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ECG Interpretation for Everyone
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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
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This edition first published 2012 © 2012 by John Wiley & Sons, Ltd.
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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
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To Dr. Edward H. Wymanand to Laura, Miya, Hana, and Aya
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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
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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
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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
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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
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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
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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
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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.)
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4 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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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.)
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6 ECG Interpretation for Everyone: An On-The-Spot Guide
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).
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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
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8 ECG Interpretation for Everyone: An On-The-Spot Guide
(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.)
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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.
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10 ECG Interpretation for Everyone: An On-The-Spot Guide
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.)
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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.
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12 ECG Interpretation for Everyone: An On-The-Spot Guide
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).
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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.
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
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14 ECG Interpretation for Everyone: An On-The-Spot Guide
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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.)
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16 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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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
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18 ECG Interpretation for Everyone: An On-The-Spot Guide
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.
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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
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20 ECG Interpretation for Everyone: An On-The-Spot Guide
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).
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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
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22 ECG Interpretation for Everyone: An On-The-Spot Guide
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.
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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
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24 ECG Interpretation for Everyone: An On-The-Spot Guide
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).
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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
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26 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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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.)
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28 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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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.
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30 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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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.
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32
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.
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
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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.
Kusumoto_c03.indd 33Kusumoto_c03.indd 33 11/30/2011 6:35:03 PM11/30/2011 6:35:03 PM
34 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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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).
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36 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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37
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.
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
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38 ECG Interpretation for Everyone: An On-The-Spot Guide
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).
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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
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40 ECG Interpretation for Everyone: An On-The-Spot Guide
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).
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Abnormal Repolarization: ST Segment Elevation 41
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.”
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42 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Abnormal Repolarization: ST Segment Elevation 43
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.
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44 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Abnormal Repolarization: ST Segment Elevation 45
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.
Kusumoto_c04.indd 45Kusumoto_c04.indd 45 11/19/2011 6:57:09 PM11/19/2011 6:57:09 PM
46 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 46Kusumoto_c04.indd 46 11/19/2011 6:57:10 PM11/19/2011 6:57:10 PM
Abnormal Repolarization: ST Segment Elevation 47
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.
Kusumoto_c04.indd 47Kusumoto_c04.indd 47 11/19/2011 6:57:10 PM11/19/2011 6:57:10 PM
48 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 48Kusumoto_c04.indd 48 11/19/2011 6:57:10 PM11/19/2011 6:57:10 PM
Abnormal Repolarization: ST Segment Elevation 49
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.
Kusumoto_c04.indd 49Kusumoto_c04.indd 49 11/19/2011 6:57:11 PM11/19/2011 6:57:11 PM
50 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 50Kusumoto_c04.indd 50 11/19/2011 6:57:11 PM11/19/2011 6:57:11 PM
Abnormal Repolarization: ST Segment Elevation 51
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.
Kusumoto_c04.indd 51Kusumoto_c04.indd 51 11/19/2011 6:57:11 PM11/19/2011 6:57:11 PM
52 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 52Kusumoto_c04.indd 52 11/19/2011 6:57:11 PM11/19/2011 6:57:11 PM
Abnormal Repolarization: ST Segment Elevation 53
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.
Kusumoto_c04.indd 53Kusumoto_c04.indd 53 11/19/2011 6:57:12 PM11/19/2011 6:57:12 PM
54 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c04.indd 54Kusumoto_c04.indd 54 11/19/2011 6:57:12 PM11/19/2011 6:57:12 PM
Abnormal Repolarization: ST Segment Elevation 55
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.
Kusumoto_c04.indd 55Kusumoto_c04.indd 55 11/19/2011 6:57:13 PM11/19/2011 6:57:13 PM
56 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c04.indd 56Kusumoto_c04.indd 56 11/19/2011 6:57:13 PM11/19/2011 6:57:13 PM
Abnormal Repolarization: ST Segment Elevation 57
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.
Kusumoto_c04.indd 57Kusumoto_c04.indd 57 11/19/2011 6:57:13 PM11/19/2011 6:57:13 PM
58 ECG Interpretation for Everyone: An On-The-Spot Guide
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
)
Kusumoto_c04.indd 58Kusumoto_c04.indd 58 11/19/2011 6:57:13 PM11/19/2011 6:57:13 PM
Abnormal Repolarization: ST Segment Elevation 59
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
.
Kusumoto_c04.indd 59Kusumoto_c04.indd 59 11/19/2011 6:57:14 PM11/19/2011 6:57:14 PM
60 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 60Kusumoto_c04.indd 60 11/19/2011 6:57:14 PM11/19/2011 6:57:14 PM
Abnormal Repolarization: ST Segment Elevation 61
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”).
Kusumoto_c04.indd 61Kusumoto_c04.indd 61 11/19/2011 6:57:14 PM11/19/2011 6:57:14 PM
62 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 62Kusumoto_c04.indd 62 11/19/2011 6:57:14 PM11/19/2011 6:57:14 PM
Abnormal Repolarization: ST Segment Elevation 63
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
.
Kusumoto_c04.indd 63Kusumoto_c04.indd 63 11/19/2011 6:57:14 PM11/19/2011 6:57:14 PM
64 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 64Kusumoto_c04.indd 64 11/19/2011 6:57:14 PM11/19/2011 6:57:14 PM
Abnormal Repolarization: ST Segment Elevation 65
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.
Kusumoto_c04.indd 65Kusumoto_c04.indd 65 11/19/2011 6:57:15 PM11/19/2011 6:57:15 PM
66 ECG Interpretation for Everyone: An On-The-Spot Guide
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”
Kusumoto_c04.indd 66Kusumoto_c04.indd 66 11/19/2011 6:57:15 PM11/19/2011 6:57:15 PM
Abnormal Repolarization: ST Segment Elevation 67
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
.
Kusumoto_c04.indd 67Kusumoto_c04.indd 67 11/19/2011 6:57:16 PM11/19/2011 6:57:16 PM
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
Abnormal Repolarization: ST Segment Elevation 69
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
.
Kusumoto_c04.indd 69Kusumoto_c04.indd 69 11/19/2011 6:57:16 PM11/19/2011 6:57:16 PM
70 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 70Kusumoto_c04.indd 70 11/19/2011 6:57:16 PM11/19/2011 6:57:16 PM
Abnormal Repolarization: ST Segment Elevation 71
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.
Kusumoto_c04.indd 71Kusumoto_c04.indd 71 11/19/2011 6:57:17 PM11/19/2011 6:57:17 PM
72 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 72Kusumoto_c04.indd 72 11/19/2011 6:57:17 PM11/19/2011 6:57:17 PM
Abnormal Repolarization: ST Segment Elevation 73
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.
Kusumoto_c04.indd 73Kusumoto_c04.indd 73 11/19/2011 6:57:17 PM11/19/2011 6:57:17 PM
74 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c04.indd 74Kusumoto_c04.indd 74 11/19/2011 6:57:17 PM11/19/2011 6:57:17 PM
Abnormal Repolarization: ST Segment Elevation 75
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.
Kusumoto_c04.indd 75Kusumoto_c04.indd 75 11/19/2011 6:57:18 PM11/19/2011 6:57:18 PM
76 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 76Kusumoto_c04.indd 76 11/19/2011 6:57:18 PM11/19/2011 6:57:18 PM
Abnormal Repolarization: ST Segment Elevation 77
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.
Kusumoto_c04.indd 77Kusumoto_c04.indd 77 11/19/2011 6:57:18 PM11/19/2011 6:57:18 PM
78 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 78Kusumoto_c04.indd 78 11/19/2011 6:57:18 PM11/19/2011 6:57:18 PM
Abnormal Repolarization: ST Segment Elevation 79
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
Kusumoto_c04.indd 79Kusumoto_c04.indd 79 11/19/2011 6:57:19 PM11/19/2011 6:57:19 PM
80 ECG Interpretation for Everyone: An On-The-Spot Guide
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.
Kusumoto_c04.indd 80Kusumoto_c04.indd 80 11/19/2011 6:57:19 PM11/19/2011 6:57:19 PM
Abnormal Repolarization: ST Segment Elevation 81
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
Kusumoto_c04.indd 81Kusumoto_c04.indd 81 11/19/2011 6:57:19 PM11/19/2011 6:57:19 PM
82 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 82Kusumoto_c04.indd 82 11/19/2011 6:57:19 PM11/19/2011 6:57:19 PM
Abnormal Repolarization: ST Segment Elevation 83
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.
Kusumoto_c04.indd 83Kusumoto_c04.indd 83 11/19/2011 6:57:19 PM11/19/2011 6:57:19 PM
84 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c04.indd 84Kusumoto_c04.indd 84 11/19/2011 6:57:20 PM11/19/2011 6:57:20 PM
Abnormal Repolarization: ST Segment Elevation 85
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.
Kusumoto_c04.indd 85Kusumoto_c04.indd 85 11/19/2011 6:57:20 PM11/19/2011 6:57:20 PM
86 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c04.indd 86Kusumoto_c04.indd 86 11/19/2011 6:57:20 PM11/19/2011 6:57:20 PM
Abnormal Repolarization: ST Segment Elevation 87
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.
Kusumoto_c04.indd 87Kusumoto_c04.indd 87 11/19/2011 6:57:21 PM11/19/2011 6:57:21 PM
88 ECG Interpretation for Everyone: An On-The-Spot Guide
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
)
Kusumoto_c04.indd 88Kusumoto_c04.indd 88 11/19/2011 6:57:21 PM11/19/2011 6:57:21 PM
Abnormal Repolarization: ST Segment Elevation 89
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
.
Kusumoto_c04.indd 89Kusumoto_c04.indd 89 11/19/2011 6:57:21 PM11/19/2011 6:57:21 PM
90 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c04.indd 90Kusumoto_c04.indd 90 11/19/2011 6:57:21 PM11/19/2011 6:57:21 PM
Abnormal Repolarization: ST Segment Elevation 91
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.
Kusumoto_c04.indd 91Kusumoto_c04.indd 91 11/19/2011 6:57:22 PM11/19/2011 6:57:22 PM
92 ECG Interpretation for Everyone: An On-The-Spot Guide
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
)
Kusumoto_c04.indd 92Kusumoto_c04.indd 92 11/19/2011 6:57:22 PM11/19/2011 6:57:22 PM
Abnormal Repolarization: ST Segment Elevation 93
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.
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94 ECG Interpretation for Everyone: An On-The-Spot Guide
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
)
Kusumoto_c04.indd 94Kusumoto_c04.indd 94 11/19/2011 6:57:22 PM11/19/2011 6:57:22 PM
Abnormal Repolarization: ST Segment Elevation 95
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.
Kusumoto_c04.indd 95Kusumoto_c04.indd 95 11/19/2011 6:57:23 PM11/19/2011 6:57:23 PM
96 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Abnormal Repolarization: ST Segment Elevation 97
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.
Kusumoto_c04.indd 97Kusumoto_c04.indd 97 11/19/2011 6:57:23 PM11/19/2011 6:57:23 PM
98
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.
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
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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?
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100 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Abnormal Repolarization: ST Segment Depression 101
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
.
Kusumoto_c05.indd 101Kusumoto_c05.indd 101 11/19/2011 6:57:57 PM11/19/2011 6:57:57 PM
102 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c05.indd 102Kusumoto_c05.indd 102 11/19/2011 6:57:57 PM11/19/2011 6:57:57 PM
Abnormal Repolarization: ST Segment Depression 103
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
.
Kusumoto_c05.indd 103Kusumoto_c05.indd 103 11/19/2011 6:57:58 PM11/19/2011 6:57:58 PM
104 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c05.indd 104Kusumoto_c05.indd 104 11/19/2011 6:57:58 PM11/19/2011 6:57:58 PM
Abnormal Repolarization: ST Segment Depression 105
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.
Kusumoto_c05.indd 105Kusumoto_c05.indd 105 11/19/2011 6:57:59 PM11/19/2011 6:57:59 PM
106 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c05.indd 106Kusumoto_c05.indd 106 11/19/2011 6:57:59 PM11/19/2011 6:57:59 PM
Abnormal Repolarization: ST Segment Depression 107
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
.
Kusumoto_c05.indd 107Kusumoto_c05.indd 107 11/19/2011 6:57:59 PM11/19/2011 6:57:59 PM
108 ECG Interpretation for Everyone: An On-The-Spot Guide
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
)
Kusumoto_c05.indd 108Kusumoto_c05.indd 108 11/19/2011 6:57:59 PM11/19/2011 6:57:59 PM
Abnormal Repolarization: ST Segment Depression 109
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.
Kusumoto_c05.indd 109Kusumoto_c05.indd 109 11/19/2011 6:57:59 PM11/19/2011 6:57:59 PM
110 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c05.indd 110Kusumoto_c05.indd 110 11/19/2011 6:57:59 PM11/19/2011 6:57:59 PM
Abnormal Repolarization: ST Segment Depression 111
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.
Kusumoto_c05.indd 111Kusumoto_c05.indd 111 11/19/2011 6:57:59 PM11/19/2011 6:57:59 PM
112 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c05.indd 112Kusumoto_c05.indd 112 11/19/2011 6:57:59 PM11/19/2011 6:57:59 PM
Abnormal Repolarization: ST Segment Depression 113
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.
Kusumoto_c05.indd 113Kusumoto_c05.indd 113 11/19/2011 6:58:00 PM11/19/2011 6:58:00 PM
114 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c05.indd 114Kusumoto_c05.indd 114 11/19/2011 6:58:00 PM11/19/2011 6:58:00 PM
Abnormal Repolarization: ST Segment Depression 115
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.
Kusumoto_c05.indd 115Kusumoto_c05.indd 115 11/19/2011 6:58:00 PM11/19/2011 6:58:00 PM
117
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.
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
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118 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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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.
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120 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Abnormal Repolarization: T Wave Changes and the QT Interval 121
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.
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122 ECG Interpretation for Everyone: An On-The-Spot Guide
“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
Kusumoto_c06.indd 122Kusumoto_c06.indd 122 11/19/2011 7:14:21 PM11/19/2011 7:14:21 PM
Abnormal Repolarization: T Wave Changes and the QT Interval 123
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.
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124 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Abnormal Repolarization: T Wave Changes and the QT Interval 125
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.
Kusumoto_c06.indd 125Kusumoto_c06.indd 125 11/19/2011 7:14:21 PM11/19/2011 7:14:21 PM
126 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c06.indd 126Kusumoto_c06.indd 126 11/19/2011 7:14:21 PM11/19/2011 7:14:21 PM
Abnormal Repolarization: T Wave Changes and the QT Interval 127
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.
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128 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c06.indd 128Kusumoto_c06.indd 128 11/19/2011 7:14:22 PM11/19/2011 7:14:22 PM
Abnormal Repolarization: T Wave Changes and the QT Interval 129
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.
Kusumoto_c06.indd 129Kusumoto_c06.indd 129 11/19/2011 7:14:22 PM11/19/2011 7:14:22 PM
130 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c06.indd 130Kusumoto_c06.indd 130 11/19/2011 7:14:22 PM11/19/2011 7:14:22 PM
Abnormal Repolarization: T Wave Changes and the QT Interval 131
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.
Kusumoto_c06.indd 131Kusumoto_c06.indd 131 11/19/2011 7:14:23 PM11/19/2011 7:14:23 PM
132 ECG Interpretation for Everyone: An On-The-Spot Guide
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
)
Kusumoto_c06.indd 132Kusumoto_c06.indd 132 11/19/2011 7:14:23 PM11/19/2011 7:14:23 PM
Abnormal Repolarization: T Wave Changes and the QT Interval 133
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
.
Kusumoto_c06.indd 133Kusumoto_c06.indd 133 11/19/2011 7:14:24 PM11/19/2011 7:14:24 PM
134 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c06.indd 134Kusumoto_c06.indd 134 11/19/2011 7:14:24 PM11/19/2011 7:14:24 PM
Abnormal Repolarization: T Wave Changes and the QT Interval 135
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.
Kusumoto_c06.indd 135Kusumoto_c06.indd 135 11/19/2011 7:14:24 PM11/19/2011 7:14:24 PM
136 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c06.indd 136Kusumoto_c06.indd 136 11/19/2011 7:14:24 PM11/19/2011 7:14:24 PM
Abnormal Repolarization: T Wave Changes and the QT Interval 137
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.
Kusumoto_c06.indd 137Kusumoto_c06.indd 137 11/19/2011 7:14:25 PM11/19/2011 7:14:25 PM
138 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c06.indd 138Kusumoto_c06.indd 138 11/19/2011 7:14:25 PM11/19/2011 7:14:25 PM
Abnormal Repolarization: T Wave Changes and the QT Interval 139
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.
Kusumoto_c06.indd 139Kusumoto_c06.indd 139 11/19/2011 7:14:25 PM11/19/2011 7:14:25 PM
140 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c06.indd 140Kusumoto_c06.indd 140 11/19/2011 7:14:25 PM11/19/2011 7:14:25 PM
Abnormal Repolarization: T Wave Changes and the QT Interval 141
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
+.
Kusumoto_c06.indd 141Kusumoto_c06.indd 141 11/19/2011 7:14:25 PM11/19/2011 7:14:25 PM
142 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c06.indd 142Kusumoto_c06.indd 142 11/19/2011 7:14:26 PM11/19/2011 7:14:26 PM
Abnormal Repolarization: T Wave Changes and the QT Interval 143
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.
Kusumoto_c06.indd 143Kusumoto_c06.indd 143 11/19/2011 7:14:26 PM11/19/2011 7:14:26 PM
144 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c06.indd 144Kusumoto_c06.indd 144 11/19/2011 7:14:26 PM11/19/2011 7:14:26 PM
Abnormal Repolarization: T Wave Changes and the QT Interval 145
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.
Kusumoto_c06.indd 145Kusumoto_c06.indd 145 11/19/2011 7:14:26 PM11/19/2011 7:14:26 PM
146 ECG Interpretation for Everyone: An On-The-Spot Guide
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
)
Kusumoto_c06.indd 146Kusumoto_c06.indd 146 11/19/2011 7:14:26 PM11/19/2011 7:14:26 PM
Abnormal Repolarization: T Wave Changes and the QT Interval 147
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.
Kusumoto_c06.indd 147Kusumoto_c06.indd 147 11/19/2011 7:14:27 PM11/19/2011 7:14:27 PM
148
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.
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
Kusumoto_c07.indd 148Kusumoto_c07.indd 148 11/19/2011 6:59:47 PM11/19/2011 6:59:47 PM
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.”
Kusumoto_c07.indd 149Kusumoto_c07.indd 149 11/19/2011 6:59:47 PM11/19/2011 6:59:47 PM
150 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Abnormal Depolarization: A Prominent R Wave in V1 151
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”
Kusumoto_c07.indd 151Kusumoto_c07.indd 151 11/19/2011 6:59:47 PM11/19/2011 6:59:47 PM
152 ECG Interpretation for Everyone: An On-The-Spot Guide
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.
Kusumoto_c07.indd 152Kusumoto_c07.indd 152 11/19/2011 6:59:47 PM11/19/2011 6:59:47 PM
Abnormal Depolarization: A Prominent R Wave in V1 153
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.
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154 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c07.indd 154Kusumoto_c07.indd 154 11/19/2011 6:59:48 PM11/19/2011 6:59:48 PM
Abnormal Depolarization: A Prominent R Wave in V1 155
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.
Kusumoto_c07.indd 155Kusumoto_c07.indd 155 11/19/2011 6:59:48 PM11/19/2011 6:59:48 PM
156 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c07.indd 156Kusumoto_c07.indd 156 11/19/2011 6:59:48 PM11/19/2011 6:59:48 PM
Abnormal Depolarization: A Prominent R Wave in V1 157
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.
Kusumoto_c07.indd 157Kusumoto_c07.indd 157 11/19/2011 6:59:49 PM11/19/2011 6:59:49 PM
158 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c07.indd 158Kusumoto_c07.indd 158 11/19/2011 6:59:49 PM11/19/2011 6:59:49 PM
Abnormal Depolarization: A Prominent R Wave in V1 159
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.
Kusumoto_c07.indd 159Kusumoto_c07.indd 159 11/19/2011 6:59:49 PM11/19/2011 6:59:49 PM
160 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c07.indd 160Kusumoto_c07.indd 160 11/19/2011 6:59:49 PM11/19/2011 6:59:49 PM
Abnormal Depolarization: A Prominent R Wave in V1 161
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
.
Kusumoto_c07.indd 161Kusumoto_c07.indd 161 11/19/2011 6:59:50 PM11/19/2011 6:59:50 PM
162 ECG Interpretation for Everyone: An On-The-Spot Guide
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”)
Kusumoto_c07.indd 162Kusumoto_c07.indd 162 11/19/2011 6:59:50 PM11/19/2011 6:59:50 PM
Abnormal Depolarization: A Prominent R Wave in V1 163
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.
Kusumoto_c07.indd 163Kusumoto_c07.indd 163 11/19/2011 6:59:50 PM11/19/2011 6:59:50 PM
164 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c07.indd 164Kusumoto_c07.indd 164 11/19/2011 6:59:50 PM11/19/2011 6:59:50 PM
Abnormal Depolarization: A Prominent R Wave in V1 165
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
.
Kusumoto_c07.indd 165Kusumoto_c07.indd 165 11/19/2011 6:59:51 PM11/19/2011 6:59:51 PM
166 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c07.indd 166Kusumoto_c07.indd 166 11/19/2011 6:59:51 PM11/19/2011 6:59:51 PM
Abnormal Depolarization: A Prominent R Wave in V1 167
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.
Kusumoto_c07.indd 167Kusumoto_c07.indd 167 11/19/2011 6:59:51 PM11/19/2011 6:59:51 PM
168 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c07.indd 168Kusumoto_c07.indd 168 11/19/2011 6:59:51 PM11/19/2011 6:59:51 PM
Abnormal Depolarization: A Prominent R Wave in V1 169
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.
Kusumoto_c07.indd 169Kusumoto_c07.indd 169 11/19/2011 6:59:52 PM11/19/2011 6:59:52 PM
170 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c07.indd 170Kusumoto_c07.indd 170 11/19/2011 6:59:52 PM11/19/2011 6:59:52 PM
Abnormal Depolarization: A Prominent R Wave in V1 171
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)
.
Kusumoto_c07.indd 171Kusumoto_c07.indd 171 11/19/2011 6:59:52 PM11/19/2011 6:59:52 PM
172 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c07.indd 172Kusumoto_c07.indd 172 11/19/2011 6:59:52 PM11/19/2011 6:59:52 PM
Abnormal Depolarization: A Prominent R Wave in V1 173
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.
Kusumoto_c07.indd 173Kusumoto_c07.indd 173 11/19/2011 6:59:52 PM11/19/2011 6:59:52 PM
174 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c07.indd 174Kusumoto_c07.indd 174 11/19/2011 6:59:53 PM11/19/2011 6:59:53 PM
Abnormal Depolarization: A Prominent R Wave in V1 175
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.
Kusumoto_c07.indd 175Kusumoto_c07.indd 175 11/19/2011 6:59:53 PM11/19/2011 6:59:53 PM
176 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c07.indd 176Kusumoto_c07.indd 176 11/19/2011 6:59:53 PM11/19/2011 6:59:53 PM
Abnormal Depolarization: A Prominent R Wave in V1 177
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
.
Kusumoto_c07.indd 177Kusumoto_c07.indd 177 11/19/2011 6:59:53 PM11/19/2011 6:59:53 PM
178 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c07.indd 178Kusumoto_c07.indd 178 11/19/2011 6:59:54 PM11/19/2011 6:59:54 PM
Abnormal Depolarization: A Prominent R Wave in V1 179
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.
Kusumoto_c07.indd 179Kusumoto_c07.indd 179 11/19/2011 6:59:54 PM11/19/2011 6:59:54 PM
180 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c07.indd 180Kusumoto_c07.indd 180 11/19/2011 6:59:54 PM11/19/2011 6:59:54 PM
Abnormal Depolarization: A Prominent R Wave in V1 181
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.
Kusumoto_c07.indd 181Kusumoto_c07.indd 181 11/19/2011 6:59:54 PM11/19/2011 6:59:54 PM
182 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c07.indd 182Kusumoto_c07.indd 182 11/19/2011 6:59:54 PM11/19/2011 6:59:54 PM
Abnormal Depolarization: A Prominent R Wave in V1 183
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.
Kusumoto_c07.indd 183Kusumoto_c07.indd 183 11/19/2011 6:59:55 PM11/19/2011 6:59:55 PM
184
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.
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
Kusumoto_c08.indd 184Kusumoto_c08.indd 184 11/19/2011 7:02:22 PM11/19/2011 7:02:22 PM
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.
Kusumoto_c08.indd 185Kusumoto_c08.indd 185 11/19/2011 7:02:22 PM11/19/2011 7:02:22 PM
186 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c08.indd 186Kusumoto_c08.indd 186 11/19/2011 7:02:23 PM11/19/2011 7:02:23 PM
Abnormal Depolarization 187
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.
Kusumoto_c08.indd 187Kusumoto_c08.indd 187 11/19/2011 7:02:23 PM11/19/2011 7:02:23 PM
188 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c08.indd 188Kusumoto_c08.indd 188 11/19/2011 7:02:23 PM11/19/2011 7:02:23 PM
Abnormal Depolarization 189
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
.
Kusumoto_c08.indd 189Kusumoto_c08.indd 189 11/19/2011 7:02:23 PM11/19/2011 7:02:23 PM
190 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c08.indd 190Kusumoto_c08.indd 190 11/19/2011 7:02:23 PM11/19/2011 7:02:23 PM
Abnormal Depolarization 191
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.
Kusumoto_c08.indd 191Kusumoto_c08.indd 191 11/19/2011 7:02:23 PM11/19/2011 7:02:23 PM
192 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c08.indd 192Kusumoto_c08.indd 192 11/19/2011 7:02:23 PM11/19/2011 7:02:23 PM
Abnormal Depolarization 193
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.
Kusumoto_c08.indd 193Kusumoto_c08.indd 193 11/19/2011 7:02:24 PM11/19/2011 7:02:24 PM
194 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c08.indd 194Kusumoto_c08.indd 194 11/19/2011 7:02:24 PM11/19/2011 7:02:24 PM
Abnormal Depolarization 195
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).
Kusumoto_c08.indd 195Kusumoto_c08.indd 195 11/19/2011 7:02:24 PM11/19/2011 7:02:24 PM
196 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c08.indd 196Kusumoto_c08.indd 196 11/19/2011 7:02:24 PM11/19/2011 7:02:24 PM
Abnormal Depolarization 197
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
.
Kusumoto_c08.indd 197Kusumoto_c08.indd 197 11/19/2011 7:02:24 PM11/19/2011 7:02:24 PM
198 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c08.indd 198Kusumoto_c08.indd 198 11/19/2011 7:02:24 PM11/19/2011 7:02:24 PM
Abnormal Depolarization 199
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.
Kusumoto_c08.indd 199Kusumoto_c08.indd 199 11/19/2011 7:02:25 PM11/19/2011 7:02:25 PM
200 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c08.indd 200Kusumoto_c08.indd 200 11/19/2011 7:02:25 PM11/19/2011 7:02:25 PM
Abnormal Depolarization 201
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.
Kusumoto_c08.indd 201Kusumoto_c08.indd 201 11/19/2011 7:02:25 PM11/19/2011 7:02:25 PM
202 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c08.indd 202Kusumoto_c08.indd 202 11/19/2011 7:02:25 PM11/19/2011 7:02:25 PM
Abnormal Depolarization 203
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.
Kusumoto_c08.indd 203Kusumoto_c08.indd 203 11/19/2011 7:02:25 PM11/19/2011 7:02:25 PM
204 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c08.indd 204Kusumoto_c08.indd 204 11/19/2011 7:02:25 PM11/19/2011 7:02:25 PM
Abnormal Depolarization 205
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
.
Kusumoto_c08.indd 205Kusumoto_c08.indd 205 11/19/2011 7:02:26 PM11/19/2011 7:02:26 PM
206 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c08.indd 206Kusumoto_c08.indd 206 11/19/2011 7:02:26 PM11/19/2011 7:02:26 PM
Abnormal Depolarization 207
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.
Kusumoto_c08.indd 207Kusumoto_c08.indd 207 11/19/2011 7:02:26 PM11/19/2011 7:02:26 PM
208 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c08.indd 208Kusumoto_c08.indd 208 11/19/2011 7:02:26 PM11/19/2011 7:02:26 PM
Abnormal Depolarization 209
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.
Kusumoto_c08.indd 209Kusumoto_c08.indd 209 11/19/2011 7:02:26 PM11/19/2011 7:02:26 PM
210 ECG Interpretation for Everyone: An On-The-Spot Guide
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
)
Kusumoto_c08.indd 210Kusumoto_c08.indd 210 11/19/2011 7:02:26 PM11/19/2011 7:02:26 PM
Abnormal Depolarization 211
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.
Kusumoto_c08.indd 211Kusumoto_c08.indd 211 11/19/2011 7:02:27 PM11/19/2011 7:02:27 PM
212 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c08.indd 212Kusumoto_c08.indd 212 11/19/2011 7:02:27 PM11/19/2011 7:02:27 PM
Abnormal Depolarization 213
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.
Kusumoto_c08.indd 213Kusumoto_c08.indd 213 11/19/2011 7:02:27 PM11/19/2011 7:02:27 PM
214
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.
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
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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)
.
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216 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c09.indd 216Kusumoto_c09.indd 216 11/30/2011 6:36:24 PM11/30/2011 6:36:24 PM
Arrhythmias: Normal Rates and Skips 217
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.
Kusumoto_c09.indd 217Kusumoto_c09.indd 217 11/30/2011 6:36:24 PM11/30/2011 6:36:24 PM
218 ECG Interpretation for Everyone: An On-The-Spot Guide
*
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)
Kusumoto_c09.indd 218Kusumoto_c09.indd 218 11/30/2011 6:36:24 PM11/30/2011 6:36:24 PM
Arrhythmias: Normal Rates and Skips 219
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
.
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220 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Normal Rates and Skips 221
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.
Kusumoto_c09.indd 221Kusumoto_c09.indd 221 11/30/2011 6:36:25 PM11/30/2011 6:36:25 PM
222 ECG Interpretation for Everyone: An On-The-Spot Guide
II aV
R
P w
ave
s?
Re
gu
lar
Rh
yth
m
Jun
ctio
na
l Rh
yth
m
Kusumoto_c09.indd 222Kusumoto_c09.indd 222 11/30/2011 6:36:25 PM11/30/2011 6:36:25 PM
Arrhythmias: Normal Rates and Skips 223
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.
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224 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Normal Rates and Skips 225
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).
Kusumoto_c09.indd 225Kusumoto_c09.indd 225 11/30/2011 6:36:27 PM11/30/2011 6:36:27 PM
226 ECG Interpretation for Everyone: An On-The-Spot Guide
**
**
**
Irre
gu
lar
Rh
yth
m
Sin
us
arr
hyt
hm
ia
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Arrhythmias: Normal Rates and Skips 227
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.
Kusumoto_c09.indd 227Kusumoto_c09.indd 227 11/30/2011 6:36:27 PM11/30/2011 6:36:27 PM
228 ECG Interpretation for Everyone: An On-The-Spot Guide
“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
Kusumoto_c09.indd 228Kusumoto_c09.indd 228 11/30/2011 6:36:27 PM11/30/2011 6:36:27 PM
Arrhythmias: Normal Rates and Skips 229
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).
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230 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c09.indd 230Kusumoto_c09.indd 230 11/30/2011 6:36:27 PM11/30/2011 6:36:27 PM
Arrhythmias: Normal Rates and Skips 231
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
.
Kusumoto_c09.indd 231Kusumoto_c09.indd 231 11/30/2011 6:36:28 PM11/30/2011 6:36:28 PM
232 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c09.indd 232Kusumoto_c09.indd 232 11/30/2011 6:36:28 PM11/30/2011 6:36:28 PM
Arrhythmias: Normal Rates and Skips 233
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
.
Kusumoto_c09.indd 233Kusumoto_c09.indd 233 11/30/2011 6:36:28 PM11/30/2011 6:36:28 PM
234 ECG Interpretation for Everyone: An On-The-Spot Guide
“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)
Kusumoto_c09.indd 234Kusumoto_c09.indd 234 11/30/2011 6:36:28 PM11/30/2011 6:36:28 PM
Arrhythmias: Normal Rates and Skips 235
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)
.
Kusumoto_c09.indd 235Kusumoto_c09.indd 235 11/30/2011 6:36:28 PM11/30/2011 6:36:28 PM
236 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c09.indd 236Kusumoto_c09.indd 236 11/30/2011 6:36:28 PM11/30/2011 6:36:28 PM
Arrhythmias: Normal Rates and Skips 237
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
.
Kusumoto_c09.indd 237Kusumoto_c09.indd 237 11/30/2011 6:36:29 PM11/30/2011 6:36:29 PM
238 ECG Interpretation for Everyone: An On-The-Spot Guide
Irre
gu
lar
Rh
yth
m
Atr
ial fi
bri
llati
on
Kusumoto_c09.indd 238Kusumoto_c09.indd 238 11/30/2011 6:36:29 PM11/30/2011 6:36:29 PM
Arrhythmias: Normal Rates and Skips 239
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.
Kusumoto_c09.indd 239Kusumoto_c09.indd 239 11/30/2011 6:36:30 PM11/30/2011 6:36:30 PM
241
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.
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
Kusumoto_c10.indd 241Kusumoto_c10.indd 241 11/30/2011 6:37:31 PM11/30/2011 6:37:31 PM
242 ECG Interpretation for Everyone: An On-The-Spot Guide
(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.
Kusumoto_c10.indd 242Kusumoto_c10.indd 242 11/30/2011 6:37:31 PM11/30/2011 6:37:31 PM
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
Kusumoto_c10.indd 243Kusumoto_c10.indd 243 11/30/2011 6:37:31 PM11/30/2011 6:37:31 PM
244 ECG Interpretation for Everyone: An On-The-Spot Guide
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.
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Arrhythmias: Bradycardia 245
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.
Kusumoto_c10.indd 245Kusumoto_c10.indd 245 11/30/2011 6:37:32 PM11/30/2011 6:37:32 PM
246 ECG Interpretation for Everyone: An On-The-Spot Guide
Sin
us
No
de
dys
fun
ctio
n (
No
t e
no
ug
h P
wav
es)
Art
ifa
ct
Kusumoto_c10.indd 246Kusumoto_c10.indd 246 11/30/2011 6:37:32 PM11/30/2011 6:37:32 PM
Arrhythmias: Bradycardia 247
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
.
Kusumoto_c10.indd 247Kusumoto_c10.indd 247 11/30/2011 6:37:32 PM11/30/2011 6:37:32 PM
248 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c10.indd 248Kusumoto_c10.indd 248 11/30/2011 6:37:32 PM11/30/2011 6:37:32 PM
Arrhythmias: Bradycardia 249
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.
Kusumoto_c10.indd 249Kusumoto_c10.indd 249 11/30/2011 6:37:33 PM11/30/2011 6:37:33 PM
250 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c10.indd 250Kusumoto_c10.indd 250 11/30/2011 6:37:33 PM11/30/2011 6:37:33 PM
Arrhythmias: Bradycardia 251
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
.
Kusumoto_c10.indd 251Kusumoto_c10.indd 251 11/30/2011 6:37:34 PM11/30/2011 6:37:34 PM
252 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
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Arrhythmias: Bradycardia 253
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.
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254 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
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Arrhythmias: Bradycardia 255
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.
Kusumoto_c10.indd 255Kusumoto_c10.indd 255 11/30/2011 6:37:34 PM11/30/2011 6:37:34 PM
256 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Bradycardia 257
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
.
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258 ECG Interpretation for Everyone: An On-The-Spot Guide
“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
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Arrhythmias: Bradycardia 259
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.
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260 ECG Interpretation for Everyone: An On-The-Spot Guide
II
PP
PP
??
Atr
iove
ntr
icu
lar
blo
ck
(P’s
wit
ho
ut
QR
S’s
)
2:1
2°
AV
blo
ck
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Arrhythmias: Bradycardia 261
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
.
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262 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Bradycardia 263
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
.
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264 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
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Arrhythmias: Bradycardia 265
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.
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266 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Bradycardia 267
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
.
Kusumoto_c10.indd 267Kusumoto_c10.indd 267 11/30/2011 6:37:37 PM11/30/2011 6:37:37 PM
268 ECG Interpretation for Everyone: An On-The-Spot Guide
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
)
Kusumoto_c10.indd 268Kusumoto_c10.indd 268 11/30/2011 6:37:37 PM11/30/2011 6:37:37 PM
Arrhythmias: Bradycardia 269
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.
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270 ECG Interpretation for Everyone: An On-The-Spot Guide
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
)
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Arrhythmias: Bradycardia 271
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).
Kusumoto_c10.indd 271Kusumoto_c10.indd 271 11/30/2011 6:37:38 PM11/30/2011 6:37:38 PM
272
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.
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
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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.)
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274 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Tachycardia 275
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
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276 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Tachycardia 277
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)
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278 ECG Interpretation for Everyone: An On-The-Spot Guide
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.
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Arrhythmias: Tachycardia 279
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.
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280 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Tachycardia 281
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.
Kusumoto_c11.indd 281Kusumoto_c11.indd 281 11/19/2011 7:07:24 PM11/19/2011 7:07:24 PM
282 ECG Interpretation for Everyone: An On-The-Spot Guide
**
AF
Irre
gu
lar
Na
rro
w Q
RS
ta
chyc
ard
ia
Atr
ial fi
bri
llati
on
(in
itia
tio
n)
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Arrhythmias: Tachycardia 283
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)
.
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284 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Tachycardia 285
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
).
Kusumoto_c11.indd 285Kusumoto_c11.indd 285 11/19/2011 7:07:25 PM11/19/2011 7:07:25 PM
286 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Tachycardia 287
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
.
Kusumoto_c11.indd 287Kusumoto_c11.indd 287 11/19/2011 7:07:25 PM11/19/2011 7:07:25 PM
288 ECG Interpretation for Everyone: An On-The-Spot Guide
Irre
gu
lar
Na
rro
w Q
RS
ta
chyc
ard
ia
Atr
ial fi
bri
llati
on
(”c
oa
rse”
)
Kusumoto_c11.indd 288Kusumoto_c11.indd 288 11/19/2011 7:07:26 PM11/19/2011 7:07:26 PM
Arrhythmias: Tachycardia 289
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
.
Kusumoto_c11.indd 289Kusumoto_c11.indd 289 11/19/2011 7:07:26 PM11/19/2011 7:07:26 PM
290 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c11.indd 290Kusumoto_c11.indd 290 11/19/2011 7:07:27 PM11/19/2011 7:07:27 PM
Arrhythmias: Tachycardia 291
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.
Kusumoto_c11.indd 291Kusumoto_c11.indd 291 11/19/2011 7:07:27 PM11/19/2011 7:07:27 PM
292 ECG Interpretation for Everyone: An On-The-Spot Guide
Re
gu
lar
Na
rro
w Q
RS
ta
chyc
ard
ia
Foca
l atr
ial t
ach
yca
rdia
PP
PP
?
V1
Kusumoto_c11.indd 292Kusumoto_c11.indd 292 11/19/2011 7:07:27 PM11/19/2011 7:07:27 PM
Arrhythmias: Tachycardia 293
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.
Kusumoto_c11.indd 293Kusumoto_c11.indd 293 11/19/2011 7:07:27 PM11/19/2011 7:07:27 PM
294 ECG Interpretation for Everyone: An On-The-Spot Guide
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’
**
**
**
**
*
Kusumoto_c11.indd 294Kusumoto_c11.indd 294 11/19/2011 7:07:27 PM11/19/2011 7:07:27 PM
Arrhythmias: Tachycardia 295
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.
Kusumoto_c11.indd 295Kusumoto_c11.indd 295 11/19/2011 7:07:28 PM11/19/2011 7:07:28 PM
296 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c11.indd 296Kusumoto_c11.indd 296 11/19/2011 7:07:28 PM11/19/2011 7:07:28 PM
Arrhythmias: Tachycardia 297
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.
Kusumoto_c11.indd 297Kusumoto_c11.indd 297 11/19/2011 7:07:29 PM11/19/2011 7:07:29 PM
298 ECG Interpretation for Everyone: An On-The-Spot Guide
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
*
* **
Kusumoto_c11.indd 298Kusumoto_c11.indd 298 11/19/2011 7:07:29 PM11/19/2011 7:07:29 PM
Arrhythmias: Tachycardia 299
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.
Kusumoto_c11.indd 299Kusumoto_c11.indd 299 11/19/2011 7:07:29 PM11/19/2011 7:07:29 PM
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
)
Kusumoto_c11.indd 300Kusumoto_c11.indd 300 11/19/2011 7:07:30 PM11/19/2011 7:07:30 PM
Arrhythmias: Tachycardia 301
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.
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302 ECG Interpretation for Everyone: An On-The-Spot Guide
Kusumoto_c11.indd 302Kusumoto_c11.indd 302 11/19/2011 7:07:30 PM11/19/2011 7:07:30 PM
Arrhythmias: Tachycardia 303
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.)
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304 ECG Interpretation for Everyone: An On-The-Spot Guide
Mo
no
mo
rph
ic V
TP
oly
mo
rph
ic V
T
(Ve
ntr
icu
lar
Fib
rilla
tio
n)
Kusumoto_c11.indd 304Kusumoto_c11.indd 304 11/19/2011 7:07:31 PM11/19/2011 7:07:31 PM
Arrhythmias: Tachycardia 305
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.
Kusumoto_c11.indd 305Kusumoto_c11.indd 305 11/19/2011 7:07:31 PM11/19/2011 7:07:31 PM
306 ECG Interpretation for Everyone: An On-The-Spot Guide
**
**
**
**
**
“Wid
e Q
RS
ta
chyc
ard
ia”
Art
ifa
ct
Kusumoto_c11.indd 306Kusumoto_c11.indd 306 11/19/2011 7:07:31 PM11/19/2011 7:07:31 PM
Arrhythmias: Tachycardia 307
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.
Kusumoto_c11.indd 307Kusumoto_c11.indd 307 11/19/2011 7:07:32 PM11/19/2011 7:07:32 PM
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
Kusumoto_c11.indd 308Kusumoto_c11.indd 308 11/19/2011 7:07:32 PM11/19/2011 7:07:32 PM
Arrhythmias: Tachycardia 309
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.
Kusumoto_c11.indd 309Kusumoto_c11.indd 309 11/19/2011 7:07:33 PM11/19/2011 7:07:33 PM
310 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c11.indd 310Kusumoto_c11.indd 310 11/19/2011 7:07:33 PM11/19/2011 7:07:33 PM
Arrhythmias: Tachycardia 311
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
.
Kusumoto_c11.indd 311Kusumoto_c11.indd 311 11/19/2011 7:07:33 PM11/19/2011 7:07:33 PM
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)
Kusumoto_c11.indd 312Kusumoto_c11.indd 312 11/19/2011 7:07:33 PM11/19/2011 7:07:33 PM
Arrhythmias: Tachycardia 313
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)
.
Kusumoto_c11.indd 313Kusumoto_c11.indd 313 11/19/2011 7:07:34 PM11/19/2011 7:07:34 PM
314 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c11.indd 314Kusumoto_c11.indd 314 11/19/2011 7:07:34 PM11/19/2011 7:07:34 PM
Arrhythmias: Tachycardia 315
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
.
Kusumoto_c11.indd 315Kusumoto_c11.indd 315 11/19/2011 7:07:35 PM11/19/2011 7:07:35 PM
316 ECG Interpretation for Everyone: An On-The-Spot Guide
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
)
Kusumoto_c11.indd 316Kusumoto_c11.indd 316 11/19/2011 7:07:35 PM11/19/2011 7:07:35 PM
Arrhythmias: Tachycardia 317
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.
Kusumoto_c11.indd 317Kusumoto_c11.indd 317 11/19/2011 7:07:35 PM11/19/2011 7:07:35 PM
318 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c11.indd 318Kusumoto_c11.indd 318 11/19/2011 7:07:35 PM11/19/2011 7:07:35 PM
Arrhythmias: Tachycardia 319
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.
Kusumoto_c11.indd 319Kusumoto_c11.indd 319 11/19/2011 7:07:36 PM11/19/2011 7:07:36 PM
320 ECG Interpretation for Everyone: An On-The-Spot Guide
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
)
Kusumoto_c11.indd 320Kusumoto_c11.indd 320 11/19/2011 7:07:36 PM11/19/2011 7:07:36 PM
Arrhythmias: Tachycardia 321
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).
Kusumoto_c11.indd 321Kusumoto_c11.indd 321 11/19/2011 7:07:36 PM11/19/2011 7:07:36 PM
322 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c11.indd 322Kusumoto_c11.indd 322 11/19/2011 7:07:36 PM11/19/2011 7:07:36 PM
Arrhythmias: Tachycardia 323
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.
Kusumoto_c11.indd 323Kusumoto_c11.indd 323 11/19/2011 7:07:37 PM11/19/2011 7:07:37 PM
324 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c11.indd 324Kusumoto_c11.indd 324 11/19/2011 7:07:37 PM11/19/2011 7:07:37 PM
Arrhythmias: Tachycardia 325
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.
Kusumoto_c11.indd 325Kusumoto_c11.indd 325 11/19/2011 7:07:37 PM11/19/2011 7:07:37 PM
326 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c11.indd 326Kusumoto_c11.indd 326 11/19/2011 7:07:37 PM11/19/2011 7:07:37 PM
Arrhythmias: Tachycardia 327
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.
Kusumoto_c11.indd 327Kusumoto_c11.indd 327 11/19/2011 7:07:38 PM11/19/2011 7:07:38 PM
328 ECG Interpretation for Everyone: An On-The-Spot Guide
Ve
ntr
icu
lar
Tach
yca
rdia
Tre
ate
d w
ith
Ca
rdio
vers
ion
*
Kusumoto_c11.indd 328Kusumoto_c11.indd 328 11/19/2011 7:07:38 PM11/19/2011 7:07:38 PM
Arrhythmias: Tachycardia 329
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.
Kusumoto_c11.indd 329Kusumoto_c11.indd 329 11/19/2011 7:07:38 PM11/19/2011 7:07:38 PM
330 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c11.indd 330Kusumoto_c11.indd 330 11/19/2011 7:07:38 PM11/19/2011 7:07:38 PM
Arrhythmias: Tachycardia 331
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.
Kusumoto_c11.indd 331Kusumoto_c11.indd 331 11/19/2011 7:07:39 PM11/19/2011 7:07:39 PM
332 ECG Interpretation for Everyone: An On-The-Spot Guide
**
**
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
)
Kusumoto_c11.indd 332Kusumoto_c11.indd 332 11/19/2011 7:07:39 PM11/19/2011 7:07:39 PM
Arrhythmias: Tachycardia 333
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.
Kusumoto_c11.indd 333Kusumoto_c11.indd 333 11/19/2011 7:07:40 PM11/19/2011 7:07:40 PM
334
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.
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
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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.
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336 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Pacing 337
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.
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338 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Pacing 339
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
.
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340 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Arrhythmias: Pacing 341
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.
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342 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c12.indd 342Kusumoto_c12.indd 342 11/19/2011 7:08:28 PM11/19/2011 7:08:28 PM
Arrhythmias: Pacing 343
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.
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344 ECG Interpretation for Everyone: An On-The-Spot Guide
Biv
en
tric
ula
r p
aci
ng
Ca
rdia
c re
syn
chro
niz
ati
on
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Arrhythmias: Pacing 345
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
.
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347
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.
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
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348 ECG Interpretation for Everyone: An On-The-Spot Guide
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.
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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.
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350 ECG Interpretation for Everyone: An On-The-Spot GuideS
up
ine
Sta
nd
ing
**
**
*
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Clinical Use of the ECG: Stress Testing 351
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.
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352 ECG Interpretation for Everyone: An On-The-Spot Guide
Ba
selin
eE
xerc
ise
Re
cove
ry
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Clinical Use of the ECG: Stress Testing 353
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.
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354 ECG Interpretation for Everyone: An On-The-Spot Guide
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Clinical Use of the ECG: Stress Testing 355
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.
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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)
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Clinical Use of the ECG: Stress Testing 357
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
.
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358 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Clinical Use of the ECG: Stress Testing 359
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.
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360 ECG Interpretation for Everyone: An On-The-Spot Guide
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Clinical Use of the ECG: Stress Testing 361
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.
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362 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Clinical Use of the ECG: Stress Testing 363
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.
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364 ECG Interpretation for Everyone: An On-The-Spot Guide
aV
R
aV
L
aV
F
*
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Clinical Use of the ECG: Stress Testing 365
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.
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366
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.
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
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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.
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368 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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Clinical Use of the ECG: Clinical Problems 369
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.
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370 ECG Interpretation for Everyone: An On-The-Spot Guide
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.
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Clinical Use of the ECG: Clinical Problems 371
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.
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372 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c14.indd 372Kusumoto_c14.indd 372 11/19/2011 7:10:31 PM11/19/2011 7:10:31 PM
Clinical Use of the ECG: Clinical Problems 373
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
.
Kusumoto_c14.indd 373Kusumoto_c14.indd 373 11/19/2011 7:10:32 PM11/19/2011 7:10:32 PM
374 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
Kusumoto_c14.indd 374Kusumoto_c14.indd 374 11/19/2011 7:10:32 PM11/19/2011 7:10:32 PM
Clinical Use of the ECG: Clinical Problems 375
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
.
Kusumoto_c14.indd 375Kusumoto_c14.indd 375 11/19/2011 7:10:32 PM11/19/2011 7:10:32 PM
376 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c14.indd 376Kusumoto_c14.indd 376 11/19/2011 7:10:33 PM11/19/2011 7:10:33 PM
Clinical Use of the ECG: Clinical Problems 377
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
.
Kusumoto_c14.indd 377Kusumoto_c14.indd 377 11/19/2011 7:10:33 PM11/19/2011 7:10:33 PM
378 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Kusumoto_c14.indd 378Kusumoto_c14.indd 378 11/19/2011 7:10:33 PM11/19/2011 7:10:33 PM
Clinical Use of the ECG: Clinical Problems 379
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.
Kusumoto_c14.indd 379Kusumoto_c14.indd 379 11/19/2011 7:10:33 PM11/19/2011 7:10:33 PM
380
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.
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
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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
Source: FM Kusumoto, ECG Interpretation: From Pathophysiology to Clinical Application, Springer, New York, NY, 2009.
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382 ECG Interpretation for Everyone: An On-The-Spot Guide
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
Source: FM Kusumoto, ECG Interpretation: From Pathophysiology to Clinical Application, Springer, New York, NY, 2009.
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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)
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384 ECG Interpretation for Everyone: An On-The-Spot Guide
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
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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
Kusumoto_bapp.indd 385Kusumoto_bapp.indd 385 11/30/2011 6:39:54 PM11/30/2011 6:39:54 PM
386 ECG Interpretation for Everyone: An On-The-Spot Guide
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)
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387
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.
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
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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
Kusumoto_bindex.indd 388Kusumoto_bindex.indd 388 11/19/2011 7:11:48 PM11/19/2011 7:11:48 PM
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
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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
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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
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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
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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
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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
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