Ebook ECG rounds: Part 1

ECG ROUNDS


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ECG ROUNDS
Thomas S. Metkus

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CONTENTS BY DIFFICULTY LEVEL
Contributors, vii
Dedication, ix
Foreword, xi
Preface, xiii

Introduction: A focused step-wise guide to ECG interpretation, 1
Level I (Cases 1-50), 3
Level II (Cases 51-100), 209
Level III (Cases 101-150), 419
Index, 641

v


vi

n CONTENTS

CONTENTS BY SUBJECT MATTER
Tracings arranged by subject matter
Contributors, vii
Dedication, ix
Foreword, xi
Preface, xiii

Normals, normal variants and artifacts
Thomas S. Metkus, MD and Sammy Zakaria, MD, MPH
4, 12, 60, 68, 254, 308, 388, 466

Chamber enlargement and hypertrophy
Ramon A. Partida, MD and Dipan A. Desai, DO
52, 88, 140, 166, 336, 452, 518, 544

Ischemia
Thomas S. Metkus, MD
16, 24, 48, 112, 128, 144, 148, 174, 186, 194, 204, 226, 246, 264, 280, 316, 348, 376,
414, 436, 478, 484, 526, 556, 572, 614, 624, 636

Myocardium, pericardium, and pulmonary artery
Narrow complex tachycardias
Samuel C. Volo, MD and Sammy Zakaria, MD, MPH

32, 100, 124, 132, 178, 198, 258, 290, 360, 400, 420, 448, 536, 584, 600

Thomas S. Metkus, MD and Glenn A. Hirsch, MD, MHS, FACC
36, 80, 116, 182, 190, 234, 324, 368, 424, 462, 492

Pacemakers
Wide complex tachycardias
Yee-Ping Sun, MD and Dipan A. Desai, DO
104, 242, 304, 320, 332, 404, 456, 500, 514, 596, 628

Thomas S. Metkus, MD and Sammy Zakaria, MD, MPH
64, 136, 272, 352, 380, 408, 476, 548, 564, 620

Ingestions, electrolyte abnormalities, and exposures
Bradycardias and blocks
Jonathan W. Waks, MD and Dipan A. Desai, DO
8, 20, 72, 84, 92, 96, 120, 162, 218, 276, 294, 340, 364, 384, 428, 440, 470, 496, 510,
530, 560, 588, 610

Matthew I. Tomey, MD and Thomas S. Metkus, MD
56, 76, 108, 152, 170, 222, 230, 268, 284, 372, 392, 396, 432, 504, 552, 568, 604

Syndromes, riddles, and miscellaneous arrhythmia
Thomas S. Metkus, MD and Sammy Zakaria, MD, MPH
28, 40, 44, 158, 210, 214, 238, 250, 298, 312, 328, 344, 356, 444, 488, 522, 540, 580, 592


CONTRIBUTORS
Dipan A. Desai, DO
Clinical Associate

Division of Cardiology
Johns Hopkins University School of Medicine
Johns Hopkins Bayview Medical Center
Baltimore, Maryland
Glenn A. Hirsch, MD, MHS, FACC
Adjunct Assistant Professor of Medicine
Division of Cardiology
Johns Hopkins University School of Medicine
Associate Professor of Medicine
Division of Cardiovascular Medicine
Department of Medicine
University of Louisville
Louisville, Kentucky
Thomas S. Metkus, Jr, MD
Fellow in Cardiovascular Medicine
Division of Cardiology
The Johns Hopkins Hospital
Baltimore, Maryland
Ramon A. Partida, MD
Fellow in Cardiovascular Medicine
Division of Cardiology
Massachusetts General Hospital
Harvard Medical School
Boston, Massachusetts

Yee-Ping Sun, MD
Clinical Cardiology Fellow
Division of Cardiology
Department of Medicine
Columbia University Medical Center

New York-Presbyterian Hospital
New York, New York
Matthew I. Tomey, MD
Chief Fellow
Department of Cardiology
The Mount Sinai Hospital
New York, New York
Samuel C. Volo, MD
Cardiology Fellow
Division of Cardiology
New York-Presbyterian Hospital Weill Cornell Medical Center
New York, New York
Jonathan W. Waks, MD
Clinical Cardiology Fellow
Division of Cardiovascular Disease
Beth Israel Deaconess Medical Center
Clinical Fellow in Medicine
Harvard Medical School
Boston, Massachusetts
Sammy Zakaria, MD, MPH
Assistant Professor of Medicine
Division of Cardiology
Johns Hopkins University School of Medicine
Baltimore, Maryland
vii


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Dedication
To my parents: you are my first role models both as physicians and as people.
To mentors too numerous to list here, in particular Drs. Joseph Loscalzo, Steve Schulman, and the late Ken Baughman: thank you!!
For Kate and for Hailey: it’s all for you, always.

ix


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FOREWORD
Over the past 25 years I have rounded with countless numbers of wonderful house
staff in the Coronary Care Unit. In the CCU and the wards, the electrocardiogram
tells a story for each patient. From acute coronary syndrome, cardiomyopathy, hypertrophy, and electrolyte and drug toxicities, the electrocardiogram helps us link a
patient’s symptoms and exam findings with a diagnosis. Asking a house officer to
not only describe the electrocardiogram, but interpret the findings is a particularly

effective method of bedside teaching. I find that this method of electrocardiographic
teaching helps house officers and students learn and remember important electrocardiographic findings. This book brings bedside electrocardiographic teaching to these
pages. Everyone who enjoys clinical care will enjoy these ECG-based cases.
Steven Schulman, MD

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PREFACE

On several occasions during residency, a junior colleague approached me with some
variation of the following request: “I’m starting a cardiology rotation soon, and I feel
uncomfortable reading ECGs ... can you recommend a resource?” I have spent a lot of
time since then considering the mechanism by which residents and students learn the
art and science of ECG interpretation.
First, what are the ECG abnormalities that most physicians should be comfortable recognizing, or, put differently, “what do I need to know?” Second, in what context is this information best delivered? I was taught to read ECGs in a fairly haphazard
fashion using several different exercises. A faculty member would host the occasional
workshop or lecture (during which I would invariably embarrass myself!). A random
assortment of ECG tracings would invariably appear on in-service, shelf, and board
examinations. Much learning necessarily happened in the context of clinical care—
myself and fellow interns intently studying the ECGs of our patients, often in the wee
hours of the morning and without senior staff guidance. Finally, many of us have had
the privileged experience of a truly gifted clinical teacher reading an ECG with us
on morning rounds, skillfully linking ECG abnormalities to the patient in the bed in
front of us.
It is this final method of learning that this book attempts to replicate. I endeavor
to present a set of tracings, which, taken together, demonstrate most abnormalities
that a generalist physician trainee would “need to know.” Each tracing is followed by

clinical questions meant to reinforce electrocardiographic concepts and simulate the
experience of rounding with a master clinician teaching in the Socratic Method. At
the conclusion of the book, I hope you will have been exposed to a wide array of ECG
abnormalities relevant to your current practice.
Practical interpretation, cogitation, and cognition are the focus rather than memorizing vast arrays of criteria. You can choose to interpret the tracings by level of
difficulty, by teaching topic, or sequentially as presented (see Table of Contents). I assume a basic knowledge of the skills of ECG interpretation, which will be reviewed
only briefly; readers are referred to several excellent texts for a more in-depth review
of basic interpretation skills and the physiology of the ECG. Likewise, this book is not
a comprehensive reference text for ECG criteria, and readers are referred to several
excellent texts for this purpose.
I hope you find this book useful and enjoyable. Interpreting ECGs connects us to

our roots as medical physiologists, clinicians, and teachers, and I hope that sense of
joy and purpose shows through in this work.
Warm regards,
TM

Disclaimer: The cases presented herein are fictional and created by the authors solely for illustrative teaching purposes alone. Any resemblance of cases
to actual patients in any context is purely coincidental. This book does not purport to offer medical advice nor management guidance on specific cases.
As always, all ECG interpretation and clinical decisions rendered in the context of patient care are solely at the discretion of the treating physician.
xiii


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ECG ROUNDS


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INTRODUCTION:

A focused step-wise guide to ECG interpretation

Reading an ECG is like juggling fire while riding a unicycle: performing the fundamentals systematically, the same way, every time, will prevent you from getting
burned. Presented here is the authors’ approach to reading an ECG. It is less important
to follow 1 particular approach; rather, choose 1 validated approach that works for you
and apply it the same way, every time, to every tracing.

Step 3: Axis

Consider first if the axis is normal or not. Recall that lead I is located at 0 degrees, lead
II at +60 degrees, and lead aVF at +90 degrees:

aVL: –30

Step 1: Rate
Recall that each “little box” on the time axis of a tracing is 0.04 seconds in duration,
with each “big box” comprising 5 little boxes and equal to 0.2 seconds. Thus, calculate
the rate as 300 divided by the number of big boxes between complexes (300/1 = rate of
300; 300/2 = rate of 150; etc). Alternatively (more accurate and more difficult math),
calculate the rate as 1500 divided by the number of little boxes between complexes
(1500/5 = rate of 300; 1500/17 = rate of 88; etc).
The above methods are accurate only if the rhythm is regular. A second approach
to calculate rate is to recall that the rhythm strip is 10 seconds in duration. Count the
number of complexes present in the rhythm strip and multiply by 6, yielding the rate.
This method is accurate whether the rhythm is regular or irregular.
Using your choice of these methods, calculate the atrial rate (P waves) and the
ventricular rate (QRS complexes).

Step 2: Rhythm analysis
First, search for atrial activity. Are there P waves? The best place to find P waves is in
the inferior leads (II, III, and aVF) and V1.
Second, are the P waves sinus P waves or nonsinus P waves? Sinus P waves should
be upright in the inferior leads and biphasic in lead V1. If the atrial activity is not a
sinus P wave, what is it? Atrial flutter? Atrial tachycardia? Is there no organized atrial
activity suggesting atrial fibrillation?
Finally, what is the relationship between the atrial activity and the ventricular activity? Does the atrial activity precede the ventricular activity with a constant interval?
Does the atrial activity follow the ventricular activity, suggesting retrograde conduction? Are the atrial and ventricular depolarizations independent of each other? Is A-V
block present?

I: 0

II: +60
aVF: +90

If the QRS complex is more positive than negative in leads I, II, and aVF, the axis
is normal, defined as axis between +100 and −30 degrees.
If the QRS complex is positive in aVF but predominantly negative in lead I, a
rightward axis is present.
If the QRS complex is negative in aVF but positive in lead I, assess lead II. If the
QRS complex is positive in lead II, a normal axis is present. If the QRS complex is
more negative than positive in lead II, a leftward axis is present.
One can be more sophisticated and can calculate the axis exactly by finding the
lead in which the QRS complex is isoelectric: the axis must be 90 degrees to this lead.

Step 4: Intervals
Assess the PR interval: is it normal, prolonged, or shortened?
Assess the QRS width: is it narrow or widened? If widened, is the morphology for
a diagnosis of bundle branch block or conduction delay present?
1


2

n INTRODUCTION
Assess the QT interval: is it prolonged or shortened? Is the morphology consistent with a particular diagnosis?
We will review criteria for the above diagnoses in the context of the tracings
to come.

Step 5: Chamber enlargement and hypertrophy

As the next step in ECG interpretation, evaluate sequentially the left atrium, the right
atrium, the left ventricle, and the right ventricle for chamber abnormality, enlargement, or hypertrophy. We will review criteria for each of these diagnoses in the context of tracings to come.

Ischemic changes should be regional; therefore, look sequentially for Q waves,
ST-segment depression, ST-segment elevation, and T-wave changes (inverted? pseudo-normalized? peaked? hyperacute?) in the inferior leads, septal leads, anterior
leads, and lateral leads.
Identify any reciprocal changes. Abnormalities spanning the distribution of more
than 1 coronary artery could be due to global ischemia (such as those occurring in
aortic stenosis, tachycardia, or anemia), multivessel disease, or secondary to disorders
such as pericardial disease. ST-segment abnormalities with morphology that appears
atypical for ischemia may be due to early repolarization, ventricular hypertrophy,
electrolyte disturbances, or other disorders that we will review.

Step 7: Additional findings
Step 6: Ischemia and infarction
Reading for ischemia and infarction as well as related abnormalities of ST segments
and T waves requires evaluating the presence of Q waves, ST-segment changes, and
T-wave abnormalities in groups of leads.
Recall that:
Leads II, III, and aVF represent the inferior aspect of the heart.
Leads I, aVL, V5, and V6 represent the lateral aspect of the heart.
Leads V1 and V2 represent the septum.
Leads V3 through V5 represent the anterior wall of the heart.
In addition, infarction of the posterior wall of the heart can manifest electrocardiographically as reciprocal anterior changes. ST-segment elevation in lead V1,
usually associated with inferior infarction, can suggest right ventricular infarction.

Look for additional findings depending on your clinical suspicion. Additional waves
seen in some clinical disorders include epsilon waves, U waves, or the J waves of
Osborn.

Step 8: Synthesize
William Osler famously noted that, along with the 4 classic physical examination maneuvers of inspection, percussion, palpation, and auscultation, a fifth maneuver was
perhaps the most critical: cogitation. Re-stated, it is important to gather the data,
but one must also consider what it means in the clinical context. So, after careful
assessment of the tracing, take time to consider the clinical history and the findings
together, opining on their relation to each other. What is the impact of your findings
on diagnosis and treatment?


Section I

LEVEL 1


4

n DIFFICULTY LEVEL 1

Case #1. A 47-year-old man presenting for preoperative evaluation
prior to knee arthroscopy.


DIFFICULTY LEVEL 1 n

QUESTIONS
1-1. What are the ECG findings?
1-2. What ECG findings would concern you during a preoperative evaluation?

5

6

n DIFFICULTY LEVEL 1


DIFFICULTY LEVEL 1 n

ANSWERS
1-1. What are the ECG findings?
This tracing demonstrates sinus rhythm at a rate of about 80 beats/min. The axis and
intervals are normal. There is no evidence of chamber enlargement, hypertrophy, or
ischemia. This is a normal ECG.

1-2. What ECG findings would concern you during a preoperative evaluation?
The preoperative ECG should first be assessed for any unstable cardiac conditions
that would preclude elective surgery. These include active ischemia, ventricular
tachycardia, or uncontrolled atrial arrhythmias such as rapid atrial fibrillation. Other

findings of importance may include the presence of Q waves in a coronary distribution suggesting occult coronary disease and prior myocardial infarction, and chamber
enlargement possibly suggesting occult valvular disease.

7


8

n DIFFICULTY LEVEL 1

Case #2. An asymptomatic 56-year-old gentleman presents for routine

follow-up.