Ebook ECG rounds: Part 1

(BQ) Part 1 book ECG rounds presents the following contents: 47-year-old man presenting for preoperative evaluation prior to knee arthroscopy, 43-year-old asymptomatic man, 65-year-old woman complaining of 3 hours of severe epigastric “bloating.”,...

ECG ROUNDS

authors and the publisher of this work have checked with sources believed to be reliable in their eff orts to provide information that is complete and generally in cord with the standards accepted at the time of publication However, in view of the possibility of human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained

ac-in this work Readers are encouraged to confi rm the ac-information contaac-ined hereac-in with other sources For example and ac-in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration Th is recommendation is of particular importance in connection with new or infrequently used drugs

Thomas S Metkus

ECG ROUNDS

New York Chicago San Francisco Athens London Madrid

Mexico City Milan New Delhi Singapore Sydney Toronto

This is a copyrighted work and McGraw-Hill Education and its licensors reserve all rights in and to the work Use of this work is subject to these terms Except as permitted under the Copyright Act of 1976 and the right

to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill Education’s prior consent You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited Your right to use the work may be terminated if you fail to comply with these terms.

THE WORK IS PROVIDED “AS IS.” McGRAW-HILL EDUCATION AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS

OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HYPERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE McGraw-Hill Education and its licensors do not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free Neither McGraw-Hill Education nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom McGraw-Hill Education has no responsibility for the content of any information accessed through the work Under no circumstances shall McGraw-Hill Education and/or its licensors be liable for any indirect, incidental, special, punitive, consequential

or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise.

Contributors, vii

Dedication, ix

Foreword, xi

Preface, xiii

Normals, normal variants and artifacts

Th omas S Metkus, MD and Sammy Zakaria, MD, MPH

4, 12, 60, 68, 254, 308, 388, 466

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

Wide complex tachycardias

Yee-Ping Sun, MD and Dipan A Desai, DO

104, 242, 304, 320, 332, 404, 456, 500, 514, 596, 628

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

Chamber enlargement and hypertrophy

Ramon A Partida, MD and Dipan A Desai, DO

Myocardium, pericardium, and pulmonary artery

Th omas S Metkus, MD and Glenn A Hirsch, MD, MHS, FACC

36, 80, 116, 182, 190, 234, 324, 368, 424, 462, 492

Pacemakers

Th omas S Metkus, MD and Sammy Zakaria, MD, MPH

64, 136, 272, 352, 380, 408, 476, 548, 564, 620

Ingestions, electrolyte abnormalities, and exposures

Matthew I Tomey, MD and Th omas 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

Th omas 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

CONTENTS BY SUBJECT MATTER

Tracings arranged by subject matter

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

Massachusetts General Hospital

Harvard Medical School

Boston, Massachusetts

Yee-Ping Sun, MD

Clinical Cardiology FellowDivision of CardiologyDepartment of MedicineColumbia University Medical CenterNew York-Presbyterian HospitalNew York, New York

Matthew I Tomey, MD

Chief FellowDepartment of Cardiology

Th e Mount Sinai HospitalNew York, New York

Samuel C Volo, MD

Cardiology FellowDivision of CardiologyNew York-Presbyterian Hospital Weill Cornell Medical CenterNew York, New York

Jonathan W Waks, MD

Clinical Cardiology FellowDivision of Cardiovascular DiseaseBeth Israel Deaconess Medical CenterClinical Fellow in Medicine

Harvard Medical SchoolBoston, Massachusetts

For Kate and for Hailey: it’s all for you, always.

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,

hyper-trophy, and electrolyte and drug toxicities, the electrocardiogram helps us link a

patient’s symptoms and exam fi ndings with a diagnosis Asking a house offi cer to

not only describe the electrocardiogram, but interpret the fi ndings is a particularly

eff ective method of bedside teaching I fi nd that this method of electrocardiographic teaching helps house offi cers and students learn and remember important electrocar-diographic fi ndings Th is book brings bedside electrocardiographic teaching to these pages Everyone who enjoys clinical care will enjoy these ECG-based cases

Steven Schulman, MD

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

comfort-able recognizing, or, put diff erently, “what do I need to know?” Second, in what

con-text is this information best delivered? I was taught to read ECGs in a fairly haphazard

fashion using several diff erent 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, oft en in the wee

hours of the morning and without senior staff guidance Finally, many of us have had

the privileged experience of a truly gift ed 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 fi nal 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 orizing vast arrays of criteria You can choose to interpret the tracings by level of diffi culty, by teaching topic, or sequentially as presented (see Table of Contents) I as-sume a basic knowledge of the skills of ECG interpretation, which will be reviewed only briefl y; readers are referred to several excellent texts for a more in-depth review

mem-of basic interpretation skills and the physiology mem-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 fi nd 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: Th e cases presented herein are fi ctional and created by the authors solely for illustrative teaching purposes alone Any resemblance of cases

to actual patients in any context is purely coincidental Th is book does not purport to off er medical advice nor management guidance on specifi c 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.

ECG ROUNDS

Reading an ECG is like juggling fi re while riding a unicycle: performing the

fun-damentals 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 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 Th us, 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 diffi cult 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)

Th e 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

Th is 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? Th e best place to fi nd 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 fl utter? Atrial tachycardia? Is there no organized atrial

activity suggesting atrial fi brillation?

Finally, what is the relationship between the atrial activity and the ventricular

ac-tivity? Does the atrial activity precede the ventricular activity with a constant interval?

Does the atrial activity follow the ventricular activity, suggesting retrograde

conduc-tion? Are the atrial and ventricular depolarizations independent of each other? Is A-V

block present?

Step 3: Axis

Consider fi rst 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

aVF: +90

I: 0

II: +60

If the QRS complex is more positive than negative in leads I, II, and aVF, the axis

is normal, defi ned 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 left ward axis is present

One can be more sophisticated and can calculate the axis exactly by fi nding 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?

Assess the QT interval: is it prolonged or shortened? Is the morphology

consis-tent 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,

enlarge-ment, or hypertrophy We will review criteria for each of these diagnoses in the

con-text of tracings to come

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

electro-cardiographically as reciprocal anterior changes ST-segment elevation in lead V1,

usually associated with inferior infarction, can suggest right ventricular infarction

Ischemic changes should be regional; therefore, look sequentially for Q waves, ST-segment depression, ST-segment elevation, and T-wave changes (inverted? pseu-do-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 fi ndings

Look for additional fi ndings 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 neuvers of inspection, percussion, palpation, and auscultation, a fi ft h 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, aft er careful assessment of the tracing, take time to consider the clinical history and the fi ndings together, opining on their relation to each other What is the impact of your fi ndings

ma-on diagnosis and treatment?

LEVEL 1

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

ANSWERS

1-1 What are the ECG fi ndings?

Th is tracing demonstrates sinus rhythm at a rate of about 80 beats/min Th e axis and

intervals are normal Th ere is no evidence of chamber enlargement, hypertrophy, or

ischemia Th is is a normal ECG

1-2 What ECG fi ndings would concern you during a preoperative evaluation?

Th e preoperative ECG should fi rst be assessed for any unstable cardiac conditions

that would preclude elective surgery Th ese include active ischemia, ventricular

tachycardia, or uncontrolled atrial arrhythmias such as rapid atrial fi brillation Other

fi ndings of importance may include the presence of Q waves in a coronary tion suggesting occult coronary disease and prior myocardial infarction, and chamber enlargement possibly suggesting occult valvular disease

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

2-1 What abnormalities are present on the ECG?

2-2 What is the diff erential diagnosis for left-axis deviation?

QUESTIONS

ANSWERS

2-1 What abnormalities are present on the ECG?

Th ere is sinus rhythm at 66 beats/min Th e axis is deviated left ward, evidenced by

the positive QRS complex in lead I and the negative QRS complex in leads II and

aVF Th is left -axis deviation is associated with small q waves and large R waves in

leads I and aVL, and small r waves and large S waves in the inferior leads Th ere is

no evidence of left ventricular hypertrophy or other chamber abnormalities Th ere

are no pathologic Q waves suggesting prior infarction, and no ST-segment or T-wave

abnormalities Th e presence of left ward axis deviation in the absence of left

ventricu-lar hypertrophy or prior infarction with this pattern of qR complexes in leads I and

aVL and rS complexes in the inferior leads is consistent with left anterior hemiblock,

also known as left anterior fascicular block Recall that the His bundle bifurcates into the left and right bundle branches Th e left bundle branch further branches into the left anterior fascicle and the left posterior fascicle Block in the left anterior fascicle is more common than block in the left posterior fascicle Hypertension, ischemic heart disease, cardiomyopathy, and degenerative conduction system disease of the elderly (Lev’s syndrome) are all associated with left anterior hemiblock Th e QRS duration is normal when left anterior hemiblock alone is present, although a delayed intrins icoid defl ection (the duration between the onset of the QRS and the peak of the R wave) of greater than 45 milliseconds should be observed in lead aVL as is present in this case

2-2 What is the diff erential diagnosis for left-axis deviation?

Left -axis deviation can be associated with left anterior hemiblock (as in this case), left

ventricular hypertrophy, prior myocardial infarction, Wolff -Parkinson-White

syn-drome, and atrial septal defect

Case # 3 A 43-year-old asymptomatic man

QUESTIONS

3-1 What abnormalities are present?

3-2 What would you do next?

ANSWERS

3-1 What abnormalities are present?

Sinus rhythm is present at approximately 85 beats/min Th e axis is normal as are the

intervals Th ere is no evidence of chamber enlargement, hypertrophy, or ischemia

Th e ninth P–QRS complex occurs earlier than expected, and the P wave has a slightly

diff erent morphology than the other P waves Th is beat represents a premature atrial

contraction Th e P–P interval (amount of time between P waves) following the ectopic beat is longer than the sinus P–P interval, a compensatory pause Overall, this ECG can be classifi ed as a normal ECG, as a single premature atrial beat is not pathologic

3-2 What would you do next?

If no symptoms are present, no further action is indicated Frequent premature atrial

contractions can sometimes occur as a manifestation of hyperthyroidism, electrolyte

abnormalities, or medication toxicity, none of which are supported by this history

β-Blockers can be prescribed for symptomatic atrial ectopy, but in this case, no ther treatment is necessary

Case # 4 A 65-year-old woman complaining of 3 hours of severe epigastric “bloating.”

QUESTIONS

4-1 What abnormalities are present?

4-2 What is the cause of her abdominal symptoms?

4-3 Which coronary artery is most likely aff ected?

ANSWERS

4-1 What abnormalities are present?

Baseline artifact is present in lead V1 Th ere is sinus rhythm at a rate of

approxi-mately 90 beats/min Th e axis is left ward Intervals are normal Th ere are broad, deep

Q waves present in leads II, III, and aVF consistent with inferior myocardial infarction

of undetermined age In addition, there are Q waves and striking ST-segment tion in the anterior leads V3, V4, and V5 consistent with acute myocardial injury and infarction in this territory

4-2 What is the cause of her abdominal symptoms?

Patients with myocardial infarction can present with a range of symptoms, from

typi-cal substernal chest discomfort to other more atypitypi-cal symptoms Dyspnea,

abdomi-nal pain, neck or jaw discomfort, nausea and vomiting, and arm pain can all signify

myocardial infarction Older patients and patients with diabetes oft en present with atypical symptoms Th is patient’s abdominal discomfort was the presenting feature of her myocardial infarction

4-3 Which coronary artery is most likely aff ected?

Th e ischemic changes including ST-segment elevation and Q-wave formation in leads

V2 through V4 are present in the anterior leads and most likely represent occlusion of

the left anterior descending coronary artery

Case # 5 A 68-year-old male with a history of diet-controlled diabetes and well-controlled hypertension presents for follow-up

QUESTIONS

5-1 Interpret this ECG What abnormalities are present on this tracing?

5-2 Explain why the QRS complex has this particular morphology

ANSWERS

5-1 Interpret this ECG What abnormalities are present on this tracing?

Th is tracing demonstrates sinus bradycardia with a heart rate of 56 beats/min Th e

axis is normal Th e PR interval is prolonged to 360 milliseconds and the QRS

dura-tion is prolonged to approximately 150 milliseconds with a right bundle branch

block (rSRʹ pattern with a wide terminal Rʹ wave in lead V1; RS wave with a wide

and slurred terminal S wave in leads I, aVL, V5, and V6) Th e QT interval is normal

Th ere are T-wave inversions in leads V1 to V3 (the leads with terminal Rʹ waves) that are secondary to the right bundle branch block

5-1 Explain why the QRS complex has this particular morphology

Right bundle branch block causes delayed activation of the right ventricle because

activation of the entire ventricular myocardium proceeds via the left bundle branch

and thereaft er through ventricular myocardium Th e fi rst portion of the QRS

com-plex is unaff ected because initial septal activation normally proceeds via part of the

left bundle branch On the surface ECG, this is manifest as a normal r wave in lead

V1 and a normal q wave in leads V5 to V6 (normal septal activation is in the left

to right direction) Th is septal activation is followed by the S wave in lead V1 and

R waves in leads I, aVL, and V6 because the normal left ventricular activation vector points toward the left -sided leads Finally, there is delayed depolarization of the right ventricle (a rightward structure), which corresponds to the wide terminal Rʹ wave in rightward leads such as V1, and the wide terminal S wave in left ward leads such as I, aVL, and V6