo

rtan

t cl

ue

that

sig

nific

ant

myo

card

ial i

njur

y is

pre

sent

.

Clin

ical

Issu

es:

Aga

in it

is im

port

ant

to r

emem

ber

that

the

ex

tent

of

ST s

egm

ent

elev

atio

n co

rrel

ates

rou

ghly

with

the

am

ount

of

m

yoca

rdiu

m

that

is

at

ris

k.

How

ever

, si

nce

the

late

ral w

all i

s “c

over

ed”

by fe

wer

lead

s th

an th

e an

terio

r w

all,

estim

atin

g m

yoca

rdiu

m

at

risk

can

som

etim

es

be

diff

icul

t.



II, II

I, a

VF,

V5

, an

d V

6 ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

V1

ST

se

gm

en

t d

ep

ress

ion

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Pre

cord

ial a

nd

La

tera

l ST

Se

gm

en

t E

lev

ati

on

Infe

rola

tera

l Myo

card

ial I

nfa

rcti

on



Fig

ure

4.2

0:

Bac

kgro

un

d:

As

disc

usse

d fo

r the

pre

viou

s tw

o fig

ures

, lat

-er

al m

yoca

rdia

l inf

arct

ion

can

be c

ause

s by

lesi

ons

in a

ny o

f th

e th

ree

maj

or v

ascu

latu

re s

yste

ms.

Thi

s ex

ampl

e is

a la

tera

l M

I due

to

a rig

ht c

oron

ary

arte

ry le

sion

.

ECG

: In

thi

s ca

se S

T se

gmen

t el

evat

ion

is p

rom

inen

t in

the

la

tera

l lea

ds w

ith t

he a

dditi

on o

f ea

rly r

epol

ariz

atio

n (n

otic

e th

e “h

ooks

” at

the

end

of

the

QRS

com

plex

). In

man

y m

yoca

rdia

l in

farc

tions

th

at

invo

lve

the

late

ral

wal

l, th

e

infe

rior

ST s

egm

ent

elev

atio

n is

mos

t pr

omin

ent

in L

ead

II an

d le

ss p

rom

inen

t in

aV

F an

d III

. The

pre

senc

e of

rec

ipro

cal

ST d

epre

ssio

n in

lea

ds V

1 an

d V

2 is

an

impo

rtan

t cl

ue t

hat

acut

e m

yoca

rdia

l in

jury

is

th

e ca

use

for

the

exte

nsiv

e in

fero

late

ral S

T se

gmen

t el

evat

ion.

Clin

ical

Issu

es:

The

sam

e cl

inic

al p

robl

ems

as f

or t

he p

rior

two

figur

es.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V2

-V6

II, II

I, a

VF

ST s

egm

ent

elev

atio

n

No

Q w

ave

s

PR

de

pre

ssio

n

aV

R

PR

ele

va

tio

n

ST s

egm

ent

dep

ress

ion

Pre

cord

ial a

nd

La

tera

l ST

Se

gm

en

t E

lev

ati

on

Pe

rica

rdit

is



Fig

ure

4.2

1:

Bac

kgro

un

d:

Peric

ardi

tis i

s th

e in

flam

mat

ion

of t

he p

eri-

card

ium

. Per

icar

ditis

can

be

obse

rved

in a

num

ber

of c

ondi

-tio

ns, m

ost

com

mon

ly a

fter

car

diac

sur

gery

. Oth

er c

ause

s of

pe

ricar

ditis

inc

lude

vira

l, ba

cter

ial,

and

imm

unol

ogic

dis

or-

ders

. Mos

t fre

quen

tly n

o sp

ecifi

c ca

use

can

be id

entif

ied

and

the

peric

ardi

tis is

ter

med

“id

iopa

thic

.”

ECG

: C

lass

ical

ly, t

here

are

fou

r st

ages

of

peric

ardi

tis t

hat

can

evol

ve o

ver a

per

iod

of ti

me

that

can

var

y fr

om w

eeks

to

mon

ths.

The

re a

re s

peci

fic v

entr

icul

ar re

pola

rizat

ion

chan

ges

that

occ

ur in

eac

h st

age:

Stag

e 1:

Con

cave

ST

segm

ent

elev

atio

nSt

age

2: S

T se

gmen

t re

turn

s to

bas

elin

eSt

age

3: T

wav

e in

vers

ion

Stag

e 4:

Gra

dual

res

olut

ion

of T

wav

es.

The

ST

segm

ent

elev

atio

n ge

nera

lly i

s ob

serv

ed i

n th

e pr

ecor

dial

lead

s an

d th

e in

ferio

r le

ads.

Impo

rtan

tly t

here

are

no

lea

ds w

ith r

ecip

roca

l ST

seg

men

t de

pres

sion

exc

ept

for

aVR.

Per

icar

ditis

can

als

o af

fect

atr

ial t

issu

e, s

o th

ere

will

be

PR s

egm

ent

depr

essi

on b

est

seen

in

the

infe

rola

tera

l le

ads

and

PR s

egm

ent

elev

atio

n in

aV

R. In

com

paris

on t

o th

e re

st

of t

he le

ads,

lead

aV

R ha

s as

opp

osite

res

pons

e ST

seg

men

t an

d PR

resp

onse

bec

ause

it is

the

only

EC

G le

ad th

at “

look

s”

at t

he h

eart

fro

m t

he r

ight

sid

e an

d th

e in

side

sur

face

of

the

hear

t. S

ince

the

per

icar

dium

ove

rlies

the

hea

rt,

all

of t

he

lead

s ex

cept

for

aV

R lo

ok “

dire

ctly

” at

the

inj

ured

per

icar

-di

um r

esul

ting

in w

ides

prea

d ST

seg

men

t el

evat

ion.

Lea

d aV

R is

pro

babl

y th

e be

st l

ead

for

iden

tifyi

ng p

eric

ardi

tis

beca

use

of it

s ch

arac

teris

tic p

rese

ntat

ion:

PR

segm

ent e

leva

-tio

n an

d th

e on

ly le

ad w

ith S

T se

gmen

t de

pres

sion

. Th

e ST

se

gmen

t el

evat

ion

has

been

des

crib

ed a

s “s

aggi

ng”

rath

er

than

the

“do

med

” ST

seg

men

t el

evat

ion

obse

rved

in

a ST

EMI.

Im

port

antly

in

peric

ardi

tis v

entr

icul

ar d

epol

ariz

atio

n w

ill

not

be a

ffec

ted

so Q

wav

es w

ill n

ot b

e se

en u

nles

s th

e pa

tient

has

Q w

aves

for

ano

ther

rea

son.

The

im

port

ant

teac

hing

poi

nt is

tha

t Q

wav

es a

ssoc

iate

d w

ith S

T se

gmen

t el

evat

ion

are

an im

port

ant

clue

tha

t m

yoca

rdia

l inj

ury

is p

re-

sent

. Th

e EC

G

diff

eren

ces

betw

een

peric

ardi

tis

and

an



Fig

ure

4.2

1: (

Con

t’d)

infe

rola

tera

l m

yoca

rdia

l in

farc

tion

are

easi

ly i

dent

ified

and

ar

e su

mm

ariz

ed in

Tab

le 4

.2.

Patie

nts

with

per

icar

ditis

may

de

velo

p si

gnifi

cant

atr

ial

arrh

ythm

ias

with

atr

ial

fibril

latio

n as

the

mos

t co

mm

only

obs

erve

d ab

norm

al r

hyth

m.

Clin

ical

Is

sues

: O

ne

of

the

mos

t co

mm

on

prob

lem

s en

coun

tere

d in

clin

ical

med

icin

e is

eva

luat

ing

the

patie

nt

with

che

st p

ain.

Thi

s is

cov

ered

in d

etai

l in

Cha

pter

14

but

for

the

sake

of

this

sho

rt d

iscu

ssio

n it

is i

mpo

rtan

t to

re

mem

ber t

hat s

ince

cor

onar

y ar

teria

l occ

lusi

on is

pot

entia

lly

life-

thre

aten

ing

and

ofte

n ha

s m

ore

sign

ifica

nt l

ong-

term

co

nseq

uenc

es th

an p

eric

ardi

tis, i

n ge

nera

l, po

ssib

le c

oron

ary

arte

ry o

cclu

sion

sho

uld

alw

ays

be t

he “

wor

king

dia

gnos

is”

for

any

patie

nt w

ith c

hest

pai

n.



Tab

le 4

.2:

Peric

ardi

tis v

s. In

fero

late

ral I

sche

mia

ECG

fin

din

gPe

rica

rdit

isIn

fero

late

ral I

sch

emia

ST S

egm

ent

elev

atio

n

●In

fero

late

ral S

T se

gmen

t el

evat

ion

●

Infe

rola

tera

l ST

segm

ent

elev

atio

nST

Seg

men

t de

pres

sion

●

ST s

egm

ent

depr

essi

on o

nly

in a

VR

●

Reci

proc

al S

T se

gmen

t de

pres

sion

in V

1–V

3T

wav

es

●N

o in

vert

ed T

wav

es w

hen

the

ST

segm

ent

is e

leva

ted

●

T w

aves

may

be

inve

rted

whe

n th

e ST

seg

men

t is

el

evat

edPR

seg

men

t

●PR

seg

men

t el

evat

ion

in a

VR

●

Isoe

lect

ric P

R se

gmen

t

●PR

seg

men

t de

pres

sion

in t

he

infe

rola

tera

l lea

dsQ

RS c

ompl

ex

●

No

Q w

aves

●

Q w

aves

may

be

pres

ent

in t

he in

fero

late

ral l

eads



Infe

rio

r S

T S

eg

me

nt

Ele

va

tio

n

No

rma

l va

ria

nt

I II III

aV

R

aV

L

aV

F

V1

V2

V3

V4

V5

V6

aV

F

V1

, V2

,

V3

, or

V4

Mild

ST

se

gm

en

t e

lev

ati

on

(usu

ally

< 2

mm

)

Sm

all

sep

tal

R w

ave

(No

Q w

ave

)

II, II

I, a

VF

Su

btl

e “n

otc

h”

in

the

te

rmin

al Q

RS



Fig

ure

4.2

2:

Bac

kgro

un

d:

“Nor

mal

” ST

seg

men

t el

evat

ion

is n

orm

ally

m

ost

prom

inen

t in

lead

s V

1 an

d V

2 al

thou

gh m

inor

ST

seg-

men

t el

evat

ion

may

be

seen

in

any

lead

par

ticul

arly

in

the

pres

ence

of

early

rep

olar

izat

ion.

ECG

: ST

seg

men

t el

evat

ion

less

tha

n or

equ

al t

o 1

mm

may

be

nor

mal

ly o

bser

ved

in a

ny le

ad.

In le

ads

V1

and

V2

whe

re

“nor

mal

” ST

seg

men

t ele

vatio

n is

mos

t com

mon

ly o

bser

ved,

ST

seg

men

t ele

vatio

n up

to 2

mm

is s

till w

ithin

nor

mal

lim

its.

It is

impo

rtan

t to

eva

luat

e an

y ST

seg

men

t ch

ange

s re

lativ

e to

the

T-P

segm

ent.

In th

is e

xam

ple,

ST

segm

ent “

elev

atio

n”

is m

ost

prom

inen

t in

the

inf

erio

r le

ads

with

the

lar

gest

ap

pare

nt d

efle

ctio

n in

lead

aV

F. N

otic

e th

at w

hen

a ho

rizon

-ta

l lin

e is

dra

wn,

the

ST

segm

ent

is a

ctua

lly r

easo

nabl

y is

oe-

lect

ric w

hen

com

pare

d to

the

T-P

seg

men

t an

d th

e ap

pare

nt

ST d

epre

ssio

n is

act

ually

due

to

PR s

egm

ent

depr

essi

on.

Clin

ical

Iss

ues

: EC

G f

indi

ngs

mus

t al

way

s be

eva

luat

ed in

th

e co

ntex

t of

pat

ient

sym

ptom

s. H

owev

er,

eval

uatio

n of

th

e EC

G i

n a

patie

nt w

ith e

arly

rep

olar

izat

ion

who

is

also

co

mpl

aini

ng

of

ches

t pa

in,

care

ful

clin

ical

ev

alua

tion

is

requ

ired.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

II, II

I, a

nd

aV

F

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

Oth

er

ST

se

gm

en

t ch

an

ge

s

de

pe

nd

en

t o

n e

xte

nt

of

infa

rct

V1

ST

se

gm

en

t d

ep

ress

ion

Infe

rio

r S

T S

eg

me

nt

Ele

va

tio

n

Infe

rio

r W

all

Myo

card

ial I

nfa

rcti

on



Fig

ure

4.2

3:

Bac

kgro

un

d:

The

post

erio

r de

scen

ding

co

rona

ry

arte

ry

trav

els

alon

g th

e in

terv

entr

icul

ar g

roov

e pa

ralle

l to

the

left

an

terio

r de

scen

ding

art

ery

but

on t

he m

ost

infe

rior

port

ion

of t

he h

eart

and

is

mos

t co

mm

only

a b

ranc

h of

the

rig

ht

coro

nary

art

ery

alth

ough

in s

ome

case

s it

can

aris

e fr

om t

he

circ

umfle

x co

rona

ry a

rter

y.

ECG

: Th

e ha

llmar

k of

an

infe

rior

MI i

s in

ferio

r ST

seg

men

t el

evat

ion.

In t

his

exam

ple

the

ST s

egm

ent

elev

atio

n is

ver

y su

btle

(c

ompa

re

it to

Fi

gure

4.

19).

Not

ice

that

th

e ST

se

gmen

t is

ele

vate

d in

rel

atio

n to

the

T-P

seg

men

t an

d th

at

reci

proc

al S

T se

gmen

t de

pres

sion

is

obse

rved

in

lead

aV

L an

d V

1. In

this

exa

mpl

e, Q

wav

es in

the

infe

rior l

eads

are

not

ob

serv

ed.

Clin

ical

Iss

ues

: In

ferio

r w

all

myo

card

ial

infa

rctio

n in

mos

t ca

ses

is d

ue t

o oc

clus

ion/

sten

osis

of

the

right

cor

onar

y ar

tery

. G

ener

ally

pat

ient

s w

ith a

n in

ferio

r w

all

myo

card

ial

infa

rctio

n ha

ve a

bet

ter

prog

nosi

s th

an t

hose

pat

ient

s w

ith

an a

nter

ior

wal

l m

yoca

rdia

l in

farc

tion

but

in e

ither

cas

e,

step

s ai

med

at

rees

tabl

ishi

ng b

lood

flo

w t

o th

e in

jure

d ar

ea

is in

dica

ted.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

II, II

I, a

nd

aV

F

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

Oth

er

ST

se

gm

en

t ch

an

ge

s

de

pe

nd

en

t o

n e

xte

nt

of

infa

rct

V1

ST

se

gm

en

t d

ep

ress

ion

* *Infe

rio

r S

T S

eg

me

nt

Ele

va

tio

n

Infe

rio

r W

all

Myo

card

ial I

nfa

rcti

on

(w

ith

firs

t d

eg

ree

AV

blo

ck)



Fig

ure

4.2

4:

Bac

kgro

un

d:

In a

ny m

yoca

rdia

l inf

arct

ion

ther

e is

evo

lutio

n of

EC

G f

indi

ngs.

In a

dditi

on in

ferio

r w

all m

yoca

rdia

l inf

arc-

tion

may

be

asso

ciat

ed w

ith a

trio

vent

ricul

ar (

AV

) bl

ock

at

leas

t in

par

t be

caus

e th

e A

V n

ode

rece

ives

its

bloo

d su

pply

fr

om t

he A

V n

odal

bra

nch

from

the

rig

ht c

oron

ary

arte

ry.

ECG

: Th

e EC

G w

ill d

ispl

ay d

iffer

ent

char

acte

ristic

s as

the

m

yoca

rdia

l inf

arct

ion

“evo

lves

” (C

hapt

er 1

4, F

igur

e 14

.7).

In

this

cas

e th

e ST

seg

men

ts a

re e

leva

ted

in t

he in

ferio

r le

ads

and

a Q

wav

e is

obs

erve

d in

lead

III.

Alth

ough

Q w

aves

may

be

obs

erve

d in

lead

III u

nder

nor

mal

con

ditio

ns, t

he p

rese

nce

of S

T se

gmen

t el

evat

ion

with

an

acco

mpa

nyin

g Q

wav

e sh

ould

alw

ays

arou

se s

uspi

cion

tha

t th

e Q

wav

e re

pres

ents

m

yoca

rdia

l in

jury

and

abn

orm

al v

entr

icul

ar d

epol

ariz

atio

n.

In t

he e

xam

ple

the

PR i

nter

val

(the

P w

ave

is d

enot

ed b

y th

e *)

is

prol

onge

d. V

aryi

ng d

egre

es o

f A

V b

lock

can

be

obse

rved

dur

ing

infe

rior

wal

l myo

card

ial i

nfar

ctio

n.

Clin

ical

Issu

es:

In g

ener

al th

e A

V c

ondu

ctio

n ab

norm

aliti

es

asso

ciat

ed w

ith a

n in

ferio

r wal

l myo

card

ial i

nfar

ctio

n re

solv

e w

ith ti

me

afte

r the

acu

te in

jury

, but

in s

ome

case

s th

e re

cov-

ery

can

be p

rolo

nged

last

ing

wee

ks.



II, II

I, a

nd

aV

F

ST

se

gm

en

t e

lev

ati

on

(oft

en

less

pro

no

un

ced

)

Q w

ave

(usu

ally

pre

sen

t)

Oth

er

ST

se

gm

en

t ch

an

ge

s

de

pe

nd

en

t o

n e

xte

nt

of

infa

rct

T w

ave

inve

rsio

n

Infe

rio

r S

T S

eg

me

nt

Ele

va

tio

n

Infe

rio

r W

all

Myo

card

ial I

nfa

rcti

on

(E

volv

ing

)



Fig

ure

4.2

5:

Bac

kgro

un

d:

The

evol

utio

n of

EC

G c

hang

es in

an

infe

rior

wal

l myo

card

ial i

nfar

ctio

n is

fai

rly p

redi

ctab

le b

ut t

he t

imin

g of

the

pro

gres

sion

of

chan

ges

can

be v

ery

varia

ble.

ECG

: In

thi

s ex

ampl

e of

an

infe

rior

wal

l myo

card

ial i

nfar

c-tio

n, Q

wav

es d

ue t

o ab

norm

al v

entr

icul

ar d

epol

ariz

atio

n ar

e pr

esen

t in

all

thre

e of

the

infe

rior

lead

s (II

, III

, an

d aV

F).

The

ST s

egm

ents

rem

ain

elev

ated

in

the

infe

rior

lead

s bu

t th

e T

wav

es a

re n

ow in

vert

ed.

In t

he s

ettin

g of

myo

card

ial

infa

rctio

n, S

T se

gmen

t el

evat

ion

is i

nitia

lly a

ssoc

iate

d w

ith

uprig

ht T

wav

es b

ut a

fter

a v

aria

ble

amou

nt o

f tim

e (u

sual

ly

hour

s) t

he T

wav

es b

ecom

e in

vert

ed w

hile

the

ST

segm

ent

rem

ains

ele

vate

d. In

this

exa

mpl

e, a

bnor

mal

ities

in V

5 and

V6

are

also

ob

serv

ed,

prob

ably

du

e to

la

rge

post

erol

ater

al

bran

ches

tha

t pr

ovid

e bl

ood

to t

he lo

wer

por

tion

of t

he la

t-er

al w

all o

f th

e le

ft v

entr

icle

.

Clin

ical

Iss

ues

: A

lthou

gh t

he p

rese

nce

of T

wav

e in

ver-

sion

and

Q w

aves

sug

gest

s th

at i

nitia

l oc

clus

ion

of t

he

arte

ry o

ccur

red

seve

ral

hour

s ag

o, t

he p

rimar

y tr

eatm

ent

rem

ains

re

esta

blis

hing

ad

equa

te

bloo

d fl

ow

to

the

inju

red

area

.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

II, II

I, a

nd

aV

F

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

V1

ST

se

gm

en

t d

ep

ress

ion

Pro

min

en

t

R w

ave

Infe

rio

r S

T S

eg

me

nt

Ele

va

tio

n

Infe

rio

r W

all

Myo

card

ial I

nfa

rcti

on

(”P

ost

eri

or”

ext

en

sio

n)



Fig

ure

4.2

6:

Bac

kgro

un

d:

Aft

er

the

post

erio

r de

scen

ding

ar

tery

br

anch

es o

ff t

o pr

ovid

e bl

ood

to t

he m

ore

apic

al r

egio

ns o

f th

e in

ferio

r w

all

the

right

cor

onar

y ar

tery

oft

en c

ontin

ues

tow

ard

the

late

ral w

all o

f th

e he

art

and

may

giv

e of

f la

rge

post

erol

ater

al b

ranc

hes.

ECG

: Th

e la

rger

pos

tero

late

ral b

ranc

hes

prov

ide

bloo

d to

the

post

erio

r w

all.

The

post

erio

r w

all i

s co

mm

only

ref

erre

d to

in

ECG

tex

ts a

lthou

gh re

cent

doc

umen

ts a

re t

ryin

g to

elim

inat

e th

is w

ord.

Sin

ce t

here

is n

o EC

G le

ad t

hat

is d

irect

ly o

ver

the

“pos

terio

r” w

all,

inju

ry a

nd i

nfar

ctio

n in

thi

s ar

ea i

s us

ually

as

sess

ed b

y ev

alua

ting

lead

V1

whi

ch is

orie

nted

180

° fr

om

the

post

erio

r w

all.

Sinc

e it

is o

ppos

ite, Q

wav

es a

re m

anife

st

as a

larg

e R

wav

e, S

T se

gmen

t ele

vatio

n ap

pear

s as

ST

depr

es-

sion

, an

d an

inve

rted

T w

ave

appe

ars

as a

n up

right

T w

ave.

Fo

r the

se re

ason

s th

e di

agno

sis

of a

“po

ster

ior”

wal

l myo

car-

dial

infa

rctio

n is

sug

gest

ed b

y th

e pr

esen

ce o

f an

R w

ave,

ST

segm

ent

depr

essi

on, a

nd a

n up

right

T w

ave

in le

ad V

1.

Clin

ical

Iss

ues

: Th

e ch

ange

s de

scrib

ed f

or i

dent

ifyin

g a

post

erio

r w

all m

yoca

rdia

l inf

arct

ion

are

gene

rally

late

in t

he

cour

se

of

the

myo

card

ial

infa

rctio

n/in

jury

bu

t ag

ain

man

agem

ent

focu

ses

on r

eest

ablis

hing

blo

od f

low

to

the

abno

rmal

reg

ion.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3V2

II, II

I, a

nd

aV

F

ST

se

gm

en

t e

lev

ati

on

Q w

ave

(may

be

pre

sen

t)

Oth

er

ST

se

gm

en

t ch

an

ge

s

de

pe

nd

en

t o

n e

xte

nt

of

infa

rct

an

d t

ho

se d

ue

to

LB

BB

V1

ST

se

gm

en

t e

lev

ati

on

Infe

rio

r S

T S

eg

me

nt

Ele

va

tio

n

Infe

rio

r W

all

Myo

card

ial I

nfa

rcti

on

(W

ith

left

bu

nd

le b

ran

ch b

lock

)



Fig

ure

4.2

7:

Bac

kgro

un

d:

Eval

uatio

n of

the

EC

G c

an b

e ve

ry d

iffic

ult

in

left

bun

dle

bran

ch b

lock

sin

ce b

oth

depo

lariz

atio

n an

d re

pola

rizat

ion

are

abno

rmal

in

the

sett

ing

of l

eft

bund

le

bran

ch b

lock

.

ECG

: In

gen

eral

, le

ft b

undl

e br

anch

blo

ck i

s as

soci

ated

w

ith S

T ab

norm

aliti

es t

hat

are

“opp

osite

” th

e di

rect

ion

of

depo

lariz

atio

n: A

lea

d w

ith a

neg

ativ

e Q

RS c

ompl

ex w

ill

have

ST

segm

ent

elev

atio

n an

d a

lead

with

a p

ositi

ve Q

RS

com

plex

will

hav

e ST

seg

men

t de

pres

sion

. Th

e pr

esen

ce o

f an

ST

segm

ent

chan

ge t

hat

is “

conc

orda

nt”

with

the

QRS

co

mpl

ex w

ould

be

unex

pect

ed a

nd m

ay re

pres

ent

abno

rmal

repo

lariz

atio

n du

e to

myo

card

ial

inju

ry.

In t

his

exam

ple,

ab

norm

al S

T se

gmen

t el

evat

ion

is o

bser

ved

in t

he i

nfer

ior

lead

s (s

ince

the

QRS

com

plex

es a

re p

ositi

ve w

e w

ould

exp

ect

ST s

egm

ent

depr

essi

on in

the

se le

ads)

. In

left

bun

dle

bran

ch

bloc

k,

abno

rmal

de

pola

rizat

ion

mak

es

eval

uatio

n of

de

pola

rizat

ion

abno

rmal

ities

(Q w

aves

) im

poss

ible

.

Clin

ical

Iss

ues

: Th

e pr

esen

ce o

f le

ft b

undl

e br

anch

blo

ck

mak

es e

valu

atio

n of

the

EC

G f

or m

yoca

rdia

l in

jury

ver

y pr

oble

mat

ic.

For

this

rea

son,

the

clin

icia

n m

ust

depe

nd

alm

ost

excl

usiv

ely

on s

ympt

oms

and

phys

ical

exa

min

atio

n fin

ding

s.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

II

ST

se

gm

en

t e

lev

ati

on

Tran

sien

t Q

wav

e

(may

be

pre

sen

t)

Oth

er

ST

se

gm

en

t ch

an

ge

s

de

pe

nd

en

t o

n t

he

sit

e o

f sp

asn

Infe

rio

r S

T S

eg

me

nt

Ele

va

tio

n

Co

ron

ary

art

ery

sp

asm

(ri

gh

t co

ron

ary

art

ery

)



Fig

ure

4.2

8:

Bac

kgro

un

d:

In a

dditi

on t

o at

hero

scle

rosi

s an

d th

rom

bus,

an

othe

r cau

se o

f myo

card

ial i

njur

y/in

farc

tion

is s

pasm

of t

he

coro

nary

art

ery.

The

EC

G c

hang

es a

re a

lmos

t in

dist

ingu

ish-

able

but

oft

en t

he E

CG

cha

nges

ass

ocia

ted

with

spa

sm a

re

mor

e tr

ansi

ent.

ECG

: Th

e EC

G c

hang

es a

ssoc

iate

d w

ith c

oron

ary

arte

ry

spas

m a

re t

he s

ame

as f

or a

n ac

ute

myo

card

ial

infa

rctio

n (n

ot s

urpr

isin

g si

nce

both

lead

to

cess

atio

n of

blo

od f

low

to

an a

rea

of m

yoca

rdiu

m).

In t

his

case

of

spas

m o

f th

e rig

ht

coro

nary

art

ery,

pro

foun

d ST

seg

men

t el

evat

ion

is o

bser

ved

in th

e in

ferio

r lea

ds w

ith re

cipr

ocal

ST

segm

ent d

epre

ssio

n in

th

e an

terio

r an

d la

tera

l lea

ds.

Clin

ical

Iss

ues

: G

ener

ally

cor

onar

y ar

tery

spa

sm r

esol

ves

afte

r se

vera

l min

utes

and

the

EC

G c

hang

es r

esol

ve a

s bl

ood

flow

is

rees

tabl

ishe

d. T

he t

reat

men

t fo

r sp

asm

is

gene

rally

m

edic

al t

hera

py s

uch

as c

alci

um c

hann

el b

lock

ers

that

pro

-m

ote

vaso

dila

tion.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3V

2

V6

ST

se

gm

en

t

Ele

va

tio

n in

aV

R

ST

se

gm

en

t d

ep

ress

ion

(oft

en

in m

ost

of

the

pre

cord

ium

)

aV

R

De

pre

sse

d J

po

int

ST

Se

gm

en

t E

lev

ati

on

in a

VR

Cri

tica

l Le

ft M

ain



Fig

ure

4.2

9: L

eft

Mai

n

Bac

kgro

un

d:

Alth

ough

th

ere

are

man

y an

atom

ic

varia

tions

, th

e le

ft m

ain

coro

nary

art

ery

begi

ns a

t th

e ao

rta

and

is u

sual

ly a

bout

1 t

o 2

cm lo

ng b

efor

e it

divi

des

into

the

le

ft a

nter

ior

desc

endi

ng a

nd c

ircum

flex

coro

nary

art

erie

s.

Occ

lusi

on o

f th

e le

ft m

ain

coro

nary

art

ery

lead

s to

lar

ge

area

s of

myo

card

ial i

njur

y an

d is

chem

ia.

ECG

: A

crit

ical

left

mai

n co

rona

ry a

rter

y le

sion

oft

en r

esul

ts

in p

rom

inen

t ST

segm

ent d

epre

ssio

n in

mul

tiple

lead

s. In

the

exam

ple,

ST

depr

essi

on is

obs

erve

d in

mul

tiple

lead

s: II

I, aV

L an

d V

2 th

roug

h V

6. S

T se

gmen

t el

evat

ion

is o

bser

ved

in t

he

lead

s th

at a

re o

rient

ed o

n th

e rig

ht o

f th

e he

art:

V1,

III,

and

aVR.

In p

artic

ular

ST

segm

ent

elev

atio

n is

ver

y pr

omin

ent

in

aVR.

In

any

patie

nt w

ith S

T se

gmen

t el

evat

ion

in a

VR,

st

enos

is o

r a

criti

cal

lesi

on i

n th

e le

ft m

ain

coro

nary

art

ery

shou

ld b

e su

spec

ted.

Lea

d aV

R is

the

onl

y le

ad t

hat

“loo

ks”

dire

ctly

at

the

endo

card

ial

surf

ace

(“in

side

”) o

f th

e le

ft

vent

ricle

. Si

nce

the

endo

card

ial

surf

ace

is

the

mos

t do

wns

trea

m a

rea

in t

he c

oron

ary

arte

ry c

ircul

atio

n, li

miti

ng

bloo

d flo

w a

t th

e le

ft m

ain

coro

nary

art

ery

lead

s to

glo

bal

isch

emia

tha

t is

mos

t pr

omin

ent

on t

he e

ndoc

ardi

um.

Clin

ical

Issu

es:

Patie

nts

with

a s

uspe

cted

lesi

on o

f th

e le

ft

mai

n co

rona

ry a

rter

y re

quire

rapi

d an

d ag

gres

sive

dia

gnos

tic

and

ther

apeu

tic m

anag

emen

t. I

n m

ost

case

s an

em

erge

nt

card

iac

cath

eter

izat

ion

to c

onfir

m t

he p

rese

nce

of a

lef

t m

ain

coro

nary

art

ery

lesi

on a

nd t

o de

fine

the

anat

omy

of

the

coro

nary

art

erie

s is

per

form

ed.

Alth

ough

a p

ercu

tane

-ou

s co

rona

ry a

rter

y an

giop

last

y m

ay b

e us

eful

for

man

agin

g th

e pa

tient

in

the

acut

e se

ttin

g, u

ltim

atel

y co

rona

ry a

rter

y by

pass

gra

ftin

g is

oft

en r

equi

red.


98


ST segment depression is also an important finding when evaluating the patient with chest pain. ST segment depression generally represents myo-cardial ischemia rather than myocardial injury. In this case, often a critical lesion is present, but some blood flow is reaching the endangered portions of the heart. Like ST segment elevation, ST segment depression can be observed in the anterior leads, the lateral leads, or the inferior leads. Unlike ST segment elevation, the location of ST segment depression does not cor-relate with the location of the myocardium at risk. For example, the pres-ence of lateral ST segment depression can be due to significant lesions in the anterior descending, circumflex, or right coronary arteries. Isolated ST segment depression is most commonly observed in the lateral leads, but isolated inferior ST segment depression can also be observed. Isolated ante-rior ST segment depression is much less common (if anterior ST segment depression is observed, always check aVR for ST segment elevation and the possibility of a critical left main lesion or severe disease in all three coronary arteries (left anterior descending coronary artery, circumflex coronary artery, and right coronary artery) which some have called “left main equivalent”).

The problem with using isolated ST segment depression as a specific sign for ischemia is that it may be present in some patients with left ventricular hypertrophy. High blood pressure or hypertension is an extremely common problem, with over 70% of people affected by age 70 years. Hypertension itself is not an issue; do you really feel the differ-ence between a blood pressure of 140/90 and a blood pressure of 120/70? The problem is that hypertension causes damage to many organs including the heart, kidney, and brain. When contracting against higher pressures for an extended period of time, the heart responds by

CHAPTER 5

Abnormal Repolarization: ST Segment Depression


Abnormal Repolarization: ST Segment Depression 99

becoming larger and thicker. The larger and thicker heart leads to a characteristic set of changes that can be identified by ECG (Figure 5.6; Figures 8.12–8.14) but one of the changes is ST segment depression in the lateral leads. So here’s the problem in a nutshell. Since hypertension is so common and some of these patients have left ventricular hypertro-phy, if you were to evaluate 100 patients with ST segment depression the great majority would have lateral ST segment depression due to left ventricular hypertrophy rather than due to myocardial ischemia. In a patient complaining of chest pain, lateral ST segment depression becomes much more suspicious, particularly since hypertension is a risk factor for developing coronary artery disease. Clues for the evaluation of a patient with chest pain are summarized in Chapter 14.

ST segment depression is usually evaluated by determining the location of the J point, which is the point between the end of the QRS complex and the beginning of the ST segment. The threshold values for ST segment depression are the opposite of the threshold values for ST segment elevation. Since ST segment depression is extremely uncom-mon in V2 and V3, J point depression > 0.5 mm is considered significant, while J point depression > 1 mm is considered significant for the rest of the leads. The characteristics of abnormal ST depression and clues for identifying whether ST depression is due to myocardial ischemia are summarized in Table 5.1. The reader will note that often deciding whether ST depression is due to ischemia often depends on compari-son between ECGs: New vs. old; presence or absence of symptoms.

Table 5.1: Factors determining whether abnormal ST segment depression is present and whether abnormal ST segment depression is more likely due to ischemia

Is abnormal ST segment depression present?(Yes to any questions means abnormal)

● Is ST segment depression > 0.5 mm in V2 and V3, or > 1 mm in the other leads?

● Is the ST segment elevation present in two “adjacent” (contiguous) leads?

Is the abnormal ST segment depression due to myocardial injury?(Yes to any questions means that myocardial ischemia is a likely cause)

● Is the ST depression new when compared to prior ECGs? ● Does the magnitude ST depression correlate with symptoms? ● Is the patient complaining of chest pain? ● Are Q waves present?



I II III

aV

R

aV

L

aV

F

V1

V6V5

V4

V3V2

ST

se

gm

en

t d

ep

ress

ion

ST

se

gm

en

t d

ep

ress

ion

du

e t

o is

che

mia

(wit

h T

wa

ve

inv

ers

ion

)

II, I

II, a

VF

V5

-V6 S

T s

eg

me

nt

de

pre

ssio

nIn

vert

ed

T w

ave

J p

oin

t



Fig

ure

5.1

:

Bac

kgro

un

d:

Infe

rola

tera

l ST

seg

men

t de

pres

sion

may

be

asso

ciat

ed w

ith is

chem

ia. I

n fa

ct th

e pr

esen

ce o

f ST

segm

ent

depr

essi

on i

s on

e of

the

im

port

ant

ECG

crit

eria

use

d fo

r st

ress

tes

ting

to id

entif

y is

chem

ia.

ECG

: ST

seg

men

t de

pres

sion

due

to

infe

rola

tera

l is

chem

ia

can

have

man

y m

anife

stat

ions

. In

thi

s ex

ampl

e th

ere

is

horiz

onta

l ST

depr

essi

on a

ssoc

iate

d w

ith T

wav

e in

vers

ion

in

lead

s II,

V5,

and

V6.

Abn

orm

al T

wav

e in

vers

ion

is a

lso

pres

ent

in I

and

aVL.

The

J p

oint

is t

he p

oint

whe

re t

he Q

RS

ends

and

the

T w

ave

begi

ns a

nd is

whe

re t

he m

agni

tude

of

ST d

epre

ssio

n sh

ould

be

mea

sure

d.

Clin

ical

Iss

ues

: ST

seg

men

t de

pres

sion

can

be

seen

in

a nu

mbe

r of

diff

eren

t co

nditi

ons.

As

disc

usse

d in

Cha

pter

14,

flu

ctua

tion

of t

he S

T ch

ange

s w

ith w

axin

g an

d w

anin

g of

ch

est

pain

(“d

ynam

ic E

CG

cha

nges

”) s

houl

d ra

ise

conc

ern

that

the

EC

G c

hang

es r

epre

sent

isch

emia

.



I II III

aV

RV

1

ST

se

gm

en

t d

ep

ress

ion

ST

se

gm

en

t d

ep

ress

ion

du

e t

o is

che

mia

(Up

rig

ht

T w

ave

s a

nd

Q w

ave

s)

aV

L

aV

F

V6

V5

V4

V3

V2

An

y le

ad

ST

se

gm

en

t d

ep

ress

ion

Up

rig

ht

T w

ave

J p

oin

t

Q w

ave



Fig

ure

5.2

:

Bac

kgro

un

d:

ST d

epre

ssio

n is

mor

e lik

ely

due

to is

chem

ia

if th

ere

is o

ther

evi

denc

e th

at c

oron

ary

arte

ry d

isea

se i

s pr

esen

t.

ECG

: In

thi

s ex

ampl

e ST

dep

ress

ion

is o

bser

ved

in t

he in

fe-

rior

lead

s, I

I, III

, an

d aV

F. A

lthou

gh t

he S

T se

gmen

ts a

re

“sco

oped

” in

the

late

ral l

eads

the

J p

oint

is o

nly

min

imal

ly

depr

esse

d if

at a

ll. U

nlik

e Fi

gure

5.1

, ST

dep

ress

ion

is n

ot

asso

ciat

ed w

ith c

hang

es in

the

T w

ave.

In th

is e

xam

ple

ther

e ar

e ab

norm

al Q

wav

es in

V1

and

V2.

A Q

wav

e is

any

initi

al

nega

tive

wav

e. T

he Q

wav

e in

aV

R is

a n

orm

al f

indi

ng s

ince

ve

ntric

ular

de

pola

rizat

ion

occu

rs

from

rig

ht

to

left

. In

addi

tion

Q w

aves

in I

and

aVL

may

be

seen

in 3

0–40

% o

f as

ympt

omat

ic p

atie

nts

with

no

card

iac

dise

ase.

How

ever

, th

e Q

wav

es in

tw

o ad

jace

nt le

ads

V1

and

V2

are

abno

rmal

an

d su

gges

t th

e po

ssib

ility

of

a pr

ior

myo

card

ial i

nfar

ctio

n.

Evid

ence

for

prio

r m

yoca

rdia

l inf

arct

ion

alw

ays

incr

ease

s th

e lik

elih

ood

that

the

ST

segm

ent

depr

essi

on (

and

for

that

m

atte

r an

y as

soci

ated

rep

olar

izat

ion

chan

ges)

rep

rese

nts

isch

emia

.

Clin

ical

Issu

es:

Aga

in, i

f the

pat

ient

is c

ompl

aini

ng o

f che

st

pain

any

EC

G c

hang

es s

houl

d be

con

side

red

susp

icio

us f

or

isch

emia

.



V6

ST

se

gm

en

t

Ele

va

tio

n in

aV

R

ST

se

gm

en

t d

ep

ress

ion

(oft

en

in m

ost

of

the

pre

cord

ium

)

aV

R

De

pre

sse

d J

po

int

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

ST

se

gm

en

t d

ep

ress

ion

ST

se

gm

en

t d

ep

ress

ion

du

e t

o is

che

mia

(cri

tica

l le

ft m

ain

ste

no

sis)



Fig

ure

5.3

:

Bac

kgro

un

d:

The

left

mai

n co

rona

ry a

rter

y pr

ovid

es b

lood

to

mos

t of

the

ant

erio

r w

all

and

late

ral

wal

l of

the

lef

t ve

ntric

le.

Alth

ough

lef

t m

ain

coro

nary

art

ery

occl

usio

n is

as

soci

ated

w

ith

ST

segm

ent

elev

atio

n in

le

ad

aVR

(see

C

hapt

er 4

, Fi

gure

4.2

9),

it is

inc

lude

d he

re b

ecau

se t

he

late

ral

ST

depr

essi

on

is

ofte

n ex

trem

ely

prom

inen

t an

d be

caus

e of

the

sev

erity

of

the

prob

lem

.

ECG

: Th

e EC

G in

left

mai

n co

rona

ry a

rter

y oc

clus

ion

is c

har-

acte

rized

by

ST s

egm

ent

elev

atio

n in

lead

aV

R bu

t pr

ofou

nd

ST s

egm

ent

depr

essi

on in

the

res

t of

the

lead

s, p

artic

ular

ly

the

ante

rola

tera

l pre

cord

ium

(V4

to V

6).

Clin

ical

Iss

ues

: Pa

tient

s w

ith p

ossi

ble

left

mai

n co

rona

ry

arte

ry

lesi

ons

mus

t be

tr

eate

d ag

gres

sive

ly

and

usua

lly

requ

ire u

rgen

t ca

rdia

c ca

thet

eriz

atio

n to

def

ine

the

coro

-na

ry a

rter

y an

atom

y.



I, a

VL,

V5

, V6

Po

siti

ve Q

RS

Do

wn

slo

pin

g S

T

seg

me

nts

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

ST

se

gm

en

t d

ep

ress

ion

ST

se

gm

en

t d

ep

ress

ion

du

e t

o le

ft b

un

dle

bra

nch

blo

ck



Fig

ure

5.4

:

Bac

kgro

un

d:

In t

he p

rese

nce

of l

eft

bund

le b

ranc

h bl

ock

the

ECG

can

be

very

diff

icul

t to

inte

rpre

t si

nce

ST s

egm

ent

chan

ges

are

very

com

mon

.

ECG

: In

gen

eral

, in

the

pre

senc

e of

lef

t bu

ndle

bra

nch

bloc

k, t

he S

T se

gmen

ts w

ill b

e el

evat

ed i

n th

e le

ads

with

a

nega

tive

QRS

com

plex

and

dep

ress

ed in

tho

se le

ads

with

a

posi

tive

QRS

com

plex

. For

exa

mpl

e in

this

cas

e th

e do

wns

lop-

ing

ST s

egm

ents

and

inve

rted

T w

aves

in I,

aV

L, a

nd V

6 ar

e al

l exp

ecte

d fin

ding

s.

Clin

ical

Issu

es:

ST s

egm

ent

chan

ges

are

extr

emel

y di

ffic

ult

to e

valu

ate

in t

he s

ettin

g of

bun

dle

bran

ch b

lock

, pa

rtic

u-la

rly in

left

bun

dle

bran

ch b

lock

.



An

y p

reco

rdia

l

lea

d w

ith

a Q

S c

om

ple

x

ST

se

gm

en

t

de

pre

ssio

n

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

ST

se

gm

en

t d

ep

ress

ion

ST

se

gm

en

t d

ep

ress

ion

du

e t

o is

che

mia

(in

th

e p

rese

nce

of

left

bu

nd

le b

ran

ch b

lock

)



Fig

ure

5.5

:

Bac

kgro

un

d:

In t

he p

rese

nce

of l

eft

bund

le b

ranc

h bl

ock

the

ECG

can

be

very

diff

icul

t to

inte

rpre

t.

ECG

: In

gen

eral

, in

the

pres

ence

of l

eft b

undl

e br

anch

blo

ck,

the

ST s

egm

ents

will

be

elev

ated

in th

e le

ads

with

a n

egat

ive

QRS

com

plex

and

dep

ress

ed i

n th

ose

lead

s w

ith a

pos

itive

Q

RS c

ompl

ex.

The

pres

ence

of

ST s

egm

ent

depr

essi

on in

a

lead

with

a n

egat

ive

QRS

com

plex

wou

ld b

e “u

nexp

ecte

d”

and

shou

ld a

rous

e su

spic

ion

for

isch

emia

, pa

rtic

ular

ly if

the

pa

tient

is c

ompl

aini

ng o

f ch

est

pain

. In

the

exa

mpl

e, t

he S

T se

gmen

t de

pres

sion

in

lead

s I

and

aVL

wou

ld b

e ex

pect

ed

sinc

e th

e Q

RS c

ompl

ex is

pos

itive

; how

ever

, the

ST

segm

ent

depr

essi

on in

lead

s V

2 th

roug

h V

5 is

wor

risom

e fo

r is

chem

ia

sinc

e th

e Q

RS c

ompl

ex is

neg

ativ

e.

Clin

ical

Issu

es:

In le

ft b

undl

e br

anch

blo

ck, t

he p

rese

nce

of

ST

segm

ent

depr

essi

on

in

a le

ad

with

a

nega

tive

QRS

co

mpl

ex s

houl

d ar

ouse

sus

pici

on if

the

pat

ient

is c

ompl

ain-

ing

of c

hest

pai

n. T

he c

linic

ian

shou

ld a

lway

s re

mem

ber

the

limita

tions

of

the

ECG

for

eva

luat

ing

ST s

egm

ent

chan

ges

in

the

sett

ing

of le

ft b

undl

e br

anch

blo

ck.



Do

wn

slo

pin

g S

T

Inve

rte

d T

wav

e

Larg

e R

wav

e

V6

De

pre

sse

d J

po

int

V6

V5

IIIa

VF

aV

LII

aV

RV

1

V4

V3

I

V2

ST

se

gm

en

t d

ep

ress

ion

ST

se

gm

en

t d

ep

ress

ion

du

e t

o le

ft v

en

tric

ula

r h

ype

rtro

ph

y



Fig

ure

5.6

:

Bac

kgro

un

d:

Left

ven

tric

ular

hyp

ertr

ophy

, us

ually

due

to

hype

rten

sion

, can

be

asso

ciat

ed w

ith re

pola

rizat

ion

chan

ges

and

late

ral S

T se

gmen

t de

pres

sion

.

ECG

: Th

e ST

seg

men

t de

pres

sion

in

left

ven

tric

ular

hyp

er-

trop

hy is

usu

ally

dow

nslo

ping

. In

thi

s ex

ampl

e, S

T se

gmen

t de

pres

sion

is

note

d in

V5

and

V6

and

aVL.

The

key

to

iden

tifyi

ng

left

ve

ntric

ular

hy

pert

roph

y as

th

e ca

use

of

late

ral S

T se

gmen

t de

pres

sion

gen

eral

ly in

clud

es id

entif

ying

ot

her

ECG

sig

ns o

f le

ft v

entr

icul

ar h

yper

trop

hy,

incl

udin

g

prom

inen

t Q

RS v

olta

ges

in t

he l

ater

al l

eads

with

lar

ge R

w

aves

and

the

pre

senc

e of

a b

ipha

sic

P w

ave

in le

ad V

1. In

th

is c

ase,

the

patie

nt is

in a

tria

l fib

rilla

tion

so P

wav

es a

re n

ot

pres

ent.

Clin

ical

Iss

ues

: Th

e pr

esen

ce o

f le

ft v

entr

icul

ar h

yper

tro-

phy

sugg

ests

tha

t th

e le

ft v

entr

icle

is c

ontr

actin

g ag

ains

t a

larg

e af

terlo

ad (

syst

emic

hyp

erte

nsio

n, a

ortic

ste

nosi

s) t

hat

lead

s to

a c

ompe

nsat

ory

incr

ease

in

left

ven

tric

ular

wal

l th

ickn

ess.



Sym

me

tric

de

ep

ly

Inv

ert

ed

T w

av

eV

6

aV

RI II III

aV

L

aV

F

V1

V6

V5

V4

V3

V2

ST

se

gm

en

t d

ep

ress

ion

ST

se

gm

en

t d

ep

ress

ion

du

e t

o h

ype

rtro

ph

ic c

ard

iom

yop

ath

y



Fig

ure

5.7

:

Bac

kgro

un

d:

Ther

e ar

e se

vera

l diff

eren

t fo

rms

of h

yper

-tr

ophi

c ca

rdio

myo

path

y (C

hapt

er 4

, Fi

gure

4.1

4) t

hat

are

clas

sifi

ed b

y th

e lo

cati

on o

f th

e th

icke

st r

egio

n of

the

le

ft

vent

ricl

e.

The

mos

t co

mm

on

form

is

ge

nera

lized

hy

pert

roph

y bu

t so

met

imes

the

hyp

ertr

ophy

is d

ispr

opor

-ti

onat

ely

prom

inen

t in

spe

cifi

c ar

eas

such

as

the

sept

um

or a

pex.

The

api

cal

hype

rtro

phy

form

is

asso

ciat

ed w

ith

late

ral

T w

ave

inve

rsio

n an

d m

ay

have

ST

se

gmen

t de

pres

sion

.

ECG

: D

eep

sym

met

ric T

wav

e in

vers

ion

in V

5 an

d V

6 is

cha

r-ac

teris

tic a

nd m

ay b

e as

soci

ated

with

mild

ST

segm

ent

depr

essi

on (u

sual

ly le

ss t

han

1 m

V).

Clin

ical

Iss

ues

: Pa

tient

s w

ith a

pica

l hy

pert

roph

ic c

ardi

o-m

yopa

thy

may

be

asym

ptom

atic

or c

ompl

ain

of s

hort

ness

of

brea

th d

ue t

o th

e st

iffer

left

ven

tric

le a

nd lu

ng c

onge

stio

n du

e to

incr

ease

d le

ft a

tria

l and

pul

mon

ary

veno

us p

ress

ures

. Pa

tient

s al

so a

re a

t hi

gher

ris

k fo

r ve

ntric

ular

arr

hyth

mia

s.



V6

“Sco

op

ed

” S

T s

eg

me

nt

Inve

rte

d T

wav

e

No

rma

l R w

ave

siz

e

(Un

less

LV

H a

lso

pre

sen

t)I II III

aV

R

aV

L

aV

F

V1

V6

V5V4

V3

V2

ST

se

gm

en

t d

ep

ress

ion

ST

se

gm

en

t d

ep

ress

ion

du

e t

o d

igo

xin



Fig

ure

5.8

:

Bac

kgro

un

d:

Dig

oxin

is a

dru

g th

at is

use

d to

con

trol

hea

rt

rate

in

patie

nts

with

atr

ial

fibril

latio

n an

d no

w,

muc

h le

ss

com

mon

ly f

or t

he t

reat

men

t of

hea

rt f

ailu

re.

ECG

: A

lthou

gh le

ss c

omm

only

use

d to

day,

dig

oxin

is a

ssoc

i-at

ed

with

ch

arac

teris

tic

ECG

ch

ange

s,

in

part

icul

ar,

dow

nslo

ping

of

the

late

ral

ST s

egm

ents

sim

ilar

to w

hat

is

obse

rved

in

left

ven

tric

ular

hyp

ertr

ophy

but

has

a f

airly

char

acte

ristic

“ro

unde

d” o

r “s

coop

ed”

appe

aran

ce.

Not

ice

that

the

J p

oint

its

elf

is n

ot d

epre

ssed

– r

athe

r th

ere

is

“sag

ging

” of

the

mid

dle

of t

he S

T se

gmen

t.

Clin

ical

Iss

ues

: Th

e EC

G c

hang

es a

ssoc

iate

d w

ith d

igox

in

are

very

com

mon

ly o

bser

ved.

Dig

oxin

can

be

used

in p

atie

nts

with

he

art

failu

re,

part

icul

arly

if

they

al

so

have

at

rial

fibril

latio

n.


117


The ST segment correlates with the plateau phase of the ventricular action potential where all of the ventricular cells are depolarized and the voltages in the inside and outside of the cell are close to the same. However, over time the cell begins to repolarize and the voltage inside of the cell becomes negative compared to the outside. The T wave is produced as the ventricular cells repolarize. Think of the beginning of the T wave as the point where the first cells are repolarizing, the peak of the T wave when the greatest number of ventricular cells are repolarizing and the end of the T wave as the point when the last cells are repolarizing. As described in Chapter 2, repolarization occurs more gradually than depolarization, which leads to a “flatter” and more broad-based T wave. Since depolarization starts in the endocardium and repolarization starts in the epicardium, the normal “T wave follows the QRS complex.”

In general, abnormal T waves are classified as either “peaked and prominent” or inverted. Inverted T waves are the most common T wave abnormality observed in clinical medicine. Identification of the cause of abnormal T waves can be extremely problematic because many medical problems can be associated with T wave inversion. Repolarization abnormalities follow a hierarchy of importance: ST segment elevation > ST segment depression > T wave inversion. For this reason, when evaluating ECGs look for ST elevation first, then ST segment depression, and only after isoelectric ST segments have been confirmed should you look for abnormal T waves.

Early repolarization is associated with ST segment elevation and prominent T waves, although in some cases the ST segment changes will be minimal. Peaked T waves can occur in two important abnormal

CHAPTER 6

Abnormal Repolarization: T Wave Changes and the QT Interval



conditions. First peaked T waves can represent the first signs of injury to the heart and second, peaked T waves are usually described in the context of hyperkalemia. The two conditions can generally be separated electrocardiographically by the extent of the prominent T waves. In myocardial injury the peaked T waves are localized to a specific region supplied by the coronary artery while in hyperkalemia peaking of the T waves is more generalized.

Usually the direction of the QRS complex and the T wave are the same because depolarization and repolarization occur in opposite directions. From a practical standpoint, since ventricular depolarization occurs from right to left which leads to positive QRS complexes in aVL, I, II, and aVF in the frontal plane and V4 through V6 in the precordial plane, the T waves are positive in these leads in the setting of normal depolarization.

In addition to the shape of the T wave, the timing of the T wave relative to the QRS complex should be evaluated by measuring the QT interval. The QT interval is measured from the beginning of the QRS complex to the end of the T wave and provides a rough estimate of the duration of ventricular depolarization until the end of repolarization.

A prolonged QT interval can be observed under several conditions (Table 6.1). First, the QT interval can be prolonged because of a hereditary disorder called the Long QT Syndrome. Second, a number of drugs can cause QT interval prolongation (Table 6.2). Third, electrolyte disorders such as hypocalcemia and hypokalemia can cause QT interval prolongation.

Table 6.1: Causes of QT interval prolongation

Etiology Specific causes/issuesHereditary Long QT syndromeDrug Table 2Metabolic Hypokalemia

HypocalcemiaHypomagnesemiaHypothermia

Endocrine HypothyroidismCentral Nervous System Subarachnoid hemorrhage


Abnormal Repolarization: T Wave Changes and the QT Interval 119

Table 6.2: Drugs associated with QT interval prolongation

Drug Class Specific DrugsAntiarrhythmics Amiodarone*

Sotalol*Dofetilide*Ibutilide*Procainamide*Disopyramide*

Antihistamines TerfenadineAnti-infectives Erythromycin

ClarithromycinPentamidine

Antimalarials ChloroqiuineAntipsychotics Thioridazine*

ChlorpromazineHaloperidol

Antidepressants AmitryptylineDesipramineImipramine

Opiates MethadoneOther Probucol Droperidol

* More likely to prolong the QT interval.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Pro

min

en

t T

wav

es

in le

ad

s w

ith

larg

er

R w

ave

s

V3

-V6

,

II, II

I, a

VF

“Ho

ok

” a

t th

e

term

ina

l QR

S

Pro

min

en

t T

wav

es

Ea

rly

rep

ola

riza

tio

n



Fig

ure

6.1

:

Bac

kgro

un

d:

Patie

nts

with

ear

ly r

epol

ariz

atio

n w

ill o

ften

ha

ve p

rom

inen

t T

wav

es.

ECG

: In

ear

ly r

epol

ariz

atio

n th

e pr

omin

ent

T w

aves

will

be

obse

rved

in

th

e in

fero

late

ral

lead

s.

Early

re

pola

rizat

ion

shou

ld b

e su

spec

ted

if th

ere

is t

he c

hara

cter

istic

“ho

ok”

on

the

term

inal

por

tion

of t

he Q

RS c

ompl

ex.

In m

ost

case

s, S

T

segm

ent

elev

atio

n w

ill b

e ob

serv

ed i

n th

e le

ads

with

the

m

ost

prom

inen

t T

wav

es.

Clin

ical

Iss

ues

: Ea

rly r

epol

ariz

atio

n is

fai

rly c

omm

on,

and

is

obse

rved

in

ab

out

7–12

%

of

the

gene

ral

popu

latio

n.

Inte

rest

ingl

y, e

arly

rep

olar

izat

ion

may

be

mor

e co

mm

on i

n at

hlet

es w

ith a

pre

vale

nce

of 3

0% in

som

e st

udie

s.



“Lo

caliz

ed

” T w

ave

pe

ak

ing

in t

he

are

a o

f is

che

mia

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Pro

min

en

t T

wav

es

Myo

card

ial I

nju

ry



Fig

ure

6.2

:

Bac

kgro

un

d:

T w

ave

peak

ing

may

be

the

first

sig

n of

myo

-ca

rdia

l inj

ury

on t

he E

CG

. Usu

ally

isol

ated

T w

ave

peak

ing

is

rapi

dly

repl

aced

by

ST s

egm

ent

elev

atio

n (a

lthou

gh t

he T

w

aves

rem

ain

prom

inen

t).

ECG

: T

wav

e pe

akin

g as

soci

ated

with

myo

card

ial

inju

ry i

s lo

caliz

ed t

o a

regi

on s

uppl

ied

by a

spe

cific

cor

onar

y ar

tery

an

d of

ten,

reci

proc

al S

T se

gmen

t cha

nges

are

als

o ob

serv

ed.

In t

he e

xam

ple,

pro

min

ent

T w

aves

are

not

ed in

V2

and

V3

due

to a

sig

nific

ant

lesi

on i

n th

e le

ft a

nter

ior

desc

endi

ng

coro

nary

art

ery.

In a

dditi

on, n

otic

e th

e ac

com

pany

ing

subt

le

ST s

egm

ent

depr

essi

on in

the

late

ral l

eads

(V4−

V6

and

I) an

d th

e in

ferio

r le

ads

(II a

nd a

VF)

.

Clin

ical

Issu

es:

The

pres

ence

of l

ocal

ized

T w

ave

peak

ing

is

very

sug

gest

ive

of a

sig

nific

ant

coro

nary

art

ery

lesi

on a

nd in

th

e pa

tient

com

plai

ning

of

ches

t pa

in,

seria

l EC

Gs

and

aggr

essi

ve d

iagn

ostic

eva

luat

ion

is e

ssen

tial.



P w

ave

s?

Pre

cord

ial

lea

ds

QR

S w

ide

nin

g

T w

ave

pe

ak

ing

P w

ave

s

ab

sen

t o

r

att

en

ua

ted

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

II

Pro

min

en

t T

wav

es

Hyp

erk

ale

mia



Fig

ure

6.3

:

Bac

kgro

un

d:

Gen

eral

ized

T w

ave

peak

ing

is t

he f

irst

sign

of

hy

perk

alem

ia.

Peak

ing

usua

lly

is

obse

rved

w

hen

the

seru

m K

+ is

> 5

.5 m

M.

ECG

: Th

e fir

st E

CG

sig

n in

hyp

erka

lem

ia is

T w

aves

pea

king

. If

the

hype

rkal

emia

wor

sens

(>

6.5

mM

) th

e Q

RS c

ompl

ex

begi

ns t

o w

iden

and

ST

segm

ent

elev

atio

n m

ay b

e ob

serv

ed

(Cha

pter

4, F

igur

e 4.

17).

In th

is e

xam

ple,

pro

min

ent T

wav

es

are

note

d in

V3

thro

ugh

V6

and

lead

s II

and

I. In

add

ition

to

the

prom

inen

t T

wav

es t

he Q

RS c

ompl

ex is

wid

e w

ithou

t Q

w

aves

du

e to

ab

norm

al

depo

lariz

atio

n.

With

ca

refu

l ob

serv

atio

n, S

T se

gmen

t el

evat

ion

in le

ads

V1

and

V2

is a

lso

pres

ent.

Fin

ally,

atr

ial t

issu

e is

mor

e se

nsiti

ve to

hyp

erka

lem

ia

than

ven

tric

ular

tis

sue.

Thi

s di

ffer

ence

lead

s to

loss

of

visi

ble

P w

ave

activ

ity

part

icul

arly

at

ex

trem

ely

high

K

+

leve

ls

(> 8

mM

). In

tere

stin

gly

the

sinu

s no

de i

s st

ill “

driv

ing”

the

he

art a

nd th

is c

ondi

tion

is c

alle

d a

“sin

oven

tric

ular

” rh

ythm

. A

lthou

gh it

wou

ld b

e un

usua

l for

myo

card

ial i

njur

y to

hav

e th

is c

ombi

natio

n of

EC

G c

hang

es,

agai

n th

e cl

inic

ian

mus

t al

so

take

th

e pa

tient

s sy

mpt

oms

into

ac

coun

t.

In

hype

rkal

emia

, che

st p

ain

is u

sual

ly a

bsen

t al

thou

gh p

atie

nts

may

com

plai

n of

nau

sea

and

gene

raliz

ed w

eakn

ess.

Clin

ical

Is

sues

: Em

erge

nt

trea

tmen

t of

hy

perk

alem

ia

is

revi

ewed

in C

hapt

er 4

, Fig

ure

4.17

. In

gene

ral o

nce

a bl

ood

sam

ple

is s

ent

off,

glu

cose

and

insu

lin a

re g

iven

. If

the

ECG

ch

ange

s ar

e du

e to

hyp

erka

lem

ia,

the

ECG

cha

nges

will

ra

pidl

y im

prov

e.



V1

-V4

(Usu

ally

V2

&V

3)

Sym

me

tric

T w

ave

Inve

rsio

n

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

T w

ave

Inve

rsio

n

Myo

card

ial I

sch

em

ia



Fig

ure

6.4

:

Bac

kgro

un

d:

Isch

emia

may

als

o ca

use

T w

ave

inve

rsio

n.

ECG

: T

wav

e in

vers

ion

is

a ve

ry

nons

peci

fic

findi

ng

part

icul

arly

in

th

e la

tera

l le

ads

beca

use

left

ve

ntric

ular

hy

pert

roph

y is

com

mon

. H

owev

er,

T w

ave

inve

rsio

n in

V3

and

V4

shou

ld a

rous

e su

spic

ion

of is

chem

ia in

a p

atie

nt w

ith

ches

t pa

in a

nd h

as b

een

asso

ciat

ed w

ith d

isea

se in

the

left

ante

rior

desc

endi

ng a

rter

y. T

he T

wav

e in

vers

ion

is u

sual

ly

sym

met

ric a

nd f

airly

pro

min

ent.

Clin

ical

Iss

ues

: T

wav

e in

vers

ion

shou

ld a

rous

e su

spic

ion

for

isch

emia

in t

he p

atie

nt w

ith c

hest

pai

n pa

rtic

ular

ly if

it is

ne

w w

hen

com

pare

d to

prio

r EC

Gs.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V1

-V4

Asy

mm

etr

ic T

wav

e

Inve

rsio

n

Ev

ide

nce

fo

r LV

H

such

as

ST

de

pre

ssio

n

an

d a

ssym

me

tric

T w

ave

Inve

rsio

n

an

d p

rom

ine

nt

volt

ag

eV

6

T w

ave

Inve

rsio

n

Left

ve

ntr

icu

lar

hyp

ert

rop

hy



Fig

ure

6.5

:

Bac

kgro

un

d:

Left

ven

tric

ular

hyp

ertr

ophy

can

als

o ca

use

ante

rior

T w

ave

inve

rsio

n bu

t is

gen

eral

ly a

ssoc

iate

d w

ith

acco

mpa

nyin

g la

tera

l wal

l T w

ave

inve

rsio

n an

d ST

seg

men

t de

pres

sion

.

ECG

: In

thi

s ex

ampl

e, i

nver

ted

T w

aves

are

pre

sent

in

the

entir

e pr

ecor

dium

but

not

ice

that

asy

mm

etric

dow

nslo

ping

ST

seg

men

t de

pres

sion

is

note

d in

the

lat

eral

lea

ds I

and

aV

L. T

he c

riter

ia fo

r lef

t ven

tric

ular

hyp

ertr

ophy

are

revi

ewed

in d

etai

l in

Cha

pter

8,

Figu

res

8.12

–14,

but

in

gene

ral

are

char

acte

rized

by

larg

e Q

RS c

ompl

exes

(due

to

incr

ease

d le

ft

vent

ricul

ar

mas

s)

and

abno

rmal

re

pola

rizat

ion

with

ST

de

pres

sion

and

T w

ave

inve

rsio

n. N

otic

e in

thi

s ex

ampl

e th

e Q

RS in

aV

L is

ext

rem

ely

larg

e (a

ppro

xim

atel

y 20

mm

).

Clin

ical

Iss

ues

: Th

e pr

esen

ce o

f re

pola

rizat

ion

abno

rmal

i-tie

s as

soci

ated

with

left

ven

tric

ular

hyp

ertr

ophy

is a

ssoc

iate

d w

ith a

wor

se p

rogn

osis

in la

rge

popu

latio

n st

udie

s.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V1

-V3

(Usu

ally

V2

&V

3)

Sym

me

tric

T w

ave

Inve

rsio

n

Ep

silo

n w

ave

s

T w

ave

Inve

rsio

n

Arr

hyt

hm

og

en

ic r

igh

t ve

ntr

icu

lar

card

iom

yop

ath

y (A

RV

C)



Fig

ure

6.6

:

Bac

kgro

un

d:

Arr

hyth

mog

enic

rig

ht

vent

ricul

ar

card

io-

myo

path

y (A

RVC

) is

a h

ered

itary

dis

ease

tha

t le

ads

to f

atty

in

filtr

atio

n of

the

rig

ht v

entr

icle

and

is

asso

ciat

ed w

ith t

he

deve

lopm

ent

of v

entr

icul

ar a

rrhy

thm

ias.

ECG

: Th

e EC

G in

ARV

C h

as s

ever

al c

hara

cter

istic

fin

ding

s.

Ant

erio

r T

wav

e in

vers

ion

is p

rese

nt a

nd is

oft

en a

ssoc

iate

d w

ith a

rig

ht b

undl

e br

anch

blo

ck p

atte

rn (

rSR’

in

V1)

. In

addi

tion,

in s

ome

case

s di

scre

te s

harp

“sp

ikes

” w

ill b

e se

en

in t

he S

T se

gmen

t of

lea

ds V

1 an

d V

2. T

hese

are

cal

led

epsi

lon

wav

es a

nd re

pres

ent e

xtre

mel

y la

te d

epol

ariz

atio

n of

a

smal

l par

t of

the

rig

ht v

entr

icul

ar o

utflo

w t

ract

.

Clin

ical

Issu

es:

Patie

nts

with

ARV

C a

re a

t hi

gh r

isk

for

the

deve

lopm

ent

of v

entr

icul

ar a

rrhy

thm

ias

and

sudd

en c

ardi

ac

deat

h.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Lim

b

lea

ds

No

rma

l

QT

inte

rva

l

V1

-V3

T w

ave

U w

ave

“Pro

lon

ge

d”

QT

Ap

pa

ren

t p

rolo

ng

ed

QT

inte

rva

l (p

rom

ine

nt

U w

ave

)



Fig

ure

6.7

:

Bac

kgro

un

d:

Aft

er t

he T

wav

e, a

noth

er d

efle

ctio

n ca

lled

the

U w

ave

can

be o

bser

ved.

ECG

: Th

e U

wav

e is

usu

ally

obs

erve

d in

you

ng a

dults

and

is

mos

t co

mm

only

see

n as

a p

ositi

ve w

ave

afte

r th

e T

wav

e in

le

ads

V2

or V

3. T

he U

wav

e is

due

to

myo

card

ial

stre

tch

rath

er t

han

vent

ricul

ar r

epol

ariz

atio

n an

d fo

r th

is r

easo

n m

ost e

xper

ts d

o no

t inc

lude

the

U w

ave

in th

e m

easu

rem

ent

of th

e Q

T in

terv

al. T

he Q

T in

terv

al c

an b

e di

ffic

ult t

o m

easu

re

beca

use

the

end

of t

he T

wav

e m

ay b

e di

ffic

ult

to id

entif

y.

Whe

n ca

lcul

atin

g th

e Q

T in

terv

al,

the

stee

pest

slo

pe o

f th

e te

rmin

al d

owns

trok

e or

ups

trok

e sh

ould

be

used

to

draw

a

“tan

gent

.” W

here

the

tan

gent

cro

sses

the

bas

elin

e sh

ould

be

use

d as

the

endp

oint

of t

he T

wav

e. T

he Q

T in

terv

al m

ust

be c

orre

cted

to

rate

to

calc

ulat

e th

e Q

Tc (C

hapt

er 3

).

Clin

ical

Is

sues

: A

ccur

ate

iden

tific

atio

n of

pa

tient

s w

ith

prol

onge

d Q

T in

terv

als

is i

mpo

rtan

t be

caus

e Q

T in

terv

al

prol

onga

tion

is a

ssoc

iate

d w

ith in

crea

sed

risk

of v

entr

icul

ar

arrh

ythm

ias

and

sudd

en c

ardi

ac d

eath

.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

All

lea

ds

No

rma

l

QT

inte

rva

l

P w

ave

V1 II V5

“Pro

lon

ge

d”

QT

Ap

pa

ren

t p

rolo

ng

ed

QT

inte

rva

l (p

rolo

ng

ed

PR

inte

rva

l)



Fig

ure

6.8

:

Bac

kgro

un

d:

Som

etim

es t

he P

wav

e w

ill b

e m

ista

ken

as

the

term

inal

por

tion

of t

he T

wav

e.

ECG

: In

pat

ient

s w

ith s

igni

fican

t di

seas

e of

the

ir A

V n

ode,

PR

int

erva

l pr

olon

gatio

n m

ay b

e ob

serv

ed (

first

deg

ree

AV

bl

ock)

. In

thi

s ex

ampl

e a

prol

onge

d PR

inte

rval

lead

s to

a P

w

ave

that

occ

urs

just

aft

er t

he T

wav

e (d

oubl

e he

aded

arro

ws)

. Thi

s si

tuat

ion

can

usua

lly b

e id

entif

ied

by th

e ap

par-

ent

abse

nce

of a

P w

ave

in f

ront

of

the

QRS

com

plex

.

Clin

ical

Issu

es:

PR in

terv

al p

rolo

ngat

ion

occu

rs w

hen

ther

e is

AV

nod

e di

seas

e th

at c

ause

s sl

ower

con

duct

ion

thro

ugh

the

AV

nod

e.



Pro

lon

ge

d Q

T

Lon

g Q

T S

ynd

rom

e All

lea

ds

Lon

g Q

T in

terv

al

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Me

asu

rin

g t

he

QT

inte

rva

l

1.

Dra

w a

“ta

ng

en

t” f

rom

th

e p

ea

k

of

the

T w

ave

to

th

e b

ase

line

2.

Me

asu

re f

rom

th

e b

eg

inn

ing

of

the

QR

S



Fig

ure

6.9

:

Bac

kgro

un

d:

The

Long

Q

T Sy

ndro

me

is

a fa

mily

of

he

redi

tary

dis

ease

s as

soci

ated

with

abn

orm

aliti

es in

the

ion

chan

nels

res

pons

ible

for

rep

olar

izat

ion.

ECG

: Th

ere

are

man

y su

btle

EC

G f

indi

ngs

asso

ciat

ed w

ith

the

Long

Q

T Sy

ndro

me

but

all

are

asso

ciat

ed

with

pr

olon

gatio

n of

the

QT

inte

rval

. D

elay

ed r

epol

ariz

atio

n is

of

ten

due

to a

bnor

mal

fun

ctio

n of

ion

chan

nels

(par

ticul

arly

K

+ c

hann

els)

. On

ECG

the

QT

is p

rolo

nged

. In

gene

ral t

he Q

T in

terv

al (s

olid

arr

ow) s

houl

d be

less

tha

n ha

lf th

e RR

inte

rval

(das

hed

arro

w);

in o

ther

wor

ds,

you

shou

ld b

e ab

le t

o fit

tw

o Q

T in

terv

als

into

one

RR

inte

rval

. The

Lon

g Q

T Sy

ndro

me

is g

ener

ally

not

ass

ocia

ted

with

any

QRS

cha

nges

.

Clin

ical

Iss

ues

: Th

e Lo

ng Q

T Sy

ndro

me

is a

ssoc

iate

d w

ith

incr

ease

d ris

k of

ven

tric

ular

arr

hyth

mia

s. P

rolo

ngat

ion

of th

e ac

tion

pote

ntia

l ap

pear

s to

rea

ctiv

ate

the

Na+

and

Ca2+

ch

anne

ls

used

fo

r de

pola

rizat

ion

and

lead

to

re

petit

ive

vent

ricul

ar d

epol

ariz

atio

n.



Pro

lon

ge

d Q

T

Dru

g (

Ibu

tilid

e)

All

lea

ds

Lon

g Q

T in

terv

al

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2



Fig

ure

6.1

0:

Bac

kgro

un

d:

A n

umbe

r of

dru

gs c

an c

ause

QT

inte

rval

pr

olon

gatio

n (T

able

6.2

).

ECG

: Q

T in

terv

al

prol

onga

tion

due

to

drug

s m

ay

be

asso

ciat

ed w

ith a

bnor

mal

T w

aves

suc

h as

lat

eral

T w

ave

inve

rsio

n as

in

this

cas

e or

may

sim

ply

be d

ue c

ause

QT

inte

rval

pro

long

atio

n. In

thi

s ca

se t

he a

nti-a

rrhy

thm

ic d

rug

ibut

ilide

led

to a

tem

pora

ry in

crea

se in

the

QT

inte

rval

.

Clin

ical

Issu

es:

Any

cau

se o

f pr

olon

ged

QT

inte

rval

(her

ed-

itary

, dr

ugs,

met

abol

ic d

isor

ders

, et

c.)

can

be a

ssoc

iate

d w

ith t

he d

evel

opm

ent

of v

entr

icul

ar a

rrhy

thm

ias

(Cha

pter

11

, Fi

gure

11.

28).

Ant

i-arr

hyth

mic

med

icat

ions

(pa

rtic

ular

ly

thos

e th

at b

lock

K+ c

hann

els)

are

the

mos

t co

mm

on c

ause

of

QT

inte

rval

pro

long

atio

n.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Lim

b

lea

ds

Lon

g Q

T in

terv

al

V1

-V3

“U w

ave”

is

act

ua

lly a

bip

ha

sic

T

wav

e

Bip

ha

sic

T w

ave

Pro

lon

ge

d Q

T

Hyp

ok

ale

mia



Fig

ure

6.1

1:

Bac

kgro

un

d:

Hyp

okal

emia

can

cau

se Q

T pr

olon

gatio

n.

ECG

: Tr

aditi

onal

ly Q

T pr

olon

gatio

n du

e to

a la

rge

“U w

ave”

ha

s be

en d

escr

ibed

as

the

clas

sic

sign

for h

ypok

alem

ia. M

ore

rece

nt s

tudi

es h

ave

show

n th

at t

he “

U w

ave”

is a

ctua

lly a

“d

oubl

e hu

mpe

d”

or

bifid

T

wav

e.

The

ECG

ch

ange

s as

soci

ated

with

hyp

okal

emia

are

mor

e lik

ely

to b

e ob

serv

ed

with

pro

gres

sive

dec

reas

es i

n K

+.

Whe

n th

e K

+ i

s be

twee

n 3.

0 an

d 3.

5 m

M,

ECG

ch

ange

s w

ill

be

obse

rved

in

ap

prox

imat

ely

10%

of

peop

le,

whi

le 8

0% o

f pe

ople

will

de

mon

stra

te E

CG

cha

nges

onc

e th

e K

+ is

< 2

.7 m

M.

Clin

ical

Iss

ues

: H

ypok

alem

ia r

equi

res

care

ful

repl

acem

ent

of K

+.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Lim

b

lea

ds

Lon

g Q

T in

terv

al

du

e t

o a

pro

lon

ge

d

ST

se

gm

en

t

Pro

lon

ge

d Q

T

Hyp

oca

lce

mia



Fig

ure

6.1

2:

Bac

kgro

un

d:

Hyp

ocal

cem

ia

can

caus

e Q

T in

terv

al

prol

onga

tion.

ECG

: Th

e cl

assi

c EC

G c

hang

e as

soci

ated

with

hyp

ocal

cem

ia

is p

rolo

ngat

ion

of t

he S

T se

gmen

t w

ith n

o ch

ange

in

the

shap

e of

the

T w

ave.

Clin

ical

Iss

ues

: Th

e m

ain

trea

tmen

t is

cor

rect

ing

the

low

se

rum

cal

cium

with

car

eful

Ca2+

rep

lace

men

t.



Pro

lon

ge

d Q

T

Hyp

om

ag

ne

sem

ia

All

lea

ds

Lon

g Q

T in

terv

al

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2



Fig

ure

6.1

3:

Bac

kgro

un

d:

Hyp

omag

nese

mia

may

be

pres

ent i

n a

varie

ty

of c

ondi

tions

inc

ludi

ng a

lcho

hol

abus

e an

d w

ith m

edic

a-tio

ns, p

artic

ular

ly d

iure

tics.

ECG

: H

ypom

agne

sem

ia c

an a

lso

caus

e Q

T in

terv

al p

rolo

-ng

atio

n. T

he th

ree

elec

trol

yte

diso

rder

s ha

ve s

light

ly d

iffer

ent

ECG

man

ifest

atio

ns.

The

QT

inte

rval

pro

long

atio

n du

e to

hy

poka

lem

ia

is

asso

ciat

ed

with

a

biph

asic

T

wav

e.

In

hypo

calc

emia

, Q

T in

terv

al p

rolo

ngat

ion

is m

ainl

y du

e to

ST

segm

ent

prol

onga

tion.

No

spec

ific

ECG

man

ifest

atio

ns f

or

hypo

mag

nese

mia

ha

ve

been

de

scrib

ed

othe

r th

an

gene

raliz

ed p

rolo

ngat

ion

of a

ll co

mpo

nent

s of

the

QT

inte

rval

(S

T se

gmen

t an

d T

wav

e)

alth

ough

so

me

stud

ies

have

su

gges

ted

that

hyo

pom

agne

sem

ia i

s as

soci

ated

with

mor

e pr

omin

ent

T w

aves

. It

shou

ld b

e no

ted

that

man

y pa

tient

s w

ill h

ave

seve

ral m

etab

olic

dis

orde

rs, e

.g. b

oth

hypo

kale

mia

an

d hy

pom

agne

sem

ia,

so t

hat

spec

ific

ECG

pat

tern

s ot

her

than

a p

rolo

nged

QT

inte

rval

will

be

diff

icul

t to

iden

tify.

Clin

ical

Iss

ues

: G

ener

ally,

the

tre

atm

ent

of h

ypom

agne

-se

mia

is

mag

nesi

um s

ulfa

te (

MgS

O4)

, us

ually

1–3

gra

ms

give

n in

trav

enou

sly.



Pro

lon

ge

d Q

T

Su

ba

rach

no

id h

em

mo

rha

ge

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V3

- V

6

Lon

g Q

T in

terv

al

Inve

rte

d T

wav

es

(usu

ally

sym

me

tric

)



Fig

ure

6.1

4:

Bac

kgro

un

d:

Suba

rach

noid

he

mor

rhag

e ca

n ca

use

QT

inte

rval

pro

long

atio

n.

ECG

: In

sub

arac

hnoi

d he

mor

rhag

e, E

CG

cha

nges

may

be

obse

rved

in

up t

o 80

% o

f pa

tient

s w

ith Q

T pr

olon

gatio

n w

ith s

ymm

etric

T w

ave

inve

rsio

n as

soci

ated

with

bra

dyca

r-di

a th

e ch

arac

teris

tic f

indi

ng.

The

spec

ific

mec

hani

sm f

or

thes

e EC

G

chan

ges

is

not

wel

l un

ders

tood

al

thou

gh

incr

ease

d sy

mpa

thet

ic a

nd p

aras

ympa

thet

ic t

one

has

been

su

gges

ted.

Clin

ical

Is

sues

: Th

e Q

T in

terv

al

prol

onga

tion

does

no

t re

quire

spe

cific

tre

atm

ent.

The

pre

senc

e of

EC

G a

bnor

mal

i-tie

s do

es n

ot a

ffec

t pr

ogno

sis.


148


So if you have gotten to this point you have finished evaluating the ST segment and the T wave. Remember that these two portions of the ECG represent ventricular repolarization. Since evaluation of patients with chest pain is one of the principal emergent clinical uses for the ECG, we have focused our initial discussion on ventricular repolarization. However, evaluation of ventricular depolarization is the other important compo-nent for evaluating ECG morphology (all the stuff other than rhythm), it is just that it can often be done at a more leisurely pace once active myocardial injury has been ruled out.

The easiest way to quickly assess ventricular depolarization is to examine lead V1. The normal QRS is “narrow” (QRS < 0.12 s), and in lead V1 the complex is usually characterized by an rS complex (Figure 7.1). With this in mind the two initial questions are: Is the QRS < 0.12 seconds? And is the QRS predominantly negative? If the answer to both of these questions is yes, the “general sequence and direction” of ventricular depolarization is probably normal. Once this has been established the ECG can be evaluated for frontal axis, Q waves, and other more subtle abnormalities of ventricular depolarization.

A narrow QRS is evidence that the ventricles are being activated simultaneously. However, if a wide QRS complex is present the ventricles are taking longer to depolarize because of relative delays in depolarization of some portions of the ventricles. The most common cause of a wide QRS complex is conduction block or delay in the left or right bundle (Figure 7.2). Block or delay in left bundle leads to depolarization of the right ventricle followed by depolarization in the left ventricle. Conversely, block or delay in the right bundle leads to initial left ventricular depolarization

CHAPTER 7

Abnormal Depolarization: A Prominent R Wave in V1


Abnormal Depolarization: A Prominent R Wave in V1 149

No

rma

lW

ide

Ne

ga

tive

Wid

e P

osi

tive

Na

rro

w P

osi

tive

QR

S M

orp

ho

log

y in

Le

ad

V1

Left

bu

nd

le b

ran

ch b

lock

Rig

ht

sid

ed

acc

ess

ory

pa

thw

ay

Rig

ht

bu

nd

le b

ran

ch b

lock

Left

sid

ed

acc

ess

ory

pa

thw

ay

Rig

ht

ven

tric

ula

r h

ype

rtro

ph

y

Po

ste

rio

r w

all

myo

card

ial I

nfa

rcti

on

Hyp

ert

rop

hic

ca

rdio

myo

pa

thy

De

xtro

card

ia

Du

che

nn

es

mu

scu

lar

dys

tro

ph

y

Fig

ure

7.1

:In

itial

eva

luat

ion

of v

entr

icul

ar d

epol

ariz

atio

n is

bes

t do

ne in

lead

V1.

The

nor

mal

dep

olar

izat

ion

is “

narr

ow a

nd n

egat

ive.

” W

ith t

his

in m

ind,

abn

orm

al d

epol

ariz

atio

n ca

n be

“w

ide

and

nega

tive,

” “n

arro

w a

nd p

ositi

ve,”

or

“wid

e an

d po

sitiv

e.”



AV node

Right bundle

Left bundle

Bundle of His

AV node

Right bundle

Left bundle

Bundle of His

AV node

Right bundle

Left bundle

Bundle of His

Normal Depolarization

Left bundle branch block

Right bundle branch block



Figure 7.2:This schematic shows ventricular depolarization (dotted arrows) and the resultant ECG forces (solid arrows) with normal ventricular depolarization, right bundle branch block, and left bundle branch block. During normal ven-tricular depolarization, after AV node and His bundle depolariza-tion the septum is depolarized from left to right due to depolari-zation from the left bundle (shorter solid arrow). Near simultaneous

depo larization of the left and right ventricles leads to a net leftward depolarization due to the larger left ventricular mass (longer solid arrow). In right bundle branch block, septal and left ventricular depolarization is unchanged but late depolarization of the right ventricle leads to a late rightward force. In left bundle branch block both the septal regions and the rest of the left ventricle are depo-larized from right to left.

followed by right ventricular depolarization. Usually, because of its smaller mass, depolarization of the right ventricle is not observed on the ECG due to “canceling out” from depolarization of the larger left ventricle in the opposite direction. However, in right bundle branch block, depolarization of the right ventricle is late so it is “unopposed” (left ventricular depolarization has already occurred) and a late positive deflection (an R wave) is seen in V1 and a corresponding late negative deflection (S wave) in V6 (Figure 7.3). A much rarer cause of a wide QRS complex is early depolarization of a portion of the ventricles. Usually the AV node and His bundle form the only way for atrioventricular conduction because the valvular annulus (the fibrous rings that provide the structure for the valves) is electrically inert. In some patients the valvular annulus does not form completely and there is a residual thread of tissue called an accessory pathway that provides an additional electrical connection between the atria and the ventricles. In this case early depolarization of ventricular tissue near the insertion point leads to a wide QRS.

A predominantly negative QRS complex in lead V1 means that ventricular depolarization is directed away from the right anterior chest (the location of V1). This is the normally observed direction of depolariza-tion because anatomically the left ventricle is located behind the right ventricle (Chapter 2, Figure 2.7). If the QRS is positive (a prominent R wave) in lead V1, it means that a large portion of the ventricles is being depolarized from “back to front” (Figure 7.3). A “prominent R wave in V1”



Rightventricle

Leftventricle

V6

V1

Rightatrium

Leftatrium

Sinusnode

Narrow Negative

V6

V1

Rightventricle

Leftventricle

Rightatrium

Leftatrium

Sinusnode

Narrow Positive

Figure 7.3:The direction and timing of ven-tricular depolarization will change the QRS morphologies in V1 and V6. The easiest way to evaluate ventricular depolarization is to examine the QRS morphology in lead V1 because this will give the clinician a sense for whether depolarization is directed toward the front of the chest or to the back. The most common cause

of a wide negative QRS complex is left bundle branch block where there is sequential activation of the right ventricle followed by the left ventricle. The most com-mon cause of a wide positive QRS complex is right bundle branch block where late depo-larization of the right ventricles leads to a late positive wave (R’) in lead V1.



Rightventricle

Leftventricle

V6

V1

Rightatrium

Leftatrium

Sinusnode

Wide Negative(left bundle branch block)

Figure 7.3: (Cont’d)

Rightventricle

Leftventricle

Rightatrium

Leftatrium

Sinusnode

V6

V1

Wide Positive(right bundle branch block)

is most commonly due to right bundle branch block but is also observed in conditions that are associated with an increase in right ventricular size. However, right bundle branch block will always be characterized by a wide QRS. The common possible causes of a prominent R wave in V1 are summarized in Figures 7.4 to 7.18.



Righ

t Bun

dle

Bran

ch B

lock

QR

S >

0.1

2 s

Late

R’ w

ave

PR

inte

rva

l is

no

t sh

ort

Left

-sid

ed A

cces

sory

Pat

hway

QR

S >

0.1

2 s

Sh

ort

PR

De

lta

wav

e

Righ

t Ven

tric

ular

Hyp

ertr

ophy

Larg

e R

wav

e

T w

ave

inve

rsio

n

De

ep

S in

V6

Post

erio

r Myo

card

ial I

nfar

ctio

n

Larg

e R

wav

e

Up

rig

ht

T w

ave

No

rma

l R in

V6

Hyp

ertr

ophi

c Ca

rdio

myo

path

y (s

epta

l)

Se

pta

l an

d in

feri

or

Q w

ave

s

No

rma

l R in

V6



Fig

ure

7.4

: Th

ere

are

seve

ral E

CG

clu

es t

hat

can

help

iden

tify

som

e of

the

com

mon

cau

ses

of a

pro

min

ent

R w

ave

in V

1.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V1 II

RS

Pre

serv

ed

R w

ave

No

rma

l axi

s

(dis

reg

ard

th

e t

erm

ina

l S)

rSR

’

Larg

e t

erm

ina

l

R w

ave

Pro

min

en

t R

Wav

e (

Wid

e)

Rig

ht

Bu

nd

le B

ran

ch B

lock



Fig

ure

7.5

:

Bac

kgro

un

d:

The

mos

t co

mm

on c

ause

of

a pr

omin

ent

R w

ave

in V

1 is

the

pre

senc

e of

rig

ht b

undl

e br

anch

blo

ck.

Righ

t bu

ndle

bra

nch

bloc

k m

ay b

e ob

serv

ed i

n 1%

of

heal

thy

popu

lati

ons

and

gene

rally

ha

s no

cl

inic

al

cons

eque

nce.

ECG

: Th

e EC

G in

righ

t bun

dle

bran

ch b

lock

is c

hara

cter

istic

. La

te a

ctiv

atio

n of

the

rig

ht v

entr

icle

lea

ds t

o a

late

for

ce

dire

cted

ant

erio

rly a

nd t

owar

d th

e rig

ht c

hest

(si

nce

this

is

whe

re t

he r

ight

ven

tric

le is

loca

ted)

. Thi

s le

ads

to a

late

pos

-iti

ve R

wav

e in

lead

V1

and

a la

te n

egat

ive

S w

ave

in V

6 an

d an

ove

rall

QRS

wid

th t

hat

is ≥

0.1

2 s.

Clin

ical

Iss

ues

: In

gen

eral

the

re a

re n

o ad

ditio

nal

clin

ical

is

sues

with

rig

ht b

undl

e br

anch

blo

ck a

nd n

o ad

ditio

nal

eval

uatio

n is

req

uire

d.



V2

, V3

, V4

,

V5

, or

V6

Q w

ave

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Pro

min

en

t R

Wav

e (

Wid

e)

Rig

ht

Bu

nd

le B

ran

ch B

lock

(w

ith

Q w

ave

s)



Fig

ure

7.6

:

Bac

kgro

un

d:

As

show

n in

Fi

gure

7.

2,

initi

al

sept

al

activ

atio

n is

no

rmal

in

rig

ht

bund

le

bran

ch

bloc

k.

As

disc

usse

d in

Cha

pter

8, o

ne o

f the

EC

G s

igns

of a

myo

card

ial

infa

rctio

n in

the

past

is a

Q w

ave

or in

itial

neg

ativ

e de

flect

ion

in t

he Q

RS c

ompl

ex.

ECG

: Si

nce

initi

al l

eft

vent

ricul

ar a

ctiv

atio

n is

via

the

lef

t bu

ndle

, in

isol

ated

righ

t bun

dle

bran

ch b

lock

abn

orm

al d

epo-

lariz

atio

n fr

om a

prio

r myo

card

ial i

nfar

ctio

n m

ay b

e ob

serv

ed.

In t

he e

xam

ple,

Q w

aves

are

pre

sent

in

lead

s V

1 an

d V

2.

Rem

embe

r tha

t Q w

aves

are

sim

ply

an in

itial

neg

ativ

e de

flec-

tion

in th

e Q

RS c

ompl

ex. A

lthou

gh in

itial

neg

ativ

e de

flect

ions

ar

e ex

pect

ed in

som

e le

ads

such

as

aVR,

in s

ome

case

s th

ey

are

abno

rmal

. In

thi

s ca

se t

he Q

wav

es r

epre

sent

a p

rior

ante

rose

ptal

myo

card

ial

infa

rctio

n. R

emem

ber

that

in

thes

e le

ads

a sm

all s

epta

l r w

ave

wou

ld b

e no

rmal

ly o

bser

ved.

The

lo

ss o

f th

e se

ptal

r w

aves

and

the

pre

senc

e of

the

abn

orm

al

Q w

aves

is d

ue t

o a

scar

fro

m t

he m

yoca

rdia

l inf

arct

ion

that

le

ads

to a

rela

tive

abse

nce

of e

lect

rical

act

ivity

in t

hese

lead

s.

Clin

ical

Iss

ues

: Th

e pr

esen

ce o

f ne

w a

bnor

mal

Q w

aves

sh

ould

alw

ays

arou

se s

uspi

cion

of

a pr

ior

myo

card

ial i

nfar

c-tio

n. M

any

myo

card

ial i

nfar

ctio

ns a

re “

sile

nt”

eith

er b

ecau

se

of t

rue

abse

nce

of s

ympt

oms

or,

mor

e lik

ely,

the

pat

ient

th

ough

t ch

est

pain

was

not

due

to

a ca

rdia

c ca

use

and

did

not

seek

med

ical

att

entio

n.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V1 II

rS

Att

en

ua

ted

R w

ave

Left

axi

s d

ev

iati

on

(dis

reg

ard

th

e t

erm

ina

l S)

rSR

’

Larg

e t

erm

ina

l

R w

ave

Pro

min

en

t R

Wav

e (

Wid

e)

Rig

ht

Bu

nd

le B

ran

ch B

lock

(w

ith

left

an

teri

or

fasc

icu

lar

blo

ck)



Fig

ure

7.7

:

Bac

kgro

un

d:

The

left

bu

ndle

di

vide

s in

to

two

maj

or

divi

sion

s: a

left

ant

erio

r fa

scic

le a

nd a

left

pos

terio

r fa

scic

le.

The

right

bun

dle

is l

ocat

ed a

djac

ent

to t

he l

eft

ante

rior

fasc

icle

and

as

a di

seas

e or

deg

ener

ativ

e pr

oces

s pr

ogre

sses

rig

ht b

undl

e br

anch

blo

ck a

nd le

ft a

nter

ior

fasc

icul

ar b

lock

m

ay o

ccur

tog

ethe

r. O

bvio

usly

if

bloc

k oc

curs

in

the

right

bu

ndle

, an

d bo

th d

ivis

ions

of

the

left

bun

dle

no a

trio

ven-

tric

ular

con

duct

ion

occu

rs (

and

a ve

ry s

low

hea

rt r

ate

– se

e C

hapt

er 1

0).

ECG

: In

the

set

ting

of c

ombi

ned

right

bun

dle

bran

ch b

lock

an

d le

ft a

nter

ior

fasi

cula

r bl

ock,

the

left

pos

terio

r bu

ndle

is

prov

idin

g in

itial

ven

tric

ular

act

ivat

ion.

For

thi

s re

ason

the

right

ven

tric

le a

nd t

he s

uper

ior

port

ion

of t

he le

ft v

entr

icle

ar

e ac

tivat

ed l

ate.

Thi

s le

ads

not

only

to

the

char

acte

ristic

fin

ding

s of

righ

t bun

dle

bran

ch b

lock

but

the

vent

ricul

ar a

xis

in t

he f

ront

al p

lane

is d

irect

ed u

pwar

d.

Clin

ical

Iss

ues

: W

hen

right

bun

dle

bran

ch b

lock

and

lef

t an

terio

r fa

scic

ular

blo

ck a

re b

oth

pres

ent,

the

pat

ient

is

depe

nden

t on

th

e le

ft

post

erio

r fa

scic

le

for

vent

ricul

ar

activ

atio

n. F

ortu

nate

ly t

he l

eft

post

erio

r fa

scic

ular

blo

ck i

s “s

hort

, fat

, and

stu

bby,

” so

tha

t it

is g

ener

ally

fai

rly r

elia

ble

and

patie

nts

can

do v

ery

wel

l ove

r ex

tend

ed p

erio

ds o

f tim

e w

ith

both

rig

ht

bund

le

bran

ch

bloc

k an

d le

ft

ante

rior

fasc

icul

ar b

lock

.



V1 II

rS

Att

en

ua

ted

R w

ave

Left

axi

s d

ev

iati

on

(dis

reg

ard

th

e t

erm

ina

l S)

rSR

’

Larg

e t

erm

ina

l

R w

ave

P

rolo

ng

ed

PR

inte

rva

l

Pro

min

en

t R

Wav

e (

Wid

e)

Rig

ht

Bu

nd

le B

ran

ch B

lock

(w

ith

left

an

teri

or

fasc

icu

lar

blo

ck

an

d a

pro

lon

ge

d P

R in

terv

al:

“tri

fasc

icu

lar

blo

ck”)



Fig

ure

7.8

:

Bac

kgro

un

d:

Evid

ence

for

ext

ensi

ve d

elay

s/bl

ock

in t

he

AV

con

duct

ion

syst

em h

as o

ften

bee

n ca

lled

“ trif

asci

cula

r”

bloc

k. A

lthou

gh t

his

term

has

bee

n us

ed f

or m

any

year

s,

rece

nt g

uide

lines

hav

e di

scou

rage

d its

use

sin

ce t

his

term

is

ofte

n no

t ac

cura

te a

nd h

as m

any

ECG

man

ifest

atio

ns.

ECG

: Tr

ifas

cicu

lar

bloc

k is

rig

ht b

undl

e br

anch

blo

ck a

nd

left

ant

erio

r fa

scic

ular

blo

ck c

ombi

ned

wit

h a

prol

onge

d PR

int

erva

l. In

the

exa

mpl

e a

biza

rre

RBBB

pat

tern

is

pres

ent

in le

ad V

1, w

ith

an a

lmos

t co

mpl

etel

y po

siti

ve Q

RS

com

plex

and

left

ant

erio

r fa

scic

ular

blo

ck (

left

axi

s de

via-

tion

wit

h th

e la

rges

t fr

onta

l pla

ne R

wav

e in

aV

L an

d aV

L w

ith

a qR

mor

phol

ogy)

. In

add

itio

n, t

he P

R in

terv

al i

s pr

olon

ged.

Com

pare

thi

s EC

G t

o th

e EC

G i

n Fi

gure

7.7

.

Not

ice

that

the

QRS

is s

igni

fican

tly w

ider

(0.2

1 s)

com

pare

d to

Fig

ure

7.7

(0.1

6 s)

.

Clin

ical

Is

sues

: A

s a

gene

ral

rule

th

e w

ider

th

e Q

RS

com

plex

the

mor

e se

vere

the

His

Pur

kinj

e di

seas

e an

d m

yo-

card

ial d

isea

se.

In f

act

seve

ral s

tudi

es h

ave

show

n a

roug

h co

rrel

atio

n be

twee

n Q

RS w

idth

and

left

ven

tric

ular

func

tion:

w

ider

QRS

com

plex

es a

re a

ssoc

iate

d w

ith w

orse

eje

ctio

n fr

actio

ns.

Inst

ead

of u

sing

the

ter

m t

rifas

cicu

lar

bloc

k, i

t is

be

tter

to

sim

ply

unde

rsta

nd t

hat

with

mor

e ev

iden

ce f

or

cond

uctio

n tis

sue

(AV

nod

e, H

is B

undl

e, a

nd t

he b

undl

e br

anch

es)

dise

ase

such

as

acco

mpa

nyin

g fa

scic

ular

blo

ck,

prol

onga

tion

of t

he P

R in

terv

al, o

r Q

RS w

iden

ing,

the

mor

e lik

ely

that

pro

blem

s w

ill a

rise

in t

he f

utur

e.



V1 aV

L

I II

III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

De

lta

wav

e

(sh

ort

PR

)

Ne

ga

tive

De

lta

wav

e

(Q w

ave

)

Pro

min

en

t R

Wav

e (

Wid

e)

Acc

ess

ory

Pat

hw

ay (

WP

W)

(le

ft la

tera

l acc

ess

ory

pa

thw

ay)



Fig

ure

7.9

:

Bac

kgro

un

d:

Nor

mal

ly t

he A

V n

ode

and

His

bun

dle

form

th

e on

ly e

lect

rical

con

nect

ion

betw

een

the

atria

and

the

ve

ntric

les

beca

use

the

annu

lus

that

for

ms

the

supp

ort

for

the

mitr

al a

nd tr

icus

pid

valv

es is

ele

ctric

ally

iner

t. In

app

roxi

mat

ely

1/1,

000

peop

le t

here

is

anot

her

mus

cula

r co

nnec

tion

(an

acce

ssor

y pa

thw

ay) b

etw

een

the

atria

and

ven

tric

les

beca

use

of in

com

plet

e fo

rmat

ion

of t

he v

alvu

lar

annu

lus.

Thi

s co

ndi-

tion

is u

sual

ly c

alle

d th

e W

olff

Par

kins

on W

hite

Syn

drom

e to

ho

nor

the

thre

e ph

ysic

ians

tha

t pr

ovid

ed t

he m

ost

com

plet

e EC

G d

escr

iptio

n of

thi

s co

llect

ion

of f

indi

ngs

in t

he 1

920s

.

ECG

: N

orm

ally

the

AV

nod

e an

d H

is b

undl

e ar

e th

e so

le

sour

ce fo

r ven

tric

ular

dep

olar

izat

ion

but i

n th

e pr

esen

ce o

f an

acce

ssor

y pa

thw

ay t

he v

entr

icle

can

be

depo

lariz

ed f

rom

tw

o si

tes

so t

he Q

RS c

ompl

ex r

epre

sent

s a

“fus

ion”

of

activ

atio

n be

twee

n th

ese

two

sour

ces.

Sin

ce m

ost

acce

ssor

y pa

thw

ays

cond

uct

rapi

dly

rela

tive

to t

he A

V n

ode

and

His

bun

dle,

the

PR

inte

rval

is s

hort

and

the

re is

an

initi

al “

delta

” w

ave

due

to

activ

atio

n vi

a th

e ac

cess

ory

path

way

. Re

mem

ber

that

al

thou

gh

AV

no

de

cond

uctio

n is

sl

ow,

depo

lariz

atio

n is

ex

trem

ely

rapi

d vi

a th

e H

is P

urki

nje

syst

em s

o th

at in

gen

eral

the

acce

ssor

y pa

thw

ay s

till a

ctiv

ates

a r

elat

ivel

y sm

all p

art

of

the

vent

ricle

s ev

en t

houg

h it

got

a “h

ead

star

t.”

In p

atie

nts

with

a le

ft s

ided

acc

esso

ry p

athw

ay, s

ince

the

left

ven

tric

le is

lo

cate

d be

hind

the

rig

ht v

entr

icle

, th

is in

itial

ven

tric

ular

act

i-va

tion

from

the

acc

esso

ry p

athw

ay l

eads

to

a pr

omin

ent

R w

ave

in V

1. T

he b

est w

ay to

iden

tify

the

pres

ence

of a

n ac

ces-

sory

pat

hway

is a

sho

rt P

R in

terv

al a

nd a

n ab

norm

al Q

RS c

om-

plex

due

to

the

pres

ence

of

the

delta

wav

e. In

thi

s ex

ampl

e,

the

patie

nt’s

acce

ssor

y pa

thw

ay is

loca

ted

in th

e la

tera

l wal

l so

the

delta

wav

e is

neg

ativ

e (a

q w

ave)

in le

ad a

VL.

Clin

ical

Iss

ues

: Pa

tient

s w

ith a

cces

sory

pat

hway

s ar

e at

hi

gher

ris

k fo

r th

e de

velo

pmen

t of

abn

orm

al f

ast

hear

t rh

ythm

s (t

achy

card

ias

or t

achy

arrh

ythm

ias)

. N

orm

ally

sin

ce

the

AV

nod

e an

d H

is b

undl

e fo

rm t

he o

nly

conn

ectio

n be

twee

n th

e at

ria a

nd v

entr

icle

s, v

entr

icul

ar d

epol

ariz

atio

n ca

nnot

af

fect

su

bseq

uent

at

rial

cont

ract

ion

(fee

dbac

k).

How

ever

with

tw

o co

nnec

tions

bet

wee

n th

e at

ria a

nd v

en-

tric

les,

it is

pos

sibl

e th

at v

entr

icul

ar d

epol

ariz

atio

n fr

om t

he

AV

nod

e co

uld

“ech

o” b

ack

to t

he a

triu

m b

y de

pola

rizat

ion

of t

he a

cces

sory

pat

hway

.



V1

II,III

,aV

F

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

De

lta

wav

e

(sh

ort

PR

)

Ne

ga

tive

De

lta

wav

e

(Q w

ave

)

Pro

min

en

t R

Wav

e (

Wid

e)

Acc

ess

ory

Pat

hw

ay (

WP

W)

(le

ft in

feri

or

acc

ess

ory

pa

thw

ay)



Fig

ure

7.1

0:

Bac

kgro

un

d:

An

acce

ssor

y pa

thw

ay c

an b

e lo

cate

d in

an

y sp

ot b

etw

een

the

atria

and

ven

tric

les.

The

mos

t co

m-

mon

loca

tion

for

an a

cces

sory

pat

hway

is t

he le

ft v

entr

icle

w

ith t

he l

ater

al w

all

a m

ore

com

mon

loc

atio

n th

an t

he

infe

rior

wal

l.

ECG

: Re

gard

less

of

the

loca

tion

of t

he a

cces

sory

pat

hway

th

e PR

inte

rval

is g

ener

ally

sho

rt b

ut t

he m

orph

olog

y of

the

Q

RS c

ompl

ex w

ill d

epen

d on

the

loca

tion

of t

he a

cces

sory

pa

thw

ays.

Lef

t si

ded

acce

ssor

y pa

thw

ays

caus

e po

sitiv

e R

wav

es in

V1

and

the

spec

ific

loca

tion

of t

he a

cces

sory

pat

h-w

ay c

an b

e de

term

ined

by

the

mor

phol

ogy

of t

he d

elta

w

ave.

In g

ener

al th

e de

lta w

ave

will

be

nega

tive

in th

e le

ads

that

are

loc

ated

nea

r th

e si

te o

f th

e ac

cess

ory

path

way

beca

use

initi

al

vent

ricul

ar

depo

lariz

atio

n ra

diat

es

away

fr

om t

he a

cces

sory

pat

hway

. In

thi

s ex

ampl

e, a

n ac

cess

ory

path

way

in th

e in

ferio

r wal

l of t

he le

ft v

entr

icle

will

be

asso

-ci

ated

with

a n

egat

ive

delta

wav

e in

the

infe

rior

lead

s (II

, III,

an

d aV

F).

Clin

ical

Iss

ues

: Th

e im

port

ant

findi

ngs

on t

he E

CG

tha

t ar

e su

gges

tive

of a

n ac

cess

ory

path

way

are

a s

hort

PR

inte

r-va

l an

d an

abn

orm

al Q

RS d

ue t

o th

e pr

esen

ce o

f a

delta

w

ave.

Acc

esso

ry p

athw

ays

loca

ted

at th

e in

ferio

r wal

l of t

he

hear

t (n

eare

st t

o th

e di

aphr

agm

) ha

ve o

ften

bee

n ca

lled

post

erio

r ac

cess

ory

path

way

s be

caus

e th

ey a

re lo

cate

d fa

r-th

est a

way

from

the

ante

rior c

hest

usi

ng a

car

diac

sur

geon

’s pe

rspe

ctiv

e.



V1

I II III

aV

R

aV

L

aV

F

V1

V6V5

V4

V3V2

R w

ave

< 6

mm

No

oth

er

ass

oci

ate

d a

bn

orm

alit

ies

Rig

ht

axi

s d

ev

iati

on

QR

S a

bn

orm

alit

ies

ST

se

gm

en

t ch

an

ge

s

T w

ave

ch

an

ge

s

“Pro

min

en

t” R

Wav

e (

Na

rro

w)

No

rma

l se

pta

l R w

ave



Fig

ure

7.1

1:

Bac

kgro

un

d:

A “

sept

al”

R w

ave

up t

o 6

mm

may

be

seen

un

der

norm

al

cond

ition

s in

V

1.

The

R w

ave

is

mor

e pr

omin

ent

in c

hild

ren.

In

fact

, in

new

born

s th

e R

wav

e is

of

ten

quite

larg

e be

caus

e th

e rig

ht v

entr

icle

and

left

ven

tric

le

are

pum

ping

aga

inst

sim

ilar

“loa

ds”

(rem

embe

r in

ute

ro,

the

lung

s ar

e no

t ex

pand

ed a

nd h

ave

a re

lativ

ely

high

re

sist

ance

). W

ith a

ging

, th

e R

wav

e gr

adua

lly d

ecre

ases

so

that

by

the

time

som

eone

is o

ver

40 y

ears

old

the

R w

ave

will

be

1–2

mm

with

an

uppe

r ra

nge

of 4

–5 m

m.

Men

hav

e la

rger

sep

tal R

wav

es t

han

wom

en.

ECG

: A

s ab

ove

an R

wav

e <

6 m

m i

s no

rmal

in

lead

V1,

al

thou

gh

an

R w

ave

> 3

–4 m

m

shou

ld

be

eval

uate

d cl

osel

y. In

gen

eral

a n

orm

al R

wav

e ca

n be

iden

tifie

d by

the

“ c

ompa

ny i

t ke

eps”

so

it sh

ould

not

be

asso

ciat

ed w

ith

abno

rmal

dep

olar

izat

ion

such

as

abno

rmal

Q w

aves

or

axis

de

viat

ion

nor

shou

ld

ther

e be

as

soci

ated

re

pola

rizat

ion

chan

ges

such

as

ST s

egm

ent d

evia

tion

or a

bnor

mal

T w

aves

. A

s a

coro

llary

to

the

norm

al p

rom

inen

t R

wav

e in

V1,

whi

le

mos

t in

divi

dual

s ha

ve a

pre

cord

ial t

rans

ition

zon

e w

here

the

R

wav

e an

d S

wav

e ar

e eq

ual

at V

3 or

V4,

abo

ut 2

–6%

of

peop

le w

ill h

ave

a tr

ansi

tion

zone

at

V1

and

12%

of

wom

en

and

up t

o 25

% o

f m

en w

ill h

ave

a tr

ansi

tion

zone

at

V2.

In

this

exa

mpl

e, t

he R

wav

e is

abo

ut 4

mm

with

a t

rans

ition

zo

ne a

t V

1. T

he s

mal

l inf

erol

ater

al Q

wav

es a

re f

rom

sep

tal

activ

atio

n an

d ar

e no

rmal

.

Clin

ical

Use

s: O

bvio

usly

it is

impo

rtan

t to

kno

w t

he u

pper

lim

its o

f no

rmal

for

an

R w

ave

in V

1 an

d th

e no

rmal

pre

cor-

dial

tra

nsiti

on z

one.



V1 V6

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

QR

S <

0.1

2 s

Term

ina

l S

Term

ina

l r’

rSr’

com

ple

x

“Pro

min

en

t” R

Wav

e (

Na

rro

w)

Rig

ht

inta

ven

tric

ula

r co

nd

uct

ion

de

lay

(rS

r’ co

mp

lex)



Fig

ure

7.1

2:

Bac

kgro

un

d:

In s

ome

case

s a

smal

l lat

e r’

will

be

obse

rved

in

lead

V1

but

the

QRS

will

be

< 0

.12

s. In

man

y ca

ses

this

re

pres

ents

slig

htly

del

ayed

act

ivat

ion

of t

he r

ight

ven

tric

le

(or

rela

tivel

y ea

rly n

orm

al a

ctiv

atio

n of

the

lef

t ve

ntric

le).

This

is

gene

rally

a n

orm

al f

indi

ng a

nd i

s pr

esen

t in

abo

ut

2–3%

of

heal

thy

indi

vidu

als.

ECG

: A

lthou

gh n

ot t

echn

ical

ly a

“pr

omin

ent

R w

ave,

” it

is

conv

enie

nt t

o ta

lk a

bout

thi

s EC

G f

indi

ng h

ere

beca

use

it ha

s a

sim

ilar

mec

hani

sm a

s rig

ht b

undl

e br

anch

blo

ck.

The

ECG

will

hav

e a

rSr’

sig

nal

with

a n

orm

al Q

RS w

idth

with

th

e r’

< 5

mm

and

the

r’ w

ave

will

alw

ays

be s

mal

ler t

han

the

S w

ave.

Gen

eral

ly t

he a

ccom

pany

ing

fron

tal a

xis

is n

orm

al.

If th

ere

is a

ccom

pany

ing

fron

tal a

xis

devi

atio

n (e

ither

left

or

right

) th

e po

ssib

ility

of

an a

tria

l sep

tal d

efec

t (a

con

geni

tal

“hol

e”

betw

een

the

left

an

d ri

ght

atri

a)

shou

ld

be

cons

ider

ed. I

n th

e ex

ampl

e, a

late

for

war

d de

pola

rizat

ion

of

the

right

ven

tric

le le

ads

to a

sm

all r

’ si

gnal

in le

ad V

1 an

d a

corr

espo

ndin

g sm

all s

wav

e in

V6.

The

pat

ient

has

a s

light

ly

left

war

d bu

t st

ill n

orm

al f

ront

al a

xis

abou

t 0°

with

the

la

rges

t R

wav

e re

cord

ed in

lead

I.

Clin

ical

Issu

es:

Gen

eral

ly th

ere

are

no c

linic

al c

onse

quen

ces

from

a r

ight

intr

aven

tric

ular

con

duct

ion

dela

y. H

owev

er, t

he

clin

icia

n sh

ould

car

eful

ly e

xclu

de t

he p

rese

nce

of a

n at

rial

sept

al d

efec

t if

sign

ifica

nt l

eft

or r

ight

axi

s de

viat

ion

is

pres

ent

(usu

ally

by

phys

ical

exa

min

atio

n an

d in

som

e ca

ses

by e

choc

ardi

ogra

phy)

.



V1 III

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Tall

P w

ave

Larg

e R

wav

e

Rig

ht

Axi

s D

ev

iati

on

ST

de

pre

ssio

n

T w

ave

inve

rsio

n

Pro

min

en

t R

Wav

e (

Na

rro

w)

Rig

ht

ven

tric

ula

r h

ype

rtro

ph

y



Fig

ure

7.1

3:

Bac

kgro

un

d:

Ther

e ar

e se

vera

l co

ndit

ions

th

at

are

asso

ciat

ed w

ith r

ight

ven

tric

ular

hyp

ertr

ophy

incl

udin

g lu

ng

dise

ases

an

d co

ngen

ital

hear

t di

seas

e.

Gen

eral

ly

right

ve

ntric

ular

hyp

ertr

ophy

dev

elop

s in

any

con

ditio

n in

whi

ch

the

right

ven

tric

le m

ust

cont

ract

aga

inst

hig

her

pres

sure

s.

ECG

: W

hen

sign

ifica

nt

right

ve

ntric

ular

hy

pert

roph

y is

pr

esen

t, i

f se

vere

eno

ugh,

the

for

ces

prod

uced

by

right

ve

ntric

ular

dep

olar

izat

ion

will

be

mor

e pr

omin

ent

than

the

fo

rces

pro

duce

d by

left

ven

tric

ular

dep

olar

izat

ion.

Thi

s si

tu-

atio

n le

ads

to a

mar

ked

chan

ge in

the

dire

ctio

n of

ven

tric

u-la

r de

pola

rizat

ion

to le

ft t

o rig

ht in

the

pre

cord

ial p

lane

and

a

right

war

d sh

ift o

f th

e ca

rdia

c ax

is in

the

fro

ntal

pla

ne. F

or

this

rea

son

the

hallm

ark

of r

ight

ven

tric

ular

hyp

ertr

ophy

is a

pr

omin

ent

narr

ow R

wav

e in

lea

d V

1 an

d rig

ht a

xis

devi

a-tio

n. In

thi

s ex

ampl

e, r

ight

axi

s de

viat

ion

is p

rese

nt w

ith t

he

larg

est

R w

ave

in t

he f

ront

al le

ads

reco

rded

in le

ad II

I. Th

e ot

her

impo

rtan

t fin

ding

ass

ocia

ted

with

rig

ht v

entr

icul

ar

hype

rtro

phy

is a

lso

show

n in

thi

s ex

ampl

e: t

he p

rom

inen

t R

wav

e w

ith a

nor

mal

QRS

dur

atio

n in

lead

V1.

Oft

en in

sev

ere

right

ven

tric

ular

hyp

ertr

ophy

the

T w

ave

will

be

inve

rted

in

lead

V1;

in

olde

r te

xtbo

oks

this

will

oft

en b

e ca

lled

right

vent

ricul

ar “

stra

in.”

The

rig

htw

ard

dire

ctio

n of

pre

cord

ial

depo

lariz

atio

n al

so le

ads

to a

dee

p S

wav

e in

lead

V6

as in

th

is e

xam

ple

whe

re t

he S

wav

e is

lar

ger

than

the

R w

ave.

Fi

nally

rig

ht v

entr

icul

ar h

yper

trop

hy w

ill o

ften

lead

to

right

at

rial e

nlar

gem

ent

and

the

P w

ave

will

bec

ome

mor

e pr

omi-

nent

. In

this

exa

mpl

e no

tice

how

dee

ply

nega

tive

the

P w

ave

is in

aV

R an

d ve

ry t

all a

nd “

peak

ed”

in le

ad V

1.

Clin

ical

Iss

ues

: Th

e pr

esen

ce o

f rig

ht v

entr

icul

ar h

yper

tro-

phy

by E

CG

is

asso

ciat

ed w

ith s

igni

fican

t di

seas

e. I

n fa

ct,

even

tho

ugh

the

left

ven

tric

le i

s re

spon

sibl

e fo

r pu

mpi

ng

bloo

d to

the

bod

y an

d th

e rig

ht v

entr

icle

res

pons

ible

for

tr

ansp

ortin

g bl

ood

to

the

lung

, th

e pr

esen

ce

of

right

ve

ntric

ular

hyp

ertr

ophy

has

a f

ar w

orse

pro

gnos

is t

han

left

ve

ntric

ular

hyp

ertr

ophy

. In

part

thi

s is

bec

ause

und

er n

orm

al

cond

ition

s th

e pu

lmon

ary

circ

ulat

ion

offe

rs v

ery

little

res

ist-

ance

to

flow

. A u

sefu

l ana

logy

is t

o th

ink

of t

he p

ulm

onar

y ci

rcul

atio

n as

a l

arge

riv

er d

elta

, w

hen

flood

ing

occu

rs

upst

ream

the

del

ta e

asily

acc

omm

odat

es t

he e

xces

s w

ater

. Th

e de

velo

pmen

t of

rig

ht v

entr

icul

ar h

yper

trop

hy i

s a

late

ev

ent

in m

ost

dise

ases

and

oft

en h

eral

ds a

ver

y di

ffic

ult

futu

re c

linic

al c

ours

e.



V1 III

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Q w

ave

(Usu

ally

)

Left

axi

s d

ev

iati

on

may

be

pre

sen

t

Up

rig

ht

T w

ave

Pro

min

en

t R

Wav

e (

Na

rro

w)

Po

ste

rio

r w

all

myo

card

ial i

nfa

rcti

on



Fig

ure

7.1

4:

Back

grou

nd:

The

use

of t

he t

erm

“po

ster

ior”

myo

card

ial

infa

rctio

n is

no l

onge

r en

cour

aged

alth

ough

it

will

stil

l be

fr

eque

ntly

enc

ount

ered

in c

linic

al m

edic

ine.

The

pos

terio

r w

all

was

nam

ed b

ecau

se i

t w

as t

he w

all

fart

hest

way

fro

m a

su

rgeo

n lo

okin

g at

the

hea

rt f

rom

the

fro

nt o

f th

e ch

est.

In

refe

renc

e to

the

hea

rt,

this

regi

on i

s be

twee

n/pa

rt o

f th

e in

ferio

r an

d la

tera

l w

alls

near

the

mitr

al a

nnul

us.

Post

erio

r in

farc

tion

is us

ually

due

to o

cclu

sion

of th

e rig

ht c

oron

ary

arte

ry

or m

ore

rare

ly o

cclu

sion

of th

e ci

rcum

flex

coro

nary

art

ery.

ECG

: A

cute

pos

terio

r wal

l myo

card

ial i

nfar

ctio

n is

dis

cuss

ed

in C

hapt

er 4

Fig

ure

26 a

s th

ere

are

usua

lly a

ssoc

iate

d ST

ch

ange

s. A

pos

terio

r wal

l myo

card

ial i

nfar

ctio

n th

at o

ccur

red

in t

he p

ast

ofte

n do

es n

ot h

ave

asso

ciat

ed S

T se

gmen

t ch

ange

s, ra

ther

the

mai

n fin

ding

is a

pro

min

ent R

wav

e in

V1

asso

ciat

ed w

ith a

n up

right

T w

ave.

Rem

embe

r th

at le

ad V

1 is

dire

ctly

opp

osite

the

pos

terio

r w

all

and

the

R w

ave

and

uprig

ht T

wav

e ac

tual

ly r

epre

sent

an

abno

rmal

Q w

ave

and

T w

ave

inve

rsio

n if

an e

lect

rode

was

pla

ced

dire

ctly

ove

r th

e in

jure

d ar

ea. G

ener

ally

occ

lusi

on o

f th

e rig

ht c

oron

ary

arte

ry

caus

es a

n ac

com

pany

ing

infe

rior

wal

l myo

card

ial i

nfar

ctio

n so

Q w

aves

in t

he in

ferio

r le

ads

supp

ort

the

diag

nosi

s of

an

old

post

erio

r w

all m

yoca

rdia

l inf

arct

ion.

In t

his

exam

ple,

the

pa

tient

has

bot

h a

post

erio

r an

d an

infe

rior

wal

l myo

card

ial

infa

rctio

n (in

ferio

r Q

s in

II,

III,

and

aVF)

. Th

e in

ferio

r w

all

myo

card

ial

infa

rctio

n le

ads

to l

eft

axis

dev

iatio

n w

ith t

he

larg

est

R w

ave

obse

rved

in a

VL.

Bot

h a

post

erio

r ac

cess

ory

path

way

and

a p

oste

rior

wal

l myo

card

ial i

nfar

ctio

n w

ill h

ave

a pr

omin

ent

R w

ave

in V

1 as

soci

ated

with

infe

rior

Q w

aves

. H

owev

er,

a po

ster

ior

wal

l myo

card

ial i

nfar

ctio

n ca

n be

dif-

fere

ntia

ted

from

a le

ft p

oste

rior

acce

ssor

y pa

thw

ay b

ecau

se

the

PR i

nter

val

will

be

norm

al a

nd d

elta

wav

es w

ill n

ot b

e se

en.

Sinc

e hy

pert

ensi

on is

a r

isk

fact

or f

or c

oron

ary

arte

ry

dise

ase,

in

man

y ca

ses,

as

in t

his

exam

ple,

an

inve

rted

or

biph

asic

P w

ave

will

be

obse

rved

in le

ad V

1.

Clin

ical

Is

sues

: Th

e pr

esen

ce

of

an

old

post

erio

r w

all

myo

card

ial i

nfar

ctio

n re

quire

s th

e cl

inic

ian

to m

ake

sure

that

he

or

she

is a

ggre

ssiv

ely

trea

ting

risk

fact

ors

for

coro

nary

ar

tery

dis

ease

suc

h as

hyp

erte

nsio

n or

hig

h ch

oles

tero

l.



V1

aV

L

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

No

rma

l PR

inte

rva

l

Inve

rte

d

P w

ave

Rig

ht

axi

s d

ev

iati

on

No

pre

cord

ial R

wav

es

in V

4-V

6

Pro

min

en

t R

Wav

e (

Na

rro

w)

De

xtro

card

ia



Fig

ure

7.1

5:

Bac

kgro

un

d:

Nor

mal

ly in

the

deve

lopi

ng e

mbr

yo, t

he h

eart

fo

rms

on t

he le

ft b

ecau

se o

f lo

opin

g of

the

vas

cula

r tu

be. I

n so

me

case

s, th

e he

art l

oops

in th

e op

posi

te d

irect

ion

lead

ing

to t

he h

eart

loc

ated

in

the

right

che

st o

r de

xtro

card

ia.

Dex

troc

ardi

a is

rar

e an

d is

pre

sent

in le

ss t

han

0.01

% o

f th

e po

pula

tion.

ECG

: In

so

me

case

s of

de

xtro

card

ia

the

hear

t is

m

orph

olog

ical

ly

norm

al

and

the

left

ve

ntric

le

is

sim

ply

orie

nted

to

the

right

(thi

s co

nditi

on is

usu

ally

ass

ocia

ted

with

si

tus

inve

rsus

whe

re a

ll of

the

orga

ns a

re o

n th

e op

posi

te s

ide

they

are

nor

mal

ly l

ocat

ed).

Dex

troc

ardi

a le

ads

to r

ight

axi

s de

viat

ion

in t

he f

ront

al le

ads,

a p

rom

inen

t R

wav

e in

lead

V1,

an

d S

wav

es in

the

late

ral l

eads

(sin

ce v

entr

icul

ar a

ctiv

atio

n is

tr

avel

ling

away

fro

m t

he l

eft

side

). W

hen

dext

roca

rdia

is

asso

ciat

ed w

ith s

itus

inve

rsus

, the

sin

us n

ode

is lo

cate

d to

the

left

and

the

atr

ia a

re a

ctiv

ated

fro

m le

ft t

o rig

ht. I

n th

is c

ase

the

P w

ave

is n

egat

ive

in a

VL

(rat

her

than

in a

VR)

alth

ough

si

nce

the

sinu

s no

de i

s st

ill i

n th

e up

per

part

of

the

right

at

rium

the

P w

aves

are

stil

l upr

ight

in th

e in

ferio

r lea

ds. I

n th

is

exam

ple

of d

extr

ocar

dia

the

fron

tal a

xis

is a

bout

−15

0° s

ince

th

e la

rges

t R

wav

e is

obs

erve

d in

aV

R. T

he n

egat

ive

P w

ave

and

QS

com

plex

in

aVL

are

the

findi

ngs

that

with

usu

al

anat

omy

are

foun

d in

aV

R. S

ince

the

R w

ave

is la

rger

in V

1 co

mpa

red

to V

2, th

e pr

ecor

dial

tran

sitio

n is

in th

e rig

ht c

hest

.

Clin

ical

Issu

es:

Gen

eral

ly t

here

are

no

spec

ific

clin

ic is

sues

as

soci

ated

with

dex

troc

ardi

a un

less

oth

er c

ardi

ac a

bnor

mal

-iti

es a

re p

rese

nt.

Whe

n ob

tain

ing

the

ECG

som

e re

com

-m

end

reve

rsin

g th

e lim

b le

ads

and

plac

ing

the

prec

ordi

al

lead

s in

the

ir us

ual p

ositi

on b

ut in

the

rig

ht c

hest

; if

this

is

done

the

EC

G w

ill lo

ok r

elat

ivel

y no

rmal

.



V1

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

No

rma

l

T w

ave

s

Hig

h f

req

ue

ncy

de

fle

ctio

n a

t th

e

term

ina

l QR

S

Pro

min

en

t R

Wav

e (

Na

rro

w)

Du

che

nn

e M

usc

ula

r D

ystr

op

hy



Fig

ure

7.1

6:

Bac

kgro

un

d:

Duc

henn

e m

uscu

lar

dyst

roph

y is

a h

ered

itary

di

seas

e th

at is

due

to

a m

utat

ion

in t

he g

ene

that

cod

es f

or

dyst

roph

in,

a pr

otei

n th

at is

impo

rtan

t fo

r m

aint

aini

ng t

he

cellu

lar

arch

itect

ure

in m

yocy

tes.

ECG

: D

uche

nne

mus

cula

r dys

trop

hy le

ads

to s

carr

ing

of th

e po

ster

ior

wal

l of

the

left

ven

tric

le le

adin

g to

a p

rom

inen

t R

wav

e in

V1

just

as

scar

ring

from

a p

oste

rior

wal

l myo

card

ial

infa

rctio

n ca

uses

a p

ositi

ve R

wav

e in

V1.

In a

dditi

on, i

n so

me

case

s la

te a

ctiv

atio

n of

the

post

erio

r lef

t ven

tric

le w

ill le

ad to

a

“spi

ke”

in

the

term

nal

port

ion

of

the

QRS

co

mpl

ex

alth

ough

thi

s is

a r

elat

ivel

y un

com

mon

fin

ding

. N

ow t

hat

we

have

int

rodu

ced

som

e of

the

cau

ses

of a

pro

min

ent

R w

ave

in V

1 we

can

see

that

an

incr

ease

d rig

htw

ard

forc

e ca

n be

see

n in

tw

o si

tuat

ions

. Fi

rst,

con

ditio

ns s

uch

as r

ight

ve

ntric

ular

hyp

ertr

ophy

and

dex

troc

ardi

a w

here

the

re i

s la

rger

mas

s to

the

rig

ht o

f th

e ch

est

and

seco

nd, c

ondi

tions

su

ch a

s D

uche

nne

mus

cula

r dy

stro

phy

or a

pos

terio

r w

all

myo

card

ial

infa

rctio

n in

whi

ch t

here

is

loss

of

myo

card

ial

tissu

e in

the

pos

terio

r po

rtio

n of

the

left

ven

tric

le.

Clin

ical

Issu

es:

Duc

henn

e m

uscu

lar d

ystr

ophy

can

be

asso

-ci

ated

with

hea

rt f

ailu

re i

n so

me

case

s du

e to

pro

gres

sive

di

seas

e an

d al

so s

igni

fican

t ar

rhyt

hmia

s.



V1

II,III

, aV

F

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3V

2

No

rma

l PR

inte

rva

l

Q w

ave

Up

rig

ht

T w

ave

Pro

min

en

t R

Wav

e (

Na

rro

w)

Hyp

ert

rop

hic

ca

rdio

myo

pa

thy



Fig

ure

7.1

7:

Bac

kgro

un

d:

Hyp

ertr

ophi

c ca

rdio

myo

path

y is

a

gene

tic

diso

rder

due

to

mut

atio

ns o

f pr

otei

ns o

f th

e sa

rcom

ere

(the

ac

tual

str

uctu

re t

hat

caus

es c

ontr

actio

n).

ECG

: In

som

e ca

ses

the

hype

rtro

phic

car

diom

yopa

thy

is

mos

t pr

omin

ent

in t

he le

ft v

entr

icul

ar s

eptu

m le

adin

g to

a

larg

e in

itial

left

to

right

for

ce t

hat

is a

lso

ofte

n or

ient

ed in

fe-

rior

to s

uper

ior.

This

abn

orm

al in

itial

dep

olar

izat

ion

lead

s to

a

larg

er t

han

expe

cted

sep

tal

r w

ave

in V

1, a

lar

ger

than

ex

pect

ed s

epta

l q w

ave

in V

6, a

nd a

bnor

mal

Q w

aves

in t

he

infe

rior

lead

s. C

ompa

re t

his

ECG

to

the

norm

al v

aria

nt E

CG

(F

igur

e 7.

11).

Q w

aves

in t

he in

fero

late

ral l

eads

are

pre

sent

in

bot

h, b

ut in

thi

s ca

se o

f hy

pert

roph

ic c

ardi

omyo

path

y th

e Q

wav

es a

re e

xtre

mel

y de

ep (

4 m

m;

as w

ill b

e di

scus

sed

in

Cha

pter

8,

abno

rmal

Q w

aves

are

def

ined

by

lead

, w

idth

, an

d de

pth)

and

ther

e ar

e as

soci

ated

ST

segm

ent e

leva

tion

in

lead

s V

1 an

d V

2, a

bnor

mal

lef

t ax

is d

evia

tion,

and

T w

ave

inve

rsio

n in

aV

L. A

lway

s re

mem

ber

to e

valu

ate

a pr

omin

ent

R w

ave

in t

he c

onte

xt o

f th

e “c

ompa

ny it

kee

ps,”

so

this

R

wav

e in

V1,

alth

ough

“no

rmal

” by

vol

tage

crit

eria

, wou

ld b

e co

nsid

ered

abn

orm

al.

Clin

ical

Is

sues

: H

yper

trop

hic

card

iom

yopa

thy

can

be

asso

ciat

ed

with

si

gnifi

cant

sh

ortn

ess

of

brea

th

due

to

pulm

onar

y co

nges

tion

from

ele

vate

d le

ft a

tria

l pr

essu

res

due

to a

thi

cken

ed s

tiff

left

ven

tric

le.

In a

dditi

on,

patie

nts

with

hyp

ertr

ophi

c ca

rdio

myo

path

y ar

e at

hig

her

risk

for

the

deve

lopm

ent

of v

entr

icul

ar a

rrhy

thm

ias.



V1

V2

,V3

,V4

,

V5

,V6

I II III

aV

R

aV

L

aV

F

V1

V6

V5V4

V3

V2

“Biz

arr

e”

R w

ave

s

(Osb

orn

wav

es)

Late

term

ina

l R w

ave

Pro

min

en

t R

Wav

e (

Wid

e)

Hyp

oth

erm

ia (

Osb

orn

Wav

e)



Fig

ure

7.1

8:

Bac

kgro

un

d:

In

seve

re

case

s of

hy

perc

alce

mia

an

d hy

poth

erm

ia,

a di

stin

ctiv

e bi

zarr

e la

te w

ave

of d

epol

ariz

a-tio

n ca

n be

obs

erve

d th

at is

oft

en c

alle

d an

Osb

orn

wav

e.

ECG

: Th

e O

sbor

n w

ave

is u

sual

ly s

een

in t

he p

reco

rdia

l le

ads

as l

arge

lat

e po

siti

ve d

efle

ctio

n ju

st a

fter

the

QRS

co

mpl

ex.

Sinc

e it

coi

ncid

es w

ith

the

J po

int

(rem

embe

r ou

r di

scus

sion

of

ST s

egm

ent

depr

essi

on;

the

J po

int

is

the

poin

t be

twee

n th

e en

d of

the

QRS

and

the

beg

inni

ng

of t

he S

T se

gmen

t),

the

Osb

orn

wav

e is

als

o ca

lled

a J

wav

e.

The

Osb

orn

wav

e be

com

es

prog

ress

ivel

y m

ore

prom

inen

t as

bod

y te

mpe

ratu

re d

ecre

ases

and

is

seen

ve

ry c

omm

only

whe

n th

e bo

dy t

empe

ratu

re i

s be

low

25

° C

. Th

e sp

ecif

ic c

ause

of

the

Osb

orn

wav

e ha

s no

t be

en c

ompr

ehen

sive

ly s

tudi

ed b

ut d

oes

appe

ar t

o be

m

edia

ted

by a

bnor

mal

fun

ctio

n of

K+ c

hann

els.

In

the

lead

s w

here

the

Osb

orn

wav

e is

obs

erve

d th

e T

wav

e is

us

ually

inve

rted

.

Clin

ical

Iss

ues

: If

an O

sbor

n w

ave

is p

rese

nt o

n th

e EC

G,

the

unde

rlyin

g ca

use-

hypo

ther

mia

or

hy

perc

alce

mia

is

ge

nera

lly e

asily

iden

tifie

d.


184


Although a prominent R wave in lead V1 is the easiest depolarization abnormality to quickly identify, obviously there are other QRS abnormali-ties that should be identified. If the QRS complex in lead V1 is predomi-nantly negative, the three remaining major parameters that have to be evaluated are: QRS width, frontal axis, identifying the presence of abnor-mal Q waves, and the overall size (voltage) of the QRS complex.

If the QRS is > 0.12 seconds then the ventricles are not being activated simultaneously and it suggests that the two ventricles are not being depolarized by the His Purkinje system in the normal fashion. By far and away the most common cause of a wide QRS complex is abnormal conduction in either the right bundle or the left bundle. As discussed in Chapter 7, in right bundle branch block delayed activation of the right ventricle leads to a late positive force directed toward lead V1 and often results in a triphasic QRS in lead V1 characterized by a large terminal R’ wave.

In left bundle branch block, the septum is activated abnormally and more importantly the left ventricle is activated very late (Chapter 7, Figure 7.3). This results in a wide very negative QRS complex in lead V1. A wide negative QRS complex is usually due to late activation of the lateral wall of the left ventricle due to left bundle branch block. Far rarer, a wide negative QRS complex in lead V1 can be due to early depolarization of the right ventricle due to the presence of a right sided accessory pathway (Figure 8.1). Finally, another common cause of a wide negative QRS complex in lead V1 is a pacemaker using a right ventricular lead.

CHAPTER 8

Abnormal Depolarization: Wide QRS Complexes and Other Depolarization Abnormalities


Abnormal Depolarization 185

Pacemakers are small, specialized computers/devices that transmit an electrical impulse to the heart via specialized leads. Pacemakers are typically used for the treatment of patients with slow heart rates.

Pacemakers are more comprehensively discussed in Chapter 12, but for this discussion it is important to note that most leads are placed in the right ventricle. With right ventricular pacing, ventricular depolarization travels from right to left and from front to back that does not utilize the

AV node

Right bundle

Left bundle

Bundle of His

Left Bundle Branch Block

AV node

Right bundle

Left bundle

Bundle of His

Right sided Accessory Pathway

Accessory pathway

Figure 8.1:Schematic showing the three most common causes of a wide negative QRS complex in lead V1. As can be seen from the schematic, all three are asso-ciated with relatively late activation of the lateral wall of the left ventricle.



His Purkinje system. For this reason, right ventricular pacing is associated with a wide negative QRS complex.

Once you have established that the QRS is narrow and negative in V1 the final things that need to be evaluated are the frontal axis, the presence of any abnormal Q waves, and the relative size of the QRS complex (Table 8.1). As described in Chapter 2, the frontal axis is generally from −35° to −110°. Left axis deviation is present if the axis is more negative (more leftward) than −35° and right axis deviation is present if the axis is more positive (more rightward) than 110°. The most common causes of left axis deviation are left ventricular hypertrophy and left anterior fascicular block. The most common causes of right axis deviation are left posterior fascicular block and right ventricular hypertrophy.

Q waves are any abnormal initial negative deflection in the QRS complex. A QS complex (thus a deep Q wave by definition) is expected in lead aVR and small q waves due to septal activation are expected in V5 and V6. Abnormal Q waves are “plump” (> 0.04 s or 1 little box wide) and “deep” (> 1 mV or 1 little box deep). Q waves can be observed in a number of conditions but where they have been historically important is for the identification of old myocardial infarctions. In a myocardial infarction, absence of depolarization in the affected area leads to net depolarization away from the affected region or a Q wave. Thus Q waves will be present in the leads that overly the affected area, so that in a patient with an old

AV node

Right bundle

Left bundle

Bundle of His

Right Ventricular Pacing

*

Figure 8.1: (Cont’d)



inferior wall myocardial infarction, Q waves will be present in leads II, III, and aVF. Q waves will also be present in I and aVL in left anterior fascicular block and in II, III, and aVF in left posterior fascicular block. Finally, a Q wave associated with an inverted T wave in lead III and an S wave in lead I has been called the S1Q3T3 pattern and has been linked to pulmonary embolus and right ventricular “strain” or “stress.” It is important to keep in mind that abnormal Q waves can be seen in a variety of conditions and simply mean that ventricular depolarization is directed away from that specific lead.

The last depolarization abnormality to be evaluated is QRS size. As in the case of right ventricular hypertrophy, left ventricular hypertrophy leads to an increase in QRS size.

Table 8.1: Evaluation of depolarization

Parameter Specific ECG QuestionQRS width Is the QRS < 0.12 s?QRS shape in V1 Is the QRS predominantly negative?Frontal axis Is the axis between −35° and 110°?Q waves Are abnormal Q waves absent?QRS size (voltage) Is the QRS voltage normal?

Any “No” answer is abnormal and the specific cause for the abnormal finding must be evaluated.



V1 a

VL

Iso

ele

ctri

c P

R

Inte

rva

l

Wid

e

mo

no

ph

asi

c

R w

ave

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2W

ide

Ne

ga

tive

QR

S in

V1

Left

Bu

nd

le B

ran

ch B

lock



Fig

ure

8.2

:

Bac

kgro

un

d:

Left

bun

dle

bran

ch b

lock

dev

elop

s in

abo

ut

1–2%

of

peop

le w

ho a

re f

ollo

wed

for

20

year

s. I

n th

e U

nite

d St

ates

lef

t bu

ndle

bra

nch

bloc

k is

ass

ocia

ted

with

hy

pert

ensi

on

and

coro

nary

ar

tery

di

seas

e al

thou

gh

wor

ldw

ide

the

mos

t co

mm

on

caus

e ha

s be

en

Cha

gas

dise

ase.

ECG

: Le

ft b

undl

e br

anch

blo

ck le

ads

to a

bnor

mal

act

ivat

ion

of t

he s

eptu

m a

nd la

tera

l wal

l and

sin

ce t

he le

ft v

entr

icle

is

not

activ

ated

ove

r th

e H

is P

urki

nje

syst

em,

the

QRS

is w

ide

and

deep

ly n

egat

ive

in le

ad V

1 and

pos

itive

in le

ad V

6. N

otic

e th

at

left

bu

ndle

br

anch

bl

ock

prod

uces

ch

arac

teris

tic

chan

ges

in r

epol

ariz

atio

n ev

en in

the

abs

ence

of

isch

emia

. A

s a

gene

ral g

uide

, the

ST

segm

ents

and

T w

aves

will

be

in

the

oppo

site

di

rect

ion

as

the

mai

n Q

RS

com

plex

: Pr

edom

inan

tly n

egat

ive

QRS

com

plex

es w

ill b

e as

soci

ated

with

ups

lopi

ng S

T se

gmen

t el

evat

ion

and

uprig

ht T

wav

es

and

pred

omin

antly

po

sitiv

e Q

RS

com

plex

es

will

ha

ve

dow

nslo

ping

ST

segm

ent

depr

essi

on a

nd in

vert

ed T

wav

es.

Like

man

y EC

G “

rule

s,”

this

one

als

o ha

s m

any

exce

ptio

ns

and

shou

ld n

ot b

e co

nsid

ered

abs

olut

e; t

he u

prig

ht T

wav

es

in l

ead

II an

d th

e la

tera

l le

ads

I, V

5, a

nd V

6 co

nstit

utes

a

norm

al f

indi

ng. C

ompa

re t

his

left

bun

dle

bran

ch b

lock

EC

G

to t

he E

CG

in

Cha

pter

5,

Figu

re 5

.4 w

here

the

T w

ave

is

inve

rted

in a

VL.

Clin

ical

Iss

ues

: Th

e le

ft b

undl

e br

anch

is

larg

er t

han

the

right

bun

dle

so t

hat

alth

ough

iso

late

d le

ft b

undl

e br

anch

w

ithou

t an

y ac

com

pany

ing

card

iac

dise

ase

has

not

been

as

soci

ated

with

a w

orse

pro

gnos

is in

som

e la

rge

popu

latio

n st

udie

s, i

dent

ifica

tion

of l

eft

bund

le b

ranc

h bl

ock

requ

ires

mor

e de

taile

d ev

alua

tion

for

any

card

iac

abno

rmal

ities

.



V1

aV

R

I II III

aV

R

aV

L

aV

F

V1

V6V5

V4

V3

V2

De

lta

wav

e

(sh

ort

PR

)

Ne

ga

tive

De

lta

wav

e

(Q w

ave

)

Wid

e N

eg

ati

ve Q

RS

in V

1

Rig

ht

sid

ed

acc

ess

ory

pa

thw

ay



Fig

ure

8.3

:

Bac

kgro

un

d:

In

the

Wol

ff

Park

inso

n W

hite

Sy

ndro

me,

pa

tient

s ha

ve a

n ac

cess

ory

path

way

tha

t co

nnec

ts t

he a

tria

an

d ve

ntric

les

(Cha

pter

7, F

igur

es 7

.9 a

nd 7

.10)

.

ECG

: In

pat

ient

s w

ith r

ight

sid

ed a

cces

sory

pat

hway

s, t

he

right

ven

tric

le i

s ac

tivat

ed f

irst

at t

he l

ater

al w

all

of t

he

tric

uspi

d an

nulu

s. T

his

lead

s to

ini

tial

depo

lariz

atio

n fr

om

right

to

left

and

a w

ide

nega

tive

QS

com

plex

is o

bser

ved

in

lead

V

1 an

d a

wid

e po

sitiv

e Q

RS

com

plex

(u

sual

ly

a m

onop

hasi

c R)

in V

6. S

ince

the

rig

ht v

entr

icle

is d

epol

ariz

ed

early

, the

PR

inte

rval

is s

hort

. Dep

olar

izat

ion

of th

e ve

ntric

les

in th

e W

olff

Par

kins

on W

hite

Syn

drom

e is

from

two

sour

ces-

the

acce

ssor

y pa

thw

ay a

nd th

e A

V n

ode/

His

Pur

kinj

e sy

stem

. Th

e in

itial

por

tion

of th

e Q

RS c

ompl

ex is

due

to th

e ac

cess

ory

path

way

and

is u

sual

ly c

alle

d th

e de

lta w

ave.

The

sha

pe o

f th

e de

lta w

ave

prov

ides

a c

lue

for

the

loca

tion

of t

he

acce

ssor

y pa

thw

ay.

In r

ight

sid

ed a

cces

sory

pat

hway

s th

e de

lta w

ave

is n

egat

ive

in le

ad a

VR

beca

use

initi

al v

entr

icul

ar

depo

lariz

atio

n is

dire

cted

aw

ay f

rom

thi

s le

ad.

Clin

ical

Iss

ues

: Pa

tient

s w

ith t

he W

olff

Par

kins

on W

hite

Sy

ndro

me

are

at h

ighe

r ris

k fo

r ta

chya

rrhy

thm

ias.



V1 aV

L

Pa

cem

ake

r “sp

ike”

fo

llow

s P

wav

e

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Left

bu

nd

le

bra

nch

blo

ck

mo

rph

olo

gy

V1

PP

PP

Wid

e N

eg

ati

ve Q

RS

in V

1

Rig

ht

ven

tric

ula

r p

aci

ng



Fig

ure

8.4

:

Bac

kgro

un

d:

In

man

y ca

ses

the

only

tr

eatm

ent

for

brad

ycar

dia

is im

plan

tatio

n of

a p

erm

anen

t pac

emak

er. S

ince

ve

ntric

ular

dep

olar

izat

ion

is c

ritic

al f

or p

rodu

cing

eff

ectiv

e m

ovem

ent

of b

lood

to

the

syst

emic

circ

ulat

ion

a pa

cing

lead

in

the

vent

ricle

is re

quire

d. V

entr

icul

ar p

acin

g ha

s tr

aditi

onal

ly

been

per

form

ed b

y pl

acin

g a

lead

in

the

right

ven

tric

ular

ap

ex s

ince

this

cha

mbe

r can

be

acce

ssed

from

the

larg

e ve

ins

of t

he b

ody

(usu

ally

the

larg

e ve

in in

the

sho

ulde

r, an

d th

e le

ad is

thr

eade

d th

roug

h th

e su

perio

r ve

na c

ava

thro

ugh

the

right

atr

ium

and

tric

uspi

d va

lve

to t

he r

ight

ven

tric

le).

ECG

: Ve

ntric

ular

pac

ing

from

the

rig

ht v

entr

icle

pro

vide

s a

char

acte

ristic

Q

RS

com

plex

. Si

nce

the

right

ve

ntric

le

is

activ

ated

firs

t, t

he Q

RS c

ompl

ex u

sual

ly h

as a

lef

t bu

ndle

bran

ch m

orph

olog

y pa

tter

n (a

mon

opha

sic

QS

com

plex

in

lead

V1)

. Ven

tric

ular

pac

ing

can

be m

ost

easi

ly d

iffer

entia

ted

from

left

bun

dle

bran

ch b

lock

by

iden

tifyi

ng t

he p

acem

aker

sp

ike

(the

ele

ctric

al o

utpu

t th

at d

epol

ariz

ed t

he v

entr

icle

). In

ad

ditio

n si

nce

the

paci

ng le

ad in

oft

en p

lace

d in

the

infe

rior

port

ion

of t

he r

ight

ven

tric

ular

ape

x, s

ince

dep

olar

izat

ion

is

activ

ated

aw

ay f

rom

the

pre

cord

ium

and

upw

ard

the

QRS

co

mpl

exes

are

oft

en n

egat

ive

in a

ll of

the

prec

ordi

al le

ads

V1

thro

ugh

V6

and

nega

tive

in t

he i

nfer

ior

lead

s. L

eft

bund

le

bran

ch b

lock

is n

ot a

ssoc

iate

d w

ith n

egat

ive

QRS

com

plex

es

in t

he in

ferio

r le

ads.

Clin

ical

Issu

es:

Paci

ng is

mor

e co

mpr

ehen

sive

ly c

over

ed in

C

hapt

er 1

2.



Q w

ave

s

No

rma

l Q w

ave

s

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Na

rro

w

q w

ave

No

rma

l Q w

ave

s

(< 0

.04

s, “

1 li

ttle

bo

x”)

Usu

ally

ass

oci

ate

d

wit

h a

no

rma

l T w

ave

Q w

ave

of a

ny d

urat

ion

may

be

seen

in II

I, aV

R, a

nd V

1



Fig

ure

8.5

:

Bac

kgro

un

d:

Smal

l sl

ende

r Q

wav

es c

an b

e ob

serv

ed i

n so

me

lead

s.

ECG

: N

orm

al Q

wav

es u

sual

ly a

re d

ue to

sept

al d

epol

ariz

atio

n an

d ar

e us

ually

obs

erve

d in

the

lat

eral

pre

cord

ial

lead

s.

Abn

orm

al Q

wav

es r

epre

sent

abn

orm

al i

nitia

l ve

ntric

ular

de

pola

rizat

ion

away

fro

m a

spe

cific

lead

and

mus

t be

wid

er

than

0.0

4 s

or 1

“lit

tle”

box

to b

e co

nsid

ered

sig

nific

ant.

Thi

s cr

iterio

n on

ly re

fers

to le

ads

in w

hich

a Q

wav

e w

ould

not

be

expe

cted

. Si

nce

vent

ricul

ar d

epol

ariz

atio

n oc

curs

fro

m r

ight

to

lef

t, Q

wav

es a

re a

lway

s pr

esen

t in

aV

R an

d m

ay b

e ob

serv

ed in

lead

III.

In fa

ct s

ince

the

iden

tific

atio

n of

Q w

aves

ha

ve a

lway

s im

plie

d th

e pr

esen

ce o

f abn

orm

al d

epol

ariz

atio

n,

trad

ition

ally

the

ini

tial

nega

tive

defle

ctio

n in

aV

R is

nev

er

refe

rred

to

as a

Q w

ave.

In t

his

exam

ple,

the

arr

ows

show

Q

wav

es i

n le

ads

II, I

II, a

nd V

6. T

he Q

wav

e in

III

is a

nor

mal

fin

ding

and

wou

ld n

ot b

e co

nsid

ered

abn

orm

al e

ven

thou

gh

it is

0.0

4 s

wid

e. T

he Q

wav

e in

lea

d II

is n

ot c

omm

only

ob

serv

ed b

ut in

thi

s ca

se is

ver

y na

rrow

and

sm

all a

nd is

not

pa

thol

ogic

. A

s m

entio

ned

earli

er,

the

smal

l q

wav

e in

V6

repr

esen

ts n

orm

al s

epta

l dep

olar

izat

ion.

A Q

wav

e m

ay a

lso

be o

bser

ved

in l

ead

V1

(rem

embe

r it

is c

ontig

uous

to

lead

aV

R) b

ut a

ny Q

wav

e in

lead

V2

is a

bnor

mal

.

Clin

ical

Iss

ues

: N

orm

al Q

wav

es a

re im

port

ant

to id

entif

y an

d m

ay b

e co

nfus

ed w

ith p

atho

logi

c Q

wav

es. I

n th

e en

d it

is i

mpo

rtan

t to

do

a co

mpr

ehen

sive

eva

luat

ion

in a

nyon

e w

ith a

n “u

nexp

ecte

d” Q

wav

e. T

he d

iffer

entia

l dia

gnos

is o

f Q

wav

es is

larg

e an

d a

mor

e co

mpl

ete

listin

g is

pro

vide

d in

th

e A

ppen

dice

s (s

ee C

hapt

er 1

5, T

able

15.

2).



I II III

aV

L

V3

, V4

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Left

Axi

s D

ev

iati

on

Term

ina

l S

q w

ave

Q w

ave

s (L

eft

Axi

s D

ev

iati

on

)

Left

an

teri

or

fasc

icu

lar

blo

ck



Fig

ure

8.6

:

Bac

kgro

un

d:

The

left

bun

dle

divi

des

into

mul

tiple

bra

nche

s bu

t ge

nera

lly i

s co

nsid

ered

to

have

tw

o m

ajor

bra

nche

s:-a

lo

nger

le

ft

ante

rior

fasc

icle

an

d a

shor

ter

thic

ker

left

po

ster

ior

fasc

icle

. A

blo

ck in

one

of

thes

e fa

scic

les

will

lead

to

cha

ract

eris

tic E

CG

pat

tern

s be

caus

e of

the

abn

orm

al

activ

atio

n pa

tter

n of

the

left

ven

tric

le.

ECG

: In

left

ant

erio

r fa

scic

ular

blo

ck t

here

is in

itial

infe

rior

depo

lariz

atio

n of

the

lef

t ve

ntric

le (

from

the

lef

t po

ster

ior

fasc

icle

) bu

t th

e re

st o

f th

e le

ft v

entr

icle

-late

ral

wal

l an

d an

terio

r w

all i

s ac

tivat

ed in

an

infe

rior

to s

uper

ior

dire

ctio

n.

This

lead

s to

a c

hara

cter

istic

QRS

pat

tern

in t

he f

ront

al le

ads

with

left

axi

s de

viat

ion

and

qR c

ompl

exes

in le

ads

I and

aV

L an

d rS

com

plex

es i

n th

e in

ferio

r le

ads.

The

ini

tial

infe

riorly

di

rect

ed d

epol

ariz

atio

n pr

oduc

es t

he s

mal

l inf

erio

r q

wav

es

in t

he l

ater

al l

eads

and

the

sm

all

r w

aves

in

the

infe

rior

lead

s. T

he s

ubse

quen

t in

ferio

r to

sup

erio

r de

pola

rizat

ion

of

the

maj

ority

of t

he le

ft v

entr

icle

lead

s to

larg

e R

wav

es in

the

late

ral l

eads

and

dee

p S

wav

es in

the

infe

rior

lead

s. T

he Q

RS

axis

is s

hift

ed le

ftw

ard.

Alth

ough

bot

h −3

0° a

nd −

45°

have

been

use

d as

“cu

t-of

fs”

for a

bnor

mal

left

axi

s de

viat

ion,

it is

im

port

ant

to

rem

embe

r th

at

left

war

d (m

ore

supe

rior)

ro

tatio

n of

le

ft

vent

ricul

ar

depo

lariz

atio

n re

pres

ents

a

cont

inuu

m. I

n ot

her

wor

ds a

lthou

gh −

45°

is m

ore

abno

rmal

th

an −

30°

bloc

k in

the

left

ant

erio

r fa

scic

le is

pro

babl

y no

t an

“al

l or

none

” ph

enom

enon

. Lik

e a

tree

, the

left

ant

erio

r fa

scic

le h

as m

any

bran

ches

and

the

re w

ill b

e pr

ogre

ssiv

ely

mor

e su

perio

r rot

atio

n as

mor

e br

anch

es a

re lo

st. T

he Q

RS is

w

iden

ed s

light

ly in

left

ant

erio

r fas

cicu

lar b

lock

but

sin

ce th

e le

ft a

nd r

ight

ven

tric

les

are

activ

ated

sim

ulta

neou

sly,

the

Q

RS c

ompl

ex is

usu

ally

< 0

.12

s. In

this

exa

mpl

e, th

e Q

wav

es

in I

and

aVL

are

less

than

0.0

4 s

and

wou

ld n

ot b

e co

nsid

ered

ab

norm

al.

Clin

ical

Issu

es:

Isol

ated

left

ant

erio

r fa

scic

ular

blo

ck in

and

of

itse

lf is

of

no c

linic

al c

onse

quen

ce a

lthou

gh o

ne is

alw

ays

conc

erne

d th

at t

he p

roce

ss t

hat

caus

ed t

he l

eft

ante

rior

fasc

icul

ar

bloc

k is

pr

ogre

ssiv

e.

Left

ax

is

devi

atio

n is

a

com

mon

fin

ding

, an

axi

s m

ore

left

war

d th

an −

30°

will

be

seen

in 2

–5%

of

asym

ptom

atic

men

.



III V3

, V4

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Rig

ht

Axi

s D

ev

iati

on

Term

ina

l S

q w

ave

Q w

ave

s (R

igh

t A

xis

De

via

tio

n)

Left

po

ste

rio

r fa

scic

ula

r b

lock



Fig

ure

8.7

:

Bac

kgro

un

d:

Prob

ably

bas

ed o

n its

ana

tom

y (s

hort

and

st

ubby

), le

ft p

oste

rior

fasc

icul

ar b

lock

is

far

less

com

mon

th

an le

ft a

nter

ior

fasc

icul

ar b

lock

.

ECG

: In

lef

t po

ster

ior

fasc

icul

ar b

lock

, in

itial

act

ivat

ion

of

the

vent

ricle

s is

via

the

lef

t an

terio

r fa

scic

le w

ith i

nitia

l ac

tivat

ion

of t

he a

nter

ior

wal

l and

with

late

act

ivat

ion

of t

he

infe

rior a

nd la

tera

l wal

ls o

f the

left

ven

tric

le. T

he E

CG

sho

ws

right

axi

s de

viat

ion

and

qR c

ompl

exes

in

the

infe

rior

lead

s an

d rS

com

plex

es i

n th

e la

tera

l le

ads.

Aga

in,

alth

ough

an

axis

of

120°

has

bee

n us

ed a

s a

“cut

-off

” fo

r id

entif

ying

abno

rmal

rig

ht a

xis

devi

atio

n, a

ny a

xis

mor

e rig

htw

ard

than

90

° sh

ould

aro

use

susp

icio

n. In

the

pre

cord

ial l

eads

, the

re is

of

ten

a de

ep S

wav

e in

the

ant

erio

r pr

ecor

dium

due

to

depo

lariz

atio

n di

rect

ed a

way

fro

m t

he f

ront

of

the

ches

t. In

th

is e

xam

ple,

a Q

wav

es a

re o

bser

ved

in l

ead

III (

norm

al

findi

ng) a

nd a

VF

(< 0

.04

s), b

ut n

eith

er w

ould

be

cons

ider

ed

abno

rmal

.

Clin

ical

Issu

es:

As

in le

ft a

nter

ior

fasc

icul

ar b

lock

, is

olat

ed

left

pos

terio

r fas

cicu

lar b

lock

is g

ener

ally

not

ass

ocia

ted

with

an

y sp

ecifi

c pr

oble

ms,

but

is m

uch

rare

r.



aV

L

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Inve

rte

d T

wav

e

Bro

ad

q w

ave

R w

ave

is n

ot

pro

min

en

t

(Le

ft a

xis

de

via

tio

n n

ot

pre

sen

t)

Q w

ave

s (A

bn

orm

al)

Old

late

ral w

all

myo

card

ial i

nfa

rcti

on



Fig

ure

8.8

:

Bac

kgro

un

d:

The

mai

n re

ason

for

iden

tifyi

ng a

bnor

mal

Q

wav

es is

tha

t th

ey m

ay re

pres

ent

a si

gn o

f an

old

myo

card

ial

infa

rctio

n. T

he g

enes

is o

f Q

wav

es is

com

plic

ated

but

the

y de

velo

p in

lead

s th

at o

verly

dam

aged

myo

card

ium

. Sca

r and

a

rela

tive

redu

ctio

n in

dep

olar

izin

g m

yoca

rdia

l cel

ls r

esul

t in

a

net

forc

e of

dep

olar

izat

ion

that

app

ears

to

be d

irect

ed

away

fro

m t

he in

jure

d ar

ea.

ECG

: A

bnor

mal

Q w

aves

due

to a

prio

r myo

card

ial i

nfar

ctio

n ar

e ge

nera

lly p

rese

nt i

n re

gion

s th

at a

re s

uppl

ied

by a

sp

ecifi

c co

rona

ry a

rter

y or

maj

or b

ranc

h. A

lat

eral

wal

l m

yoca

rdia

l in

farc

tion

may

lea

d to

abn

orm

al Q

wav

es i

n I,

aVL,

V

5 an

d V

6,

whi

le

a pr

ior

infe

rior

wal

l m

yoca

rdia

l in

farc

tion

may

res

ult

in Q

wav

es in

the

infe

rior

lead

s (II

, III

, an

d aV

F).

In t

his

exam

ple,

abn

orm

al Q

wav

es a

re o

bser

ved

in I,

aV

L, V

5, a

nd V

6. Q

wav

es o

bser

ved

in I

and

aVL

may

be

due

to e

ither

lef

t an

terio

r fa

scic

ular

blo

ck o

r a

late

ral

wal

l

myo

card

ial i

nfar

ctio

n. In

a la

tera

l wal

l myo

card

ial i

nfar

ctio

n th

e ax

is w

ill b

e no

rmal

or

even

rig

htw

ard

(due

to

loss

of

myo

card

ium

) an

d lo

ss o

f R

wav

es m

ay b

e ev

iden

t in

the

la

tera

l pre

cord

ial l

eads

. In

this

exa

mpl

e, th

ere

is n

o R

wav

e in

V

5 and

eve

n in

V6 w

here

an

R w

ave

is p

rese

nt, t

he a

mpl

itude

is

ext

rem

ely

atte

nuat

ed a

nd t

he a

xis

is e

xtre

mel

y rig

htw

ard

with

a p

redo

min

antly

pos

itive

QRS

in

aVR.

Bot

h of

the

se

findi

ngs

are

com

pelli

ng e

vide

nce

that

the

lat

eral

Q w

aves

ar

e du

e to

a p

rior

myo

card

ial i

nfar

ctio

n.

Clin

ical

Iss

ues

: A

n ol

d la

tera

l w

all

myo

card

ial

infa

rctio

n m

ay b

e as

soci

ated

with

hea

rt fa

ilure

and

oth

er s

ympt

oms.

In

part

icul

ar, l

ater

al w

all c

ontr

actio

n of

ten

prov

ides

sup

port

to

the

papi

llary

mus

cle

of t

he m

itral

val

ve.

In s

ome

case

s a

late

ral w

all m

yoca

rdia

l inf

arct

ion

can

lead

to th

e de

velo

pmen

t of

sev

ere

mitr

al re

gurg

itatio

n du

e to

the

loss

of t

his

supp

ort.



An

y p

reco

rdia

l

lea

d o

the

r th

an

V1

Ab

no

rma

l

Q w

ave

s a

re

wid

er

an

d m

ay

hav

e a

no

tch

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Q w

ave

s (A

bn

orm

al)

Old

an

teri

or

wa

ll m

yoca

rdia

l in

farc

tio

n



Fig

ure

8.9

:

Bac

kgro

un

d:

Q w

aves

may

dev

elop

aft

er a

n an

terio

r w

all

myo

card

ial i

nfar

ctio

n.

ECG

: In

thi

s ca

se, l

ead

V1 h

as a

nor

mal

con

figur

atio

n w

ith a

sm

all s

epta

l r w

ave.

How

ever

, lea

d V

3 is

mar

kedl

y ab

norm

al

with

a d

eep

Q w

ave

and

abse

nce

of a

n R

wav

e. A

lso

notic

e th

at t

here

is

acco

mpa

nyin

g ST

seg

men

t el

evat

ion.

Not

ice

that

the

pre

cord

ial

tran

sitio

n w

here

the

pos

itive

R w

ave

is

equa

l to

the

nega

tive

S w

ave

is le

ad V

5 (o

r pe

rhap

s “V

4 an

d th

ree

quar

ters

” si

nce

the

R w

ave

is s

light

ly la

rger

than

the

S).

The

norm

al R

wav

e tr

ansi

tion

is V

2 th

roug

h V

4 an

d so

me

have

des

crib

ed a

lat

e tr

ansi

tion

zone

(V

5 or

V6)

as

“Poo

r R

wav

e Pr

ogre

ssio

n.”

Poor

R w

ave

prog

ress

ion

may

be

due

to

post

erio

r ro

tatio

n of

the

hea

rt a

nd c

an b

e se

en in

pat

ient

s

with

lef

t ve

ntric

ular

hyp

ertr

ophy

but

can

als

o be

due

to

a re

lativ

e lo

ss o

f m

yoca

rdia

l mas

s du

e to

an

old

ante

rior

wal

l m

yoca

rdia

l inf

arct

ion.

Gen

eral

ly a

bnor

mal

Q w

aves

, lik

e ST

se

gmen

t ch

ange

s, a

re g

ener

ally

pre

sent

in t

wo

cont

iguo

us

lead

s. H

owev

er,

in t

his

exam

ple,

alth

ough

the

re m

ay b

e a

smal

l “n

ubbi

n” o

f an

R w

ave

in V

3 th

e ex

trem

ely

deep

S

wav

e is

pro

babl

y du

e to

an

ante

rior

scar

and

is

a Q

wav

e “e

quiv

alen

t.”

In t

he a

nter

osep

tal l

eads

the

Q w

ave

may

be

obse

rved

as

a “n

otch

” in

the

dow

nstr

oke.

The

pre

senc

e of

a

notc

h in

the

ini

tial

dow

nstr

oke

is s

tron

g ev

iden

ce t

hat

an

abno

rmal

Q w

ave

is p

rese

nt.

Clin

ical

Iss

ues

: Th

e pr

esen

ce o

f an

ant

erio

r Q

wav

e(s)

sh

ould

alw

ays

spur

add

ition

al e

valu

atio

n.



V2

-V4

Q w

ave

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Q w

ave

s (A

bn

orm

al)

Infi

ltra

tive

dis

ea

se (

am

ylo

ido

sis)



Fig

ure

8.1

0:

Bac

kgro

un

d:

Alth

ough

abn

orm

al Q

wav

es a

re m

ost

ofte

n du

e to

a p

rior

myo

card

ial i

nfar

ctio

n, a

nter

ior

Q w

aves

may

be

obs

erve

d in

any

con

ditio

n th

at le

ads t

o lo

ss o

f myo

card

ium

su

ch a

s am

yloi

dosi

s, s

arco

idos

is, o

r he

mac

hrom

atos

is.

ECG

: In

thi

s ex

ampl

e Q

wav

es a

nd a

ccom

pany

ing

loss

of

R w

aves

is o

bser

ved

in t

he a

nter

ior

lead

s V

2 th

roug

h V

4. A

gain

po

or

R w

ave

prog

ress

ion

is

pres

ent

with

a

prec

ordi

al

tran

sitio

n be

twee

n V

4 an

d V

5. A

lthou

gh lo

ss o

f R

wav

es in

th

e an

terio

r pr

ecor

dium

(o

ften

ca

lled

“poo

r R

wav

e pr

ogre

ssio

n”) m

ay b

e du

e to

pos

terio

r ro

tatio

n of

the

hea

rt,

the

pres

ence

of

a

QS

com

plex

in

le

ad

V4

is

defin

itely

ab

norm

al. O

ften

tim

es, a

nter

ior

Q w

aves

in t

he s

ettin

g of

a

prio

r myo

card

ial i

nfar

ctio

n ar

e as

soci

ated

with

acc

ompa

nyin

g ST

se

gmen

t el

evat

ion

due

to

the

form

atio

n of

a

left

ve

ntric

ular

ane

urys

m (

Cha

pter

4,

Figu

re 4

.12)

. In

thi

s ca

se

the

abse

nce

of

acco

mpa

nyin

g ST

se

gmen

t el

evat

ion

sugg

ests

an

infil

trat

ive

dise

ase

as t

he c

ause

for

the

EC

G

abno

rmal

ities

. Th

is

patie

nt

had

amyl

oido

sis,

w

here

an

ab

norm

al p

rote

in c

alle

d tr

anst

hyre

tin i

s de

posi

ted

in t

he

hear

t w

ith lo

ss o

f m

yocy

tes.

Clin

ical

Iss

ues

: By

far

and

aw

ay t

he m

ost

com

mon

cau

se

of a

nter

ior

Q w

aves

is

coro

nary

art

ery

dise

ase

and

an o

ld

prio

r m

yoca

rdia

l inf

arct

ion

but

may

be

due

to o

ther

dis

ease

s th

at a

ffec

t th

e ve

ntric

ular

myo

card

ium

.



III

Inve

rte

d T

wav

eQ

wav

e

I

S w

ave

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Q w

ave

s (A

bn

orm

al?

)

Pu

lmo

na

ry e

mb

olu

s (S

1Q

3T

3)



Fig

ure

8.1

1:

Bac

kgro

un

d:

Pulm

onar

y em

bolu

s is

a c

omm

on c

ause

for

th

e su

dden

dev

elop

men

t of

che

st p

ain.

Thi

s di

agno

sis

is

gene

rally

mad

e by

tes

ts o

ther

tha

n th

e EC

G.

ECG

: Th

e m

ost c

omm

on fi

ndin

g on

EC

G is

sim

ple

incr

ease

d he

art

rate

du

e to

ge

nera

lized

sy

mpa

thet

ic

activ

atio

n in

re

spon

se t

o th

e hy

poxi

a du

e to

the

pul

mon

ary

embo

lus.

O

ne E

CG

pat

tern

tha

t ha

s be

en a

ssoc

iate

d w

ith p

ulm

onar

y em

bolu

s is

the

S1Q

3T3

patt

ern

that

is c

hara

cter

ized

by

an S

w

ave

in le

ad I,

and

a Q

wav

e an

d an

inve

rted

T w

ave

in le

ad

III. T

he d

epol

ariz

atio

n pa

tter

n is

thou

ght t

o be

due

to a

mor

e rig

htw

ard

orie

ntat

ion

of

the

fron

tal

axis

. Th

e T

wav

e in

vers

ion

is t

houg

ht t

o be

due

to

hypo

xia.

In t

his

exam

ple

of

a pa

tient

with

a p

rove

n la

rge

pulm

onar

y em

bolu

s, a

dee

p S

wav

e is

not

ed in

I, a

nd a

dee

p Q

wav

e in

lead

III.

The

T w

ave

is

uprig

ht

but

ther

e is

so

me

very

su

btle

ST

se

gmen

t de

pres

sion

.

Clin

ical

Issu

es:

Pulm

onar

y em

bolu

s (u

sual

ly d

ue t

o a

bloo

d cl

ot th

at h

as b

roke

n of

f fro

m a

clo

t in

the

leg

and

trav

eled

to

the

pulm

onar

y ar

terie

s)

shou

ld

be

in

the

diff

eren

tial

diag

nosi

s of

any

one

com

plai

ning

of

sudd

en o

nset

of

ches

t pa

in

part

icul

arly

w

ith

asso

ciat

ed

shor

tnes

s of

br

eath

. A

lthou

gh t

he S

1Q3T

3 pa

tter

n is

mor

e co

mm

only

obs

erve

d in

pu

lmon

ary

embo

lus

and

shou

ld

arou

se

susp

icio

n if

pres

ent,

in g

ener

al t

he E

CG

has

ver

y lit

tle, i

f an

y, u

se f

or t

he

iden

tific

atio

n of

pul

mon

ary

embo

lus.



aV

L

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

R >

11

mm

Pro

min

en

t V

olt

ag

e

Left

ve

ntr

icu

lar

hyp

ert

rop

hy

(aV

L)



Fig

ure

8.1

2:

Bac

kgro

un

d:

One

of

th

e pr

inci

pal

prob

lem

s as

soci

ated

w

ith h

yper

tens

ion

is t

he d

evel

opm

ent

of l

eft

vent

ricul

ar

hype

rtro

phy.

Thi

cken

ing

of t

he le

ft v

entr

icle

is a

way

for

the

he

art

to r

espo

nd t

o co

ntra

ctin

g ag

ains

t hi

gher

pre

ssur

es

(als

o ca

lled

high

er a

fter

load

) in

hype

rten

sion

.

ECG

: Le

ft v

entr

icul

ar h

yper

trop

hy i

s as

soci

ated

with

bot

h de

pola

rizat

ion

and

repo

lariz

atio

n ch

ange

s. S

ince

the

lef

t ve

ntric

le is

larg

er a

nd t

hick

er, t

he v

olta

ges

mea

sure

d on

the

EC

G a

re u

sual

ly l

arge

r. A

bnor

mal

dep

olar

izat

ion

lead

s to

ab

norm

al r

epol

ariz

atio

n m

ost

ofte

n as

soci

ated

with

lat

eral

ST d

epre

ssio

n an

d T

wav

e in

vers

ion.

One

of

the

olde

st c

rite-

ria f

or le

ft v

entr

icul

ar h

yper

trop

hy is

an

R w

ave

> 1

1 m

m in

le

ad a

VL,

as

show

n in

thi

s ex

ampl

e.

Clin

ical

Is

sues

: Id

entif

icat

ion

of

ECG

cr

iteria

fo

r le

ft

vent

ricul

ar

hype

rtro

phy

shou

ld

spur

fu

rthe

r ca

rdia

c ev

alua

tion.

Oft

en a

n ec

hoca

rdio

gram

is re

quire

d to

eva

luat

e th

e se

verit

y of

left

ven

tric

ular

hyp

ertr

ophy

and

rul

e ou

t an

y va

lvul

ar c

ause

s of

left

ven

tric

ular

hyp

ertr

ophy

, suc

h as

aor

tic

valv

e st

enos

is.



V6

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V1

R w

ave

in V

6

S w

ave

in V

1

+}>

35

mm

(7 “

big

bo

xes”

)

Pro

min

en

t V

olt

ag

e

Left

ve

ntr

icu

lar

hyp

ert

rop

hy

(V1

, V6

)



Fig

ure

8.1

3:

Bac

kgro

un

d:

Sinc

e id

entif

icat

ion

of

left

ve

ntric

ular

hy

pert

roph

y ca

n be

an

im

port

ant

clin

ical

is

sue,

se

vera

l di

ffer

ent

crite

ria

for

iden

tific

atio

n of

le

ft

vent

ricul

ar

hype

rtro

phy

have

bee

n de

velo

ped.

ECG

: In

add

ition

to

a la

rge

R w

ave

in a

VL,

larg

e vo

ltage

s in

th

e pr

ecor

dial

lea

ds h

ave

also

bee

n us

ed a

s cr

iteria

for

id

entif

icat

ion

of l

eft

vent

ricul

ar h

yper

trop

hy.

If th

e su

m o

f

the

volta

ge o

f th

e S

wav

e in

V1

and

the

R w

ave

in V

6 is

> 3

5 m

m, l

eft

vent

ricul

ar h

yper

trop

hy is

pre

sent

.

Clin

ical

Issu

es:

The

pres

ence

of l

eft v

entr

icul

ar h

yper

trop

hy

by E

CG

in a

pat

ient

with

hyp

erte

nsio

n is

evi

denc

e th

at t

he

hype

rten

sion

is

si

gnifi

cant

an

d pr

obab

ly

has

not

been

op

timal

ly c

ontr

olle

d.



V6

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V1

ST

de

pre

ssio

n a

nd

T w

ave

inve

rsio

n

“LV

str

ain

”

Inve

rte

d P

wav

e

“Le

ft a

tria

l ab

no

rma

lity

”

Pro

min

en

t V

olt

ag

e

Left

ve

ntr

icu

lar

hyp

ert

rop

hy

(Ro

mh

ilt-E

ste

s)



Fig

ure

8.1

4:

Bac

kgro

un

d:

In

addi

tion

to

incr

ease

d vo

ltage

du

e to

in

crea

sed

left

ven

tric

ular

siz

e an

d th

ickn

ess,

the

pre

senc

e of

re

pola

rizat

ion

chan

ges

and

othe

r in

dire

ct e

vide

nce

for

left

ve

ntric

ular

hyp

ertr

ophy

hav

e al

so b

een

used

to

iden

tify

left

ve

ntric

ular

hyp

ertr

ophy

.

ECG

: In

an

effo

rt t

o in

crea

se t

he a

bilit

y of

the

EC

G t

o id

entif

y pa

tient

s w

ith

left

ve

ntric

ular

hy

pert

roph

y,

som

e m

etho

ds

use

a co

mbi

natio

n of

di

ffer

ent

ECG

fin

ding

s to

geth

er.

In t

he m

ost

com

mon

ly u

sed

syst

em,

nam

ed t

he

Rom

hilt

Este

s cr

iteria

for

the

tw

o in

vest

igat

ors

who

initi

ally

de

scrib

ed t

he m

etho

d, p

oint

s ar

e aw

arde

d fo

r di

ffer

ent

findi

ngs.

Alth

ough

QRS

vol

tage

is u

sed,

poi

nts

are

also

giv

en

for

the

pres

ence

of

re

pola

rizat

ion

abno

rmal

ities

(S

T de

pres

sion

and

T w

ave

inve

rsio

n) o

r a

left

atr

ial a

bnor

mal

ity.

The

pres

ence

of

left

atr

ial a

bnor

mal

ity s

ugge

sts

that

the

left

at

rium

has

enl

arge

d/th

icke

ned

in r

espo

nse

to c

ontr

actin

g ag

ains

t a

thic

k le

ft v

entr

icle

. The

Rom

hilt

Este

s po

int

syst

em

is s

umm

ariz

ed i

n in

the

App

endi

ces

(see

Tab

le 1

5.4)

. It

is

diff

icul

t to

rem

embe

r all

of th

e po

ints

for e

ach

of th

e sp

ecifi

c EC

G f

indi

ngs

but

from

a p

ract

ical

sta

ndpo

int,

a p

atie

nt h

as

left

ven

tric

ular

hyp

ertr

ophy

if

both

lef

t at

rial

abno

rmal

ity

and

repo

lariz

atio

n ab

norm

aliti

es a

re p

rese

nt.


214


Arrhythmias are classified by their rate (Figure 9.1). Abnormally slow heart rhythms are called bradycardias from the Greek root “brady,” which means slow. Chapter 10 provides a comprehensive discussion of bradycardia. Abnormally fast hearts are called tachycardias from the Greek root “tachy,” which means “fast” and are covered in Chapter 11 (good luck when you come to this chapter, this is the most complicated of the arrhythmia topics). In between these two extremes are a diverse collection of arrhythmias with normal heart rates that will be the subject of this chapter.

We discussed normal rhythm in Chapter 3, Figure 3.4. In a normal rhythm the sinus node is generating the cardiac impulse and initiating atrial depolarization and every atrial depolarization is followed by a timely ventricular depolarization. The source of atrial depolarization is identified by examining the shape of the P wave. Since the sinus node is located at the superior vena cava/right atrial junction, it is positive in lead II and negative in aVR. If the AV node and His bundle are conducting normally, ventricular depolarization (a QRS complex) will follow the P wave. With normal conduction through the AV node and His bundle, the PR interval (the interval measured from the beginning of the P wave to the beginning of the QRS complex) will be < 0.20 s.

If the patient is having an abnormal heart rhythm (arrhythmia) at a normal rate there are two basic questions that must be answered. First, is the basic rhythm being generated by the sinus node? Second, are there irregular heart beats?

CHAPTER 9

Arrhythmias: Normal Rates and Skips


Arrhythmias: Normal Rates and Skips 215

Rat

e

Slo

w H

ea

rt R

ate

(Bra

dyc

ard

ia)

No

rma

l Rat

eR

ap

id H

ea

rt R

ate

(Ta

chyc

ard

ia)

1.

Are

th

ere

en

ou

gh

P w

ave

s?

2.

Do

th

e P

wav

es

pro

du

ce a

QR

S?

Ch

ap

ter

10

1.

Is t

he

ba

sic

rhyt

hm

sin

us?

2.

Re

gu

lar

or

irre

gu

lar?

Ch

ap

ter

9

1.

Wid

e o

r n

arr

ow

QR

S?

2.

Re

gu

lar

or

irre

gu

lar?

Ch

ap

ter

11

Fig

ure

9.1

: Th

e ba

sic

algo

rithm

for

abn

orm

al h

eart

rhy

thm

s (a

rrhy

thm

ias)

.



II

III III

aV

R

aV

R

aV

L

aV

F

Ne

ga

tive

P w

ave

in a

VR

Po

siti

ve P

wav

e

in II

No

rma

l sin

us

rhyt

hm

(wit

h n

orm

al A

V c

on

du

ctio

n)

Re

gu

lar

Rh

yth

m

No

rma

l Sin

us

Rh

yth

m



Fig

ure

9.2

:W

e of

ten

shor

ten

“nor

mal

sin

us r

hyth

m w

ith n

orm

al A

V

cond

uctio

n” t

o “n

orm

al s

inus

rhy

thm

.” O

bvio

usly

the

sin

us

node

cou

ld s

till b

e ge

nera

ting

depo

lariz

atio

n bu

t if

atrio

ven-

tric

ular

con

duct

ion

was

blo

cked

eve

ry P

wav

e w

ould

not

be

asso

ciat

ed w

ith a

QRS

(th

is c

ause

of

brad

ycar

dia

is c

over

ed

in C

hapt

er 1

0).

So w

e sh

ould

alw

ays

rem

embe

r th

at w

hen

we

say

a pa

tient

has

“no

rmal

sin

us r

hyth

m,”

we

are

real

ly

sayi

ng tw

o th

ings

: the

sin

us n

ode

is g

ener

atin

g th

e be

at a

nd

atrio

vent

ricul

ar c

ondu

ctio

n is

nor

mal

. In

thi

s ex

ampl

e th

e P

wav

es a

re n

egat

ive

in a

VR

and

posi

tive

in l

ead

II. T

he P

R in

terv

al i

s 0.

20 s

, w

hich

is

the

uppe

r lim

it of

nor

mal

. It

is

hope

d th

at a

fter

rea

ding

the

firs

t po

rtio

n of

the

boo

k yo

u w

ould

hav

e no

ted

the

inve

rted

T w

ave

in le

ad II

I tha

t co

uld

still

be

a no

rmal

fin

ding

sin

ce t

here

are

no

acco

mpa

nyin

g T

wav

e ch

ange

s or

QRS

abn

orm

aliti

es i

n th

e ot

her

infe

rior

lead

s.



*

I II III aV

R

aV

L

aV

F

V1

V2

V3

V4

V5

V6

Re

gu

lar

Rh

yth

m

No

rma

l Sin

us

Rh

yth

m (

art

ifa

ct)



Fig

ure

9.3

:So

met

imes

ele

ctric

al s

igna

ls f

rom

oth

er e

lect

rical

equ

ipm

ent

will

int

erfe

re w

ith t

he E

CG

rec

ordi

ng.

In t

his

case

low

am

plitu

de fr

om a

n im

plan

ted

mus

cle

stim

ulat

or is

inte

rfer

ing

with

the

EC

G b

ut a

P w

ave

can

be o

bser

ved

(*).

This

pat

ient

ha

s a

norm

al h

eart

rhy

thm

.



aV

R

No

nn

eg

ati

ve

P w

ave

in a

VR

**

*

Re

gu

lar

Rh

yth

m

Ect

op

ic a

tria

l rh

yth

m



Fig

ure

9.4

:In

an

ecto

pic

atria

l rhy

thm

, a s

ite o

ther

tha

n th

e si

nus

node

de

pola

rizes

the

atr

ium

. In

ect

opic

atr

ial r

hyth

m t

he P

wav

e w

ill n

ot b

e po

sitiv

e in

lea

d II

and

nega

tive

in a

VR*

. Th

e sh

ape

of t

he P

wav

e w

ill b

e de

pend

ent

on t

he s

ite o

f th

e ec

topi

c at

rial f

ocus

. In

this

exa

mpl

e th

e ec

topi

c at

rial r

hyth

m

is b

eing

gen

erat

ed f

rom

a s

ite in

the

low

er p

art

of t

he a

tria

sinc

e th

e P

wav

es a

re n

egat

ive

in t

he i

nfer

ior

lead

s (a

tria

l de

pola

rizat

ion

mus

t be

tra

velli

ng a

way

fro

m t

hese

lea

ds).

Sinc

e th

e P

wav

e is

pos

itive

in

aVL

and

flat

or p

artia

lly

nega

tive

in a

VR,

the

ect

opic

site

is a

lso

prob

ably

with

in t

he

right

atr

ium

. Gen

eral

ly e

ctop

ic a

tria

l rhy

thm

is o

f no

clin

ical

co

nseq

uenc

e.



II aV

R

P w

ave

s?

Re

gu

lar

Rh

yth

m

Jun

ctio

na

l Rh

yth

m



Fig

ure

9.5

:G

ener

ally,

the

sin

us n

ode

has

the

fast

est

pace

mak

er r

ate

of

all

of

the

card

iac

tissu

es

and

“driv

es”

card

iac

activ

ity.

How

ever

, in

som

e ca

ses

the

AV

nod

al a

rea

can

depo

lariz

e fa

ster

tha

n th

e si

nus

node

and

a ju

nctio

nal r

hyth

m w

ill b

e ob

serv

ed.

In

junc

tiona

l rh

ythm

, si

nce

the

AV

no

de

is

gene

ratin

g th

e he

art

beat

, th

ere

is n

o P

wav

e be

fore

the

Q

RS c

ompl

ex.

Junc

tiona

l rh

ythm

gen

eral

ly h

as n

o cl

inic

al

cons

eque

nce

but

a sl

ow ju

nctio

nal r

hyth

m (

Cha

pter

10

on

brad

ycar

dia)

may

be

a si

gn o

f si

nus

node

dys

func

tion.



Re

gu

lar

rhyt

hm

Sin

us

rhyt

hm

wit

h fi

rst

de

gre

e A

V b

lock

**

**

**

An

y le

ad

PR

inte

rva

l > 0

.20

s



Fig

ure

9.6

:In

thi

s ex

ampl

e, t

he in

vert

ed P

wav

e in

aV

R an

d po

sitiv

e P

wav

e in

II is

evi

denc

e th

at t

he s

inus

nod

e is

res

pons

ible

for

at

rial

depo

lariz

atio

n (*

). H

owev

er,

the

PR i

nter

val

is a

bnor

-m

ally

pro

long

ed (0

.36

s). A

ny P

R in

terv

al >

0.2

0 s

is c

lass

ified

as

firs

t de

gree

AV

blo

ck. I

n th

is c

ase

ther

e is

“no

rmal

” si

nus

rhyt

hm (

the

P w

aves

are

bei

ng g

ener

ated

at

a no

rmal

rat

e)

but a

trio

vent

ricul

ar c

ondu

ctio

n is

not

“no

rmal

.” O

ften

times

, ne

w E

CG

rea

ders

look

for

a P

wav

e in

fro

nt o

f ev

ery

QRS

as

thei

r de

finiti

on o

f “n

orm

al s

inus

rhy

thm

.” A

s ill

ustr

ated

in

this

exa

mpl

e, e

valu

atin

g th

e re

latio

nshi

p be

twee

n P

wav

es

and

QRS

com

plex

es is

a m

easu

re o

f AV

nod

e an

d H

is P

urki

nje

func

tion.

Fin

ally,

this

EC

G il

lust

rate

s an

impo

rtan

t adv

anta

ge

to d

igita

l EC

G re

cord

ing

in w

hich

sig

nals

are

acq

uire

d si

mul

-ta

neou

sly.

If a

P w

ave

is e

asily

iden

tifie

d in

one

lead

(II

and

aVF)

, the

lead

s ab

ove

and

belo

w c

an b

e ev

alua

ted

and

mor

e su

btle

def

lect

ions

tha

t re

pres

ent

P w

aves

can

be

iden

tifie

d (a

rrow

s).



**

**

**

Irre

gu

lar

Rh

yth

m

Sin

us

arr

hyt

hm

ia



Fig

ure

9.7

:Th

e m

ost

com

mon

cau

se o

f an

irre

gula

r he

art

rate

in y

oung

ad

ults

is n

orm

al ir

regu

lar

depo

lariz

atio

n of

the

sin

us n

ode.

Th

e ra

te o

f si

nus

node

dep

olar

izat

ion

chan

ges

as m

etab

olic

ne

ed c

hang

es.

Whe

n w

e ex

erci

se t

he s

inus

rat

e in

crea

ses

beca

use

of m

ore

sym

path

etic

ner

ve (t

he “

adre

nalin

” sy

stem

)

activ

ity.

In y

oung

peo

ple

the

sinu

s ra

te w

ill c

hang

e fa

irly

dram

atic

ally

si

mpl

y w

ith

norm

al

brea

thin

g.

In

sinu

s ar

rhyt

hmia

all

of t

he P

wav

es (

*) h

ave

the

sam

e sh

ape

but

the

inte

rval

bet

wee

n P

wav

es v

arie

s.



“un

exp

ect

ed

”

de

fle

ctio

n

De

fle

ctio

n in

th

e T

wav

e is

a

pre

ma

ture

atr

ial c

on

tra

ctio

n

aV

RI

Sim

ilar

QR

S f

or

bo

th t

he

no

rma

l

sin

us

rhyt

hm

be

at

an

d t

he

ea

rly

be

at

II III

Irre

gu

lar

Rh

yth

m

Pre

ma

ture

atr

ial c

on

tra

ctio

ns



Fig

ure

9.8

:A

noth

er

com

mon

ca

use

of

an

irreg

ular

he

artb

eat

is

a pr

emat

ure

atria

l co

ntra

ctio

n. A

noth

er s

ite w

ithin

the

atr

ia,

othe

r tha

n th

e si

nus

node

, dep

olar

izes

ear

ly. T

his

lead

s to

an

early

P w

ave

that

oft

en c

an b

e fo

und

in t

he p

rece

ding

T

wav

e (c

ircle

d ar

eas)

. Si

nce

the

vent

ricle

s ar

e st

ill a

ctiv

ated

norm

ally

by

the

His

Pur

kinj

e sy

stem

the

QRS

com

plex

com

es

early

but

has

a n

orm

al s

hape

sim

ilar

to t

he Q

RS c

ompl

exes

pr

oduc

ed b

y th

e si

nus

beat

s. P

rem

atur

e at

rial

cont

ract

ions

ge

nera

lly h

ave

no c

linic

al c

onse

quen

ce b

ut in

som

e pe

ople

ca

n in

itiat

e at

rial f

ibril

latio

n (C

hapt

er 1

1, F

igur

e 11

.4).



Na

rro

w Q

RS

tha

t lo

oks

sim

ilar

to o

the

r Q

RS

co

mp

lexe

s

No

P w

ave

be

fore

th

e

ea

rly

QR

S a

lth

ou

gh

the

re m

ay b

e o

ne

aft

er

the

QR

S

V1 II V5

Irre

gu

lar

Rh

yth

m

Pre

ma

ture

jun

ctio

na

l co

ntr

act

ion

s



Fig

ure

9.9

:A

noth

er c

ause

of

an e

arly

bea

t is

pre

mat

ure

depo

lariz

atio

n fr

om t

he A

V n

odal

are

a. In

thi

s ca

se t

he e

arly

QRS

com

plex

w

ill b

e th

e sa

me

as t

he s

inus

rhy

thm

QRS

com

plex

es b

ut

ther

e w

ill b

e no

ear

ly P

wav

e be

fore

the

ear

ly Q

RS c

ompl

ex.

Som

etim

es t

he p

rem

atur

e ju

nctio

nal b

eat

will

lead

to

both

ve

ntric

ular

con

trac

tion

and

atria

l co

ntra

ctio

n. I

n th

is c

ase

the

atria

are

dep

olar

ized

abn

orm

ally

fro

m “

low

to

high

” so

th

e P

wav

e is

inv

erte

d. T

his

back

war

ds d

epol

ariz

atio

n is

us

ually

cal

led

retr

ogra

de c

ondu

ctio

n. If

retr

ogra

de c

ondu

ctio

n is

ver

y fa

st t

he P

wav

e m

ight

be

obse

rved

jus

t be

fore

the

Q

RS c

ompl

ex (e

xtre

mel

y ra

re),

if re

trog

rade

con

duct

ion

and

vent

ricul

ar d

epol

ariz

atio

n ar

e si

mila

r th

e sm

alle

r P

wav

e w

ill

be o

bscu

red

by t

he Q

RS c

ompl

ex (

mos

t co

mm

on),

and

if re

trog

rade

co

nduc

tion

is

slow

er

than

ve

ntric

ular

de

pola

rizat

ion

the

inve

rted

P w

ave

will

be

seen

in

the

ST

segm

ent.

A

gain

, co

mpa

ring

the

QRS

, ST

se

gmen

t an

d T

wav

e fo

r bo

th t

he n

orm

al b

eat

and

the

early

bea

t is

ex

trem

ely

usef

ul.

In t

his

case

the

ear

ly b

eat

has

a ne

gativ

e de

flect

ion

in t

he S

T se

gmen

t th

at is

not

see

n in

the

nor

mal

be

at

(circ

les)

. Th

is

“une

xpec

ted”

de

flect

ion

mus

t be

a

P w

ave

and

conf

irms

that

the

ear

ly b

eat

aros

e fr

om t

he

AV

nod

e. P

rem

atur

e ju

nctio

nal

com

plex

es h

ave

very

litt

le

clin

ical

con

sequ

ence

oth

er t

han

bein

g an

EC

G o

ddity

.



No

P w

ave

in t

he

T w

ave

;

A r

etr

og

rad

e P

wav

e m

ay b

e s

ee

n

I II III aV

R

aV

L

aV

F

“Slo

we

r” u

pst

roke

may

be

pre

sen

t

Re

tro

gra

de

P?

Irre

gu

lar

Rh

yth

m

Pre

ma

ture

ve

ntr

icu

lar

con

tra

ctio

ns



Fig

ure

9.1

0:So

met

imes

ear

ly a

ctiv

ity a

rises

fro

m v

entr

icul

ar t

issu

e to

pr

oduc

e a

prem

atur

e ve

ntric

ular

com

plex

. Si

nce

prem

atur

e ve

ntric

ular

com

plex

es d

o no

t us

e th

e no

rmal

His

Pur

kinj

e sy

stem

for

ven

tric

ular

dep

olar

izat

ion,

the

QRS

com

plex

is

wid

e an

d bi

zarr

e, a

ppea

ring

ofte

n w

ith a

n in

itial

ups

trok

e or

do

wns

trok

e th

at

is

less

st

eep

(arr

ow).

Retr

ogra

de

atria

l co

ntra

ctio

n ca

n so

met

imes

be

seen

aft

er t

he Q

RS c

ompl

ex

(ver

tical

ar

row

s)

but

may

be

ve

ry

subt

le.

Prem

atur

e

vent

ricul

ar c

ontr

actio

ns m

ay b

e a

mar

ker

for

incr

ease

d ris

k of

ven

tric

ular

arr

hyth

mia

s bu

t m

ay a

lso

be b

enig

n an

d of

no

clin

ical

con

sequ

ence

. A

gen

eral

rul

e (a

“gl

ass

bead

” ra

ther

th

an a

pea

rl) is

tha

t pr

emat

ure

vent

ricul

ar c

ontr

actio

ns a

re

“bad

” if

they

are

ass

ocia

ted

with

the

pre

senc

e of

oth

er

stru

ctur

al h

eart

dis

ease

(re

duce

d he

art

func

tion,

etc

.) an

d “N

ot m

uch

to w

orry

abo

ut”

if th

e pa

tient

has

no

othe

r hea

rt

abno

rmal

ities

.



“un

exp

ect

ed

”

de

fle

ctio

n

De

fle

ctio

n in

th

e T

wav

e is

a

pre

ma

ture

atr

ial c

on

tra

ctio

n

V1

V2

V3

Re

lati

vely

“fa

st”

up

stro

ke

Irre

gu

lar

Rh

yth

m

Pre

ma

ture

atr

ial c

on

tra

ctio

ns

(wit

h a

be

rra

nt

con

du

ctio

n)



Fig

ure

9.1

1:N

ot a

ll ea

rly Q

RS w

ide

QRS

com

plex

es a

re f

rom

pre

mat

ure

vent

ricul

ar c

ontr

actio

ns.

Ano

ther

cau

se o

f an

ear

ly w

ide

QRS

co

mpl

ex

is

a pr

emat

ure

atria

l co

ntra

ctio

n th

at

is

asso

ciat

ed w

ith a

berr

ant

or a

bnor

mal

con

duct

ion.

In

this

ca

se,

as

the

depo

lariz

atio

n fr

om

the

prem

atur

e at

rial

cont

ract

ion

reac

hes

the

His

Pur

kinj

e sy

stem

, on

e of

the

bu

ndle

br

anch

es

(usu

ally

th

e rig

ht

bund

le

bran

ch)

is

refr

acto

ry (

cann

ot c

ondu

ct)

and

the

wav

e of

dep

olar

izat

ion

only

tra

vels

dow

n on

e of

the

bun

dles

. Bu

ndle

bra

nch

bloc

k le

ads

to s

eque

ntia

l ac

tivat

ion

of t

he v

entr

icle

s an

d a

wid

e Q

RS c

ompl

ex. I

dent

ifica

tion

of a

pre

mat

ure

atria

l con

trac

tion

with

abe

rran

t co

nduc

tion

requ

ires

iden

tific

atio

n of

the

ear

ly

atria

l de

pola

rizat

ion.

A

s re

view

ed

in

Figu

re

9.8,

ca

refu

l co

mpa

rison

of t

he T

wav

es fo

r the

bea

t bef

ore

the

early

bea

t an

d a

late

r re

gula

r be

at w

ill h

elp

(circ

les)

.



Irre

gu

lar

Rh

yth

m

Co

mp

eti

ng

pa

cem

ake

rs

I II III

aV

R

aV

L

aV

F

Pe

Pe

Psr

Psr

Psr

Psr

Pf

Pe



Fig

ure

9.1

2:So

met

imes

irr

egul

ar

hear

t rh

ythm

s ca

n be

se

en

whe

n di

ffer

ent

site

s w

ithin

the

atr

ia h

ave

sim

ilar

rate

s or

irre

gula

r an

d “c

ompe

te.”

In

this

exa

mpl

e, a

site

fro

m t

he l

ower

at

rium

is f

aste

r th

an t

he s

inus

nod

e an

d pr

oduc

es a

P w

ave

that

is in

vert

ed in

the

infe

rior

lead

s (P

e) an

d an

ect

opic

atr

ial

rhyt

hm.

Whe

n th

is “

pace

mak

er”

paus

es,

the

sinu

s no

de

take

s ov

er a

nd p

rodu

ces

a no

rmal

upr

ight

P w

ave

(Psr) a

nd a

sh

ort

run

of s

inus

rhy

thm

. H

owev

er,

the

low

er a

tria

l si

te

begi

ns t

o de

pola

rize

agai

n at

a r

ate

fast

er t

han

the

sinu

s no

de a

nd g

radu

ally

tak

es o

ver.

Not

ice

that

the

re i

s on

e P

wav

e (P

f) th

at is

a “

fusi

on”

beat

whe

re a

tria

l dep

olar

izat

ion

is d

ue t

o bo

th t

he e

ctop

ic s

ite a

nd t

he s

inus

nod

e an

d th

e P

wav

e ha

s an

inte

rmed

iate

mor

phol

ogy

betw

een

the

P w

ave

from

the

ect

opic

atr

ial r

hyth

m a

nd t

he P

wav

e pr

oduc

ed b

y th

e si

nus

node

.



Irre

gu

lar

Rh

yth

m

Atr

ial fi

bri

llati

on



Fig

ure

9.1

3:A

noth

er

caus

e of

an

irr

egul

ar

rhyt

hm

with

a

rela

tivel

y no

rmal

hea

rt r

ate

is a

tria

l fib

rilla

tion.

In a

tria

l fib

rilla

tion,

the

at

ria a

re a

ctiv

ated

con

tinuo

usly

by

mul

tiple

atr

ial

wav

es o

f de

pola

rizat

ion.

Atr

ial f

ibril

latio

n is

gen

eral

ly a

ssoc

iate

d w

ith

a ra

pid

vent

ricul

ar r

ate

beca

use

rapi

d at

rial a

ctiv

atio

n le

ads

to r

apid

ven

tric

ular

rat

es b

ut in

som

e ca

ses,

if t

he A

V n

ode

does

not

con

duct

rap

idly,

atr

ial f

ibril

latio

n ca

n be

ass

ocia

ted

with

re

lativ

ely

norm

al

rate

s al

thou

gh

the

rhyt

hm

will

be

irr

egul

ar.

Atr

ial

fibril

latio

n is

co

vere

d ex

tens

ivel

y in

C

hapt

er 1

1, F

igur

es 1

1.3,

11.

4, a

nd 1

1.7

and

of a

ll th

e ar

rhyt

hmia

s it

is t

he m

ost

prev

alen

t an

d as

soci

ated

with

the

m

ost

hosp

ital a

dmis

sion

s.


241


There are only two general causes of slow heart rates: Failure of the sinus node to deliver normal impulses or depolarization is blocked between the atrium and the ventricles (atrioventricular or AV block) (Figure 10.1). Although someone new to clinical medicine might say, “who cares? A slow heart rate is a slow heart rate,” it is very important to make this distinc-tion as the management can vary dramatically. The ECG can provide definitive information on the specific site of the problem.

In sinus node dysfunction, since the sinus node does not generate an impulse at the normal rate there are fewer P waves than expected. There are many manifestations of sinus node dysfunction including sinus pauses, sinus bradycardia, ectopic atrial rhythm, or junctional rhythm. In ectopic atrial rhythm and junctional rhythm, the sinus rate is so slow that a subsidiary pacemaker, either from another region in the atrium or the AV node, must take over and “drive” the heart. We introduced ectopic atria rhythms and junctional rhythms in the last chapter. Ectopic atrial rhythms and junctional rhythms can be observed if these sites have more rapid activity than the sinus node or in the case of sinus node dysfunction if the sinus node pacemaker activity slows. These two situations can generally be differentiated by rate, the arbitrary cut-off for an abnormal sinus rate is 50 beats per minute and the AV junction has a spontaneous rate of about 35–50 beats per minute. If junctional rhythm is observed because of more rapid junctional activity the heart rate will be > 50 beats per minute and if junctional rhythm is observed because of sinus node dysfunction, the heart rate will be < 50 beats per minute.

In AV block the site of block is usually in the AV node or in the His bundle since these two structures, in most cases, form the only axis for AV conduction. Clinically AV block is classified by the relationship between the P waves and the QRS complexes. In first degree AV block

CHAPTER 10

Arrhythmias: Bradycardia



(introduced in Chapter 9, Figure 9.6) there is a one to one relationship between the P waves and the QRS complexes but the time required for AV conduction is prolonged (> 0.20 s). First degree AV block does not cause slow heart rates in and of itself since every P wave is conducted to the ventricles. In second degree AV block some but not all P waves are conducted to the ventricles and in third degree heart block there is no relationship between P waves and QRS complexes. It is important to remember that AV block is a normal response in the setting of rapid atrial activity. For example, if the atria were to suddenly start to beat at 300 times a minute (as in atrial flutter, Chapter 11, Figure 11.6), the AV node acts to limit the number of impulses that propagate to the ventricles and prevents rapid ventricular rates. Think of the AV node as a regulator that “protects” the ventricle from atrial arrhythmias. The corollary of this point is that abnormal AV conduction should only be identified if the P waves have a normal rate.

Second degree AV block is further classified into different types depending on the exact relationship between P waves and QRS com-plexes. In 1924, Woldemar Mobitz classified 2° AV blocks into Type I or Type II. In Type I block there is gradual prolongation of the PR interval until a QRS complex is dropped. Type I block is most commonly called Wenckebach block in honor of Karl Wenckebach who first described this unusual conduction pattern in the late 1800s by carefully evaluat-ing the relationship between the venous and arterial pulsations without the aid of the ECG (pretty impressive). In Type II block the PR interval remains constant and there is a sudden dropped QRS complex. The distinction between Type I and Type II block is very easy to make from the ECG. Simply measure the PR interval before and after the P wave associated with the dropped QRS complex. If the PR intervals are differ-ent Type I block is present and if they are the same Type II block is pre-sent. The distinction between Type I and Type II block is extremely important. In Type I block, the site of block is usually within the AV node so that if complete AV block develops the patient is usually left with a junctional rhythm with a heart rate of 35–50 bpm. The presence of Type II block suggests that the site of block is “below the AV node” within the His bundle (infranodal block). In this case, if complete AV block develops the patient is dependent on a pacemaker within ventricular tissues for the generation of QRS complexes. These ventricular sites are associated with very slow heart rates and are extremely unreliable and can stop suddenly.


Arrhythmias: Bradycardia 243

*

Sinus node dysfunction with junctional escape rhythm

* *•

*

Sinus rhythm

* * * * *

**

AV block with junctional escape rhythm

* * * * * * * *

Figure 10.1: Bradycardia can develop from either failure of the sinus node to initiate depolarization (sinus node dysfunction) or once the atrium is depolarized, atrioventricular block. The two forms of bradycardia can easily be differentiated by the ECG: in sinus node dysfunction not enough P waves are generated, while in AV block there are “enough” P waves, but they do not conduct

to the ventricles in a normal fashion. In the example, since the sinus node is not depolarizing normally, a subsidiary site, the AV node, “takes over” depolarizing the heart. Junctional beats in this case can be identified because the QRS complex is not preceded by a P wave. In the example of AV block, there is no AV conduction, so the AV node region also generates the QRS complexes but



Figure 10.1: (Cont’d )unlike sinus node dysfunction P waves at a normal rate are present. (With permission, taken from FM Kusumoto, ECG Interpretation:

From Pathophysiology to Clinical Application, Springer, New York, NY, 2009.)

There are two situations that do not “fit” into the Type I and Type II classification system for AV block. In the first, every other P wave is associated with a QRS complex. In 2:1 AV block although the PR intervals are the same before and after the blocked P wave, 2:1 AV block can be due to block within the AV node or infranodal. In most cases of 2:1 block the patient will have a few consecutive P waves that conduct to the ventricles so that the distinction between Type I and Type II can be made. Generally since Type I AV block is much more common than Type II block, intermittent periods with gradual prolongation of the PR interval will be observed between periods of 2:1 AV block. In the second situation called advanced AV block, two or more consecutive nonconducted P waves are present. In this case three or more P waves are presented between QRS complexes but some P waves conduct so that some AV conduction is present.

Although discussed earlier, there are two common circumstances where AV conduction is normal but are classified incorrectly as 2° degree AV block. In the first a premature atrial contraction (PAC) is not associated with a QRS complex (often called a “blocked PAC” in clinical shorthand). The second situation is an abnormal atrial rate associated with block in AV conduction. The AV node has decremental conduction properties so both of these responses are actually normal. In order to make the diagnosis of AV block, the P waves must be regular and with a normal rate.

In complete heart block (3° AV block) there is no relationship between P waves and QRS complexes. If the block is within the AV node a regular narrow QRS rhythm or junctional rhythm will be observed. This can be a source of confusion since junctional rhythm is also a manifestation of sinus node dysfunction. The difference is that in complete heart block P waves are present and do not conduct to the ventricles and in junctional rhythm due to sinus node dysfunction P waves generated by the sinus node will not be seen. If complete heart block due to infranodal block develops, the escape QRS complex will be wide.



The distinction between 2° degree AV block and complete heart block seems confusing at first glance. For example, how do I differentiate between advanced AV block and complete heart block? Actually there is a practical way for the ECG to help. In 2° AV block, generally the QRS rhythm is irregular because of some conducted P waves while in complete AV block the QRS rhythm will be regular. This practical method helps in another situation. In atrial fibrillation, the atria are activated irregularly and in turn this leads to an irregular QRS rhythm. In patients with atrial fibrillation and complete AV block, a regular slow QRS rhythm will be observed.



Sin

us

No

de

dys

fun

ctio

n (

No

t e

no

ug

h P

wav

es)

Art

ifa

ct



Fig

ure

10.

2:

Part

icul

arly

with

rhy

thm

str

ips,

art

ifact

(in

ref

eren

ce t

o th

e EC

G,

artif

act

refe

rs t

o an

y co

nditi

on i

n w

hich

an

exte

rnal

so

urce

or

prob

lem

cau

ses

a ch

ange

in

the

ECG

rec

ordi

ng

rath

er t

han

an a

ctua

l sig

nal g

ener

ated

by

card

iac

activ

ity) c

an

lead

to

appa

rent

asy

stol

e. T

he m

ost

com

mon

cau

se o

f th

is

prob

lem

is th

at o

ne o

f the

lead

s te

mpo

raril

y lo

ses

skin

con

tact

. In

th

is

case

, ar

tifac

t is

co

nfirm

ed

sinc

e th

e si

nus

rate

is

unch

ange

d be

fore

and

aft

er th

e ap

pare

nt p

ause

(the

R-R

inte

r-va

ls d

enot

ed b

y th

e do

uble

-hea

ded

arro

ws

are

cons

tant

) and

a

smal

l “pa

rtia

l” s

igna

l als

o be

iden

tifie

d. O

bvio

usly

it is

impo

r-ta

nt t

o de

term

ine

whe

ther

the

pat

ient

has

sym

ptom

s du

ring

any

“arr

hyth

mia

” ep

isod

e. A

lthou

gh a

bsen

ce o

f sy

mpt

oms

does

not

“ru

le o

ut”

arrh

ythm

ias,

in

alm

ost

all

dise

ases

the

pr

esen

ce o

f sy

mpt

oms

is a

ssoc

iate

d w

ith a

wor

se p

rogn

osis

.



Sin

us

No

de

dys

fun

ctio

n (

No

t e

no

ug

h P

wav

es)

Sin

us

pa

use

wit

h id

iove

ntr

icu

lar

rhyt

hm

P?

V1

II



Fig

ure

10.

3:In

thi

s ca

se o

f si

nus

node

dys

func

tion

, th

e si

nus

node

st

ops

depo

lari

zing

so

no P

wav

es a

re o

bser

ved

but

the

resu

ltin

g Q

RS is

wid

e an

d ve

ry s

low

bec

ause

the

sub

sidi

ary

AV

nod

e pa

cem

aker

als

o di

d no

t de

pola

rize

nor

mal

ly.

Vent

ricu

lar

pace

mak

ers

such

as

in t

his

case

are

slo

wer

and

no

tori

ousl

y un

relia

ble

(the

y ca

n st

op

sudd

enly

) an

d pa

tien

ts a

re a

t hi

gher

ris

k fo

r de

velo

ping

sig

nifi

cant

sym

p-to

ms.

Com

pare

thi

s to

the

mid

dle

pane

l of

Figu

re 1

0.1.

In

Figu

re 1

0.1,

whe

n a

sinu

s pa

use

occu

rs t

he A

V n

ode

“tak

es o

ver.”

In t

his

case

, a d

efle

ctio

n af

ter

the

QRS

com

-pl

ex d

ue t

o re

trog

rade

dep

olar

izat

ion

of t

he a

tria

can

be

obse

rved

(arr

ows)

. The

AV

nod

e is

a “

two-

way

str

eet”

and

ca

n co

nduc

t bo

th f

orw

ard

and

back

war

d. N

orm

ally

sin

ce

the

sinu

s no

de h

as t

he f

aste

st p

acem

aker

act

ivit

y, o

nly

for-

war

d co

nduc

tion

thr

ough

the

AV

nod

e an

d H

is b

undl

e is

ob

serv

ed.



P?

Sin

us

No

de

dys

fun

ctio

n (

No

t e

no

ug

h P

wav

es)

Sin

us

no

de

exi

t b

lock

V1

II III



Fig

ure

10.

4:Th

ere

are

man

y fo

rms

of s

inus

nod

e dy

sfun

ctio

n. I

n th

is

case

, in

stea

d of

a p

rolo

nged

pau

se,

a si

ngle

P w

ave

is

drop

ped.

Thi

s co

ndit

ion

is s

omet

imes

cal

led

sinu

s no

de

exit

blo

ck b

ecau

se i

t is

tho

ught

to

be d

ue t

o bl

ock

of

depo

lari

zati

on f

rom

the

sin

us n

ode

to s

urro

undi

ng a

tria

l ti

ssue

.



PP

PP

?

V1 II III

Atr

iove

ntr

icu

lar

blo

ck (

Ps

wit

ho

ut

QR

Ss)

We

nck

eb

ach

2°

AV

blo

ck (

Mo

bit

z Ty

pe

I)



Fig

ure

10.

5:Th

ere

are

seve

ral

patt

erns

of

2° A

V b

lock

tha

t ha

ve b

een

iden

tifie

d by

EC

G. I

n al

l for

ms

of 2

° A

V b

lock

som

e bu

t no

t al

l P w

aves

con

duct

to th

e ve

ntric

les

to p

rodu

ce a

QRS

com

-pl

ex.

Orig

inal

ly M

obitz

des

crib

ed t

wo

form

s: T

ype

I an

d Ty

pe I

I. Th

is i

s an

exa

mpl

e of

Typ

e I

AV

blo

ck (

mor

e co

m-

mon

ly c

alle

d W

enck

ebac

h bl

ock)

tha

t is

cha

ract

eriz

ed b

y pr

ogre

ssiv

e pr

olon

gatio

n of

the

PR

inte

rval

(ar

row

s) u

ntil

final

ly t

here

is a

dro

pped

QRS

(?)

due

to

AV

blo

ck o

f at

rial

depo

lariz

atio

n. I

n an

y ca

se o

f A

V b

lock

it

is i

mpo

rtan

t to

m

ake

a cl

inic

al g

uess

at

the

site

of

bloc

k. B

lock

with

in t

he

AV

nod

e w

hile

abn

orm

al c

arrie

s a

bett

er p

rogn

osis

tha

n bl

ock

with

in th

e H

is b

undl

e. A

lmos

t all

case

s of

Mob

itz T

ype

I bl

ock

asso

ciat

ed w

ith a

nar

row

QRS

com

plex

are

due

to

bloc

k in

the

AV

nod

e.



PP

PP

V1 II III

P

Atr

iove

ntr

icu

lar

blo

ck

(Ps

wit

ho

ut

QR

Ss)

We

nck

eb

ach

2°

AV

blo

ck

(wit

h r

igh

t b

un

dle

bra

nch

blo

ck)



Fig

ure

10.

6:Th

is is

ano

ther

exa

mpl

e of

Mob

itz T

ype

I blo

ck id

entif

ied

by

prog

ress

ive

PR i

nter

val

prol

onga

tion

befo

re t

he d

ropp

ed

QRS

com

plex

. In

this

cas

e, t

he Q

RS is

wid

e du

e to

rig

ht b

un-

dle

bran

ch b

lock

(Cha

pter

7, F

igur

e 7.

5). G

ener

ally

any

tim

e

Mob

itz T

ype

I blo

ck is

iden

tifie

d, th

e si

te o

f blo

ck is

in th

e A

V

node

, al

thou

gh in

thi

s ca

se t

he p

rese

nce

of a

ccom

pany

ing

right

bun

dle

bran

ch b

lock

is e

vide

nce

that

som

e H

is P

urki

nje

dise

ase

is p

rese

nt.



PP

PP

PP

?

Atr

iove

ntr

icu

lar

blo

ck

(Ps

wit

ho

ut

QR

Ss)

Mo

bit

z Ty

pe

II 2

° A

V b

lock



Fig

ure

10.

7:In

Mob

itz T

ype

II bl

ock,

the

PR

inte

rval

rem

ains

con

stan

t be

fore

a P

wav

e is

ass

ocia

ted

with

a d

ropp

ed Q

RS c

ompl

ex

(?).

Mob

itz T

ype

II bl

ock

is im

port

ant

to id

entif

y be

caus

e it

is

gene

rally

due

to

bloc

k in

the

His

bun

dle

regi

on a

nd c

arrie

s a

wor

se p

rogn

osis

tha

n bl

ock

in t

he A

V n

ode

(mai

nly

due

to

the

slow

er a

nd m

ore

unre

liabl

e ve

ntric

ular

pac

emak

ers

that

w

ould

hav

e to

dep

olar

ize

the

hear

t if

com

plet

e he

art

bloc

k

wer

e to

de

velo

p).

Alth

ough

m

ost

text

book

s em

phas

ize

eval

uatin

g su

cces

sive

PR

inte

rval

s pr

ior

to t

he P

wav

e w

ith

the

drop

ped

QRS

, it

is o

ften

eas

ier

to s

impl

y ev

alua

te t

he P

R in

terv

al

befo

re

and

afte

r th

e P

wav

e w

ithou

t th

e Q

RS

com

plex

. If

the

PR i

nter

vals

are

diff

eren

t, T

ype

I bl

ock

is

pres

ent,

and

if t

he P

R in

terv

als

are

the

sam

e, t

he p

atie

nt h

as

Type

II b

lock

.



“Atr

iove

ntr

icu

lar

blo

ck”

(Ps

wit

ho

ut

QR

Ss)

Blo

cke

d p

rem

atu

re a

tria

l co

ntr

act

ion

s

PP

PAC

PP

PAC

II



Fig

ure

10.

8:It

is

impo

rtan

t to

rem

embe

r th

at a

bnor

mal

AV

blo

ck c

an

gene

rally

be

iden

tifi

ed o

nly

whe

n th

e P

wav

e ra

te i

s co

nsta

nt.

In

this

ca

se

ther

e ar

e pr

emat

ure

atri

al

cont

ract

ions

(P

AC

) th

at

do

not

resu

lt

in

vent

ricu

lar

cond

ucti

on a

nd a

QRS

com

plex

bec

ause

the

AV

nod

e is

re

frac

tory

. Th

is c

ondi

tion

is

som

etim

es m

isid

enti

fied

as

abno

rmal

AV

blo

ck.

Rem

embe

r fr

om C

hapt

er 3

tha

t A

V

noda

l co

nduc

tion

del

ay i

s im

port

ant

to a

llow

eff

icie

nt

filli

ng o

f th

e ve

ntri

cles

fro

m a

tria

l con

trac

tion

. In

addi

tion

, as

we

will

lear

n in

Cha

pter

11,

by

acti

ng a

s a

“lim

iter

” th

e A

V n

ode

prev

ents

rap

id a

tria

l ac

tivi

ty f

rom

res

ulti

ng i

n ra

pid

vent

ricu

lar

cond

ucti

on.



II

PP

PP

??

Atr

iove

ntr

icu

lar

blo

ck

(P’s

wit

ho

ut

QR

S’s

)

2:1

2°

AV

blo

ck



Fig

ure

10.

9:Th

is is

an

exam

ple

of 2

:1 A

V b

lock

. The

P w

ave

rate

is re

gula

r bu

t ev

ery

othe

r P

wav

e do

es n

ot c

ondu

ct t

o th

e ve

ntric

les

and

lead

s to

an

abse

nt Q

RS c

ompl

ex (?

). W

hen

2:1

AV

blo

ck

is p

rese

nt it

is im

poss

ible

to

clas

sify

the

AV

blo

ck a

s Ty

pe I

or

Type

II

alth

ough

gen

eral

ly t

here

will

be

perio

ds w

here

tw

o

cons

ecut

ive

P w

aves

con

duct

to

the

vent

ricle

and

the

PR

inte

rval

can

be

exam

ined

for a

ny c

hang

es a

nd th

e PR

inte

rval

be

fore

and

aft

er t

he P

wav

e w

ith t

he d

ropp

ed Q

RS c

ompl

ex

can

be e

valu

ated

.



PP

PP

PP

PP

P

??

??

Atr

iove

ntr

icu

lar

blo

ck

(Ps

wit

ho

ut

QR

Ss)

Ad

va

nce

d 2

° A

V b

lock



Fig

ure

10.

10:

In a

dvan

ced

AV

blo

ck, s

ome

cond

uctio

n fr

om t

he a

triu

m t

o th

e ve

ntric

les

occu

rs b

ut s

ever

al c

onse

cutiv

e P

wav

es d

o no

t co

nduc

t to

the

ven

tric

les

(?).

Whi

le t

here

is

som

e A

V

com

mun

icat

ion,

the

pre

senc

e of

con

secu

tive

P w

aves

at

norm

al r

ates

tha

t do

not

con

duct

pro

vide

s st

rong

evi

denc

e th

at A

V c

ondu

ctio

n is

ten

uous

at

best

.



Atr

iove

ntr

icu

lar

blo

ck (

P’s

wit

ho

ut

QR

S’s

)

PP

PP

PP

PP

P

Co

mp

lete

he

art

blo

ck (

3°

AV

blo

ck)



Fig

ure

10.

11:

In c

ompl

ete

hear

t bl

ock,

the

re is

no

AV

con

duct

ion

and

the

patie

nt i

s de

pend

ent

on a

n in

trin

sic

pace

mak

er b

elow

the

si

te o

f bl

ock

for

vent

ricul

ar d

epol

ariz

atio

n. C

ompl

ete

hear

t bl

ock

will

be

asso

ciat

ed w

ith a

reg

ular

slo

w r

ate

beca

use

no

P w

aves

lea

d to

ven

tric

ular

dep

olar

izat

ion

(dou

ble-

head

ed

arro

ws)

. In

con

tras

t, in

alm

ost

all c

ases

of

2° A

V b

lock

, th

e rh

ythm

will

be

irreg

ular

due

to

varia

ble

AV

con

duct

ion.



Atr

iove

ntr

icu

lar

blo

ck (

”Ps”

wit

ho

ut

QR

Ss)

Co

mp

lete

he

art

blo

ck (

3°

AV

blo

ck)

in a

tria

l fib

rilla

tio

n

I II III



Fig

ure

10.

12:

In

atria

l fib

rilla

tion,

th

e at

ria

are

activ

ated

ra

pidl

y an

d ch

aotic

ally

usu

ally

lead

ing

to r

apid

and

irre

gula

r he

art

rate

s (C

hapt

er 1

1, F

igur

e 11

.3).

In t

he s

ettin

g of

com

plet

e he

art

bloc

k, t

he v

entr

icul

ar r

ate

will

be

regu

lar

(dou

ble-

head

ed

arro

ws)

des

pite

the

pre

senc

e of

atr

ial f

ibril

latio

n. In

the

pas

t th

is w

as a

lmos

t al

way

s du

e to

dig

oxin

tox

icity

.



PP

PP

PP

P

II

Atr

iove

ntr

icu

lar

blo

ck

(Ps

wit

ho

ut

QR

Ss)

Se

vere

ad

va

nce

d A

V b

lock

(2

° A

V b

lock

)



Fig

ure

10.

13:

Usin

g th

e st

rict d

efin

ition

of c

ompl

ete

hear

t blo

ck (n

o A

V c

on-

duct

ion)

, th

e Q

RS c

ompl

exes

will

gen

eral

ly b

e re

gula

r. In

thi

s ex

ampl

e, t

he f

ourt

h P

wav

e co

nduc

ts le

adin

g to

one

slig

htly

ea

rly Q

RS c

ompl

ex (

third

QRS

). Th

e fir

st,

seco

nd,

and

four

th

QRS

com

plex

es a

rise

from

the

jun

ctio

n sin

ce t

hey

have

a

r egu

lar s

low

rate

(dou

ble-

head

ed a

rrow

s). A

lthou

gh th

is is

not

a ca

se o

f co

mpl

ete

hear

t bl

ock,

clin

ical

ly t

his

cond

ition

wou

ld

be t

reat

ed in

exa

ctly

the

sam

e w

ay a

s co

mpl

ete

hear

t bl

ock.



PP

PP

PP

PII

RB

LBR

B

V1

V5

Atr

iove

ntr

icu

lar

blo

ck (

Ps

wit

ho

ut

QR

Ss)

Ad

va

nce

d 2

° A

V b

lock

(w

ith

bu

nd

le b

ran

ch b

lock

)



Fig

ure

10.

14:

In t

he s

ettin

g of

AV

blo

ck,

it is

im

port

ant

to e

valu

ate

the

QRS

com

plex

es-b

oth

from

low

er s

ubsi

diar

y pa

cem

aker

s an

d fo

r co

nduc

ted

beat

s. T

his

info

rmat

ion

is c

ritic

al f

or e

valu

at-

ing

shor

t-te

rm a

nd l

ong-

term

pro

gnos

is.

In t

his

case

of

adva

nced

2°

AV

blo

ck (c

onse

cutiv

e no

ncon

duct

ed P

wav

es),

whe

n at

riove

ntric

ular

co

nduc

tion

does

oc

cur

som

etim

es

only

the

rig

ht b

undl

e (R

B) c

ondu

cts

prod

ucin

g a

QRS

with

a

left

bun

dle

bran

ch b

lock

mor

phol

ogy

(wid

e ne

gativ

e Q

S co

mpl

ex)

and

at o

ther

tim

es o

nly

the

left

bun

dle

(LB)

con

-du

cts

prod

ucin

g a

QRS

with

a r

ight

bun

dle

bran

ch b

lock

m

orph

olog

y. T

his

cond

ition

is p

artic

ular

ly w

orris

ome

and

the

clin

icia

n sh

ould

be

very

con

cern

ed a

bout

the

dev

elop

men

t of

P w

aves

with

out

QRS

com

plex

es (

no h

eart

rat

e =

a b

ad

thin

g).


272


Okay, take a very deep breath as this chapter is by far and away the most difficult to get through (hopefully you are not already grumbling “Oh dear, the first ten were awfully tough”). At first glance, the material appears very dense with a lot of information. Sadly you might be right about the quantity of material, but it is hoped this chapter will provide an outline to make the material easier to organize. However, the ECG is the fundamental diagnostic tool for evaluating rapid heart rates. In fact, if at all possible (sometimes the clinician is limited because of hemodynamic collapse), any patient who is thought to have an abnormal rapid heart rate should receive a 12 lead ECG as soon as possible. Once mastered, the ability to quickly evaluate an ECG is an essential skill necessary for taking care of critically ill patients.

From an anatomic standpoint, rapid heart rates can be due to abnor-mally rapid activity from three sites: the atria, AV junction, or the ventricles. The fourth cause of tachycardia uses an abnormal muscular connection between the atria and ventricles (accessory pathway) that is used as the essential component in the tachycardia (Figure 11.1).

Although this anatomic classification is extremely helpful for remem-bering the different types of tachycardia and will be used for the remain-der of the chapter, clinically the ECG is used to make a distinction between narrow complex tachycardias and wide complex tachycardias. In narrow complex tachycardia, the QRS has a normal appearance with an rS complex in V1 and a width < 0.12 s. The normal QRS complex means that the ventricles are being activated normally using the His Purkinje tissue and generally rules out a tachycardia arising solely from ventricular tissue (ventricular tachycardia). In wide complex tachycardias, the focus will be on deciding whether the patient has ventricular

CHAPTER 11

Arrhythmias: Tachycardia


Arrhythmias: Tachycardia 273

Wide QRS

Tachycardias

Figure 11.1:Anatomic types of tachycardia. The ventricular tachycardias and the accessory pathway mediated tachycardias in which the ventri-cles are activated by the accessory pathway always are associated with a wide complex tachycardia (Wide QRS tachycardia). The other tachycardias are usually associated with a narrow QRS

tachycardia and are grouped together as supraventricular tachy-cardias. Any supraventricular tachycardia can be associated with aberrant conduction and produce a wide complex tachy-cardia. (Adapted with permission from FM Kusumoto, Cardio-vascular Pathophysiology, Hayes Barton Press, Raleigh, NC, 2004.)



tachycardia or one of the supraventricular tachycardias with abnormal or aberrant conduction. Ventricular tachycardia is generally more likely to be life-threatening, while the supraventricular tachycardia, although it may be associated with significant symptoms, is generally better tolerated. The presence of a narrow QRS on the ECG is a first form of “triage,” and essentially rules out ventricular tachycardia.

Narrow QRS tachycardias are generally grouped together and called supraventricular tachycardias, to emphasize that ventricular tachycardia is not present. If we return to our anatomic classification scheme, supraven-tricular tachycardia can have three anatomic causes: atrial tachycardias, junctional tachycardias, or accessory pathway mediated tachycardias. In atrial tachycardia, the cause of tachycardia is solely within atrial tissue. This could be a site or sites within the atria that are depolarizing (or “firing”) abnormally fast or a reentrant circuit within the atria.

We now have to take a slight “detour” and talk about the difference between automaticity and reentry (Figure 11.2). Automaticity is very easy to understand conceptually as a single or several rapidly blinking lights that cause rapid atrial activity. On the other hand, reentry is not very intuitive and can be one of the most confusing subjects for students learning about arrhythmias. However, a cursory understanding of reentry is necessary for analyzing the ECG. In reentry a “substrate” consisting of two parallel pathways with connected ends and different electrical properties is present. Generally, a wave of activation travels through both sides of the pathway equally. But a premature stimulation can lead to conduction down only one pathway, due to block in the other pathway. In some cases, the impulse can turn around and travel backwards up the parallel pathway, setting up a continual loop of depolarization. The analogy that is often used is a dog chasing its tail. The electrical activity continues to circle on the two pathways until one of the arms blocks suddenly and the tachycardia stops. Tachycardias due to reentry tend to start suddenly and stop abruptly. Although it might not first seem obvious, parallel electrical pathways are quite common in the diseased heart due to the development of scar tissue and natural barriers, e.g. the entrance of the vena cavae into the right atrium (see the discussion on atrial flutter which follows).

So now back to our discussion of atrial tachcardias. An atrial tachycardia due to a single rapidly depolarizing site is formally called a focal atrial tachycardia, although to add to the confusion these arrhythmias are often just called atrial tachycardias. If three or more sites are depolarizing



Automaticity

*

*

Premature beat

blocks in one

“pathway”

Depolarization

reenters the

“pathway” to start

a reentrant loop

Reentry

Figure 11.2:The two cellular/tissue causes of tachycardia are automaticity and reentry. In automaticity a site or sites within the heart begins to depolarize abnormally fast. In this example an automatic site is located within the atria. In reentry, a “substrate” of two parallel “pathways” is present. The path-ways can be anywhere and are separated by fibrosis or a nor-mal anatomic structure (e.g. the

inferior vena cava). In this example the two “pathways” are shown in the right atrium. A premature beat blocks in one “pathway” and conducts in only one “pathway.” The wave of depolarization turns around by depolarizing the other “pathway” and a reentrant circuit develops. Reentry requires both “substrate”-two pathways with different electrical properties and a “trigger” to initiate the reentry.

abnormally, the arrhythmia is called a multifocal atrial tachycardia. An atrial tachycardia due to reentry within atrial tissue is called atrial flutter (Figure 11.1).

Tachycardias that arise from junctional tissue are usually due to small reentrant circuits that are confined to the AV node and adjacent atrial



tissue (AV node reentrant tachycardia or AVNRT). In rare cases (usually children), an unusual arrhythmia called junctional ectopic tachycardia (JET) due to an automatic focus from junctional tissue can be observed (Figure 11.1).

The final distinct anatomic cause of supraventricular tachycardia uses an accessory pathway. Usually the AV node is the only electrical connec-tion between the atria and the ventricles, but in some cases a strand of tissue that forms an additional electrical connection between the atria and ventricles called an accessory pathway is present (Chapter 7, Figures 7.9 and 7.10 and Chapter 8, Figure 8.3). The coexistence of the AV node and an accessory pathway are the perfect conditions for the develop-ment of reentry. Under normal conditions, atrial depolarization travels down both the accessory pathway and the AV node to depolarize the ventricles. A premature atrial contraction can sometimes block in the accessory pathway and conduct solely down the AV node to activate the ventricles. Ventricular depolarization may activate the ventricular end of the accessory pathway and the depolarization can travel “backwards” up the accessory pathway to depolarize the atria and initiate a reentrant circuit (the dog chasing its tail). This type of tachycardia is called atrioven-tricular reentrant tachycardia or AVRT and leads to a rapid supraventricu-lar tachycardia since the ventricles are being depolarized normally via the AV node and His Purkinje system.

Although there are obvious complexities and subtleties, in general, when evaluating a supraventricular tachycardia there are two considera-tions: determining whether the rhythm is regular or irregular and identi-fying atrial activity.

Irregular supraventricular tachycardias are generally due to tachycar-dias from rapid atrial activity (atrial tachycardias) (Table 11.1). Rapid atrial activity can have several forms. The most common cause of an irregular supraventricular tachycardia is atrial fibribrillation where irregular, con-tinuous, and chaotic atrial activity called fibrillatory waves is observed. In atrial fibrillation, the pulse and ventricular rhythm is extremely irregular because of irregular activation of the ventricles via the AV node. Several other forms of rapid atrial activity can also cause irregular rhythms. In multifocal atrial tachycardia, several different sites within the atria alter-natively activate the atria. Think of rapidly blinking lights from different sites and rates within the atria. Both atrial fibrillation and multifocal atrial tachycardia cause irregular rapid heart rhythms, and the distinction between the two is made by the ECG. In multifocal atrial tachycardia, the



atria are depolarized as a single wave, albeit at abnormal rates and from different sites, so discrete P waves of different shapes are observed. In atrial fibrillation, the atria are not depolarized as single waves of activity and rather by continuous ever-changing smaller waves of activity. One way to think about the differences between multifocal atrial tachycardia and atrial fibrillation is the motion of water at the beach or in a rapidly flowing river. At the beach, waves break at irregular intervals but between the waves there is no activity. In contrast, in a rapidly flowing river, multi-ple different waves are continuously slowing in an ever-changing pattern with no quiescent period.

Usually focal atrial tachycardias and atrial flutters lead to regular rapid rhythms but in some cases regular rapid atrial activity can lead to some irregularity of the QRS complexes due to variable conduction. However, even in this case there will be periods of regular tachycardia, and when an irregular tachycardia develops fixed intervals will still be observed since the atria are being depolarized regularly. This pattern is often called “reg-ularly irregular” to differentiate it from atrial fibrillation and multifocal atrial tachycardia which are associated with very irregular QRS rhythms because the atria are being activated irregularly (often referred to as “irregularly irregular”). In some cases of atrial fibrillation, large areas of tissue are activated relatively regularly, leading to the appearance of larger “flutter” waves, particularly in lead V1, and this is sometimes called “coarse” atrial fibrillation. The distinction between atrial flutter and atrial fibrillation is usually made by the QRS rhythm; if the QRS rhythm is irreg-ularly irregular, it is classified as atrial fibrillation, and if there is some pattern of regularity, it is called atrial flutter or atrial tachycardia.

Table 11.1: Causes of supraventricular tachycardia

ECG Rhythm PossibilitiesIrregular Atrial tachycardias

• Atrial fibrillation• Multifocal atrial tachycardia• Atrial flutter/focal atrial tachycardia with variable AV

conductionRegular Atrial flutter/focal atrial tachycardia

Junctional tachycardia Accessory Pathway-mediated (AVRT,ORT)



A regular supraventricular tachycardia can be caused by a regular atrial tachycardia or atrial flutter, a rhythm arising from the AV junction, and finally in one of the tachycardias that use an accessory pathway. Atrial tachycardia and atrial flutter have already been described and if AV con-duction is constant, a regular tachycardia is observed. In most cases every other depolarization of atrium conducts to the ventricle (2:1 conduction). For example, the most common form of atrial flutter depolarizes the atrium at a regular rate of 300 beats per minute, if every other depolari-zation is conducted to the ventricles, the resulting ventricular rate will be 150 beats per minute. Fast but probably a lot more stable than a heart rate of 300 bpm! Careful inspection of the ECG is required to identify the P waves.

Tachycardias arising from the AV junction area are usually due to a small reentrant circuit due to small parallel inputs into or within the AV node. Since the junction is driving the heart, the ventricles are activated via the His Purkinje system and the atria are activated “backwards” from the AV node region. Since the atria and ventricles are activated simultaneously the P wave is sometimes obscured by the QRS complex or seen at the end of the QRS complex.

As discussed previously in this chapter, patients with an accessory pathway can develop supraventricular tachycardia. In contrast to tachy-cardias arising from the junction the ventricles and atria are activated sequentially one after the other. For this reason, the P waves are typically observed after the QRS complex within the ST segment. As will be emphasized in the figures, identification of the P waves can provide important clues for determining what type of tachycardia is present.

One last confusing point about supraventricular tachycardias is the “alphabet soup” of abbreviations used to describe them:

SVT: Supraventricular tachycardia – a generic term used to describe any fast heart rhythm with a normal QRS complex.

PSVT: Paroxysmal supraventricular tachycardia – an SVT that occurs sporadically and starts suddenly and stops suddenly.

AVNRT: AV node reentrant tachycardia – a reentrant tachycardia with all of the components for the reentrant circuit within the AV node and /or adjacent tissue.

AVRT: Atrioventricular reentrant tachycardia – a reentrant tachycardia that uses an accessory pathway and the AV node as two “limbs” of a reentrant circuit.



ORT: Orthodromic reciprocating tachycardia – the specific form of AVRT in which the AV node activates the ventricles and the accessory pathway activates the atria. The term “ortho” comes from the Greek word “normal or standard” and “dromic” for direction to describe the normal direction of AV conduction in this type of tachycardia that results in a narrow complex tachycardia.

A wide QRS tachycardia is also called wide complex tachycardia. In this case, the ventricles are not being activated normally by the His Purkinje system. Any of the supraventricular tachycardias can cause a wide QRS tachycardia if there is abnormal or aberrant conduction in the His Purkinje system, often collectively referred to as “SVT with aberrancy.” But wide QRS tachycardia can also be caused by rapid ventricular activation due to automaticity or a reentrant circuit within ventricular tissue. Any tachycardia that is due solely to abnormal activation of ventricular tissue is called ventricular tachycardia. Although both SVT with aberrancy and ventricular tachycardia can be associated with significant symptoms, rapid identification of ventricular tachycardia is critical since ventricular tachycardia is often unstable and can lead to sudden death. For this reason, the ECG is very useful for first identifying whether a tachycardia is wide complex or narrow complex (SVT) and second, for differentiating between ventricular tachycardia and SVT with aberrancy. The ECG clues for identifying ventricular tachycardia are provided in Figures 11.17 through 11.24.



I II

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Irre

gu

lar

QR

S r

hyt

hm

Rat

e d

ep

en

ds

on

AV

no

de

co

nd

uct

ion

An

y le

ad

III

Irreg

ular

bas

elin

e w

ith n

o di

scre

teis

oele

ctric

per

iods

V1

Irre

gu

lar

Na

rro

w Q

RS

ta

chyc

ard

ia

Atr

ial fi

bri

llati

on



Fig

ure

11.

3:

Bac

kgro

un

d:

Atr

ial

fibril

latio

n is

th

e m

ost

com

mon

ar

rhyt

hmia

in m

edic

ine.

In a

tria

l fib

rilla

tion

ther

e ar

e se

vera

l si

mul

tane

ous

wav

es o

f atr

ial d

epol

ariz

atio

n th

at c

hang

e an

d de

pola

rize

the

atria

in a

ran

dom

fas

hion

.

ECG

: Th

e EC

G

in

atria

l fib

rilla

tion

show

s ch

aotic

at

rial

activ

ity w

ith n

o “q

uies

cent

” pe

riod

at b

asel

ine

beca

use

of

cont

inuo

us

depo

lariz

atio

n of

th

e at

ria.

The

vent

ricle

s de

pola

rize

irreg

ular

ly d

ue t

o irr

egul

ar a

ctiv

atio

n of

the

AV

no

de a

nd H

is P

urki

nje

syst

em.

The

vent

ricul

ar r

ate

in a

tria

l fib

rilla

tion

depe

nds

on A

V n

ode

func

tion.

If t

he A

V n

ode

is

dise

ased

or

abno

rmal

due

to

drug

, th

e ve

ntric

ular

rat

e in

at

rial

fibril

latio

n w

ill b

e no

rmal

or

even

slo

w (

Cha

pter

9,

Figu

re 9

.13

and

Cha

pter

10,

Fig

ure

10.1

2).

Clin

ical

Iss

ues

: A

tria

l fib

rilla

tion

can

lead

to

sign

ifica

nt

tired

ness

an

d fa

tigue

du

e to

th

e ra

pid

vent

ricul

ar

rate

an

d lo

ss

of

atria

l co

ntrib

utio

n to

ve

ntric

ular

fil

ling.

H

owev

er,

in

som

e ca

ses

patie

nts

are

only

m

inim

ally

sy

mpt

omat

ic

and

in

som

e ca

ses

com

plet

ely

asym

pto-

mat

ic.

The

seve

rity

of s

ympt

oms

is m

ost

depe

nden

t on

th

e ve

ntric

ular

ra

te;

the

mor

e ra

pid

the

vent

ricul

ar

rate

th

e m

ore

likel

y th

e pa

tient

w

ill

have

sy

mpt

oms.

Th

e m

ain

clin

ical

is

sue

with

at

rial

fibril

latio

n is

in

crea

sed

risk

of

stro

ke.

Sinc

e th

e at

ria

are

not

con-

trac

ting

norm

ally,

blo

od p

oolin

g on

the

lef

t at

rium

can

fa

cilit

ate

deve

lopm

ent

of

bloo

d cl

ots.

If

the

bloo

d cl

ot

trav

els

(em

boliz

es)

to t

he b

rain

, bl

ood

supp

ly t

o a

part

of

the

bra

in is

lost

, and

a s

trok

e de

velo

ps.



**

AF

Irre

gu

lar

Na

rro

w Q

RS

ta

chyc

ard

ia

Atr

ial fi

bri

llati

on

(in

itia

tio

n)



Fig

ure

11.

4:In

itiat

ion

of a

tria

l fib

rilla

tion.

In

this

cas

e pr

emat

ure

atria

l co

ntra

ctio

ns (*

) are

eith

er is

olat

ed o

r ini

tiate

atr

ial f

ibril

latio

n.

Prem

atur

e at

rial c

ontr

actio

ns c

an b

e id

entif

ied

by id

entif

ying

“une

xpec

ted”

def

lect

ions

tha

t ar

e pr

esen

t in

som

e bu

t no

t al

l T w

aves

(circ

les)

.



Irre

gu

lar

Na

rro

w Q

RS

ta

chyc

ard

ia

Mu

ltif

oca

l atr

ial t

ach

yca

rdia Irre

gu

lar

P w

ave

rh

yth

m

lea

ds

to a

n ir

reg

ula

r Q

RS

rh

yhm

An

y

lea

d

Dis

cret

e at

rial a

ctiv

ityw

ith ≥

3 P

wav

e sh

apes

Iso

ele

ctri

c b

ase

line



Fig

ure

11.

5:

Bac

kgro

un

d:

Mul

tifoc

al

atria

l ta

chyc

ardi

a is

us

ually

ob

serv

ed in

crit

ical

ly il

l pat

ient

s in

the

set

ting

of d

ecre

ased

ox

ygen

due

to

pneu

mon

ia o

r ot

her

pulm

onar

y pr

oces

s or

se

vere

ele

ctro

lyte

dis

orde

rs. I

t is

mos

t com

mon

ly o

bser

ved

in

thos

e pa

tient

s w

ith c

hron

ic o

bstr

uctiv

e lu

ng d

isea

se.

ECG

: In

mul

tifoc

al a

tria

l ta

chyc

ardi

a th

ree

or m

ore

uniq

ue

site

s ar

e de

pola

rizin

g th

e at

rium

at d

iffer

ent r

ates

. Thi

s le

ads

to

irreg

ular

P

wav

es

of

diff

eren

t sh

apes

se

para

ted

by

isoe

lect

ric p

erio

ds.

Sinc

e at

rial

depo

lariz

atio

n is

irr

egul

ar,

vent

ricul

ar d

epol

ariz

atio

n is

als

o irr

egul

ar.

Clin

ical

Issu

es:

In a

nd o

f its

elf,

mul

tifoc

al a

tria

l tac

hyca

rdia

do

es

not

requ

ire

spec

ific

trea

tmen

t bu

t th

e un

derly

ing

caus

e, h

ypox

ia,

acid

osis

or

othe

r el

ectr

olyt

e di

sord

er m

ust

be d

eter

min

ed a

nd a

ppro

pria

tely

tre

ated

. M

ultif

ocal

atr

ial

tach

ycar

dia

may

pro

gres

s to

atr

ial f

ibril

latio

n (w

here

org

an-

ized

atr

ial d

epol

ariz

atio

n is

lost

).



I II

II

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Ne

ga

tive

flu

tte

r w

ave

s

QR

S r

ate

/rh

yth

m d

ep

en

ds

on

AV

no

de

co

nd

uct

ion

(oft

en

2:1

an

d a

he

art

ra

te 1

50

bp

m)

3:1

2:1

II, II

I, a

VF

III

Re

gu

lar

Na

rro

w Q

RS

ta

chyc

ard

ia (

or

irre

gu

lar)

Atr

ial fl

utt

er



Fig

ure

11.

6:

Bac

kgro

un

d:

In a

tria

l flu

tter

a s

tabl

e re

entr

ant

circ

uit

lead

s to

rap

id a

tria

l act

ivity

.

ECG

: Th

e at

rial

activ

ity i

s ra

pid

and

regu

lar.

In t

he m

ost

com

mon

for

m o

f at

rial

flutt

er,

the

reen

tran

t ci

rcui

t ci

rcle

s ar

ound

the

tric

uspi

d va

lve.

Fro

m o

ur p

rior

disc

ussi

on o

n re

entr

y th

e tr

icus

pid

valv

e fo

rms

an a

nato

mic

bar

rier

that

se

para

tes

two

“pat

hway

s.”

One

“pa

thw

ay”

is f

orm

ed f

rom

th

e na

rrow

str

ip o

f tis

sue

that

sep

arat

es t

he i

nfer

ior

vena

ca

va f

rom

the

tric

uspi

d va

lve

and

the

othe

r “p

athw

ay”

is

sim

ply

the

rem

aini

ng

atria

l tis

sue.

A

pr

emat

ure

atria

l co

ntra

ctio

n le

ads

to i

nitia

tion

of a

sta

ble

reen

tran

t ci

rcui

t.

Typi

cally

, dep

olar

izat

ion

of th

e in

tera

tria

l sep

tum

and

the

left

at

rium

tra

vels

fro

m “

low

to

high

” an

d de

eply

neg

ativ

e flu

tter

wav

esar

e ob

serv

ed i

n th

e in

ferio

r le

ads.

Lik

e at

rial

fibril

latio

n,

in

atria

l flu

tter

th

ere

is

cont

inuo

us

atria

l de

pola

rizat

ion,

at a

ny p

oint

in ti

me

som

e po

rtio

n of

the

atria

ar

e be

ing

depo

lariz

ed.

For

this

rea

son,

in

case

s of

typ

ical

at

rial f

lutt

er,

the

flatt

er p

erio

d be

twee

n th

e ne

gativ

e flu

tter

w

aves

act

ually

sho

ws

a sl

ight

neg

ativ

e sl

ope.

Unl

ike

atria

l fib

rilla

tion,

in a

tria

l flu

tter

dep

olar

izat

ion

of t

he a

tria

occ

urs

via

a st

able

ree

ntra

nt c

ircui

t le

adin

g th

at p

rodu

ces

regu

lar

flutt

er w

aves

. The

ven

tric

ular

rate

may

be

regu

lar o

r irr

egul

ar

depe

ndin

g on

whe

ther

the

re i

s co

nsis

tent

con

duct

ion

via

the

AV

nod

e.

Clin

ical

Iss

ues

: In

atr

ial f

lutt

er,

like

atria

l fib

rilla

tion,

tre

at-

men

t gen

eral

ly fo

cuse

s on

slo

win

g A

V c

ondu

ctio

n to

rest

ore

a m

ore

norm

al v

entr

icul

ar t

=ra

te a

nd p

rote

ctin

g ag

ains

t st

roke

with

med

icat

ions

.



Irre

gu

lar

Na

rro

w Q

RS

ta

chyc

ard

ia

Atr

ial fi

bri

llati

on

(”c

oa

rse”

)



Fig

ure

11.

7:In

som

e ca

ses

atria

l fib

rilla

tion

will

hav

e pe

riods

of

rela

tivel

y re

gula

r ac

tivity

with

rel

ativ

ely

regu

lar

wav

es t

hat

appe

ar t

o be

atr

ial f

lutt

er.

In f

act

it is

not

unc

omm

on f

or a

pat

ient

to

tran

sitio

n be

twee

n pe

riods

of

atria

l flu

tter

and

per

iods

of

atria

l fib

rilla

tion.

M

ore

com

mon

ly,

atria

l fib

rilla

tion

will

be

com

e m

ore

orga

nize

d fo

r a

perio

d so

tha

t th

e at

ria a

re

bein

g ac

tivat

ed i

n a

rela

tivel

y co

nsta

nt r

epet

itive

man

ner.

Gen

eral

ly t

he d

istin

ctio

n be

twee

n at

rial f

ibill

atio

n an

d at

rial

flutt

er i

s m

ade

indi

rect

ly b

y ev

alua

ting

the

QRS

rhy

thm

. In

atria

l flu

tter

, alth

ough

the

rhy

thm

may

be

irreg

ular

the

re a

re

rela

tivel

y fe

w c

onst

ant

inte

rval

s of

ven

tric

ular

act

ivat

ion

sinc

e ve

ntric

ular

irre

gula

rity

is d

epen

dent

onl

y on

cha

ngin

g at

riove

ntric

ular

con

duct

ion.

In

cont

rast

in

atria

l fib

rilla

tion

the

irreg

ular

ven

tric

ular

rhyt

hm is

due

to b

oth

irreg

ular

atr

ial

depo

lariz

atio

n an

d va

ryin

g at

riove

ntric

ular

con

duct

ion.

Thi

s ex

ampl

e w

ould

be

cl

assi

fied

as

atria

l fib

rilla

tion

sinc

e al

thou

gh t

here

are

a f

ew r

elat

ivel

y fix

ed Q

RS i

nter

vals

, in

ge

nera

l the

ven

tric

ular

rhy

thm

is v

ery

irreg

ular

.



Re

gu

lar

Na

rro

w Q

RS

ta

chyc

ard

ia

Foca

l atr

ial t

ach

yca

rdia

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

I II

II

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

III

II

Tach

yca

rdia

Ba

selin

e

Rapi

d an

d re

gula

r P w

aves

that

are

not a

risin

g fro

m th

e si

nus n

ode

An

y le

ad



Fig

ure

11.

8:

Bac

kgro

un

d:

Foca

l atr

ial t

achy

card

ias

are

rela

tivel

y ra

re b

ut

prob

ably

acc

ount

for

app

roxi

mat

ely

10%

of

regu

lar

rapi

d rh

ythm

s en

coun

tere

d in

clin

ical

med

icin

e.

ECG

: U

sual

ly fo

cal a

tria

l tac

hyca

rdia

s ar

e no

nsus

tain

ed b

ut in

so

me

case

s su

stai

ned

foca

l at

rial

tach

ycar

dia

is o

bser

ved.

Fo

cal

atria

l ta

chyc

ardi

as a

re g

ener

ally

ide

ntifi

ed b

y a

high

er

than

exp

ecte

d ra

te a

nd a

P w

ave

shap

e th

at s

ugge

sts

that

the

sinu

s no

de is

not

gen

erat

ing

atria

l dep

olar

izat

ion.

In th

is E

CG

, th

e pa

tient

’s he

art r

ate

is a

ppro

xim

atel

y 12

0 be

ats

per m

inut

e de

spite

res

ting

flat

on a

tab

le.

The

P w

aves

are

inve

rted

in I

and

aVL

due

to a

n ab

norm

al a

tria

l foc

us in

the

left

atr

ium

. La

ter

whe

n an

EC

G i

s re

cord

ed i

n no

rmal

sin

us r

hyth

m,

a sl

ower

hea

rt r

ate

with

a P

wav

e w

ith t

he e

xpec

ted

shap

e is

ob

serv

ed.

Com

parin

g P

wav

e m

orph

olog

ies

(circ

les)

dur

ing

tach

ycar

dia

and

durin

g si

nus

rhyt

hm is

ext

rem

ely

help

ful.

Clin

ical

Iss

ues

: G

ener

ally

atr

ial

tach

ycar

dias

are

non

sus-

tain

ed a

nd o

ften

no

spec

ific

trea

tmen

t is

req

uire

d. In

som

e ca

ses

of in

cess

ant

arrh

ythm

ias,

med

icat

ions

to

supp

ress

the

ar

rhyt

hmia

or

an a

blat

ion

proc

edur

e to

elim

inat

e th

e ta

chy-

card

ia s

ite a

re r

ecom

men

ded.



Re

gu

lar

Na

rro

w Q

RS

ta

chyc

ard

ia

Foca

l atr

ial t

ach

yca

rdia

PP

PP

?

V1



Fig

ure

11.

9:In

thi

s ex

ampl

e of

uns

usta

ined

foc

al a

tria

l ta

chyc

ardi

a, t

he

tach

ycar

dia

term

inat

es

and

allo

ws

com

paris

on

betw

een

atria

l tac

hyca

rdia

and

sin

us r

hyth

m in

the

sam

e st

rip.

If th

e ra

te o

f th

e fo

cal a

tria

l tac

hyca

rdia

is f

ast

enou

gh,

not

ever

y at

rial d

epol

ariz

atio

n w

ill c

ondu

ct to

the

vent

ricle

s to

pro

duce

a

QRS

com

plex

. Rem

embe

r th

is r

epre

sent

s no

rmal

AV

nod

e fu

nctio

n an

d do

es n

ot i

mpl

y A

V n

odal

dis

ease

. Bl

ocke

d

P w

aves

can

be

iden

tifie

d by

com

parin

g th

e Q

RS c

ompl

ex

and

T w

aves

dur

ing

tach

ycar

dia

with

the

QRS

and

T w

ave

durin

g si

nus

rhyt

hm. I

n th

is c

ase

a de

flect

ion

in t

he t

erm

inal

po

rtio

n of

the

QRS

dur

ing

tach

ycar

dia

is n

ot o

bser

ved

durin

g si

nus

rhyt

hm

(?)

and

mus

t ha

ve

repr

esen

ted

atria

l de

pola

rizat

ion

that

did

not

con

duct

to

the

vent

ricle

s.



Re

gu

lar

Na

rro

w Q

RS

ta

chyc

ard

ia

AV

no

de

re

en

tra

nt

tach

yca

rdia

(A

VN

RT

)

V1Te

rmin

al r

’ du

e t

o r

etr

og

rad

e P

wav

e

?

r’

?

r’r’

r’

**

**

**

**

*



Fig

ure

11.

10:

Bac

kgro

un

d:

AV

nod

e re

entr

ant

tach

ycar

dia

(oft

en c

alle

d A

VN

RT)

is t

he m

ost

com

mon

cau

se o

f ra

pid

regu

lar

hear

t ra

tes

in y

oung

adu

lts.

It is

mor

e co

mm

on i

n w

omen

tha

n m

en.

ECG

: In

AV

nod

e re

entr

ant

tach

ycar

dia,

a r

eent

rant

circ

uit

with

in t

he A

V n

ode

and

adja

cent

tis

sue

lead

s to

a r

apid

na

rrow

com

plex

tac

hyca

rdia

. The

rap

id a

ctiv

ity f

rom

the

AV

no

de le

ads

to r

etro

grad

e ac

tivat

ion

of t

he a

tria

and

alm

ost

sim

ulta

neou

s ac

tivat

ion

of t

he v

entr

icle

s. T

he P

wav

e is

of

ten

obsc

ured

but

may

be

seen

as

a sm

all r

’ w

ave

in le

ad

V1.

It is

ext

rem

ely

usef

ul t

o co

mpa

re t

he E

CG

in t

achy

card

ia

to t

he E

CG

in

sinu

s rh

ythm

. In

thi

s ex

ampl

e th

e to

p fo

ur

row

s sh

ow t

he E

CG

dur

ing

tach

ycar

dia

and

the

bott

om

four

row

s sh

ow t

he E

CG

dur

ing

sinu

s rh

ythm

aft

er t

he

tach

ycar

dia

has

reso

lved

. Th

e re

trog

rade

P w

ave

(*)

can

be

seen

slig

htly

aft

er t

he Q

RS c

ompl

ex.

Clin

ical

Issu

es:

AV

NRT

is n

ot a

ssoc

iate

d w

ith li

fe t

hrea

ten-

ing

prob

lem

s, b

ut if

the

epis

odes

of t

achy

card

ia a

re fr

eque

nt

enou

gh c

an l

ead

to s

igni

fican

t re

duct

ion

in q

ualit

y of

life

. Em

erge

ntly,

AV

NRT

is

trea

ted

with

int

rave

nous

ade

nosi

ne

that

will

oft

en t

erm

inat

e th

e re

entr

ant

loop

by

caus

ing

tran

-si

ent

bloc

k w

ithin

the

AV

nod

e.



PP

PP

PP

I II

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

III

V5

Re

gu

lar

Na

rro

w Q

RS

ta

chyc

ard

ia

Au

tom

ati

c ju

nct

ion

al t

ach

yca

rdia



Fig

ure

11.

11:

Bac

kgro

un

d:

The

spon

tane

ous

depo

lariz

atio

n ra

te o

f th

e A

V n

ode

is 3

5–50

bpm

. A

muc

h ra

rer

caus

e of

tac

hyca

rdia

fr

om t

he A

V n

odal

reg

ion

is in

crea

sed

auto

mat

icity

.

ECG

: In

crea

sed

auto

mat

icity

fro

m t

he A

V n

ode

resu

lts in

a

narr

ow

com

plex

ta

chyc

ardi

a th

at

is

not

prec

eded

by

P

wav

es.

By E

CG

it

is i

mpo

ssib

le t

o di

ffer

entia

te b

etw

een

incr

ease

d au

tom

atic

ity

and

reen

try

from

th

e A

V

node

. H

owev

er,

auto

mat

ic

junc

tiona

l ta

chyc

ardi

a is

m

ore

com

mon

ly a

ssoc

iate

d w

ith r

etro

grad

e at

rial

bloc

k. W

hen

retr

ogra

de b

lock

is

pres

ent

ther

e ar

e fe

wer

P w

aves

tha

n

QRS

co

mpl

exes

. In

th

is

exam

ple

P w

aves

ca

n be

se

en

betw

een

som

e bu

t no

t al

l the

QRS

com

plex

es.

Clin

ical

Issu

es:

Incr

ease

d au

tom

atic

ity o

f th

e A

V n

ode

can

be s

een

in t

wo

very

diff

eren

t co

nditi

ons.

In n

ewbo

rns

rapi

d au

tom

atic

ity f

rom

the

AV

nod

e ca

n be

obs

erve

d. It

is o

ften

tr

ansi

ent,

but

in

som

e ca

ses,

par

ticul

arly

if

it is

ass

ocia

ted

with

oth

er h

eart

abn

orm

aliti

es,

it w

ill c

ontin

ue a

nd r

equi

re

drug

tr

eatm

ent.

In

ad

ults

th

at

have

un

derg

one

card

iac

surg

ery,

tr

ansi

ent

auto

mat

icity

fr

om

the

AV

no

de

may

de

velo

p bu

t ra

rely

req

uire

s tr

eatm

ent.



Re

gu

lar

Na

rro

w Q

RS

ta

chyc

ard

ia

Atr

iove

ntr

icu

lar

ree

ntr

an

t ta

chyc

ard

ia (

AV

RT

)

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

An

y le

ad

Re

tro

gra

de

P w

ave

in t

he

ST

se

gm

en

t

*

* **



Fig

ure

11.

12:

Bac

kgro

un

d:

Atr

iove

ntric

ular

ree

ntra

nt t

achy

card

ia (A

VRT

) du

e to

an

acce

ssor

y pa

thw

ay i

s th

e se

cond

mos

t co

mm

on

caus

e of

epi

sode

s of

rap

id r

egul

ar h

eart

rat

es i

n yo

ung

adul

ts (a

fter

AV

NRT

).

ECG

: A

n ac

cess

ory

path

way

ca

n be

in

volv

ed

in

seve

ral

diff

eren

t ta

chyc

ardi

as.

In

the

mos

t co

mm

on

form

, a

reen

tran

t circ

uit d

evel

ops

whe

re th

e A

V n

ode

and

His

bun

dle

depo

lariz

e th

e ve

ntric

les

and

the

atria

are

dep

olar

ized

by

the

acce

ssor

y pa

thw

ay.

This

le

ads

to

a na

rrow

co

mpl

ex

tach

ycar

dia,

tha

t is

oft

en c

alle

d or

thod

rom

ic r

ecip

roca

ting

tach

ycar

dia

or

ORT

be

caus

e th

e A

V

node

is

ac

tivat

ed

norm

ally

(“

orth

o”)

and

the

atria

an

d ve

ntric

les

are

depo

lariz

ed in

a “

back

and

for

th”

or r

ecip

roca

ting

fash

ion.

Si

nce

the

atria

are

dep

olar

ized

aft

er t

he v

entr

icle

s, t

he

P w

ave

is u

sual

ly s

een

in t

he S

T se

gmen

t.

Clin

ical

Issu

es:

Emer

gent

ly, a

lmos

t an

y re

gula

r ta

chyc

ardi

a is

tre

ated

with

ade

nosi

ne.

Ade

nosi

ne w

ill u

sual

ly t

erm

inat

e A

VN

RT o

r A

VRT

by

bloc

king

con

duct

ion

in t

he A

V n

ode,

w

hich

will

sud

denl

y st

op t

he r

eent

rant

circ

uit.

Som

etim

es

ther

e is

con

fusi

on o

n w

heth

er a

deno

sine

can

be

used

saf

ely

in t

he s

ettin

g of

an

acce

ssor

y pa

thw

ay b

ecau

se o

f co

ncer

n ab

out

mor

e ra

pid

activ

atio

n of

the

ven

tric

les

via

the

acce

s-so

ry p

athw

ay. R

emem

ber t

his

is a

con

cern

onl

y if

the

patie

nt

has

atria

l fib

rilla

tion

or f

lutt

er a

nd t

he v

entr

icle

s ar

e ac

ti-va

ted

both

via

the

acc

esso

ry p

athw

ay a

nd t

he A

V n

ode

(Fig

ures

11.

1 an

d 11

.29)

. Th

is c

ondi

tion

lead

s to

a r

apid

irr

egul

ar ta

chyc

ardi

a w

ith a

wid

e Q

RS c

ompl

ex. I

n O

RT, s

ince

th

e ac

cess

ory

path

way

is

co

nduc

ting

“bac

kwar

ds”

and

activ

atin

g th

e at

ria i

n a

regu

lar

fash

ion,

ade

nosi

ne w

ill

usua

lly t

erm

inat

e th

e ta

chyc

ardi

a w

ithou

t an

y pr

oble

ms.


300 ECG Interpretation for Everyone: An On-The-Spot GuideR

eg

ula

r N

arr

ow

QR

S t

ach

yca

rdia

Atr

iove

ntr

icu

lar

ree

ntr

an

t ta

chyc

ard

ia (

AV

RT

)



Fig

ure

11.

13:

In a

ny p

atie

nt w

ith a

sup

rave

ntric

ular

tac

hyca

rdia

, co

mpa

r-in

g an

EC

G d

urin

g ta

chyc

ardi

a an

d si

nus

rhyt

hm is

ext

rem

ely

usef

ul. T

he lo

catio

n of

the

P w

ave

durin

g ta

chyc

ardi

a ca

n be

m

ore

easi

ly id

entif

ied

by c

aref

ully

iden

tifyi

ng a

ny d

iffer

ence

s in

the

QRS

, ST

seg

men

t, o

r T

wav

e (c

ircle

s).

In t

his

patie

nt

with

an

acce

ssor

y pa

thw

ay,

notic

e th

at t

he b

asel

ine

QRS

du

ring

sinu

s rh

ythm

ha

s a

norm

al

PR

inte

rval

an

d no

de

lta w

ave

(Cha

pter

7,

Figu

res

7.9

and

7.10

; C

hapt

er 8

,

Figu

re 8

.3).

In s

ome

case

s th

e ac

cess

ory

path

way

is a

“on

e w

ay s

tree

t” r

athe

r th

an a

“tw

o w

ay s

tree

t.”

In t

his

case

, the

ac

cess

ory

path

way

can

con

duct

ret

rogr

adel

y to

dep

olar

ize

the

atria

but

can

not

depo

lariz

e th

e ve

ntric

les

durin

g si

nus

rhyt

hm.

An

acce

ssor

y pa

thw

ay

with

th

ese

prop

ertie

s is

ca

lled

“con

ceal

ed”

beca

use

it is

onl

y is

app

aren

t du

ring

tach

ycar

dia.



Fig

ure

11.

14:

Wid

e co

mpl

ex

tach

ycar

dia

may

be

du

e to

ve

ntric

ular

ta

chyc

ardi

a (a

) or

any

type

of

supr

aven

trci

ular

tac

hyca

rdia

in

whi

ch t

he v

entr

icle

s ar

e de

pola

rized

abn

orm

ally.

The

mos

t co

mm

on f

orm

of

aber

rant

con

duct

ion

is b

lock

in o

ne o

f th

e bu

ndle

s le

adin

g to

a t

achy

card

ia w

ith r

ight

bun

dle

bran

ch

bloc

k or

lef

t bu

ndle

bra

nch

bloc

k (b

). A

rar

er f

orm

of

abno

rmal

ven

tric

ular

dep

olar

izat

ion

is t

he p

rese

nce

of a

n ac

cess

ory

path

way

(c)

. In

thi

s ca

se t

he a

cces

sory

pat

hway

al

low

s ra

pid

atria

l de

pola

rizat

ion

to b

e tr

ansm

itted

to

the

vent

ricle

s le

adin

g to

a r

apid

wid

e co

mpl

ex (

sinc

e th

e H

is

Purk

inje

sys

tem

is

not

used

) ta

chyc

ardi

a. O

f th

ese

thre

e ch

oice

s it

is im

port

ant t

o id

entif

y ve

ntric

ular

tach

ycar

dia

and

atria

l ta

chyc

ardi

a w

ith d

epol

ariz

atio

n of

the

ven

tric

les

via

an

acce

ssor

y pa

thw

ay.

Both

of

th

ese

cond

itons

if

left

un

trea

ted

can

lead

to

life-

thre

aten

ing

cons

eque

nces

. (U

sed

with

pe

rmis

sion

fr

om

FM

Kus

umot

o,

Car

diov

ascu

lar

Path

ophy

siol

ogy,

Hay

es B

arto

n Pr

ess,

Ral

eigh

, NC

, 200

4.)



Mo

no

mo

rph

ic V

TP

oly

mo

rph

ic V

T

(Ve

ntr

icu

lar

Fib

rilla

tio

n)



Fig

ure

11.

15:

Vent

ricul

ar

tach

ycar

dia

(and

at

rial

fibril

latio

n w

ith

rapi

d co

nduc

tion

via

an a

cces

sory

pat

hway

) m

ay d

eter

iora

te t

o ve

ntric

ular

fib

rilla

tion.

In

vent

ricul

ar t

achy

card

ia t

he Q

RS

com

plex

es,

alth

ough

rap

id a

nd b

izar

re,

all

have

the

sam

e m

orph

olog

y be

caus

e th

e ve

ntric

les

are

bein

g de

pola

rized

fr

om

a si

ngle

so

urce

. In

ve

ntric

ular

fib

rilla

tion,

m

ultip

le

wav

es o

f ve

ntric

ular

dep

olar

izat

ion

are

pres

ent

lead

ing

to

rapi

d an

d irr

egul

ar v

entr

icul

ar a

ctiv

ity t

hat

chan

ges

the

shap

e of

ven

tric

ular

act

ivity

reco

rded

by

the

ECG

. Som

etim

es

the

wor

d po

lym

orph

ic v

entr

icul

ar t

achy

card

ia i

s us

ed t

o de

scrib

e a

tach

ycar

dia

that

has

rapi

d an

d irr

egul

ar v

entr

icul

ar

activ

ity b

ut w

ith la

rger

sw

ings

aw

ay f

rom

the

bas

elin

e. F

or

the

prac

tical

pu

rpos

es

of

our

disc

ussi

on,

ther

e is

no

di

ffer

ence

bet

wee

n ve

ntric

ular

fib

rilla

tion

and

poly

mor

phic

ve

ntric

ular

tac

hyca

rdia

. Bo

th a

re li

fe-t

hrea

teni

ng a

nd s

igna

l im

pend

ing

deat

h.



**

**

**

**

**

“Wid

e Q

RS

ta

chyc

ard

ia”

Art

ifa

ct



Fig

ure

11.

16:

Som

etim

es e

xter

nal s

ourc

es o

r pro

blem

s ca

n le

ad to

app

aren

t w

ide

com

plex

ta

chyc

ardi

a.

The

pres

ence

of

ar

tifac

t ca

n us

ually

be

dete

rmin

ed b

y id

entif

ying

nar

row

QRS

com

plex

es

(*)

at c

onst

ant

inte

rval

s (d

oubl

e he

aded

arr

ows)

with

in t

he

“wid

e co

mpl

ex t

achy

card

ia.”

Obv

ious

ly, if

the

EC

G c

hang

es

are

due

to a

rtifa

ct t

he p

atie

nt w

ill n

ot h

ave

asso

ciat

ed

sym

ptom

s. B

ut re

mem

ber t

he o

ppos

ite s

tate

men

t is

not t

rue.

M

any

wid

e co

mpl

ex a

rrhy

thm

ias (

both

ven

tric

ular

tach

ycar

dia

and

supr

aven

tric

ular

tac

hyca

rdia

with

abe

rran

t co

nduc

tion)

m

ay b

e as

soci

ated

with

min

imal

or

no s

ympt

oms.


308 ECG Interpretation for Everyone: An On-The-Spot GuideW

ide

Co

mp

lex

Tach

yca

rdia

Is t

he

pa

tie

nt

un

sta

ble

?R

est

ore

No

rma

l Rh

yth

m

(Ca

rdio

vers

ion

)

Is A

V d

isso

ciat

ion

pre

sen

t?

(Fig

ure

18

& 1

9)

Is c

on

cord

an

ce p

rese

nt?

(Fig

ure

20

)

Ab

sen

t R

S?

(Fig

ure

21

)

No

rth

we

st A

xis?

(Fig

ure

22

)

Sti

ll U

nsu

re?

(Fig

ure

s 2

3 &

24

)

Ve

ntr

icu

lar

tach

yca

rdia

Ve

ntr

icu

lar

tach

yca

rdia

Ve

ntr

icu

lar

tach

yca

rdia

Ve

ntr

icu

lar

tach

yca

rdia

Ve

ntr

icu

lar

tach

yca

rdia

Yes

Yes

Yes

Yes

Yes

Yes



Fig

ure

11.

17:

Onc

e it

is e

stab

lishe

d th

at a

wid

e co

mpl

ex t

achy

card

ia i

s pr

esen

t, t

he E

CG

may

be

extr

emel

y va

luab

le f

or id

entif

ying

th

e pr

esen

ce

of

vent

ricul

ar

tach

ycar

dia.

A

gain

be

fore

ev

alua

ting

the

ECG

as

k “H

ow’s

the

patie

nt

doin

g?”

Obv

ious

ly

if th

e rh

ythm

is

asso

ciat

ed

with

si

gnifi

cant

hem

odyn

amic

co

mpr

omis

e (lo

w

bloo

d pr

essu

re

and

sym

ptom

s),

it re

ally

doe

sn’t

mat

ter

wha

t th

e rh

ythm

is,

no

rmal

rhy

thm

mus

t be

res

tore

d qu

ickl

y. Q

uick

res

tora

tion

of n

orm

al rh

ythm

oft

en re

quire

s ca

rdio

vers

ion

whe

re a

larg

e sh

ock

is a

pplie

d to

the

hea

rt.



II, II

I, a

VF,

V1

Do

no

t lo

ok

for

atr

iove

ntr

icu

lar

ass

oci

ati

on

:

P w

ave

s in

th

e e

xpe

cte

d lo

cati

on

Loo

k fo

r a

trio

ven

tric

ula

r d

isso

cia

tio

n:

P w

ave

s in

un

exp

ect

ed

loca

tio

ns

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

II“U

ne

xpe

cte

d D

efl

ect

ion

s”

Wid

e Q

RS

ta

chyc

ard

ia

Ve

ntr

icu

lar

Tach

yca

rdia

(A

V d

isso

cia

tio

n)



Fig

ure

11.

18:

The

best

way

to

iden

tify

vent

ricul

ar t

achy

card

ia i

s to

fin

d ev

iden

ce t

hat

atria

l an

d ve

ntric

ular

act

ivity

do

not

depe

nd

on

each

ot

her

and

are

depo

lariz

ing

inde

pend

ently

(a

trio

vent

ricul

ar

diss

ocia

tion

or

AV

di

ssoc

iatio

n).

In

the

sett

ing

of a

wid

e co

mpl

ex t

achy

card

ia,

the

pres

ence

of

atrio

vent

ricul

ar d

isso

ciat

ion

mea

ns th

at a

site

in th

e ve

ntric

les

is d

rivin

g ca

rdia

c ac

tivity

. P

wav

es a

re b

est

iden

tifie

d by

ex

amin

ing

the

infe

rior

lead

s an

d le

ad

V1

for

any

“une

xpec

ted”

def

lect

ions

. If y

ou th

ink

back

to F

igur

e 11

.11,

au

tom

atic

ju

nctio

nal

tach

ycar

dias

ca

n al

so

caus

e A

V

diss

ocia

tion,

but

in t

his

case

a n

arro

w Q

RS t

achy

card

ia w

ith

mor

e Q

RS c

ompl

exes

tha

n P

wav

es is

obs

erve

d.

It is

impo

rtan

t to

em

phas

ize

the

valu

e of

AV

dis

soci

atio

n fo

r th

e di

agno

sis

of

vent

ricul

ar

tach

ycar

dia.

O

ften

times

w

hen

eval

uatin

g th

e EC

G, t

he n

atur

al re

spon

se is

to lo

ok fo

r P

wav

es in

the

ir ex

pect

ed lo

catio

n si

nce

this

is h

ow w

e ev

al-

uate

EC

Gs

with

nor

mal

rat

es.

How

ever

, in

any

tac

hyca

rdia

th

e P

wav

es a

re o

ften

diff

icul

t to

sep

arat

e fr

om t

he T

wav

es.

Whe

n co

nfro

nted

with

a w

ide

com

plex

tac

hyca

rdia

it is

bes

t to

tak

e a

“wid

e an

gle”

vie

w o

f th

e en

tire

ECG

and

look

for

th

e “u

nexp

ecte

d de

flect

ions

” th

at re

pres

ent

AV

dis

soci

atio

n an

d co

nfirm

the

pre

senc

e of

ven

tric

ular

tac

hyca

rdia

.


312 ECG Interpretation for Everyone: An On-The-Spot GuideW

ide

QR

S t

ach

yca

rdia

Ve

ntr

icu

lar

Tach

yca

rdia

(AV

dis

soci

ati

on

ide

nti

fie

d b

y ca

ptu

re b

ea

ts)



Fig

ure

11.

19:

Atr

iove

ntric

ular

dis

soci

atio

n ca

n al

so b

e id

entif

ied

if a

QRS

co

mpl

ex

with

a

diff

eren

t sh

ape,

us

ually

m

ore

norm

al

appe

arin

g, i

s id

entif

ied.

Thi

s m

ore

norm

al Q

RS c

ompl

ex

occu

rs b

ecau

se a

P w

ave

is a

ble

to c

ondu

ct t

o th

e ve

ntric

les

are

part

ially

dep

olar

ize

the

vent

ricle

s. If

the

beat

is c

ompl

etel

y no

rmal

app

earin

g it

is c

alle

d a

“cap

ture

bea

t” a

nd i

f th

e be

at

has

an

inte

rmed

iate

sh

ape

betw

een

the

QRS

of

ve

ntric

ular

tac

hyca

rdia

and

a n

orm

al Q

RS i

t is

cal

led

a “f

usio

n be

at.”

Bot

h ca

ptur

e be

ats

and

fusi

on b

eats

are

indi

rect

evi

denc

e of

atr

iove

ntric

ular

dis

soci

atio

n an

d th

e pr

esen

ce

of

vent

ricul

ar

tach

ycar

dia.

In

th

is

exam

ple

of

vent

ricul

ar t

achy

card

ia,

the

two

mor

e no

rmal

app

earin

g be

ats

(*) w

ould

be

calle

d ca

ptur

e or

fus

ion

beat

s si

nce

QRS

ch

ange

s ca

n be

see

n in

V1

and

V2.

Thi

s ta

chyc

ardi

a al

so h

as

an a

bsen

t RS

com

plex

in

the

prec

ordi

al l

eads

whi

ch i

s an

othe

r cl

ue

that

ve

ntric

ular

ta

chyc

ardi

a is

pr

esen

t (F

igur

e 11

.21)

.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V1

th

rou

gh

V6

V1

V2

V3

V4

V5

V6

Po

siti

ve C

on

cord

an

ce

V1

V2

V3

V4

V5

V6

Ne

ga

tive

Co

nco

rda

nce

V1

Wid

e Q

RS

ta

chyc

ard

ia

Ve

ntr

icu

lar

Tach

yca

rdia

(C

on

cord

an

ce)



Fig

ure

11.

20:

If at

riove

ntric

ular

di

ssoc

iatio

n ca

nnot

be

id

entif

ied

the

clin

icia

n m

ust

depe

nd o

n ev

alua

tion

of t

he Q

RS (c

olle

ctiv

ely

calle

d m

orph

olog

y cl

ues)

to

he

lp

iden

tify

vent

ricul

ar

tach

ycar

dia.

One

of

the

mos

t us

eful

tho

ugh

unco

mm

on

mor

phol

ogy

clue

s is

the

pres

ence

of p

reco

rdia

l con

cord

ance

. In

ne

gativ

e co

ncor

danc

e al

l of

th

e Q

RS

com

plex

es

are

nega

tive

and

in

posi

tive

conc

orda

nce

all

of

the

QRS

co

mpl

exes

are

pos

itive

.



V1

th

rou

gh

V6

V4

V5

V6

V1

V2

V3

Ab

sen

t R

S

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

Wid

e Q

RS

ta

chyc

ard

ia

Ve

ntr

icu

lar

Tach

yca

rdia

(A

bse

nt

RS

)



Fig

ure

11.

21:

Ano

ther

use

ful

mor

phol

ogy

clue

is

the

abse

nce

of a

n RS

co

mpl

ex i

n th

e pr

ecor

dial

lea

ds.

This

fin

ding

is

rela

ted

to

conc

orda

nce

but

in t

his

case

som

e of

the

QRS

com

plex

es

can

be n

egat

ive

and

som

e of

the

QRS

com

plex

es p

ositi

ve.



II

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V1

aV

R

QR

S F

ron

tal A

xis:

–9

0 t

o –

18

0

Wid

e Q

RS

ta

chyc

ard

ia

Ve

ntr

icu

lar

Tach

yca

rdia

(”N

ort

hw

est

” a

xis)



Fig

ure

11.

22:

Ano

ther

use

ful

mor

phol

ogy

clue

is

a rig

ht s

uper

ior

card

iac

axis

in th

e fr

onta

l lea

ds, a

lso

collo

quia

lly c

alle

d a

“nor

thw

est”

ax

is. A

s yo

u kn

ow t

he c

ardi

ac a

xis

is n

orm

ally

bet

wee

n −3

0°

and

100°

. If

the

QRS

is

betw

een

−90°

and

−18

0° t

hen

depo

lariz

atio

n of

the

ven

tric

les

mus

t be

sta

rtin

g ne

ar t

he

apex

of

the

hear

t an

d it

is u

nlik

ely

that

any

for

m o

f ab

erra

nt

cond

uctio

n co

uld

caus

e in

itial

ve

ntric

ular

de

pola

rizat

ion

“out

the

re”

near

the

tip

(ape

x) o

f th

e he

art.



V1

, V2

Do

wn

stro

ke

is r

ap

id

R, i

f p

rese

nt,

is n

arr

ow

No

“un

exp

ect

ed

de

fle

ctio

ns”

AV

dis

soci

ati

on

is n

ot

pre

sen

t

Wid

e Q

RS

ta

chyc

ard

ia

Su

pra

ven

tric

ula

r Ta

chyc

ard

ia (

Wit

h le

ftt

bu

nd

le b

ran

ch b

lock

)



Fig

ure

11.

23:

Wid

e co

mpl

ex t

achy

card

ias

are

gene

rally

cla

ssifi

ed a

s le

ft

bund

le

bran

ch

bloc

k m

orph

olog

y if

the

QRS

in

V

1 is

pr

edom

inan

tly

nega

tive

or

right

bu

ndle

br

anch

bl

ock

mor

phol

ogy

if th

e Q

RS c

ompl

ex i

n V

1 is

pre

dom

inan

tly

posi

tive

(Cha

pter

7, F

igur

e 7.

3). S

upra

vent

ricul

ar ta

chyc

ardi

a w

ith le

ft b

undl

e br

anch

blo

ck a

berr

ancy

is a

ssoc

iate

d w

ith a

sm

all,

shar

p, a

nd t

hin

sept

al R

wav

e in

V1.

In t

his

exam

ple

of

AV

RT w

ith l

eft

bund

le b

ranc

h bl

ock

aber

ranc

y a

shar

p na

rrow

sep

tal

R w

ave

in V

1 is

pre

sent

. In

thi

s ca

se i

t is

extr

emel

y di

ffic

ult

to d

efin

itive

ly s

ay t

hat

the

patie

nt h

as

supr

aven

tric

ular

ta

chyc

ardi

a w

ith

aber

ranc

y.

Whe

neve

r th

ere

is A

NY

dou

bt,

trea

t th

e pa

tient

as

if he

or

she

has

vent

ricul

ar t

achy

card

ia.

In a

dditi

on,

the

diag

nosi

s of

AV

RT

cann

ot b

e m

ade

by e

valu

atin

g th

e EC

G.

In t

his

case

the

ex

act

mec

hani

sm o

f th

e ta

chyc

ardi

a w

as i

dent

ified

by

an

elec

trop

hsio

logy

stu

dy (

an i

nvas

ive

proc

edur

e th

at a

llow

s th

e be

st d

elin

eatio

n of

arr

hyth

mia

s by

usi

ng p

last

ic c

oate

d el

ectr

odes

pla

ced

dire

ctly

with

in t

he c

ham

bers

of

the

hear

t).



V1

rSR

’ co

mp

lex

No

“un

exp

ect

ed

de

fle

ctio

ns”

AV

dis

soci

ati

on

is n

ot

pre

sen

t

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

V1

Wid

e Q

RS

ta

chyc

ard

ia

Su

pra

ven

tric

ula

r Ta

chyc

ard

ia (

Wit

h r

igh

t b

un

dle

bra

nch

blo

ck)



Fig

ure

11.

24:

In a

wid

e co

mpl

ex t

achy

card

ia w

ith a

rig

ht b

undl

e br

anch

bl

ock

patt

ern,

sup

rave

ntric

ular

tach

ycar

dia

with

abe

rran

cy is

m

ore

likel

y if

the

ECG

has

an

rSR’

com

plex

with

the

sec

ond

posi

tive

defle

ctio

n (R

’) is

la

rger

th

an

the

first

po

sitiv

e de

flect

ion

(r).

In t

his

exam

ple

of A

VRT

with

rig

ht b

undl

e br

anch

bl

ock

aber

ranc

y (J

ust

like

Figu

re

11.2

3,

an

elec

trop

hysi

olog

y st

udy

was

req

uire

d to

mak

e a

defin

itive

di

agno

sis)

, a

larg

e w

ide

R’ i

n V

1 is

obs

erve

d. I

t is

wor

th

repe

atin

g th

at w

hene

ver

ther

e is

any

dou

bt,

it is

bes

t to

as

sum

e an

y w

ide

com

plex

ta

chyc

ardi

a is

ve

ntric

ular

ta

chyc

ardi

a.



Wid

e Q

RS

ta

chyc

ard

ia

Ve

ntr

icu

lar

Tach

yca

rdia

(In

itia

tio

n)

II (a

ny

lea

d)

Init

iate

d w

ith

ven

tric

ula

r

de

po

lari

zati

on

No

P w

ave

ob

serv

ed



Fig

ure

11.

25:

In s

ome

case

s, th

e in

itiat

ion

of th

e w

ide

com

plex

tach

ycar

dia

is a

vaila

ble

for

eval

uatio

n. V

entr

icul

ar t

achy

card

ia a

lmos

t al

way

s is

initi

ated

with

a p

rem

atur

e ve

ntric

ular

con

trac

tion.

In t

his

exam

ple,

a r

elat

ivel

y sl

ow v

entr

icul

ar t

achy

card

ia i

s in

itiat

ed w

ith a

pre

mat

ure

vent

ricul

ar d

epol

ariz

atio

n.



QR

S m

orp

ho

log

y

cha

ng

es

Sta

rts

wit

h a

“V

”

No

P w

ave

pri

or

to t

he

firs

t b

ea

t

]

PP

PP

P

aV

L

aV

F

V1



Fig

ure

11.

26:

Eval

uatio

n of

a w

ide

com

plex

tac

hyca

rdia

in t

he s

ettin

g of

a

pree

xist

ing

bund

le b

ranc

h bl

ock

can

som

etim

es b

e di

ffic

ult.

In

th

is

exam

ple,

th

e ta

chyc

ardi

a st

arts

w

ith

vent

ricul

ar

depo

lariz

atio

n an

d du

ring

the

tach

ycar

dia

AV

dis

soci

atio

n is

pr

esen

t with

mor

e Q

RS c

ompl

exes

than

P w

aves

. In

addi

tion,

no

tice

that

th

e pa

tient

ha

s le

ft

bund

le

bran

ch

bloc

k

mor

phol

ogy

at b

asel

ine

(the

firs

t ne

gativ

e Q

RS c

ompl

ex).

Whe

n ta

chyc

ardi

a st

arts

the

QRS

com

plex

has

a d

iffer

ent

mor

phol

ogy.

A w

ide

com

plex

tac

hyca

rdia

ass

ocia

ted

with

a

chan

ge in

QRS

mor

phol

ogy

mor

e lik

ely

repr

esen

ts v

entr

icul

ar

tach

ycar

dia.



Ve

ntr

icu

lar

Tach

yca

rdia

Tre

ate

d w

ith

Ca

rdio

vers

ion

*



Fig

ure

11.

27:

Vent

ricul

ar

tach

ycar

dia

requ

ires

urge

nt

trea

tmen

t w

ith

med

icat

ions

and

in

man

y ca

se r

equi

res

deliv

erin

g a

larg

e el

ectr

ical

cur

rent

bet

wee

n tw

o pa

ddle

s or

pad

s pl

aced

on

the

ches

t. T

his

larg

e el

ectr

ical

cur

rent

“re

sets

” th

e he

art a

nd

hope

fully

ext

ingu

ishe

s al

l w

aves

of

card

iac

depo

lariz

atio

n (b

oth

atria

l an

d ve

ntric

ular

). H

opef

ully

“w

hen

the

dust

cl

ears

,”

the

patie

nt’s

norm

al

rhyt

hm

resu

mes

. In

th

is

exam

ple

a pa

tient

has

ven

tric

ular

tac

hyca

rdia

due

to

a re

entr

ant

circ

uit

invo

lvin

g a

scar

fro

m a

prio

r m

yoca

rdia

l in

farc

tion.

Myo

card

ial i

nfar

ctio

ns c

an c

ause

pat

chy

scar

ring

that

inc

reas

es t

he l

ikel

ihoo

d of

hav

ing

the

subs

trat

e fo

r re

entr

y (t

wo

elec

tric

ally

iso

late

d pa

ralle

l pa

ths

that

hav

e di

ffer

ent

elec

tric

al

prop

ertie

s).

A

prem

atur

e ve

ntric

ular

co

ntra

ctio

n ac

ts a

s a

“trig

ger”

and

ini

tiate

s th

e re

entr

ant

circ

uit.

A

hi

gh

volta

ge

curr

ent

is

deliv

ered

ac

ross

th

e m

yoca

rdiu

m v

ia e

xter

nal

pads

tha

t “r

eset

s” t

he h

eart

and

th

e si

nus

node

beg

ins

to d

rive

the

hear

t (*

). Th

e sh

arp

read

er w

ill n

otic

e th

at th

e fir

st b

eat a

fter

the

shoc

k is

act

ually

fr

om v

entr

icul

ar t

issu

e w

ith a

n in

vert

ed P

wav

e in

the

ST

segm

ent

due

to r

etro

grad

e co

nduc

tion.



QT:

60

0 m

sV

en

tric

ula

r Ta

chyc

ard

ia

Irre

gu

lar

wid

e Q

RS

ta

chyc

ard

ia

wit

h a

ch

an

gin

g Q

RS

Tors

ad

es

de

Po

inte

s



Fig

ure

11.

28:

One

spe

cial

for

m o

f po

lym

orph

ic v

entr

icul

ar t

achy

card

ia i

s ca

lled

Tors

ades

de

Poin

tes

(“Tw

istin

g of

the

Poi

nts”

). In

thi

s ar

rhyt

hmia

, pr

olon

gatio

n of

the

QT

inte

rval

lead

s to

rea

cti-

vatio

n of

the

hea

rt a

nd le

ads

to a

cha

ract

eris

tic p

olym

orph

ic

vent

ricul

ar t

achy

card

ia t

hat

has

an u

ndul

atin

g pa

tter

n th

at

appe

ars

to b

e tw

istin

g ar

ound

a c

entr

al a

xis.

Alth

ough

Tors

ades

de

Poin

tes

may

term

inat

e sp

onta

neou

sly

it m

ust b

e tr

eate

d ag

gres

sive

ly b

y ev

alua

ting

any

caus

e fo

r th

e pr

o-lo

nged

QT

inte

rval

suc

h as

hyp

okal

emia

or

drug

s. I

n th

is

exam

ple

the

patie

nt h

as a

n ex

trem

ely

prol

onge

d Q

T in

terv

al

of 0

.60

s.



**

**

V1

1. W

ide

QR

S (

usu

ally

po

siti

ve in

V1

)

2. I

rre

gu

lar

3. S

ho

rt R

-R in

terv

als

(V

ery

fa

st)

Irre

gu

lar

wid

e Q

RS

ta

chyc

ard

ia w

ith

a c

ha

ng

ing

QR

S

Atr

ial fi

bri

llati

on

an

d W

PW

(R

ap

id v

en

tric

ula

r d

ep

ola

riza

tio

nv

ia t

he

AP

)



Fig

ure

11.

29:

The

final

maj

or c

ause

of

a w

ide

com

plex

tac

hyca

rdia

is a

tria

l fib

rilla

tion

in t

he p

rese

nce

of a

n ac

cess

ory

path

way

(W

olff

Pa

rkin

son

Whi

te

Synd

rom

e;

Figu

res

11.1

an

d 11

.14)

. Re

mem

ber t

hat t

he A

V n

ode

has

slow

con

duct

ion

prop

ertie

s th

at l

imit

the

vent

ricul

ar r

ate

if at

rial

fibril

latio

n or

oth

er

atria

l arr

hyth

mia

s de

velo

p. H

owev

er,

an a

cces

sory

pat

hway

al

low

s ra

pid

cond

uctio

n so

if

a pa

tient

with

the

Wol

ff

Park

inso

n W

hite

Syn

drom

e de

velo

ps a

tria

l fib

rilla

tion

very

rapi

d ve

ntric

ular

rat

es u

p to

300

bea

ts p

er m

inut

e ca

n be

in

term

itten

tly p

rese

nt.

The

tria

d of

an

irreg

ular

ver

y fa

st

wid

e co

mpl

ex t

achy

card

ia s

houl

d al

way

s ar

ouse

sus

pici

on

that

a p

atie

nt w

ith a

n ac

cess

ory

path

way

has

dev

elop

ed

atria

l fib

rilla

tion.

Sin

ce t

he v

entr

icle

s ar

e be

ing

rapi

dly

depo

-la

rized

thi

s rh

ythm

can

det

erio

rate

to

vent

ricul

ar f

ibril

latio

n an

d m

ust

be t

reat

ed u

rgen

tly w

ith e

ither

med

icat

ion

or

card

iove

rsio

n.


334


Implantable cardiac devices are now used for several different functions. Implantable cardioverter defibrillators (ICDs) are designed to automatically detect ventricular tachyarrhythmias and deliver therapy to terminate the arrhythmia by rapid pacing or by delivering a large shock. The oldest implantable cardiac device, pacemakers have been used to treat slow heart rhythms. More recently, pacing has been used to help the failing heart contract in a more normal fashion (cardiac resynchronization therapy or CRT). Most commonly, devices designed to provide CRT also have ICD capabilities. The last type of implantable cardiac device is an implantable loop recorder (ILR). The ILR is a strictly diagnostic device (it provides no therapy) and is used to evaluate patients with intermittent symptoms that are separated by longer periods of time (weeks and months). A compre-hensive discussion of implanted cardiac devices is far beyond the scope of this introductory text on ECGs, but since pacemakers are so common it is important to have some basic understanding on how they function and how they affect the ECG.

Pacemakers were first developed as a way to artificially stimulate the heart in patients with bradycardia. Depending on which chamber(s) needs to be paced lead(s) are placed in the right atrium and/or right ventricle (Figure 12.1). The first pacemakers developed used a single lead placed in the right ventricle. Although ventricular pacing prevents catastrophic bradycardia, atrioventricular synchrony is not maintained. In patients with sinus node dysfunction, atrial pacing is sufficient to treat bradycardia because atrioventricular conduction is normal. Obviously, for a patient with bradycardia due to atrioventricular block, a single chamber atrial pacing would not be effective for producing ventricular depolarization. In the United States dual chamber pacemakers are the most common type

CHAPTER 12

Arrhythmias: Pacing


Arrhythmias: Pacing 335

of pacemaker used for treating bradycardia. Although dual chamber pacemakers are more complicated, they ensure ventricular depolarization and maintain atrioventricular synchrony in patients with bradycardia due to either sinus node dysfunction or atrioventricular block.

More recently, leads have been placed in veins overlying the left ventricle to restore more normal ventricular depolarization in patients with left bundle branch block and severe heart failure.



R

PR

RLow

rate

tim

erex

pir

es

Low

rate

tim

erex

pir

es

Low

rate

tim

erex

pir

es

Low

rate

tim

erex

pir

es

retr

og

rad

e P

Sin

us

no

de

dys

fun

ctio

n(S

inu

s p

ause

)A

trio

ven

tric

ula

r blo

ck(3

° AV

B)

Sin

gle

ch

amb

erV

entr

icu

lar p

acin

g

Sin

gle

ch

amb

erA

tria

l Pac

ing

R

PR

RLow

rate

tim

erex

pir

es

AV

Iex

pir

es

PA

VI

exp

ires

PP

R

Du

al c

ham

ber

pac

ing



Fig

ure

12.

1:D

iffer

ent

pace

mak

er t

ypes

for

the

tre

atm

ent

of b

rady

card

ia.

Sing

le c

ham

ber

vent

ricul

ar p

acem

aker

s us

e a

sing

le l

ead

plac

ed in

the

right

ven

tric

le. S

ingl

e ch

ambe

r ven

tric

ular

pac

e-m

aker

s pr

even

t br

adyc

ardi

a in

bot

h si

nus

node

dys

func

tion

and

atrio

vent

ricul

ar b

lock

but

do

not

mai

ntai

n at

riove

ntric

u-la

r sy

nchr

ony

(atr

ial

cont

ract

ion

follo

wed

by

vent

ricu

lar

cont

ract

ion)

. Sin

gle

cham

ber v

entr

icul

ar p

acem

aker

s de

liver

a

stim

ulus

to

pace

the

ven

tric

les

afte

r th

e lo

w r

ate

timer

ex

pire

s. T

he lo

w ra

te ti

mer

is a

pro

gram

mab

le p

aram

eter

that

defin

es th

e lo

nges

t per

iod

of ti

me

befo

re a

pac

ing

stim

ulus

is

deliv

ered

. Si

ngle

cha

mbe

r at

rial

pace

mak

ers

oper

ate

in t

he

sam

e w

ay b

ut w

ith th

e pa

cing

lead

in th

e at

rium

. Dua

l cha

m-

ber

pace

mak

er c

an b

e qu

ite c

ompl

ex b

ut f

or t

he p

urpo

ses

of

this

func

tion

it is

sim

ply

impo

rtan

t to

know

that

they

hav

e an

A

V in

terv

al (

AV

I) tim

er t

hat

is d

esig

ned

to m

imic

the

phy

sio-

logi

c PR

int

erva

l. In

thi

s w

ay d

ual

cham

ber

pace

mak

ers

are

able

to

pr

even

t br

adyc

ardi

a an

d m

aint

ain

AV

sy

nchr

ony

rega

rdle

ss o

f th

e ca

use

of b

rady

card

ia.



Atr

ial p

aci

ng

an

d

“na

tive

” A

V n

od

e c

on

du

ctio

n

An

y le

ad

Atr

ial

Sp

ike

QR

S

aV

R

aV

L

aV

F

V1

V2

Atr

ial p

aci

ng

Atr

ial p

aci

ng

wit

h “n

ati

ve”

AV

co

nd

uct

ion



Fig

ure

12.

2:A

tria

l pac

ing

is u

sed

for p

atie

nts w

ith si

nus n

ode

dysf

unct

ion.

In

thi

s ca

se t

he s

inus

nod

e do

es n

ot d

epol

ariz

e no

rmal

ly s

o th

e pa

cem

aker

is s

et t

o de

pola

rize

at a

rat

e of

60

beat

s pe

r m

inut

e. T

he s

hape

of

the

P w

ave

give

s so

me

idea

of

the

loca

tion

of t

he p

acin

g le

ad.

In t

his

case

the

P w

ave

is

nega

tive

in a

VR

and

biph

asic

in

lead

aV

F, w

hich

sug

gest

s

that

the

ele

ctro

des

of t

he l

ead

are

plac

ed i

n th

e lo

wer

po

rtio

n of

the

rig

ht a

triu

m.

Not

ice

in t

his

exam

ple

the

patie

nt h

as c

ondu

ctio

n vi

a th

e A

V n

ode

that

pro

duce

s a

narr

ow

QRS

co

mpl

ex.

How

ever

, th

e pa

tient

do

es

have

ev

iden

ce f

or A

V n

ode

dise

ase

beca

use

of t

he p

rese

nce

of a

pr

olon

ged

PR in

terv

al a

nd f

irst

degr

ee A

V b

lock

.



Pa

ced

Fusi

on

Na

tive

PP

PP

Ve

ntr

icu

lar

pa

cin

g

Ve

ntr

icu

lar

pa

cin

g in

sin

us

no

de

dys

fun

ctio

n



Fig

ure

12.

3:Ve

ntri

cula

r pa

cing

pr

even

ts

brad

ycar

dia

but

does

no

t m

aint

ain

atrio

vent

ricul

ar s

ynch

rony

. In

this

cas

e th

e si

nus

rate

is

abo

ut t

he s

ame

as t

he p

rogr

amm

ed v

entr

icul

ar p

acin

g ra

te.

The

first

thr

ee Q

RS c

ompl

exes

are

due

to

vent

ricul

ar

paci

ng fr

om th

e in

ferio

r rig

ht v

entr

icul

ar a

pex

(the

QRS

com

-pl

exes

are

wid

e, n

egat

ive

in th

e in

ferio

r lea

ds, a

nd h

ave

a le

ft

bund

le b

ranc

h bl

ock

mor

phol

ogy)

. The

fift

h th

roug

h se

vent

h

QRS

com

plex

es a

re p

rodu

ced

from

nat

ive

cond

uctio

n du

e to

at

rial d

epol

ariz

atio

n fr

om t

he s

inus

nod

e (u

prig

ht P

wav

e in

le

ad I

I w

ith a

nar

row

QRS

and

a n

orm

al P

R in

terv

al).

The

four

th Q

RS c

ompl

ex i

s du

e to

fus

ion

betw

een

norm

al A

V

cond

uctio

n (n

otic

e th

e P

wav

e be

fore

the

QRS

) and

ven

tric

u-la

r pa

cing

. It

has

an in

term

edia

te s

hape

tha

t ha

s ch

arac

teris

-tic

s of

bot

h th

e na

tive

QRS

com

plex

es a

nd v

entr

icul

ar p

acin

g.



Du

al c

ha

mb

er

pa

cin

g

“Tra

ckin

g n

orm

al s

inu

s rh

yth

m”

Atr

ial a

nd

ve

ntr

icu

lar

pa

cin

g



Fig

ure

12.

4:D

ual

cham

ber

paci

ng.

Top.

In

this

pat

ient

P w

aves

are

“s

ense

d” b

y th

e at

rial

lead

of

a du

al c

ham

ber

pace

mak

er

and

“tra

cked

.” W

hen

P w

aves

are

“tr

acke

d,”

the

P w

ave

initi

ates

the

AV

inte

rval

and

a v

entr

icul

ar o

utpu

t is

del

iver

ed

whe

n th

e A

V i

nter

val

expi

res.

In

this

way

AV

syn

chro

ny i

s m

aint

aine

d. N

otic

e in

Fig

ure

12.3

with

sin

gle

lead

ven

tric

ular

paci

ng,

P w

aves

do

not

occu

r be

fore

the

ven

tric

ular

pac

ed

beat

s. In

the

bot

tom

str

ip, b

oth

atria

l and

ven

tric

ular

pac

ing

is p

rese

nt. T

his

patie

nt h

as b

oth

sinu

s no

de d

ysfu

nctio

n an

d at

riove

ntric

ular

con

duct

ion

abno

rmal

ities

; we

know

tha

t th

e PR

int

erva

l is

at

leas

t 0.

20 s

econ

ds b

ecau

se n

o in

trin

sic

vent

ricul

ar c

ondu

ctio

n w

as o

bser

ved

afte

r the

atr

ial s

timul

us.



Biv

en

tric

ula

r p

aci

ng

Ca

rdia

c re

syn

chro

niz

ati

on



Fig

ure

12.

5:In

pat

ient

s w

ith c

onge

stiv

e he

art

failu

re a

nd l

eft

bund

le

bran

ch b

lock

, car

diac

fun

ctio

n m

ay b

e w

orse

ned

beca

use

of

poor

tim

ing

of l

eft

vent

ricul

ar c

ontr

actio

n. I

n le

ft b

undl

e br

anch

blo

ck t

he l

ater

al l

eft

vent

ricul

ar w

all

cont

ract

s ve

ry

late

rel

ativ

e to

the

sep

tum

. In

an

effo

rt t

o pr

ovid

e m

ore

coor

dina

ted

left

ven

tric

ular

con

trac

tion,

spe

cial

ly d

esig

ned

lead

s ca

n be

pla

ced

on t

he la

tera

l wal

l of

the

left

ven

tric

le

thro

ugh

the

coro

nary

si

nus

and

veno

us

bran

ches

. Si

mul

tane

ous

paci

ng f

rom

the

lef

t ve

ntric

le a

nd t

he r

ight

ve

ntric

le le

ads

to m

ore

coor

dina

ted

cont

ract

ion.

In t

his

case

th

e Q

RS i

s na

rrow

er d

urin

g ca

rdia

c re

sync

hron

izat

ion

than

du

ring

paci

ng f

rom

the

rig

ht v

entr

icle

.


347


Since identifying myocardial ischemia or injury is one of the most useful functions of the ECG in patients with chest pain, it is not surprising that the ECG is used as a diagnostic tool during exercise stress testing to identify patients who may have significant coronary artery lesions. The concept is simple, exercise increases metabolic demand of cardiac tissue. If blood supply is limited to a region of the heart because of significant blockages that region will become ischemic and the ECG will show signs suggestive or diagnostic of ischemia. Exercise stress testing is generally a safe procedure. However, severe complications such as myocardial infarction and death have been reported in approximately 1 / 2,500 tests. Obviously, good clinical judgment and appropriate risk stratifica-tion should be considered before ordering or performing any type of stress test.

There are several protocols used for exercise testing but all employ a gradual increase in the slope and speed of a treadmill. The Bruce Protocol is the most widely used exercise protocol. It delivers an incremental workload every three minutes. This protocol is used for patients that are able to exercise and achieve at least a speed of 2.5 to 3.4 mph on an incline of 12% to 14%. For individuals where this amount of exercise is unrealistic, several protocols that use lower workloads such as the modified Bruce Protocol, the Balke Protocol, and the Naughton Protocol have been developed. Regardless of the protocol, in general patients are asked to exercise until they have to stop due to symptoms such as chest pain, shortness of breath, or generalized fatigue (symptom limited stress test). For most protocols it is important for the patient to achieve a specific heart rate, usually 85% of the maximum predicted heart rate for age.

CHAPTER 13

Clinical Use of the ECG: Stress Testing



During exercise, the ECG is constantly monitored with six leads in the standard precordial positions and the limb leads placed on the trunk. The ST segment is the principal parameter monitored during an exercise test. Specially designed ECG recording systems are used that employ specialized electronics to filter extraneous noise and motion artifact from movement and also continuously measure ST segment changes from baseline.

The most common abnormal ECG finding with stress testing is ST segment depression. In order to provide some standardization for inter-pretation of ST segment changes, the J point (the point where the QRS ends and the ST segment starts) and the J + 80 ms (2 little boxes after the J point) are used as the specific locations of the ST segment for measurement. In addition the character of the ST segment changes are described qualitatively. There are four types of ST segment depression that can occur during cardiac stress testing:

Rapid upsloping: If the ST segment returns to normal at 0.08 sec from the J point, it is a normal response.

Slowly upsloping: The ST segment returns to baseline later than 0.08 sec after the J point and it is an equivocal ST segment response to ischemia (some patients have CAD and some do not). If it only occurs in recov-ery, it may be entirely normal.

Flat (horizontal) depressed ST segment: It is definitely abnormal and if it upslopes within two to four minutes in recovery, it is much less likely to be true disease.

Downsloping ST segment depression: The possibility of a positive ECG increase with the amount of downsloping and its persistence in recovery.

Several ECG findings are particularly significant if they occur during stress testing because they may signify the presence of significant lesions in multiple coronary arteries (multivessel disease):

Marked ST segment depression greater than 2 mm, especially flat or downsloping ST segment depression.

Early ST segment depression in the first three to five minutes of the test, especially when it is persistent for four to six minutes in recovery.

Severe or increasing chest pain, especially with ST segment depression.Failure to complete at least four to six minutes of exercise.Exercise induced hypotension.Frequent ventricular ectopy in association with ST segment depression.


Clinical Use of the ECG: Stress Testing 349

In addition to ST segment changes, the amount of exercise that an individual can perform on a stress test is extremely useful. Exercise capac-ity is generally quantified with METS (metabolic equivalents). A MET is a metabolic equivalent that is used to quantify cardiovascular workload and it is used to express exercise capacity. One MET is equal to the uptake of 3.5 ml of oxygen/kg/min and is the average oxygen requirement from inspired air necessary to maintain life in the resting state. After adjusting for age and other risk factors, each increase in exercise capacity (METS) equates to 10% to 25% improvement in survival. Examples of the value of the METS achieved during exercise:

● 5 METS is associated with a poor prognosis in patients under 65 years. ● Failure to complete stage II (7 METS) is very concerning. ● 8.5 METS is common with a sedentary adult. ● 9 METS or more after a CABG indicates a good prognosis regardless of other responses.

● 10 METS is considered a degree of fitness. ● 14 METS is considered physically fit. ● 18–20 METS is considered to be a highly conditioned individual. ● 24 METS is considered a well-trained aerobic athlete.

The probability for ischemia and the likelihood of its severity is directly related to the amount of abnormal ST segment depression and inversely related to the slop of the ST segment. The severity of CAD is also related to the time of appearance of ischemic shifts. It is extremely difficult to evaluate ST segment changes in patients who have significant baseline ST segment abnormalities including left bundle branch block, left ventricular hypertrophy, the Wolff Parkinson White Syndrome, ventricular pacing, and digoxin therapy.


350 ECG Interpretation for Everyone: An On-The-Spot GuideS

up

ine

Sta

nd

ing

**

**

*



Fig

ure

13.

1:Pa

tient

s w

ill

som

etim

es

have

EC

G

chan

ges

sim

ply

with

ch

ange

s in

pos

ition

. In

thi

s pa

tient

sta

ndin

g is

ass

ocia

ted

with

att

enua

tion

of T

wav

es (*

) and

R w

aves

(arr

ows)

in t

he

infe

rola

tera

l lea

ds.



Ba

selin

eE

xerc

ise

Re

cove

ry



Fig

ure

13.

2:EC

G c

hang

es d

urin

g a

norm

al s

tres

s te

st.

Wit

h ex

erci

se

ther

e is

min

imal

ups

lopi

ng S

T se

gmen

t de

pres

sion

tha

t w

ould

not

mee

t di

agno

stic

cri

teri

a fo

r is

chem

ia.

An

ECG

ob

tain

ed i

mm

edia

tely

upo

n st

oppi

ng e

xerc

ise,

sho

ws

no

ST s

egm

ent

depr

essi

on.

This

fir

st E

CG

dur

ing

reco

very

is

crit

ical

. A

s no

ted

the

ECG

du

ring

ex

erci

se

can

have

sign

ific

ant

arti

fact

due

to

mot

ion.

ST

segm

ent

depr

essi

on

asso

ciat

ed w

ith

true

myo

card

ial i

sche

mia

is r

elat

ivel

y lo

ng

last

ing

and

shou

ld r

emai

n in

the

fir

st E

CG

dur

ing

reco

very

. In

thi

s ca

se t

here

are

no

ST s

egm

ent

chan

ges

that

mee

t cr

iter

ia f

or is

chem

ia. T

his

stre

ss t

est

wou

ld b

e cl

assi

fied

as

norm

al.



Fig

ure

13.

3:A

ll co

mm

erci

ally

ava

ilabl

e m

achi

nes

used

for

str

ess

test

ing

will

pro

vide

a s

umm

ary

of r

esul

ts.

The

form

at o

f th

e su

m-

mar

y w

ill v

ary

from

hos

pita

l to

hos

pita

l. In

thi

s ca

se,

two

sum

mar

y sh

eets

from

the

pati

ent i

n Fi

gure

13.

2 ar

e sh

own.

Top

: In

thi

s ex

ampl

e, t

he f

irst

sum

mar

y sh

eet

show

s ex

er-

cise

tim

e, c

ondi

tions

(spe

ed a

nd g

rade

), ac

hiev

ed w

orkl

oad

in M

ETS,

hem

odyn

amic

mea

sure

men

ts –

HR:

hea

rt r

ate,

BP

: bl

ood

pres

sure

; RR

P: r

ate

pres

sure

pro

duct

(he

art

rate

m

ultip

lied

by t

he p

eak

syst

olic

blo

od p

ress

ure

at a

giv

en

poin

t in

the

stu

dy);

and

ST: s

egm

ent

chan

ges.

Bo

tto

m:

Repr

esen

tativ

e EC

G r

ecor

ding

s at

crit

ical

tim

es f

or

all

12 l

eads

are

sho

wn.

Abs

olut

e va

lues

for

J p

oint

cha

nge

and

the

rela

tive

chan

ge o

f the

j+ 8

0 m

s po

int f

or e

ach

lead

are

ca

lcul

ated

by

the

com

pute

r fr

om s

tore

d di

gita

l tra

cing

s an

d di

spla

yed.

In t

his

exam

ple

ST s

egm

ent

depr

essi

on >

1 m

m is

no

ted

for

lead

s II,

III,

V3–

V5.

Com

pare

the

com

pute

r ge

ner-

ated

tra

cing

s an

d es

timat

ed v

alue

s of

ST

segm

ent

depr

essi

on

to t

he a

ctua

l tra

cing

s at

pea

k ex

erci

se a

nd im

med

iate

ly a

fter

ex

erci

sing

in

Figu

re 1

3.2.

The

wav

efor

ms

gene

rate

d by

the

tr

eadm

ill m

achi

ne t

hrou

gh it

s fil

terin

g al

gorit

hms

have

ove

r-es

timat

ed t

he S

T de

pres

sion

tha

t w

as a

ctua

lly p

rese

nt.

This

ill

ustr

ates

an

extr

emel

y im

port

ant

fact

. A

lthou

gh t

he c

om-

pute

r EC

G g

ener

ated

sum

mar

ies

are

usef

ul, e

valu

atio

n of

the

actu

al E

CG

tra

cing

s is

alw

ays

requ

ired.


356 ECG Interpretation for Everyone: An On-The-Spot GuideB

ase

line

Exe

rcis

e (

no

ch

est

pa

in)

2:3

0 R

eco

very

(ch

est

pa

in b

eg

ins)

2:4

5 R

eco

very

(ch

est

pa

in w

ors

en

s)

11

:00

Re

cove

ry (

che

st p

ain

re

solv

ed

at

7:0

0)



Fig

ure

13.

4:A

tru

e po

sitiv

e EC

G t

est.

In

this

exa

mpl

e, a

s th

e pa

tient

ex

erci

ses,

hor

izon

tal S

T se

gmen

t de

pres

sion

is n

oted

dur

ing

exer

cise

. The

nur

se s

tops

the

tes

t be

caus

e of

the

mag

nitu

de

of t

he S

T se

gmen

t de

pres

sion

(>

−2

mm

in II

and

aV

F) e

ven

in t

he a

bsen

ce o

f ch

est

pain

. Th

e pa

tient

sto

ps e

xerc

isin

g an

d af

ter

2:30

in

reco

very

the

pat

ient

dev

elop

s ch

est

pain

w

ith h

oriz

onta

l ST

seg

men

t de

pres

sion

in

the

infe

rola

tera

l le

ads.

With

in 1

5 se

cond

s, S

T se

gmen

t de

pres

sion

dee

pens

an

d be

com

es d

owns

lopi

ng.

ST s

egm

ent

depr

essi

on t

hat

is

mor

e pr

omin

ent

(> 2

mm

), do

wns

lopi

ng, o

r as

soci

ated

with

sy

mpt

oms

incr

ease

the

like

lihoo

d th

at t

he E

CG

cha

nges

are

du

e to

myo

card

ial i

sche

mia

. It

is im

port

ant

to n

ote

that

the

de

velo

pmen

t of c

hest

pai

n is

oft

en a

rela

tivel

y la

te e

vent

and

th

at

ST

segm

ent

chan

ges

asso

ciat

ed

with

is

chem

ia

are

usua

lly q

uite

pro

long

ed. I

n th

e bo

ttom

pan

el e

ven

afte

r th

e pa

in

has

reso

lved

, do

wns

lopi

ng

ST

segm

ent

depr

essi

on

pers

ists

, par

ticul

arly

in le

ad II

.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

ST

se

gm

en

t e

lev

ati

on

an

d d

ep

ress

ion

Loss

of

R w

ave

am

plit

ud

e

II

Ba

selin

eE

xerc

ise



Fig

ure

13.

5:U

nfor

tuna

tely

ST

segm

ent

depr

essi

on t

hat

mee

ts c

riter

ia f

or

isch

emia

can

als

o be

see

n in

pat

ient

s w

ithou

t si

gnifi

cant

co

rona

ry a

rter

y di

seas

e. T

his

is c

alle

d a

“fal

se p

ositi

ve”

beca

use

the

test

was

“po

sitiv

e” (

in o

ther

wor

ds,

indi

cate

s is

chem

ia)

but

“fal

se”

(bec

ause

it w

as w

rong

). Fa

lse

posi

tive

ST s

egm

ent

depr

essi

on i

s pa

rtic

ular

ly c

omm

on i

n w

omen

an

d so

me

have

que

stio

ned

whe

ther

the

EC

G p

rovi

des

any

valu

e fo

r ide

ntify

ing

isch

emia

in w

omen

. To

incr

ease

the

abil-

ity o

f th

e st

ress

tes

t to

ide

ntify

isc

hem

ia (

decr

ease

“fa

lse

nega

tive”

tes

ts)

and

to r

educ

e th

e lik

elih

ood

that

the

tes

t w

ill in

corr

ectly

iden

tify

a pa

tient

with

out s

igni

fican

t cor

onar

y ar

tery

dis

ease

(de

crea

se “

fals

e po

sitiv

e” t

ests

), ad

ditio

nal

imag

ing

test

s su

ch a

s ec

hoca

rdio

grap

hy,

nucl

ear

scan

ning

,

mag

netic

res

onan

ce im

agin

g, o

r co

mpu

ted

tom

ogra

phy

are

used

. Pa

tient

s w

ith

true

flo

w

limiti

ng

lesi

ons

will

ha

ve

chan

ges

in fu

nctio

n or

blo

od s

uppl

y th

at c

an b

e id

entif

ied

by

thes

e ad

vanc

ed im

agin

g te

chni

ques

. In

this

exa

mpl

e, p

rom

i-ne

nt u

pslo

ping

ST

segm

ent

depr

essi

on is

obs

erve

d in

II a

nd

horiz

onta

l ST

depr

essi

on n

oted

in t

he o

ther

infe

rior

lead

s III

an

d aV

F. T

he p

atie

nt h

ad n

o as

soci

ated

sym

ptom

s an

d an

ac

com

pany

ing

echo

card

iogr

am d

emon

stra

ted

no a

bnor

mal

-iti

es i

n le

ft v

entr

icul

ar f

unct

ion.

Thi

s te

st e

mph

asiz

es t

he

impo

rtan

ce o

f sy

mpt

oms

for

deci

ding

whe

ther

any

EC

G

chan

ges

are

due

to i

sche

mia

(ra

ther

tha

n th

e ot

her

way

ar

ound

). Th

is is

why

the

impo

rtan

ce o

f sy

mpt

oms

has

been

st

ress

ed t

hrou

ghou

t th

is b

ook.



Fig

ure

13.

6:A

noth

er s

ituat

ion

whe

re t

he S

T se

gmen

t de

pres

sion

can

be

obse

rved

as

a fa

lse

posi

tive

is in

the

Wol

ff P

arki

nson

Whi

te

Synd

rom

e. A

bnor

mal

ven

tric

ular

dep

olar

izat

ion

can

lead

to

abno

rmal

repo

lariz

atio

n w

ith s

tres

s te

sts.

In th

is e

xam

ple

the

patie

nt h

as a

sho

rt P

R in

terv

al a

nd a

wid

ely

nega

tive

QRS

com

plex

in le

ad V

1 co

nsis

tent

with

a r

ight

sid

ed a

cces

sory

pa

thw

ay. T

he S

T se

gmen

t de

pres

sion

is a

n ex

pect

ed f

indi

ng

with

str

ess

and

the

ECG

ess

entia

lly p

rovi

des

no in

form

atio

n on

the

pre

senc

e of

cor

onar

y ar

tery

lesi

ons.



I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

ST

se

gm

en

t e

lev

ati

on

an

d

de

pre

ssio

n L

oss

of

R w

ave

am

plit

ud

e



Fig

ure

13.

7:Th

e de

velo

pmen

t of

ST

segm

ent

elev

atio

n du

ring

stre

ss

test

ing

is e

xtre

mel

y su

gges

tive

of m

ultiv

esse

l di

seas

e. S

T se

gmen

t ele

vatio

n is

mor

e co

mm

only

see

n in

pat

ient

s w

ith a

pr

ior

myo

card

ial i

nfar

ctio

n.



aV

R

aV

L

aV

F

*



Fig

ure

13.

8:In

add

ition

to

ST s

egm

ent

chan

ges,

the

dev

elop

men

t of

ve

ntric

ular

arr

hyth

mia

s w

ith e

xerc

ise

may

iden

tify

patie

nts

at

high

er r

isk

of f

utur

e su

dden

dea

th.

In t

his

exam

ple,

dur

ing

exer

cise

, ho

rizon

tal

ST s

egm

ent

depr

essi

on i

n aV

F an

d ST

segm

ent

elev

atio

n in

aV

R ar

e pr

esen

t. T

he p

atie

nt d

evel

ops

a w

ide

com

plex

tach

ycar

dia

(firs

t bea

t mar

ked

by a

n as

teris

k)

that

ra

pidl

y de

terio

rate

s to

a

poly

mor

phic

ve

ntric

ular

ta

chyc

ardi

a.


366


The ECG is an extremely important diagnostic tool for patients who may have cardiac problems and for this “wrap-up” chapter it is useful to put the ECG in the context of its main clinical uses: Evaluating the patient with an ongoing arrhythmia, evaluating a patient who complains of symptoms in the past that may be due to arrhythmias (palpitations, dizziness), and evaluating a patient with chest pain or other symptoms suggestive of a cardiac problem.

Ongoing arrhythmiaIn the patient with an ongoing arrhythmia, simplistically the patent has a heart rate that is too slow, a heart rate that is too fast, or a heart rate that is normal but has skips or is irregular. Now that we have reviewed the different causes of arrhythmias we can modify Chapter 9, Figure 9.1 to include the specific arrhythmias (Figure 14.1). Slow heart rates (bradycar-dia) are either due to sinus node dysfunction or atrioventricular block. The ECG helps identify if enough P waves are being generated and if P waves are present do they conduct normally to the ventricles.

In a patient with a rapid heart rate, the ECG is used to quantify the rate and rhythm, and perhaps most important, determine whether or not the ventricles are being depolarized normally or abnormally (Figure 14.1). If the QRS is narrow and normal appearing, the ventricles are being depolarized normally and the patient has supraventricular tachycardia. Although supraventricular tachycardia can be associated with significant symptoms, they are usually reasonably stable and generally not associated with hemodynamic collapse. In fact if the patient has a tachycardia not associated with a pulse, it suggests that some significant process other than arrhythmia is present (severe infection, severe blood loss, etc.). In

CHAPTER 14

Clinical Use of the ECG: Clinical Problems


Clinical Use of the ECG: Clinical Problems 367

Rate

Slow Heart Rate

(Bradycardia)Normal Rate

Rapid Heart Rate

(Tachycardia)

Sinus node Dysfunction(Not enough P Waves)

AV block(P’s don’t conduct)

SkipsPACs, PVCs, PJCs

NonsinusEctopic atrial rhythm

Junctional rhythm

Atrial fibrillation

Irregular narrow QRSAtrial fibrillation

MAT

AT/Flutter w/ Variable AV

Regular narrow QRSAT/Flutter

AVNRT

Junctional tachycardia

AVRT

Regular Wide QRSVT

SVT w/aberrancy

Irregular Wide QRSTorsades

AF and WPW

VF

Arrhythmias

Figure 14.1:Flow sheet for evaluation of arrhythmias. AV: atrioventricular; PAC: premature atrial contrac-tion; PVC: premature ventricular contraction; PJC: premature junc-tional complex; MAT: multifocal atrial tachycardia; AT: atrial tachy-cardia; AVNRT: AV node reentrant

tachycardia; AVRT: atrioventricu-lar reentrant tachycardia; SVT: supraventricular tachycardia; AF: atrial fibrillation; WPW: Wolff Parkinson White Syndrome; VT: ventricular tachycardia; VF: ven-tricular fibrillation.



contrast, a wide complex tachycardia confirms that the heart is not being depolarized normally and the possibility of ventricular tachycardia must be the first thought that crosses the clinician’s mind. Specific identification of the cause of the supraventricular tachycardia or wide complex tachycardia is covered in Chapter 11.

If the patient is complaining of an irregular heart beat, the ECG can identify whether the patient is in sinus rhythm with skips (either premature atrial contractions or premature ventricular contractions) or some other arrhythmia such as atrial fibrillation is present (Figure 14.1).

Symptoms suggestive of a prior arrhythmia: syncope or palpitationsOftentimes patients come for evaluation of a problem they experienced in the past such as palpitations, dizziness, or syncope. Syncope is a medical term used for sudden loss of consciousness that is transient and often with a quick recovery. Syncope is extremely common and can have many causes. Generally most patients with syncope have a very good prognosis except for those patients that have syncope due to a cardiac problem, most commonly a transient arrhythmia. The ECG is an essential part of the initial evaluation of patients with syncope. The focus of the ECG is to identify patients who may have a cardiac cause of syncope (Figure 14.2). The ECG should be evaluated for depolarization abnormalities and repolarization abnormalities. Identification of an abnormal ECG makes a cardiac cause of syncope more likely.

Chest PainFinally, the ECG remains one of the most important diagnostic tools for evaluating the patient with symptoms that may be due to cardiac ischemia (Figure 14.3). Although this is important, remember that the patient’s description of their symptoms provides the most valuable clues for the cause of chest pain. Chest pain due to ischemia is generally described as a dull pressure in the central or left chest that may radiate to the arm or jaw. The pain lasts minutes or longer (rather than sharp stabbing pain for seconds) and generally does not change with a breath or with change in position.

The hallmark ECG changes associated with myocardial ischemia, injury, or infacrtion are changes in repolarization such as ST segment elevation, ST segment depression, or T wave changes (inversion and less commonly, peaking). The ST segment elevation associated with myocardial infarction



is present in two contiguous leads. The presence of reciprocal changes, T wave inversion or Q waves makes myocardial infarction and injury as the likely cause for ST segment elevation. Reciprocal changes (other than depression in aVR due to pericarditis) are particularly useful if they are present. But remember that the absence of reciprocal changes does not “rule out” myocardial injury as a cause of ST segment elevation, particu-larly for anterior wall myocardial infarctions. In Chapter 4, only very subtle reciprocal changes in the inferior leads are observed in Figure 4.8 and no reciprocal changes are present in Figure 4.10. Reciprocal changes are much more commonly observed in inferior wall myocardial infarctions (inferior ST segment elevation; reciprocal changes most commonly observed in V1, V2, I, and aVL) and lateral wall myocardial infarctions (lat-eral ST segment elevation; reciprocal changes in the inferior leads).

The evaluation of the ECG with only ST segment depression or T wave changes can be extremely challenging. In some cases, the ECG changes

Significant ECG abnormalitiesin Syncope or Palpitations

DepolarizationAbnormalities

Prologed PR

Bundle Branch block

Left ventricular hypertrophy

Q waves

LVH

RVH

Long QT Syndrome

Brugada Syndrome

LVH

QT interval

Brugada Syndrome

RepolarizationAbnormalities

Figure 14.2:ECG evaluation in syncope and palpitations. LVH: left ventricular hyper-trophy; RVH: right ventricular hypertrophy.



EC

G e

va

lua

tio

n in

th

e p

ati

en

t w

ith

ch

est

pa

in

ST s

egm

ent e

leva

tion

Ca

refu

l ev

alu

ati

on

of

sym

pto

ms

is

the

mo

st im

po

rta

nt

dia

gn

ost

ic t

oo

l

An

ato

mic

dis

trib

uti

on

Re

cip

roca

l ch

an

ge

s

Q w

ave

s

ST s

egm

ent d

epre

ssio

n

Ne

w o

r d

yna

mic

Q w

ave

s

T w

ave

abno

rmal

itie

s

Ne

w o

r d

yna

mic

Q w

ave

s

Loca

lize

d T

wav

e p

ea

kin

g

Left

bu

nd

le b

ran

ch b

lock

an

d L

VH

ma

ke t

he

pre

sen

ce o

f ca

rdia

c d

ise

ase

mo

re li

kely

bu

t m

ake

th

e E

CG

mo

re d

ifficu

lt a

nd

so

me

tim

es

imp

oss

ible

to

ev

alu

ate

Fig

ure

14.

3:Ev

alua

tion

of t

he E

CG

in a

pat

ient

com

plai

ning

of

ches

t pa

in.



can be extremely subtle, perhaps only present in one lead. For ST segment depression and T wave inversion, comparison with an old ECG or if the chest pain is “coming and going,” associated dynamic ST segment and T wave changes should arouse suspicion for ischemia. The presence of left bundle branch block and left ventricular hypertrophy increase the likelihood that a patient has coronary artery disease or other cardiac abnormality but also make the ECG more difficult and sometimes impossible to evaluate for ischemia. Several final thoughts may help. First, more obvious ECG changes are more worrisome. The corollary of this is that for more subtle the ECG changes, either the ischemia is in a region in an area that is not “seen well” by the ECG (lateral wall), or, more likely, that the ischemia is not severe enough to be associated with large changes in repolarization or depolarization. Second, comparison ECGs, whether old or when the patient is experiencing different symptoms, may be helpful. Finally, listen to your patient and remember that symptoms always take precedence over ECG findings.



Co

mp

ari

ng

EC

Gs

Eva

lua

te p

reco

rdia

l le

ad

pla

cem

en

t

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

RS

RS

rS

Pri

or

EC

GC

urr

en

t E

CG

(ch

est

pa

in)



Fig

ure

14.

4:W

hen

com

parin

g EC

Gs

in a

pat

ient

with

che

st p

ain,

it

is

criti

cal

to e

valu

ate

the

QRS

com

plex

, pa

rtic

ular

ly i

n th

e pr

ecor

dial

lead

s. In

thi

s ex

ampl

e, t

he T

wav

e ap

pear

s m

ore

peak

ed in

V3

whe

n co

mpa

red

to a

prio

r EC

G.

How

ever

, by

com

parin

g th

e Q

RS c

ompl

exes

(RS

rat

her

than

an

rS),

it is

ob

viou

s th

at

lead

V

3 fr

om

the

prio

r EC

G

prob

ably

co

rres

pond

s to

lead

V4

on t

he c

urre

nt E

CG

.



Co

mp

ari

ng

EC

Gs

T w

ave

ch

an

ge

s d

ue

to

isch

em

ia in

th

e s

ett

ing

of

LVH

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

RS

RS

Pri

or

EC

GC

urr

en

t E

CG

(ch

est

pa

in)



Fig

ure

14.

5:In

thi

s pa

tient

with

lef

t ve

ntric

ular

hyp

ertr

ophy

(LV

H b

y Ro

milt

Es

tes

crite

ria

with

ST

T ch

ange

s an

d le

ft

atria

l ab

norm

ality

), th

e EC

G w

ith c

hest

pai

n is

ass

ocia

ted

with

m

ore

prom

inen

t an

terio

r T

wav

e in

vers

ion.

In t

his

case

, th

e pa

tient

had

a s

igni

fican

t le

sion

in h

is r

ight

cor

onar

y ar

tery

.

The

loca

tion

of

T w

ave

abno

rmal

ities

an

d ST

se

gmen

t ch

ange

s us

ually

pr

ovid

es

very

lit

tle

info

rmat

ion

on

the

loca

tion

of t

he m

yoca

rdiu

m a

t ris

k. T

he a

bilit

y to

com

pare

th

e cu

rren

t EC

G i

s ve

ry h

elpf

ul i

n th

is p

atie

nt w

ho h

as

base

line

abno

rmal

ities

due

to

left

ven

tric

ular

hyp

ertr

ophy

.



I

II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

I II III

aV

R

aV

L

aV

F

V1

V6

V5

V4

V3

V2

No

ch

est

pa

inC

he

st p

ain

* *

* *

Co

mp

ari

ng

EC

Gs

Dyn

am

ic T

wav

e c

ha

ng

es

du

e t

o is

che

mia



Fig

ure

14.

6:In

thi

s pa

tient

with

che

st p

ain

that

is “

com

ing

and

goin

g,”

ECG

s ar

e ob

tain

ed in

the

em

erge

ncy

depa

rtm

ent

both

with

an

d w

ithou

t ch

est

pain

. D

ynam

ic E

CG

cha

nges

ass

ocia

ted

with

sym

ptom

s ar

e ex

trem

ely

usef

ul. I

n th

is c

ase

the

T w

aves

ar

e m

ore

prom

inen

t in

the

ant

erio

r le

ads

(*).

This

pat

ient

had

a cr

itica

l les

ion

in h

is le

ft a

nter

ior

desc

endi

ng c

oron

ary

arte

ry.

T w

ave

peak

ing

is a

T w

ave

chan

ge t

hat

prov

ides

a

clue

to

the

anat

omic

loca

tion

of t

he m

yoca

rdiu

m a

t ris

k. In

th

is c

ase,

ant

erio

r T w

ave

peak

ing

due

to a

nter

ior m

yoca

rdia

l in

jury

.



Baselin

eMinutes

Minutes/H

ours

Hou

rs/D

ayD

ays/

We

eks

T w

ave

pe

ak

ing

ST

se

gm

en

t e

lev

ati

on

(pro

min

en

t)

ST

se

gm

en

t e

lev

ati

on

gra

du

ally

de

cre

ase

s

T w

ave

s in

vert

Q w

ave

s d

eve

lop

ST

se

gm

en

t e

lev

ati

on

reso

lve

s

T w

ave

s re

ma

in in

vert

ed

Q w

ave

s d

ee

pe

n

Evo

luti

on

of

EC

G C

ha

ng

es

in M

yoca

rdia

l In

jury



Fig

ure

14.

7:Ev

olut

ion

of E

CG

cha

nges

in

myo

card

ial

inju

ry.

The

timin

g an

d pr

esen

ce o

f th

ese

findi

ngs

will

dep

end

dram

atic

ally

on

ther

apy.

For

exa

mpl

e, i

f bl

ood

flow

is

quic

kly

rest

ored

, ST

segm

ent

elev

atio

n m

ay re

solv

e im

med

iate

ly o

r ov

er t

he n

ext

seve

ral h

ours

and

Q w

aves

mig

ht r

esol

ve o

r ne

ver

appe

ar.


380


Additional ReferencesChou’s Electrocardiography in Clinical Practice: Adult and Pediatric. Surawicz B,

Knilans TK. Sunders, Philadelphia, PA, 2008.Goldberger AL. Clinical Electrocardiography: A Simplified Approach. Mosby,

Philadelphia, PA, 2006.Kusumoto FM, ECG Interpretation: From Pathophysiology to Clinical Application,

Springer, New York, NY, 2009.O’Keefe JH, Hammill SC, Freed MS, Pogwizd SM. The ECG Criteria Book. Jones and

Bartlett Publishers, Sudbury, MA, 2010.

Lists:

Appendices

Causes for Abnormal Axis Deviation

Left axis deviation ● Normal variant (2–5%) ● Left anterior fascicular block ● Left ventricular hypertrophy ● Inferior wall myocardial infarction ● Primum atrial septal defect ● Hyperkalemia ● Left bundle branch block

Right axis deviation ● Normal variant ● Lead misplacement ● Left posterior fascicular block ● Right ventricular hypertrophy ● Lateral wall myocardial infarction ● Dextrocardia

Kusumoto_bapp.indd 380Kusumoto_bapp.indd 380 11/30/2011 6:39:53 PM11/30/2011 6:39:53 PM

Appendices 381

(Cont’d )

● Pulmonary embolus ● Chronic obstructive lung disease ● Secundum atrial septal defect

Source: FM Kusumoto, ECG Interpretation: From Pathophysiology to Clinical Application, Springer, New York, NY, 2009.

Differential Diagnosis for Q Waves

Anterior ● Anterior wall myocardial infarction ● Left ventricular aneurysm ● Left ventricular hypertrophy ● Left bundle branch block ● Infiltrative Diseases (amyloid, sarcoid) ● Right sided accessory pathway ● Chronic obstructive lung disease ● Pneumothorax ● Dilated cardiomyopathy ● Intracranial hemorrhage ● Hyperkalemia ● Pacing

Inferior ● Inferior wall myocardial infarction ● Left posterior fascicular block ● Inferior accessory pathway ● Hypertrophic cardiomyopathy ● Pacing

Lateral ● Lateral wall myocardial infarction ● Left anterior fascicular block ● Left lateral accessory pathway




T Wave Changes and Possible Causes

Nonspecific T wave changes ● Heart disease ● Drugs ● Electrolyte abnormalities ● Hyperventilation ● Pericarditis ● Normal variant ● Left ventricular hypertrophy ● Bundle branch block ● Pancreatitits, cholecystitis, esophageal spasm ● Hypothyroid

T wave inversion ● Normal variant ● Myocardial infarction / ischemia ● Digoxin, antiarrhythmic medications ● After ventricular pacing or radiofrequency catheter ablation (cardiac memory)

● Left ventricular hypertrophy ● Bundle branch block ● Central nervous system problems

Peaked T waves ● Hyperkalemia ● Myocardial infarction/injury ● Normal variant (early repolarization) ● Intracranial hemorrhage ● Left bundle branch block ● Left ventricular hypertrophy



Appendices 383

Criteria for left ventricular hypertrophy and right ventricular hypertrophy

Left Ventricular Hypertrophy

Sokolow-Lyon Presence of either:

● R in aVL > 11 mm ● Sum of the S in V1 or V2 and the R in V5 or V6 > 35 mm

Cornell R in aVL and S in V3 > 28 mm (men) or > 20 mm (women)

Estes Point score: ≥ 5 for left ventricular hypertrophy

● Amplitude: 3 pts ❍ Largest R or S wave ≥ 20 mm in a limb lead

❍ S wave in V1 or V2 ≥ 30 mm ❍ R wave in V5 or V6 ≥ 30 mm

● Typical STT wave “strain” pattern ❍ Without dig: 3 pts ❍ With dig: 1 pt

● Left atrial enlargement: 3 pts ● Left axis deviation ≥ 30°: 2 pts ● QRS duration > 0.09 s: 1 pt ● Intrinsicoid deflection in V5 or V6 ≥ 0.05s: 1 pt

Right Ventricular Hypertrophy Suggested by the presence of one or more of the following:

● Right axis deviation > 110° ● R wave in V1 ≥ 7 mm ● S wave in V1 < 2 mm ● Sum of the R in V1 and the S in V6 > 10.5 mm

● rsR’ in V1 with R’ > 10 mm

● Right atrial enlargement

Intrinsicoid deflection: Measurement from the beginning of the QRS complex to the peak of the R wave (less commonly called the R wave peak time)



Nor

mal

rS c

om

ple

x

T w

ave

may

be

up

rig

ht

or

inve

rte

d

Abn

orm

al N

egat

ive

Defl

ecti

ons

in V

1

LBBB

QS

or

rS c

om

ple

x

QR

S >

0.1

2 s

LVH

rS c

om

ple

x

QR

S <

0.1

4

De

ep

S w

ave

Sept

al M

IQ

S c

om

ple

x

QR

S <

0.1

2 s

Do

wn

stro

ke

no

tch

Righ

t AP,

WPW

QS

co

mp

lex

QR

S >

0.1

2 s

Sh

ort

PR

De

lta

wav

e

RV p

acin

gQ

S c

om

pe

x

QR

S >

0.1

2 s

Pa

cer

stim

ulu

s

Abn

orm

al P

osit

ive

Defl

ecti

ons

in V

1

Righ

t IV

CDrS

r’ co

mp

lex

QR

S <

0.1

2 s

RBBB

rsR

’ or

rR’ c

om

ple

x

QR

S >

0.1

2 s

Brug

ada

Synd

rom

ers

R’ c

om

ple

x

ST

se

gm

en

t e

lev

ati

on

RVH

Rs

com

ple

x

QR

S <

0.1

2 s

Inve

rte

d

T w

ave

Post

erio

r MI

Rs

or

RS

co

mp

lex

QR

S <

0.1

2 s

Up

rig

ht

T w

ave

Infe

rio

r Q

s

Left

AP,

WPW

Rs

com

ple

x

QR

S >

0.1

2 s

Sh

ort

PR

De

lta

wav

e

Sept

al h

yper

trop

hyR

S w

ith

a d

ee

pe

r S

Oth

er

Cri

teri

a f

or

LVH

Nor

mal

Dep

olar

izat

ion

in V

1


Appendices 385

1. H

ow

’s t

he

pa

tie

nt?

2. I

rre

gu

lar

or

reg

ula

r?

3. C

an

yo

u fi

nd

P w

ave

s?

Re

gu

lar

Irre

gu

lar

No

P w

ave

s o

r P

wav

es

in t

he

QR

S

P w

ave

s in

th

e S

T s

eg

me

nt

P w

ave

s in

th

e T

wav

e o

r a

fte

r

P w

ave

s o

f d

iffe

ren

t sh

ap

es

Flu

tte

r w

ave

s

No

org

an

ize

d a

ctiv

ity

Flu

tte

r W

ave

s

Atr

ial A

ctiv

ity

AV

no

de

re

ee

ntr

y

AV

re

en

ty (

acc

ess

ory

pa

thw

ay)

Atr

ial t

ach

yca

rdia

Mu

ltif

oca

l atr

ial t

ach

yca

rdia

Atr

ial fl

utt

er

Atr

ial fi

bill

ati

on

Atr

ial fl

utt

erDia

gn

osi

s?R

hyt

hm

Ev

alu

ati

on

of

Su

pra

ve

ntr

icu

lar

Ta

chyc

ard

ia



1. How’s the patient?

2. Can you find “unexpected” deflections (P waves)?

3. “Really” abnormal QRS complexes?

- Concordance

- Absent RS

- “Northwest” Axis

4. “ALWAYS assume the worst”

(ventricular tachycardia)

Wide Complex Tachycardia Glass Beads

“Unexpected Deflections”

V1 V2 V3 V4 V5 V6

Concordance

or

Absent RS

aVR IIAxis –90° to –180°

V4 V5V1 V2 V3

Very Wide QRS (> 0.16–0.18s)


387


aberrant conduction, 234–5abnormal depolarization. see

depolarizationabnormal repolarization. see

repolarizationabsent RS complex, 316–17accessory pathway

prominent R wave in V1, 154, 164–7QRS complex/interval, 184–5,

190–191tachycardia, 272–4, 302–3

acute myocardial injury, 77advanced second degree AV block,

262–3, 268–71amyloidosis, 204–5aneurysms, 44–5, 60–61anterior leads, 7–8, 11–12anterior ST segment elevation, 41–3anterior wall MI, 42–3, 52–9, 61, 202–3anteroseptal MI, 159apical ballooning syndrome, 62–3apical hypertrophic cardiomyopathy, 113arrhythmias

atrial fibrillation, 238–9, 245bradycardia, 214–15, 241–71, 366–7competing pacemakers, 236–7ectopic atrial rhythm, 220–221, 237interpretation of ECGs, 32–3, 35irregular rhythm, 226–39junctional rhythm, 222–3narrow QRS tachycardia, 272–4,

280–305normal rates and skips, 214–40normal sinus rhythm, 216–19

ongoing, 366–8pacing, 334–45premature atrial contraction, 228–9,

234–5premature junctional contraction,

230–231premature ventricular contraction,

232–3regular rhythm, 216–25sinus arrhythmia, 226–7sinus node dysfunction, 241, 243,

246–51sinus rhythm with AV block, 224–5,

241–5, 252–71stress testing, 364–5ST segment elevation, 49, 61, 65–71syncope and palpitations, 368–9tachycardia, 214–15, 272–333,

364–5, 366–8wide QRS tachycardia, 272–4, 306–33

arrhythmogenic right ventricular cardiomyopathy (ARVC), 130–131

artifact, 218–19, 246–7, 306–9, 352–3ARVC. see arrhythmogenic right

ventricular cardiomyopathy (ARVC)asymmetric T wave inversion, 128–9atrial depolarization, 15–18, 248–9, 302atrial fibrillation

bradycardia, 245, 266–7normal rates and skips, 238–9tachycardia, 273, 276–7, 280–283,

288–9, 332–3atrial pacing, 334–9atrial repolarization, 18

Index

Kusumoto_bindex.indd 387Kusumoto_bindex.indd 387 11/19/2011 7:11:47 PM11/19/2011 7:11:47 PM

388 Index

atrial tachycardia (flutter), 272–8, 284–7, 290–293

atrioventricular (AV) block, 366bradycardia, 241–5, 252–71normal rates and skips, 224–5pacing, 334–7ST segment elevation, 86–7

atrioventricular (AV) conduction, 18–19, 25

atrioventricular (AV) dissociation, 310–313

atrioventricular node reentrant tachycardia (AVNRT), 273–4, 276, 294–5

atrioventricular reentrant tachycardia (AVRT), 278, 298–305, 320–323

attenuated R wave, 160–163automaticity, 274–5, 279, 296–7AV. see atrioventricular (AV) blockAVNRT. see atrioventricular node

reentrant tachycardia (AVNRT)AVRT. see atrioventricular reentrant

tachycardia (AVRT)

Balke Protocol, 347Bazett’s formula, 31biphasic T wave, 140–141, 145bipolar limb leads, 5biventricular pacing cardiac

resynchronization, 344–5bizarre R waves, 182–3blocked premature atrial contractions,

258–9bradycardia, 241–71

atrial fibrillation, 245normal rates and skips, 214–15ongoing arrhythmias, 366–7pacing, 334–7sinus node dysfunction, 241, 243,

246–51sinus rhythm with AV block, 241–5,

252–71Bruce Protocol, 347Brugada syndrome, 44–5, 66–9bundle branches, 18–19, 24–5

arrhythmias, 235, 254–5, 270–271, 302–3, 320–323

prominent R wave in V1, 148, 150, 153–4, 156–63

QRS complex/interval, 184–5, 188–9, 192–3

ST segment depression, 106–9ST segment elevation, 41, 50–51,

54–5, 92–3T wave abnormalities, 131

capture beats, 312–13cardiac axis, 21–2cardiac resynchronization therapy (CRT),

334, 344–5cardioversion, 328–9changing QRS, 330–333chest pain, 356–7, 368–77comparing ECGs, 372–7competing pacemakers, 236–7complete heart block, 244–5, 264–7concordance, 314–15continuous ECG recordings, 4coronary artery spasm, 94–5critical left main lesions, 96–7critical left main stenosis, 104–5CRT. see cardiac resynchronization

therapy (CRT)

deep symmetric T wave inversion, 112–13

deflection of T wave, 228–9, 234–5, 282–3, 310–311

delta wave, 164–7, 190–191depolarization

arrhythmias, 302, 332–3, 369atrial, 15–18, 248–9, 302chest pain, 371direction and timing, 152early, 151evaluation parameters, 187interpretation of ECGs, 35narrow positive depolarization, 149,

152, 168–81normal ECG, 16, 19–25, 149–52,

168–9pacing, 334–5prominent R wave in V1, 148–83QRS complex/interval, 184–203


Index 389

QT interval, 137Q wave anomalies, 186–7, 194–207stress testing, 360–361technical issues, 8–9wide negative depolarization, 149,

153, 156–7, 160–167wide positive depolarization, 149,

153, 156–67, 182–3dextrocardia, 176–7digoxin, 114–15, 267displaying the ECG, 9–12dizziness, 368downsloping ST segment, 106–7,

110–111drug-associated QT interval

prolongation, 119, 138–9dual chamber pacemakers, 334–7,

342–3Duchenne muscular dystrophy, 178–9dynamic ECG changes, 101, 376–7

early depolarization, 151early repolarization, 44–5, 48–9, 83,

120–121ectopic atrial rhythm, 220–221, 237electrodes

leads, 2, 4–9, 11–12placement, 2–4

electrophysiology, 1endocardial cells, 25–7epicardial cells, 25–7epsilon waves, 130–131evolving infarcts, 44–5, 87–9exercise stress testing. see stress testing

false positives/negatives, 358–9first degree AV block, 86–7, 242, 244focal atrial tachycardia, 276–7, 290–293frontal plane leads, 5–7fusion beats, 313

heart rateinterpretation of ECGs, 32PR interval, 28–30QT interval, 28, 30–31R–R interval, 27–9, 31

hemodynamic collapse, 366–7

His Purkinje systembradycardia, 252–5normal ECG, 18–19, 24–5, 29normal rates and skips, 228–9, 235QRS complex/interval, 186, 191tachycardia, 272–4, 276, 279–81,

302–3Hook pattern, 76–7, 120–121horizontal plane leads, 5–7hyperkalemia, 70–71, 118, 124–5hypertension, 98–9hypertrophic cardiomyopathy

prominent R wave in V1, 154, 180–181

ST segment depression, 112–13ST segment elevation, 64–5

hypocalcemia, 118, 142–3hypokalemia, 118, 140–141hypomagnesemia, 144–5hypothermia, 182–3

ibutilide, 138–9ICD. see implantable cardioverter

defibrillators (ICD)idioventricular rhythm, 248–9ILR. see implantable loop recorder (ILR)implantable cardioverter defibrillators

(ICD), 65, 334implantable loop recorder (ILR), 334inferior leads, 7–8, 11–12inferior wall MI, 42–3, 82–93inferolateral ST segment depression, 101inferolateral wall MI, 76–7, 80–81infiltrative disease, 204–5intercostal spaces, 2–3inverted P wave

arrhythmias, 224–5, 231prominent R wave in V1, 176–7QRS complex/interval, 212–13

inverted T wave, 117, 126–31prominent R wave in V1, 172–3QRS complex/interval, 206–11QT interval, 146–7ST segment depression, 100–101,

112–15ST segment elevation, 37, 39, 44, 73,

81, 88–92


390 Index

ischemiacomparing ECGs, 374–7stress testing, 347, 352–3, 356–9ST segment depression, 99–105,

108–9ST segment elevation, 37, 39–40T wave abnormalities, 122–3, 126–7

J point depression, 96–7, 99, 110–111, 354–5

junctional ectopic tachycardia (JET), 276junctional escape rhythm, 241, 243junctional tachycardia, 272–4, 275–6,

296–7, 311

large terminal R wave, 160–163lateral leads, 7–8, 11–12lateral ST segment depression, 111lateral wall MI, 42–3, 72–5, 200–201late terminal R wave, 182–3LBBB. see left bundle branch block (LBBB)leads, 2, 4–9, 11–12left anterior fascicular block, 160–163,

196–7left bundle branch block (LBBB)

arrhythmias, 302–3, 320–321prominent R wave in V1, 148, 150QRS complex/interval, 184–5, 188–9,

192–3ST segment depression 106–9ST segment elevation 44–5, 92–3

left posterior fascicular block, 198–9left-sided accessory pathway, 154,

164–7left ventricular aneurysm, 60–61left ventricular hypertrophy (LVH)

comparing ECGs, 374–5QRS complex/interval, 187, 208–13ST segment depression, 98, 110–111,

114–15syncope and palpitations, 369T wave abnormalities, 127–9

left ventricular strain, 212–13lipid plaques, 40localized T wave peaking, 122–3long QT syndrome, 118, 136–7LVH. see left ventricular hypertrophy

(LVH)

metabolic equivalents (METS), 348MI. see myocardial infarction (MI)mitral valve, 13modified Bruce Protocol, 347monitors, 11–12monomorphic VT, 304–5monophasic R wave, 188–9multifocal atrial tachycardia, 276–7,

284–5myocardial infarction (MI)

chest pain, 368–9prominent R wave in V1, 154, 159,

174–5QRS complex/interval, 200–203stress testing, 347, 363ST segment elevation, 39–45, 52–9,

61, 72–7, 80–93myocardial injury

comparing ECGs, 376–9interpretation of ECGs, 32–3stress testing, 347ST segment depression, 99ST segment elevation, 37–9, 77T wave abnormalities, 123

narrow negative depolarization, 149–52narrow positive depolarization, 149,

152, 168–81narrow QRS tachycardia, 272–4,

280–305native AV conducting, 338–9Naughton Protocol, 347negative concordance, 314–15negative delta wave, 164–7normal ECG, 13–31

anatomy of the heart, 13–14atrial depolarization, 15–18atrioventricular conduction, 18–19cardiac axis, 21–2characteristics, 34–6PR interval, 28–30QRS complex/interval, 19–20, 22–5,

27–8, 30QT interval, 28, 30–31Q wave, 194–5repolarization, 16, 25–7R–R interval, 27–9, 31ST segment, 25


Index 391

timing of normal cardiac activity, 27–31

ventricular depolarization, 16, 19–25, 149–52, 168–9

normal sinus rhythmartifact, 218–19with normal AV conduction, 216–17

northwest axis, 318–19Notch pattern, 82–3nubbins, 202–3

old anterior wall MI, 202–3old lateral wall MI, 200–201ongoing arrhythmias, 366–8orthodromic reciprocating tachycardia

(ORT), 279, 299Osborn waves, 182–3

PAC. see premature atrial contractions (PAC)

pacemaker cells, 15–17pacemaker spikes, 192–3pacing, 334–45

atrial, 334–9atrioventricular block, 334–7biventricular pacing cardiac

resynchronization, 344–5dual chamber, 334–7, 342–3implantable devices, 334sinus node dysfunction, 335–7,

340–341ventricular, 334–7, 340–341

palpitations, 368–9paroxysmal supraventricular tachycardia

(PSVT), 278peaked T wave, 117–18, 122–5pericarditis, 44–5, 78–81physical examination, 32–3placement of electrodes, 2–4plaque rupture, 40polymorphic VT, 304–5poor R wave progression, 56–7, 204–5positive concordance, 314–15positive QRS, 106–7, 109posterior wall MI, 90–91, 154, 174–5precordial leads

comparing ECGs, 372–3ST segment depression, 108–9

ST segment elevation, 44–81technical issues, 2, 6–7T wave abnormalities, 124–5

premature atrial contractions (PAC), 228–9, 234–5, 258–9

premature junctional contractions, 230–231

premature ventricular contractions, 232–3

PR intervalarrhythmias, 244, 256–7, 301, 338–41interpretation of ECGs, 34–5normal ECG, 28–30prolonged QT interval, 134–5prominent R wave in V1, 162–7,

176–7, 180–181QRS complex/interval, 187, 190–191,

212–13stress testing, 360–361ST segment elevation, 78–9, 81, 83, 87

prolonged QT. see QT intervalprominent R wave in V1, 148–83prominent T wave, 117, 120–125, 145prominent voltage, 208–13PSVT. see paroxysmal supraventricular

tachycardia (PSVT)pulmonary circulation, 13–14pulmonary embolus, 206–7pulmonic valve, 13P wave

bradycardia, 241–71clinical problems, 366interpretation of ECGs, 32, 35–6normal rates and skips, 214, 216–27,

230–233, 236–7pacing, 338–43prominent R wave in V1, 172–7QRS complex/interval, 192–3, 212–13QT interval, 134–5ST segment elevation, 87tachycardia, 277–8, 284–5, 290–291,

294–301, 310–311T wave abnormalities, 124, 134–5

QRS complex/intervalbradycardia, 241–5, 248–9, 252–71changing QRS, 330–333clinical problems, 366–8, 372–3


392 Index

QRS complex/interval (cont’d)depolarization, 184–203interpretation of ECGs, 32–6left bundle branch block, 184–5,

188–9, 192–3normal ECG, 19–20, 22–5, 27–8normal rates and skips, 214, 222–5,

228–35pacing, 338–41, 344–5prominent R wave in V1, 148–9,

151–2, 156–9, 162–7, 170–173, 178–9

prominent voltage, 208–13Q wave anomalies, 186–7, 194–207right-sided accessory pathway, 184–5,

190–191right ventricular pacing, 184–6, 192–3size/voltage, 187ST segment depression, 99, 106–11ST segment elevation, 41, 44, 50–51,

54–5, 58–9, 70–71, 76–7, 82–3, 92–3

tachycardia, 272–4, 277–8, 280–333T wave abnormalities, 117–18,

120–121, 124–5wide and negative, 184–93widening from bundle branch block,

50–51, 54–5widening from hyperkalemia, 70–71,

124–5QT interval

drug-associated prolongation, 119, 138–9

etiology of prolongation, 118–19, 140–147

interpretation of ECGs, 36long QT syndrome, 118, 136–7normal ECG, 28, 30–31ST segment, 142–3, 145T wave abnormalities, 118–19,

132–47Q wave

abnormal, 200–207chest pain, 369interpretation of ECGs, 35–6left axis deviation, 196–7myocardial injury, 378–9normal ECG, 194–5

prominent R wave in V1, 158–9, 164–9, 174–5, 180–181

QRS complex/interval, 186–7, 194–207

right axis deviation, 198–9ST segment depression, 99, 102–3ST segment elevation, 41, 52–63,

70–77, 79–81, 84–9, 94–5

ramus intermedius, 57, 73rapid ventricular depolarization, 332RBBB. see right bundle branch block

(RBBB)recording paper, 9–12reentry, 274–5, 278–9, 294–5, 298–305,

320–323repetitive ventricular depolarization, 137repolarization

arrhythmias, 369atrial, 18aVR lead elevation, 96–7, 98, 105chest pain, 371early, 44–5, 48–9, 83, 120–121interpretation of ECGs, 35normal ECG, 16, 25–7normal ST segment elevation, 46–9,

82–3precordial ST segment elevation, 44–81QT interval, 118–19, 132–47stress testing, 360–361ST segment depression, 37–8, 41,

72–9, 84–5, 90–91, 96–7, 98–115, 117–18, 128–9

ST segment elevation, 37–97, 117–18technical issues, 8–9T wave abnormalities, 37–40, 44–5,

70–71, 81, 88–91, 100–103, 107, 112–15, 117–47

ventricular, 16, 25–7, 35retrograde atrial depolarization, 248–9retrograde P wave, 232–3, 294–5,

298–9right bundle branch block (RBBB)

arrhythmias, 254–5, 270–271, 322–3prominent R wave in V1, 150–151,

153–4, 156–63QRS complex/interval, 184

right coronary artery spasm, 94–5


Index 393

right-sided accessory pathway, 184–5, 190–191

right ventricular conduction delay, 170–171

right ventricular hypertrophy (RVH)prominent R wave in V1, 154, 172–3QRS complex/interval, 187syncope and palpitations, 369

right ventricular pacing, 184–6, 192–3Romhilt-Estes point system, 212–13R–R interval

interpretation of ECGs, 36normal ECG, 27–9, 31prolonged QT interval, 137

RS complex, 316–17rSr’ complex, 170–171R wave

attenuated, 160–163depolarization, 148–83large terminal R wave, 160–163monophasic, 188–9prominent in V1, 148–83QRS complex/interval, 188–9, 202–5,

210–211septal, 168–9stress testing, 350–351, 358–9,

362–3ST segment depression, 110–111,

114–15ST segment elevation, 56–7, 60–61,

82–3T wave abnormalities, 120–121

saddleback pattern, 68–9sail pattern, 66–7sarcoplasmic reticulum, 17scooped pattern, 103, 114–15second degree AV block, 242, 244–5,

252–7, 260–263, 268–712:1 second degree AV block, 244,

260–261septal R wave, 168–9severe advanced second degree AV

block, 268–9single chamber pacemakers, 334–41sinoventricular rhythm, 125sinus arrhythmia, 226–7sinus node, 15–18

artifact, 246–7bradycardia, 241, 243, 246–51clinical problems, 366exit block, 250–251pacing, 335–7, 340–341sinus pause with idioventricular

rhythm, 248–9SiQ3T3 pattern 206–7standardization marks, 10–11stress testing, 347–65

exercise and recovery ECGs, 352–3, 356–7

ST segment depression, 348, 352–63

ST segment elevation, 362–3supine and standing ECGs, 350–351

ST segment, 25arrhythmias, 230–231aVR lead elevation, 96–7, 98, 105depression, 37–8, 41, 72–9, 84–5,

90–91, 96–7, 98–115chest pain, 368–71prominent R wave in V1, 172–3QRS complex/interval, 189, 208–9,

212–13stress testing, 348, 352–63T wave abnormalities, 117–18,

128–9early repolarization, 44–5, 48–9elevation, 37–97, 117–18

chest pain, 368–71QRS complex/interval, 189,

202–5stress testing, 362–3

interpretation of ECGs, 32–6normal elevation, 46–9, 82–3percordial elevation, 44–81prominent R wave in V1, 172–3, 181QT interval, 142–3, 145repolarization, 37–115T wave abnormalities, 37–40, 44–5,

70–71, 81, 88–91, 100–103, 107, 112–15

subarachnoid hemorrhage, 146–7sudden cardiac death, 49, 59, 67, 69supraventricular tachycardia (SVT),

273–4, 276–9, 303, 306–309, 320–323, 366–8


394 Index

S waveprominent R wave in V1, 169, 173QRS complex/interval, 187, 198–9,

202–203, 206–7, 210–211ST segment elevation, 65

symmetric T wave inversion, 126–7, 130–131, 146–7

syncope, 368–9systemic circulation, 13–14

tachycardia, 272–333accessory pathway, 272–4, 302–3artifact, 306–9atrial, 272–8, 284–7, 290–293automaticity and reentry, 274–5,

278–9, 294–305, 320–323changing QRS, 330–333junctional, 272–4, 275–6, 296–7, 311normal rates and skips, 214–15ongoing arrhythmias, 366–8QRS complex/interval, 272–4, 277–8,

280–333stress testing, 364–5ventricular, 272–4, 279, 302–19,

324–9, 364–5Takotsubo syndrome, 62–3technical issues, 1–12

depolarization and repolarization, 8–9displaying the ECG, 9–12electrode placement, 2–4electrodes and leads, 4–9, 11–12

third degree AV block, 244–5, 264–7thrombus formation, 40timing of normal cardiac activity, 27–31Torsade de Pointes, 330–331T–P segment/interval, 34, 83tricuspid valve, 13trifascicular block, 162–3T wave. see also inverted T wave

arrhythmias, 228–35, 282–3, 292–3, 300–301, 310–311

biphasic, 140–141, 145chest pain, 368–77deflection, 228–9, 234–5, 282–3,

310–311interpretation of ECGs, 32–6normal ECG, 25, 27–9peaked, 117–18, 122–5

prominent, 117, 120–125, 145prominent R wave in V1, 174–5,

178–81QRS complex/interval, 187, 189,

194–5QT interval, 118–19, 132–47stress testing, 350–351ST segment depression, 100–103,

107, 112–115, 117–118, 128–9ST segment elevation, 37–40, 44–5,

70–71, 81, 88–91, 117–118twelve lead ECGs, 2–12type I/II errors, 358–9

unipolar limb leads, 5U wave

normal ECG, 30QT interval, 132–3, 140–141

vena cavae, 13ventricular arrhythmias, 61, 65–9ventricular depolarization. see

depolarizationventricular hypertrophy

comparing ECGs, 374–5prominent R wave in V1, 154, 172–3QRS complex/interval, 187, 208–13ST segment depression, 98, 110–111syncope and palpitations, 369T wave abnormalities, 127–9

ventricular pacing, 334–7, 340–341ventricular repolarization. see

repolarizationventricular tachycardia (VT), 272–4, 279,

302–19, 324–9, 364–5

Wenckebach second degree AV block, 252–5

wide negative depolarization, 149, 153, 156–7, 160–167

wide negative QRS complex/interval, 184–93

wide positive depolarization, 149, 153, 156–67, 182–3

wide QRS tachycardia, 272–4, 306–33Wolff Parkinson White (WPW)

Syndrome, 164–7, 190–191, 332–3, 360–361


ecg interpretation for everyone -...

Documents