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VOLUME 2

Editors:
Mohammad Shenasa, MD • Mark E. Josephson, MD • N. A. Mark Estes III, MD
Ezra A. Amsterdam, MD • Melvin Scheinman, MD
Over 300 exceptional electrocardiogram case studies curated from the libraries of 60
internationally recognized master teachers of ECG interpretation are brought together
in this one-of-a-kind resource for student and teacher alike.
Presented in two individual volumes and organized by disease type, ECG case
studies are shown in a clinical context followed by questions and discussion. Medical
students, residents, fellows, physicians — anyone who is involved in caring for
patients with various cardiovascular diseases and other systemic pathologies — will
find this unique collection with a global perspective useful and practical in developing
the skills necessary to read ECGs.

This book should serve as an important reference, and I guarantee it will be
pulled from the shelf for decades to come.
–Francis E. Marchlinski, MD
The collection of ECGs is remarkable. Students of electrocardiography will
enjoy reading this book and teachers will utilize many of its tracings as
materials for their ECG rounds.
–Prof. Jerónimo Farré MD, PhD

3405 W. 44th Street
Minneapolis, Minnesota 55410
www.cardiotextpublishing.com
+1 (612) 925-2053

This book includes a free digital
edition for use by the first buyer.
For additional information regarding
personal or institutional use, please
visit www.cardiotextpublishing.com.

Volume 1 – 230 ECG case studies.
978-1-942909-08-8
Volume 2 - 79 ECG case studies.
978-1-942909-20-0

ECG Masters’ Collection

Favorite ECGs from Master Teachers Around the World

Favorite ECGs from Master Teachers Around the World

ECG Masters’ Collection

VOL. 2
Shenasa
Josephson
Estes
Amsterdam
Scheinman

ECG Masters’
Collection

Favorite ECGs from
Master Teachers
Around the World
VOLUME 2
Editors:
Mohammad Shenasa
Mark E. Josephson
N. A. Mark Estes III
Ezra A. Amsterdam
Melvin Scheinman
Forewords by
Francis E. Marchlinski
and Samuel Lévy

ECG Masters’ Collection
Favorite;  ECGs from Master Teachers
Around the World
Volume 2

Mohammad Shenasa,
Mark E. Josephson,
N.A. Mark Estes III,
Ezra A. Amsterdam,
Melvin Scheinman,

Minneapolis, Minnesota

MD
MD
MD
MD
MD

© 2018 Mohammad Shenasa, Mark E. Josephson, N.A. Mark Estes III, Ezra A. Amsterdam, Melvin Scheinman
Cardiotext Publishing, LLC
3405 W. 44th Street
Minneapolis, Minnesota 55410
USA
www.cardiotextpublishing.com
Any updates to this book may be found at:
www.cardiotextpublishing.com/electrophysiology-heart-rhythm-mgmt/ecg-masters-collection-volume-2
Comments, inquiries, and requests for bulk sales can be directed to the publisher at: info@cardiotextpublishing.com.
All rights reserved. No part of this book may be reproduced in any form or by any means without the prior
permission of the publisher.
All trademarks, service marks, and trade names used herein are the property of their respective owners and are
used only to identify the products or services of those owners.
This book is intended for educational purposes and to further general scientific and medical knowledge, research,
and understanding of the conditions and associated treatments discussed herein. This book is not intended to
serve as and should not be relied upon as recommending or promoting any specific diagnosis or method of
treatment for a particular condition or a particular patient. It is the reader’s responsibility to determine the proper
steps for diagnosis and the proper course of treatment for any condition or patient, including suitable and
appropriate tests, medications or medical devices to be used for or in conjunction with any diagnosis or
treatment.
Due to ongoing research, discoveries, modifications to medicines, equipment and devices, and changes in
government regulations, the information contained in this book may not reflect the latest standards,
developments, guidelines, regulations, products or devices in the field. Readers are responsible for keeping up to
date with the latest developments and are urged to review the latest instructions and warnings for any medicine,
equipment or medical device. Readers should consult with a specialist or contact the vendor of any medicine or
medical device where appropriate.
Except for the publisher’s website associated with this work, the publisher is not affiliated with and does not
sponsor or endorse any websites, organizations or other sources of information referred to herein.
The publisher and the authors specifically disclaim any damage, liability, or loss incurred, directly or indirectly,
from the use or application of any of the contents of this book.
Unless otherwise stated, all figures and tables in this book are used courtesy of the authors.
Library of Congress Control Number: 2018931463
ISBN: 978-1-942909-20-0
eISBN: 978-1-942909-21-7
Printed in The United States of America
For additional ECG case studies, please consider ECG Masters’ Collection, Volume 1
cardiotextpublishing.com/electrophysiology-heart-rhythm-mgmt/ecg-masters-collection
1 2 3 4 5 6 7 21 20 19 18

Dedication
We dedicate this book in memory of Mark E. Josephson, MD (January 27, 1943 – January 11, 2017),
who inspired and mentored many of us. He gave the electrogram a new look: “ECG as a mapping tool.”
He is also the senior editor on this book.

Contents
Contributors............................................................................................................................vii
Forewords...............................................................................................................................xiii
Dr. Francis E. Marchlinski
Dr. Samuel Lévy
Preface...................................................................................................................................xvii
Abbreviations.........................................................................................................................xix
Section 1

Introduction to the Interpretation of the Electrocardiogram���������������������������1

Section 2

Conduction Disturbances: Sinus Node Disease/Sick Sinus Syndrome,
AV Conduction Disturbances, AV Blocks, Bundle Branch Blocks, and
Fascicular Blocks....................................................................................................3

Section 3

Miscellaneous Phenomena: Concealed Conduction, Superabnormalities,
Aberrancy Conduction, Premature Atrial and Ventricular
Contractions (PACs and PVCs).............................................................................33

Section 4

Preexcitation Syndromes....................................................................................39

Section 5

Early Repolarization (ECG Pattern and the Syndrome).....................................55

Section 6

Long and Short QT Syndromes........................................................................... 61
A. Long QT Syndrome........................................................................................ 61
B. Short QT Syndrome*
C. Torsades de Pointes.......................................................................................63
D. Other Proarrhythmias*

Section 7

Brugada Syndrome..............................................................................................65

Section 8

Narrow QRS Complex Arrhythmias....................................................................79
A. Inappropriate Sinus Tachycardia*
B. Sinus Node Reentrant Tachycardia*
C. Atrial Tachycardia/Atrial Flutter....................................................................79
D. Atrioventricular Nodal Reentrant Tachycardia.............................................91
E. Atrioventricular Reentrant Tachycardia*
F.

Atrial Fibrillation*

G. Junctional Rhythms..................................................................................... 103
* Included only in Volume 1.

v

Section 9

Wide Complex Arrhythmias..............................................................................105
A. Ventricular Tachycardia/Fibrillation............................................................105
B. Supraventricular Tachycardia (SVT) with Bundle Branch Block (BBB)*
C. Preexcited Tachycardia................................................................................ 123
D. Idioventricular Rhythm*

Section 10 Ischemia and Infarction..................................................................................... 125
Section 11 Electrolyte Disturbances, Pharmacological and Recreational Agents*
Section 12 Paced Rhythms and Device Troubleshooting..................................................129
Section 13 Heart Failure, Left Ventricular Hypertrophy, and Cardiomyopathies............149
A. Arrhythmogenic Right Ventricular
Dysplasia/Cardiomyopathy (ARVD/C).......................................................... 149
B. Hypertrophic Cardiomyopathy (HCM)*
C. Dilated Cardiomyopathy (DCM)*
D. Chagas*
E. Takotsubo (Stress) Cardiomyopathy*
F.

Non-Compaction Cardiomyopathy*

G. Pericarditis.................................................................................................... 159
H. Other Cardiomyopathies*
Section 14 Congenital Heart Diseases*
Section 15 Special Considerations: Age, Race, Gender, and Athletes..............................165
Section 16 Syncope and ECG Troubleshooting..................................................................187
Appendix...............................................................................................................................195
* Included only in Volume 1.

vi u Contents

Contributors

Editors

Contributors

Mohammad Shenasa, MD, FACC, FHRS,
FAHA, FESC
Attending Physician, Department of
Cardiovascular Services, O’Conner Hospital;
Heart & Rhythm Medical Group, San Jose,
California

Ahmed Abdel Aziz, MD, PhD
Professor, Critical Care Medicine Department,
Cairo University Hospitals, Cairo, Egypt

Mark E. Josephson, MD, FACC, FHRS,
FAHA
Director, Harvard-Thorndike Electrophysiology
Institute and Arrhythmia Service;
Chief Emeritus, Division of Cardiovascular
Medicine, Beth Israel Deaconess Medical
Center; Herman C. Dana Professor of Medicine,
Harvard Medical School, Boston,
Massachusetts
N.A. Mark Estes III, MD, FACC, FHRS,
FAHA, FESC
Professor of Medicine, Tufts University School
of Medicine; Director, New England Cardiac
Arrhythmia Center, Tufts Medical Center,
Boston, Massachusetts
Ezra A. Amsterdam, MD
Distinguished Professor, Associate Chief
(academic affairs), Division of Cardiovascular
Medicine, University of California, Davis,
Medical Center, Sacramento, California
Melvin Scheinman, MD, FACC, FHRS
Professor of Medicine, Walter H. Shorenstein
Endowed Chair in Cardiology; Chief of
Cardiology Genetics Arrhythmia Program,
University of California, San Francisco,
San Francisco, California

Baris Akdemir, MD
Cardiac Electrophysiology Fellow, Cardiology,
University of Minnesota, Minneapolis,
Minnesota
Jason Andrade, BSc, MD, FRCPC, FHRS
Clinical Assistant Professor, Department of
Medicine, University of British Columbia,
Vancouver, British Columbia, Canada; Adjunct
Professor, Université de Montréal, Clinical
Electrophysiology Service, Montreal Heart
Institute, Montreal, Quebec, Canada
Adrian Baranchuk, MD, FACC, FRCPC, FCCS
Professor of Medicine (Tenure), Head, Heart
Rhythm Service, Queen’s University, Kingston,
Ontario, Canada
Antoni Bayés de Luna, MD, PhD, FESC, FACC
Senior Investigator, Catalan Institute of
Cardiovascular Sciences, St. Pau Hospital,
Barcelona, Spain
Bernard Belhassen, MD, FHRS
Department of Cardiology, Tel Aviv Sourasky
Medical Center; Sackler Faculty of Medicine,
Tel Aviv University, Tel Aviv, Israel
David G. Benditt, MD, FACC, FHRS, FRCPC,
FESC
Cardiac Arrhythmia Center, Cardiovascular
Division, University of Minnesota Medical
School, Minneapolis, Minnesota
vii

Dan Blendea, MD, PhD, FHRS
Cardiac Arrhythmia Service, Department of
Medicine, Massachusetts General Hospital,
Boston, Massachusetts

Paolo China, MD
Unit of Electrophysiology and Cardiac
Pacing, Ospedale Dell’Angelo,
Venice, Italy

Maichel Sobhy Naguib Botros, MD, PhD,
ECES
EHRA Certified Electrophysiology Specialist
Lecturer, Critical Care Medicine Department,
Cairo University Hospital
Cairo, Egypt

Jane E. Crosson, MD
Associate Professor of Pediatrics,
Johns Hopkins Hospital, Baltimore, Maryland

Jonathan Bui, MD
Internal Medicine Resident,
Billings Clinic, Billings,
Montana
Haran Burri, MD
Associate Professor, Cardiology Department,
University Hospital of Geneva,
Geneva, Switzerland
Catalin A. Buzea, MD, PhD
Cardiology Consultant, Cardiology
Department, Colentina University Hospital;
Associate Professor, “Carol Davila” University
of Medicine, Bucharest, Romania
David J. Callans, MD, FHRS
Professor of Medicine, Perelman School of
Medicine; Associate Director of
Electrophysiology, University of Pennsylvania
Health System, Philadelphia, Pennsylvania
Sanoj Chacko, MD, PhD
Heart Rhythm Service, Queen’s University,
Kingston, Ontario, Canada
Alan Cheng, MD, FACC, FAHA, FHRS
Adjunct Associate Professor of Medicine,
Adjunct Associate Professor of Pediatrics,
Johns Hopkins University School of Medicine,
Baltimore, Maryland

viii u Contributors

Andrei G. Dan, MD, PhD, FESC, FAHA,
FACC, FEHRA
Head of Cardiology Department and Internal
Medicine Clinic, Colentina University
Hospital; Professor, “Carol Davila” University of
Medicine, Bucharest, Romania
Marc Dubuc, MD, FRCPC, FACC, FHRS
Associate Professor of Medicine, Université de
Montréal; Clinical Electrophysiology Service,
Montreal Heart Institute, Montreal,
Quebec, Canada
Kenneth A. Ellenbogen, MD, FHRS
Kontos Professor of Medicine,
Chair, Division of Cardiology,
Virginia Commonwealth University,
Pauley Heart Center, Richmond, Virginia
Tamer S. Fahmy, MD, PhD
Associate Professor, Critical Care Medicine
Department, Cairo University Hospitals,
Cairo, Egypt
Miquel Fiol, MD, PhD
Balearic Islands Health Research Institute
(IdISBa) and Son Espases Hospital. Palma,
Spain; Physiopathology of Obesity and
Nutrition Networking Biomedical Research
Centre (CIBERObn), Carlos III Health Institute,
Madrid, Spain
Robert Frank, MD
Institut de Cardiologie, Hopital Pitié
Salpétrière, Paris, France

Benedict M. Glover, MD, FESC
Division of Cardiology, Queen’s University,
Kingston, Ontario, Canada
Shahriar Heidary, MD, FACC
Adjunct Clinical Instructor, Department of
Internal Medicine, Division of Cardiovascular
Medicine, Stanford University Medical School,
Stanford, California
Hein Heidbuchel, MD, PhD, FESC, FEHRA
Professor and Chair, Department of Cardiology,
Antwerp University Hospital, Antwerp,
Belgium; Guest Professor, Cardiology, Hasselt
University, Hasselt, Belgium

Bradley P. Knight, MD, FACC, FHRS
Medical Director, Center for Heart Rhythm
Disorders, Bluhm Cardiovascular Institute,
Northwestern Memorial Hospital, Cooley
Professor of Medicine, Northwestern University,
Feinberg School of Medicine,
Chicago, Illinois
Pieter Koopman, MD
Electrophysiologist, Heart Center Hasselt, Jessa
Hospital, Hasselt, Belgium
Peter R. Kowey, MD, FACC
Professor, Jefferson Medical College, Lankenau
Institute for Medical Research,
Philadelphia, Pennsylvania

Henry H. Hsia, MD, FACC, FHRS
Health Science Professor of Medicine,
University of California, San Francisco;
Chief, Arrhythmia Service, VA Medical
Center, San Francisco, California

Andrew D. Krahn, MD, FRCPC
Heart Rhythm Services, Department of
Medicine, Division of Cardiology, St. Paul’s
Hospital, University of British Columbia,
Vancouver, British Columbia, Canada

Mohammad-Ali Jazayeri, MD
Division of Cardiovascular Diseases,
University of Kansas Hospital & Medical
Center, Kansas City, Kansas

Balaji Krishnan, MD
Cardiac Arrhythmia Center, Cardiovascular
Division, University of Minnesota Medical
School, Minneapolis, Minnesota

Mohammad-Reza Jazayeri, MD
Heart, Lung & Vascular, Bellin Health,
Green Bay, Wisconsin

Gilles Lascault, MD
Cardiologist, Arrhythmia Department, Centre
Cardiologique du Nord, Saint-Denis, France

Gautham Kalahasty, MD
Program Director, Cardiology Fellowship
Program, Virginia Commonwealth University;
Associate Professor of Medicine,
Pauley Heart Center, Richmond, Virginia
Jonathan Kalman, MBBS, PhD, FRACP, FHRS
Professor of Medicine and Director of Cardiac
Arrhythmia Service, Department of Cardiology,
Royal Melbourne Hospital and Department of
Medicine, University of Melbourne, Melbourne,
Australia

Robert Lemery, MD, FHRS, FESC, FRCPC
Cardiac Electrophysiology, University of Ottawa
Heart Institute, Ottawa, Canada
Mohamed Magdy, MSc, L’AFSA, PhD, MD
Electrophysiology Fellow, Nancy CHU France;
Lecturer, Cairo University Hospital,
Egypt; Head of EP Lab, Al Qassimi Hospital,
United Arab Emirates
Moussa Mansour, MD
Cardiac Arrhythmia Service, Department of
Medicine, Massachusetts General Hospital,
Boston, Massachusetts

Contributors u ix

Robert J. Myerburg, MD
Professor of Medicine and Physiology, Division
of Cardiology, American Heart Association
Chair in Cardiovascular Research, University of
Miami Miller School of Medicine,
Miami, Florida
Yuji Nakazato, MD, PhD, FESC
Professor, Department of Cardiology, Heart
Center, Juntendo University Urayasu Hospital,
Urayasu City, Chiba, Japan

Andrés Ricardo Pérez-Riera, MD, PhD
Post Graduate Advisor at Design of Studies
and Scientific Writing Laboratory, ABC School
of Medicine, Santo André, São Paulo, Brazil
Femi Philip, MD
Division of Cardiovascular Medicine,
Kaiser Permanente, Medical Center,
Sacramento, California

Sercan Okutucu, MD
Associate Professor of Cardiology,
Department of Cardiology, MHG,
Memorial Ankara Hospital, Ankara, Turkey

Philip Podrid, MD
Professor, Boston University School of
Medicine; Lecturer in Medicine, Harvard
Medical School, Boston, Massachusetts;
Attending Physician, West Roxbury VA
Hospital, West Roxbury, Massachusetts

Ali Oto, MD, FESC, FACC, FHRS, FISHNE
Professor of Cardiology, Chairman, Department
of Cardiology, MHG, Memorial Ankara
Hospital, Ankara, Turkey

Magdi M. Saba, MD, FHRS
Consultant Cardiac Electrophysiologist,
St. George’s Hospital and University of London,
London, England

Santosh K. Padala, MD
Assistant Professor of Medicine
Division of Cardiology,
Virginia Commonwealth University,
Pauley Heart Center, Richmond, Virginia

Scott Sakaguchi, MD, FHRS, FACC, FACP
Professor, Department of Internal Medicine,
University of Minnesota,
Minneapolis, Minnesota

Gemma Parry-Williams, MBChB, MRCP (UK)
Cardiology Clinical and Academic Group,
St. George’s University of London,
London, England
Carlos Alberto Pastore, MD, PhD, FESC
Director, Clinical Unit of Electrocardiography,
Instituto do Coração (InCor), Hospital das
Clínicas FMUSP, Faculdade de Medicina,
Universidade de São Paulo,
São Paulo, Brazil
Olivier Paziaud, MD
Cardiologist, Arrhythmia Department, Centre
Cardiologique du Nord, Saint-Denis, France

x u Contributors

Nelson Samesima, MD, PhD
Supervising Physician, Clinical Unit of
Electrocardiography, Instituto do Coração
(InCor), Hospital das Clínicas (FMUSP),
Faculdade de Medicina, Universidade de São Paulo,
São Paulo, Brazil
Massimo Santini, MD, FESC, FACC
Past-President, World Society of Arrhythmias,
Rome, Italy
Sanjay Sharma, BSc (Hons), MD, FRCP (UK),
FESC
Cardiology Clinical and Academic Group,
St. George’s University of London,
London, England

Hossein Shenasa, MD, MS, FACC
Staff Cardiologist, Electrophysiologist,
Heart & Rhythm Medical Group, San Jose
Area Hospitals, San Jose, California
Mariah Smith
Heart & Rhythm Medical Group,
San Jose, California
Christian Steinberg, MD, FRCPC
Heart Rhythm Services, Department of
Medicine, Division of Cardiology, St. Paul’s
Hospital, University of British Columbia,
Vancouver, British Columbia, Canada
Sakis Themistoclakis, MD
Director, Unit of Electrophysiology and Cardiac
Pacing, Ospedale Dell’Angelo, Venice, Italy
Vassil Traykov, MD, FEHRA
Head of Department of Electophysiology and
Pacing, Clinic of Cardiology, Acibadem City
Clinic, Tokuda Hospital, Sofia, Bulgaria

Nishant Verma, MD, MPH
Assistant Professor of Medicine-Cardiology,
Cardiac Electrophysiology, Bluhm
Cardiovascular Institute, Northwestern
Memorial Hospital, Feinberg School of
Medicine, Northwestern University,
Chicago, Illinois
David E. Ward, MD, FACC
Consultant Cardiologist and
Electrophysiologist, Retired, London, England
Begüm Yetiş Sayın, MD
Department of Cardiology, Cardiology
Specialist, Memorial Ankara Hospital,
Ankara, Turkey
Li Zhang, MD
Associate Professor, Jefferson Medical College,
Lankenau Institute for Medical Research,
Philadelphia, Pennsylvania

Contributors u xi

Foreword
It is exciting to see the publication of these case-based collections of ECGs from “Masters” in
electrocardiography and electrophysiology. It is also a pleasure for me to contribute the foreword to
these important volumes. This collection should be read by both early trainees and experienced
electrocardiographers. There are pearls littered throughout and the explanations and interpretations
grounded in physiology and fundamental vector analysis. The clinical relevance is made obvious by
the case format. The outstanding group of editors has done a superb job with the organization of the
text in dividing it into focused sections to maximize ease of review and educational value. The ECG
recordings are characteristically the best from the experts’ collections. The tracings show the
incredible value of this simple yet elegant tool for diagnosing and localizing arrhythmias and
recognizing signature ECG patterns associated with unique genetically determined and acquired
arrhythmogenic syndromes.
It is important for me to also pay a special tip of the hat to one of the Co-Editors, Dr. Mark
Josephson. Not only is he the father of modern cardiac electrophysiology, but Mark has also been
inspirational in his love of the 12-lead ECG and his desire to maximize its full potential. For more
than 40 years, he has mentored a long collection of trainees on the correct interpretation of the 12-lead
ECG. Such phrases as “burn it in your brain” for a unique ECG pattern that was critical to recognize
within a second of display are always remembered with a smile throughout one’s career. I was a
lucky trainee who has many critical ECG images “burned in my brain.” His participation in
this important text adds to the glow of the other stellar editors and ECG aficionados and provides the
‘Grand Cru’ stamp to this effort.
These books should serve as important references, and I guarantee they will be pulled from the
shelf for decades to come. They are gems and should be enjoyed by even those with only a modest
interest in the 12-lead ECG and the care of patients with cardiac arrhythmias. The true fans of the
ECG will be awed by the experience.
Francis E. Marchlinski, MD, FACC, FHRS, FAHA
University of Pennsylvania School of Medicine
Philadelphia, Pennsylvania

xiii

Foreword
The father of electrocardiography is Willem Einthoven (1860–1927), who first recorded the first
human ECG in 1902 at the University of Leiden, the Netherlands, where he used to teach. He received
the Nobel Prize in 1924 for his major invention. Since then, the ECG has fascinated a number of
cardiologists by the amount of information that can be derived. Some of these famous
electrocardiographers such as Alfred Pick and Richard Langendorf have described a number of
phenomena such as “concealed conduction” or “tachycardia/bradycardia-dependent bundle branch
block,” which were found later on to be correct using invasive electrophysiology. My generation is
fortunate to have met some of them and to learn from them. It is refreshing that Mohammad Shenasa,
Mark E. Josephson, N.A. Mark Estes III, Ezra A. Amsterdam, and Melvin Scheinman, the editors of
this ECG Masters’ collection, have emphasized that the ECG remains an invaluable tool for clinicians
despite the advances made in the field of arrhythmias. This contribution, with the participation of
experts from around the world, will be extremely useful to clinicians, fellows in cardiology, and all
those who are involved in the management of cardiac arrhythmia patients.
These books are not a simple collection of ECGs. They are, in fact, reports of clinical situations in
which the ECG guides the diagnosis, signals the choice of the appropriate tests, and leads to the
appropriate management. The cases presented are not rare or unusual. They represent clinical settings
that cardiologists and clinicians will encounter in their daily practice — and this, in my view, adds to
the educational value of these books. I found it very interesting and enjoyable to read the ECG tracings
put into their clinical context.
The field of cardiac arrhythmias has been enriched by the major advances made in the last four
decades in better understanding tachycardia mechanisms due to the advent of intracardiac recordings,
invasive clinical electrophysiology, ablation, and new mapping techniques. The authors of the cases
refer to these techniques to support their interpretation and document the concepts used in their
interpretation, adding, when necessary, references and suggested reading.
I have no doubt that the authors have succeeded in providing the reader with an interesting,
enjoyable, and useful collection of clinical situations in which the correct ECG interpretation has
played a major role.
Samuel Lévy, MD, FACC, FESC, FAHA
Aix-Marseille Université
Marseille School of Medicine, France

xv

Preface
Each year, several new books or new editions are published on electrocardiography. Since the invention
of the electrocardiogram (ECG) by Willem Einthoven almost 110 years ago, the ECG has become the
most commonly used test worldwide, and its use continues to increase. The medical community has
subsequently gained a wealth of knowledge from the ECG for the diagnosis of many cardiac and noncardiac conditions, ranging from acute ischemia and infarction on the one hand to arrhythmias on the
other. Furthermore, the ECG is the first step in evaluating patients arriving at the emergency department,
as the results are immediately available. Likewise, the ECG has been used as a screening test for athletes
and is also used to identify patients at a high-risk of arrhythmias and sudden cardiac death.
Despite the emergence of other imaging modalities, the ECG remains a benchmark diagnostic test
and is an integral part of a risk stratification algorithm in almost all guidelines of all disciplines of
medicine.
Since the success of our 2015 book, The ECG Handbook of Contemporary Challenges, many of our
colleagues and friends encouraged us to provide a case-based collection of ECGs. Thus, we have
invited the most renowned physicians from around the world who read and interpret ECGs (i.e.,
electrocardiographers) to provide their most insightful examples. We also asked them to include their
interpretation of the ECG findings with appropriate, up-to-date references. All tracings are well
annotated and described. In addition, we suggested providing questions for the readers relating to the
ECGs and a discussion that makes these books useful for trainees at all levels.
Although the main theme of these two volumes is electrocardiography, other imaging techniques
are discussed to validate the authors’ interpretations. We are extremely grateful that all of our
colleagues have unanimously accepted our invitation and provided their best cases.
The cases are arranged according to topics in electrocardiography and arrhythmias. Areas of focus
include ECGs of inherited arrhythmia syndromes, athletic ECGs, and ECGs in congenital heart
disease. There is also discussion of new ECG criteria/markers and syndromes related to recently
discovered channelopathies such as Brugada syndrome, early repolarization syndrome, and the like.
We are confident that this collection of ECGs from masters of electrocardiography from around the
world will prove useful and of great educational value to clinicians in many areas of medicine. We
believe this unique collection is similar to receiving a master art collection from the Louvre or the
Metropolitan Museum of Art that should be on everyone’s shelf as an ECG museum.
Finally, we wish to thank the Cardiotext staff, namely Mike Crouchet and Carol Syverson, for their
professionalism and for providing the text and figures in a high-quality format.
The Editors

xvii

Abbreviations
ACS
AF
AP
APC
APD
ARVC/D
AT
AVNRT
AVRT

acute coronary syndrome
atrial fibrillation
accessory pathway
atrial premature contraction
action potential duration
arrhythmogenic right ventricular cardiomyopathy/dysplasia
atrial tachycardia
atrioventricular nodal reentrant tachycardia
atrioventricular reentrant tachycardia

BB
BBB
BS

bundle branch
bundle branch block
Brugada syndrome

CAD
CHF
CL

coronary artery disease
congestive heart failure
cycle length

DDD

dual-chamber pacing

EADs
ECG
EF

early afterdepolarizations
electrocardiogram
ejection fraction

HCM
HPS
HR

hypertrophic cardiomyopathy
His-Purkinje system
heart rate

ICD

implantable cardioverter-defibrillator

LA
LAD
LAFB
LBB
LBBB
LQTS

left atrial
left axis deviation
left anterior fascicular block
left bundle branch
left bundle branch block
long QT syndrome

xix

LV
LVEF
LVH
LVOT

left ventricle
left ventricular ejection fraction
left ventricular hypertrophy
left ventricular outflow tract

MI
MRI

myocardial infarction
magnetic resonance imaging

OD
ORT

once daily
orthodromic reciprocating tachycardia

PABs
PAC
PJRT
PV
PVC
PVI

premature atrial beats
premature atrial contraction
permanent form of junctional reciprocating tachycardia
pulmonary vein
premature ventricular contraction
pulmonary vein isolation

RA
RBB
RBBB
RV
RVA
RVH
RVOT

right atrial
right bundle branch
right bundle branch block
right ventricle
right ventricular apex
right ventricular hypertrophy
right ventricular outflow tract

SCD
SQTS
SR
SVT

sudden cardiac death
short QT syndrome
sinus rhythm
supraventricular tachycardia

TdP

torsades de pointes

VF
VT

ventricular fibrillation
ventricular tachycardia

WCT
WPW

wide complex tachycardia
Wolff–Parkinson–White syndrome

xx u Abbreviations

SECTION 1
Introduction to the Interpretation of the Electrocardiogram

CASE

Mohammad Shenasa, MD

1.1

The first and most important step in ECG interpretation is the differentiation between “normal”
and “abnormal.”
The second step consists of differentiation between the various abnormal ECG patterns and
their correlation with known pathologic conditions. In particular, the recent discoveries with small,
subtle, significant markers for adverse events such as early repolarization, Brugada-type ECGs, and
other channelopathies.
Information about the ECG in disease is much more complex than knowledge of normal
variation. Yet, it is in the differentiation between normal and abnormal that difficulties in ECG
interpretation frequently arise.
Below are two examples of normal ECGs.
Heart rate: 64 bpm
PR interval: 154 ms
QRS duration: 98 ms
QT/QTc: 406/415 ms
Normal ST-T wave patterns

Figure 1.1.1
ECG Masters’ Collection: Favorite ECGs from Master Teachers Around the World, Vol. 2 © 2018 Mohammad Shenasa, Mark E. Josephson,
N.A. Mark Estes III, Ezra A. Amsterdam, Melvin Scheinman. Cardiotext Publishing, ISBN: 978-1-942909-20-0.

1

Heart rate: 80 bpm
PR interval: 148 ms
QRS duration: 92 ms
QT/QTc: 364/420 ms

Figure 1.1.2

It is important to have a systematic approach when analyzing and interpreting of ECGs.
1.
2.
3.
4.
5.

Baseline findings in sinus rhythm.
Observations during tachycardias.
Analysis of the changes of the cardiographic morphologies (transient changes).
Mode of spontaneous initiation and termination.
Maneuvers during tachycardias.

In a stepwise approach to ECG or rhythm analysis, one should determine the rate of the
tachycardia (fast or slow), the QRS duration (wide or narrow) and morphology, and the relationship
of the P wave to the QRS, whether it is before, during, or after, and if there is a one-to-one
relationship between the P wave and the QRS.
Other important points regarding interpretation of the ECG.
1.
2.
3.
4.
5.
6.

Determine the origin and initiation of cardiac arrhythmias.
Look for myocardial ischemia and infarction.
Evidence of electrolyte imbalance and reversible causes.
Systemic and myocardial disorders.
Measure; do not eyeball the intervals.
Focus on the zone of transition.

References
1. Wellens HJ, Gorgels AP. The electrocardiogram 102 years after Einthoven. Circulation. 2004;109(5):562–564.
2. Yong CM, Froelicher V, Wagner G. The electrocardiogram at a crossroads. Circulation. 2013;128(1):79–82.
3. Stern S. Electrocardiogram: Still the cardiologist’s best friend. Circulation. 2006;113(19):e753–e756.

2 u Section 1: Introduction to the Interpretation of the Electrocardiogram

SECTION 2
Conduction Disturbances: Sinus Node Disease/Sick Sinus
Syndrome, AV Conduction Disturbances, AV Blocks,
Bundle Branch Blocks, and Fascicular Blocks

Mohammad-Ali Jazayeri, MD
Mohammad-Reza Jazayeri, MD

CASE

2.1

Patient History
Two cases are shown in Figure 2.1.1. The first is from a 68-year-old female with severe aortic
stenosis who underwent aortic replacement three days prior to the date that the rhythm strip (Panel
A) was obtained. Her surgery was uneventful, and her native valve was replaced with a 21-mm
Medtronic Mosaic tissue valve. The second case is an 84-year-old male with a 10-day history of
recurrent syncope who was admitted to the hospital.
The rhythm strip (Panel B) was obtained from the patient one day after admission.

Figure 2.1.1 The occurrence of block after termination of supraventricular tachycardia (SVT). Panel A shows a non-sustained run of
narrow QRS complex atrial tachycardia (AT) followed by sinus beats exhibiting left bundle branch block (LBBB). Panel B depicts termination
of a wide QRS complex AT followed by a 1440-ms pause and then a blocked sinus beat. The subsequent sinus beat is conducted with
first-degree atrioventricular (AV) block (PR interval of 300 ms) and a QRS complex similar to that during AT. All of the intervals are in ms.
The paper speed is different in these two panels.

ECG Masters’ Collection: Favorite ECGs from Master Teachers Around the World, Vol. 2 © 2018 Mohammad Shenasa, Mark E. Josephson,
N.A. Mark Estes III, Ezra A. Amsterdam, Melvin Scheinman. Cardiotext Publishing, ISBN: 978-1-942909-20-0.

3

Question
What is the probable mechanism of block in Figure 2.1.1A and B?
1.
2.
3.
4.

Pause-dependent block
His-Purkinje system (HPS) fatigue phenomenon
Functional block in the HPS
Potent vagal stimulation

Answer
The correct answer is A. The common theme in these two cases is the termination of a run of
supraventricular tachycardia (SVT), followed by a pause before the arrival of the next sinus (P wave) beat.
Subsequently, the P wave is conducted with LBBB in panel A and bilateral BBB in panel B. In other
words, the occurrence of block is preceded by a sudden short-to-long input to the AV conduction system.
It should be mentioned that the SVT, in both cases, is most likely AT with narrow QRS complex in Case 1;
and with RBBB and left anterior fascicular block (LAFB) (bifascicular block) in Case 2 (Figure 2.1.2).
Case 2 suddenly developed third-degree AV block later during the same hospital course (Figure 2.1.3).

Figure 2.1.2 Sustained AT. Seven-lead ECG of a sustained episode of AT with a cycle length (CL) of 440 ms is shown. The QRS complex
is 120 ms with RBBB and LAFB present.

Discussion
Over the past 65 years, a number of terms have been offered for this intriguing HPS block. These include
bradycardia-dependent block, Phase 4 block, (heart-rate) deceleration block, and pause-dependent block.
Spontaneous diastolic depolarization (SDD) is a normal electrophysiology property of the specialized
automatic cells including the HPS, which is normally responsible for the impulse formation. Although
the exact pathophysiologic mechanism of this type of block is still unknown, preexisting HPS
conduction disease is almost always the case even if the QRS complex appears narrow. Therefore, this is
a pathologic response that is usually not expected to occur in the normal HPS. Among several
mechanisms that have been offered, we discuss the two prevailing hypotheses as follows.
From a historical point of view, bradycardia-dependent BBB was recognized in the early years of
the 20th century, shortly after the invention of the ECG recorder.1 Bradycardia was attributed to a
4 u Section 2: Conduction Disturbances

Figure 2.1.3 Spontaneous third-degree AV block. The 8-lead ECG tracing starts with sinus bradycardia (cycle length of 1160 ms) and
1:1 AV conduction. There is first-degree AV block and RBBB plus LAFB present during sinus rhythm, the same as during the AT shown in
Figure 2.1.2. The last three sinus beats (arrows) block spontaneously without any obvious provocation.

heightened vagal tone in those patients. The first indisputable case of BBB during heart-rate
deceleration was reported in 1959.2 Subsequently, in 1967, enhanced SDD during phase 4
(Figure 2.1.4) in the HPS automatic cells was put forth as a putative mechanism of a broad
spectrum of conduction disturbances ranging from simple slowing to complete block.3 The same
investigators also proposed two other concomitant alterations in the EP characteristics of the

Figure 2.1.4 Spontaneous phase 4 depolarization. This is a schematic representation of transmembrane action potentials (AP) of the
automatic Purkinje cells shown during phase 4 depolarization. The AP on the left side of each panel shows the first impulse with normal
depolarization (phase 0) and repolarization phases 1, 2, and 3. Spontaneous depolarization of phase 4 is presumably in response to a
decrease in the frequency of stimulating impulses. The AP on the right side of each panel (dashed line) represents the second impulse
arriving at different times during diastole. In panel A, the second impulse (SI) provokes a near normal response because the membrane
potential (MP) is -80 mV, slightly less negative than the normal resting MP. In panel B, the SI is introduced at the time the MP is -60 mV
and therefore, the AP amplitude and its dv/dtmax is markedly diminished. In panel C, the SI arrives later during diastole at a time when the
MP is -40 mV. This results in a subthreshold response. (Used with permission from Singer DS et al., Circ Res 1967;21:537-558.)

Case 2.1 u 5

transmembrane action potential (TAP) in order for SDD to exert its maximal deleterious effect on
the conduction disturbances in a diseased HPS. These alterations were: (1) generalized diastolic
depolarization (hypopolarization), 3-5 which raise the resting potential to the less negative values
(>-70), giving rise to TAPs with diminished phase-0 amplitude, and (2) a shift of threshold potential
towards zero.3 In 1968, development of “bradycardia-dependent” BBB in patients was linked to
enhanced SDD during phase-4 of TAP for the first time.6 The majority of ensuing reports also
favored the same mechanism as the most plausible explanation for development of “bradycardiadependent” HPS block and the term “phase-4 block” emerged in the literature and quickly became
popular.7-13
The second hypothesis appeared in the literature in 1983.14,15 By using the sucrose gap model,
these investigators studied the frequency-dependent alterations of conduction in Purkinje fibers.
They assessed the time-dependent changes of two determining factors for conduction across a zone
of block: (1) the magnitude of the electrotonic current flow and (2) the efficacy of the electrotonic
inputs in exciting the distal site. Based on these studies, successful propagation from proximal to
distal sites required a delicate balance between these two factors. Otherwise, conduction delay or
block developed due to a source-to-sink mismatch. The resultant time-course conduction
disturbances, by appearing in early and late diastole (Figure 2.1.5), exhibited a biphasic pattern (an
early block followed by full conduction, followed by a late block). This biphasic behavior could be

Figure 2.1.5 Time-dependent biphasic (“phase 3” and “phase 4”) responses in Purkinje fiber-sucrose gap preparation. Tracings are
schematic representations of the superimposed APs across a Purkinje fiber from proximal (P) to distal (D) sites, 12 mm apart, in response
to bipolar stimulating electrodes. Ten-beat trains of stimuli were applied at a basic cycle length of 500 ms, and then the diastolic intervals
between the trains were scanned with test stimuli at progressively longer intervals. Note that the initial stimuli during basic drive (purple)
generate APs with short duration in the P sites and subthreshold responses in the D sites. Subsequent test stimuli (panel A) continue
to generate short-duration APs in the P site and subthreshold responses in the D site. This early diastolic P-to-D block may correspond
to what is also known as short-cycle (“phase 3”) block. At a critical interval, the stimulus evoking a full-fledged AP (arrow) generates a
response at the D site, which reaches threshold. All the ensuing stimuli (panel B) follow suit for the next 300 ms until the stimulus again
becomes unable to elicit fully developed AP (arrow) at the D sites. This late diastolic P-to-D block may correspond to what is also known as
long-cycle (“phase 4”) block. (Used with permission from Jalife J et al., Circulation 1983;67:912-922.)

6 u Section 2: Conduction Disturbances

interpreted as the equivalent of what had been designated previously as “phase 3” and “phase 4”
block, respectively. Furthermore, these investigators did not dismiss the SDD contribution to the
development of deceleration-dependent block, but they refuted its necessity as a prerequisite.
Although both studies have been extremely helpful in understanding the underlying mechanism of
the phenomenon observed in experimental animal models, it seems reasonable to address this type
of block as “deceleration-dependent,” “pause-dependent,” or “long-cycle” until the exact
mechanism(s) of this arrhythmia is (are) determined in humans. However, most of the current
literature accepts the phrase “pause-dependent.”
Deceleration-dependent HPS block is occasionally preceded by SVT termination as shown in
both cases presented here. More commonly, however, such a block is preceded by premature
impulses, either supraventricular (Figure 2.1.6) or ventricular (Figure 2.1.7) in origin. Occasionally,
the onset of block is sudden and without any visible premature beat as a trigger. In such cases, the
possibility of premature ventricular or junctional impulses with bidirectional block (i.e., nonpropagated impulses)16 cannot be excluded (Figure 2.1.8). Once the block occurs, it perpetuates
itself until the area of block is fully repolarized, allowing conduction to resume. Termination of
persistent HPS block may be facilitated (or mediated) by acceleration of the impulses approaching
the site of block or by premature impulses depolarizing that site (Figure 2.1.8).

Figure 2.1.6 Sudden onset of third-degree AV block preceded by a premature atrial complex (PAC). This is an 8-lead ECG taken from an
84-year-old woman with a history of prior anteroseptal myocardial infarction (MI), hypertension, and hyperlipidemia admitted with persistent
chest pain and elevated troponin consistent with an acute non-STEMI who underwent a percutaneous coronary intervention (PCI). This ECG
was obtained on the subsequent day after PCI showing two sinus beats at a rate of 100 bpm with RBBB with a right axis deviation, most likely
due to left posterior fascicular block. The presence of abnormal Q waves is compatible with a previous inferior and anteroseptal infarction. The
third beat is a conducted PAC. The subsequent sinus P wave arrives 850 ms after the PAC and blocks completely due to heart-rate deceleration,
which persist for the next 6.2 seconds. Worth noting is that the sinus PP interval remains 600 ms in duration throughout. The first QRS complex
(arrow) after the pause appear slightly different than the other complexes, which may be due to incomplete recovery of the HPS at the time of
sinus impulse arrival. Alternatively, this QRS complex could be an extrasystolic beat arising from the HPS.

Case 2.1 u 7

Figure 2.1.7 Sudden onset of third-degree AV block preceded by a premature ventricular complex (PVC). This lead II rhythm strip was obtained
from an 80-year-old man who presented with a recent-onset recurrent syncope. A 12-lead ECG showed sinus rhythm with RBBB. The rhythm strip
shows sinus bradycardia with a rate of 50 bpm. A PVC is followed by an 11-second period of third-degree AV block and ventricular asystole. The
first blocked sinus beat is most likely an encountered block in the AV node due to retrograde concealment of the PVC. However, the subsequent
sinus beat is blocked due to rate deceleration of the impulse arriving at the His-Purkinje system (HPS), approximately 1600 ms after the PVC (i.e.,
prior to HPS activation). Note that the sinus cycle length shortens to 960 ms, shortly before resumption of the AV conduction. The rhythm strip is
continuous in panel A. The noise (third tracing) is probably due to the patient’s involuntary activity during a brief episode of loss of consciousness.
Panel B shows an episode of 2:1 AV block, which had occurred approximately 2 hours before the episode shown in panel A.

Figure 2.1.8 Possible mechanisms of initiation and termination of deceleration-dependent block. The laddergram depicts sinus beats and
non-propagated premature ventricular beats (X). The first two sinus beats are conducted normally. The first X impulse is non-propagated
because it is blocked retrogradely in the AV node and antegradely in the HPS. The subsequent (third) sinus beat is blocked in the AV node
because of the retrograde concealment of the X impulse. From the time of the retrograde HPS concealment to the subsequently occurring
antegrade HPS activation during the fourth sinus beat, a pause (n) is created, which is longer than the prior HPS activation (m) CL. This
short-to-long CL variation sets the stage for deceleration-dependent AV block in the HPS. The second X impulse, by depolarizing the HPS,
resets the electrophysiological parameter(s) crucial for the persistence of the block and therefore allows resumption of HPS conduction.
The asterisks signify a lapse of time between the upper and lower laddergrams.

8 u Section 2: Conduction Disturbances

HPS fatigue (answer B) is a rare phenomenon, in which HPS block occurs after either cessation of
rapid ventricular burst pacing or termination of ventricular tachycardia. Like deceleration-dependent
block, the HPS fatigue phenomenon is also a pathological behavior of the diseased HPS.17-20 Both
situations share a common feature, and that is a pause preceding the onset of the HPS block. Thus, it
is conceivable that they also share the same underlying mechanism. Alternatively, it has been shown
in experimental animals that overdrive suppression of conduction may be due to transient block at
the Purkinje muscle junction.21 Depending upon whether or not the supraventricular impulses can
penetrate the conduction system and reach the depressed HPS as effectively as their ventricular
counterparts, rapid atrial pacing may or may not provoke suppression of conduction and HPS block.
Functional HPS block (answer C), unlike this entity, occurs physiologically when the heart rate
accelerates beyond a critical point or the HPS input is preceded by a long-to-short cycle length
variation. Potent vagal stimulation (answer D) may also cause AV block, but its potential
mechanism(s), ECG manifestations, diagnosis, and treatment are entirely different.22

References
1. Wilson FN. A case in which the vagus influenced the form of the ventricular complex of the electrocardiogram.
Arch Intern Med. 1915;16:1008–1027.
2. Dressler W. Transient bundle branch block occurring during slowing of the heartbeat and following gagging. Am
Heart J. 1959;58:760–764.
3. Singer DH, Lazzara R, Hoffman BF. Interrelationship between automaticity and conduction in Purkinje fibers. Circ
Res. 1967;21:537–558.
4. Rosenbaum MB, Elizari MV, Lázzari JO, et al. The mechanism of intermittent bundle branch block: Relationship to
prolonged recovery, hypopolarization and spontaneous diastolic depolarization. Chest. 1973;63:666–677.
5. Rosenbaum MB, Elizari MV, Levi RJ, et al. Paroxysmal atrioventricular block related to hypopolarization and
spontaneous diastolic depolarization. Chest. 1973;63:678–688.
6. Massumi RA. Bradycardia-dependent bundle-branch block. A critique and proposed criteria. Circulation.
1968;38:1066–1073.
7. El-Sherif N. Tachycardia-dependent versus bradycardia-dependent intermittent bundle-branch block. Br Heart J.
1972;34(2):167–176.
8. Elizari MV, Nau GJ, Levi RJ, et al. Experimental production of rate-dependent bundle branch block in the canine
heart. Circ Res. 1974;34(5):730–742.
9. Rosenbaum MB, Elizari MV, Chiale P, et al. Relationships between increased automaticity and depressed conduction
in the main intraventricular conducting fascicles of the human and canine heart. Circulation. 1974;49:818–828.
10. Barold SS, Ong LS, Young JA. Electrocardiographic observations in bradycardia and tachycardia-dependent
atrioventricular block. Relationship to supernormal phase of intraventricular conduction. Chest. 1975;67:450–745.
11. MB Rosenbaum, JO Lazzari, MV Elizari. The role of phase 3 and phase 4 block in clinical electrocardiography. In:
The Conduction System of the Heart. Wellens HJJ, et al., Eds. Philadelphia, PA: Lea & Febiger. 1976:126–144.
12. Cohen HC, D’Cruz I, Arbel ER, et al. Tachycardia and bradycardia-dependent bundle branch block alternans:
Clinical observations. Circulation. 1977;55:242–246.
13. Wu D, Deedwania P, Dhingra RC, et al. Electrophysiologic observations in a patient with bradycardia-dependent
atrioventricular block. Am J Cardiol. 1978;42:506–512.
14. Antzelevitch C, Jalife J, Moe GK. Frequency-dependent alterations of conduction in Purkinje fibers: A model of
phase 4 facilitation and block. In: Frontiers of Cardiac Electrophysiology. Rosenbaum MB, Elizari MV, Eds.
Amsterdam: Martinus Nijhoff. 1983:397–415.
15. Jalife J, Antzelevitch C, Lamanna V, et al. Rate-dependent changes in excitability of depressed cardiac Purkinje fibers
as a mechanism of intermittent bundle branch block. Circulation. 1983;67:912–922.
16. Rosen KM, Rahimtoola SH, Gunnar RM. Pseudo A-V block secondary to premature nonpropagated His bundle
depolarizations: Documentation by His bundle electrocardiography. Circulation. 1970;42:367–373.

Case 2.1 u 9

17. Narula DS and Runge M. Accommodation of AV nodal conduction and fatigue phenomenon in the His-Purkinje
system. In: The Conduction System of the Heart. Wellens HJJ, et al., Eds. Philadelphia, PA: Lea & Febiger. 1976:529–
544.
18. Fisch C. Bundle branch block after ventricular tachycardia: A manifestation of “fatigue” or “overdrive suppression.” J
Am Coll Cardiol. 1984;3:1562–1564.
19. DiLorenzo DR, Sellers TD. Fatigue of the His-Purkinje system during routine electrophysiologic studies. Pacing Clin
Electrophysiol. 1988;11:263–270.
20. Barold SS, Barold HS. Demonstration of a His-Purkinje fatigue phenomenon with programmed stimulation of the
right ventricular outflow tract. J Interv Card. Electrophysiol. 2000;4:489–491.
21. Gilmour RF, Jr, Davis JR, Zipes DP. Overdrive suppression of conduction at the canine Purkinje-muscle junction.
Circulation. 1987;76:1388–1396.
22. Lee S, Wellens HJ, Josephson ME. Paroxysmal atrioventricular block. Heart Rhythm. 2009;6:1229–1234.

10 u Section 2: Conduction Disturbances

Balaji Krishnan, MD
David G. Benditt, MD

CASE

2.2

Patient History
These tracings were obtained in a 21-year-old female college-level rower who had been in good
health and was on no prescription or over-the-counter medications. She presented with complaints
of intermittent palpitations but denied dizziness or loss of consciousness. Laboratory tests including
an echocardiogram and cardiac MRI were normal. An exercise stress test was well tolerated and
induced no arrhythmias.
Heart rate: 56 bpm
QRS duration: 80 ms
QT: 405 ms

Figure 2.2.1

The 12-lead ECG showed sinus bradycardia with marked sinus arrhythmia (average heart rate
56 bpm). An ambulatory ECG monitor revealed sinus arrhythmia, which correlated with her
“palpitations,” and episodes of paroxysmal complete atrioventricular (AV) block ranging from 4 to
13.6 seconds mainly at night (see Figure 2.2.2). The pauses were not associated symptoms and
there was no past medical history to suggest sleep apnea.

Case 2.2 u 11

Figure 2.2.2 Ambulatory ECG monitoring strip at the time of symptoms. Note the recording shows a gradually slowing heart rate before
there is complete AV block, resulting in a pause of 7.8 seconds. During AV block, the atrial rate remains relatively slow, strongly favoring
an autonomic etiology for the AV block.

Discussion
Due to lack of symptoms during daytime activity, including sports, and absence of guidelines to the
contrary, a pacemaker was not deemed indicated and there was no reason to restrict her activities.
12 u Section 2: Conduction Disturbances

In 5 years of annual follow-up, the patient has continued vigorous competitive rowing without
problems.
Figure 2.2.2 showed a gradually decreasing heart rate prior to transient complete AV block.
During the block the atrial rate remains slow, favoring an autonomic basis for the disturbance.1–3
In AV block due to conduction system disease, one would expect the atrial rate to increase in an
attempt to “compensate” for the hemodynamic stress (assuming absence of drug effects, such as
from beta-adrenergic blockers that may impair this response). In any case, an increased sinus rate
would not provide effective compensation if the AV block persists. In AV block due to autonomic
disturbance, as in this case, both the AV node and the sinus node are affected by presumed excess
parasympathetic influence.1,3

Disclosure
This work was supported in part by a grant from the Dr. Earl E. Bakken Family in support of HeartBrain research.

References
1. Massie B, Scheinman MM, Peters R, et al. Clinical and electrophysiologic findings in patients with paroxysmal
slowing of the sinus rate and apparent Mobitz II atrioventricular block. Circulation. 1978;58:305–314.
2. Strasberg B, Lam W, Swiryn S, et al. Symptomatic spontaneous paroxysmal AV nodal block due to localized
hyperresponsiveness of the AV node to vagotonic reflexes. Am Heart J. 1982;103:304–314.
3. Alboni P, Holz A, Brignole M. Vagally mediated atrioventricular block: Pathophysiology and diagnosis. Heart.
2013;99(13):904–908.

Case 2.2 u 13

CASE

2.3

Balaji Krishnan, MD
David G. Benditt, MD

Patient History
A 67-year-old female presented to the emergency department (ED) after an abrupt collapse with a
minor laceration on her scalp. She reported having a similar event about 1 year earlier. She had no
known cardiac disease, no previous illnesses, and no pertinent family history. She was not taking
any cardioactive medications. A witness reported the fall to have been without any apparent
warning. The patient was neither pale nor clammy and recovered promptly in less than 30 seconds.
Findings in the ED were unremarkable. A 12-lead ECG was reported to be normal with a narrow
QRS and normal QT interval (unavailable). An echocardiogram in the ED was reported as normal.

Figure 2.3.1 The tracing shows sinus rhythm with a narrow QRS and an initial PP interval of 860 ms. During subsequent high-grade AV
block the PP intervals (indicated in ms) progressively shorten. As the block begins to resolve toward the end of the tracing, the PP interval
begins to return toward baseline value.

Discussion
While being monitored in the ED, the recording shown (Figure 2.3.1) was obtained. The patient felt
lightheaded. The tracing shows sinus rhythm with a narrow QRS, which abruptly transitions to
high-grade atrioventricular (AV) block. Note that there is progressive shortening of the PP interval
(i.e., speeding of atrial rate) in response to the presumed hemodynamic stress of the conduction
disturbance. The latter observation tends to exclude an autonomically-mediated hyperparasympathetic block.1,2 A diagnosis of conduction disease was made, despite the normal QRS
duration. A pacemaker was implanted and the patient remained symptom free after 4 years of
follow-up.

14 u Section 2: Conduction Disturbances

Disclosure
This work was supported in part by a grant from the Dr. Earl E. Bakken Family in support of HeartBrain research.

References
1. Zysko D, Gajek J, Kozluk E, et al. Electrocardiographic characteristics of atrioventricular block induced by tilt
testing. Europace. 2009;11(2):225–230.
2. Barold SS, Hayes DL. Second degree atrioventricular block—A reappraisal. Mayo Clin Proc. 2001;76(1):44–57.

Case 2.3 u 15

CASE

2.4

Balaji Krishnan, MD
David G. Benditt, MD

Patient History
A 76-year-old male had been complaining of palpitations and intermittent “dizzy” spells for 6–8
months. On the day that this recording was obtained, he had collapsed while shopping. He suffered
a clavicular fracture and was admitted to the emergency department (ED) Observation Unit. He
had no prior cardiac evaluation and did not have a previous ECG on record.
During the course of the evening, he complained of his heart beating fast. His wife noticed that
he briefly slumped to the side with his eyes open. He recovered promptly. The ECG tracing (Figure
2.4.1) was recorded at the time of this in-hospital event.

Figure 2.4.1 The 2-channel rhythm strip begins with a relatively slow atrial tachycardia (approx. 95/min), which terminates abruptly,
resulting in two sequential cardiac asystolic pauses of 6.5 and 5.2 seconds, respectively. It was in association with these pauses that the
patient was symptomatic in the ED. The tracing concludes with sinus bradycardia at approximately 30–50 bpm.

Electrophysiology was consulted and a pacemaker was placed the following morning. Ablation
of his atrial tachycardia was discussed, but the patient declined. Sotalol therapy was initiated, and
the patient has been without symptomatic rapid heart rate or near-syncope for 3 years.

Discussion
Sinus node dysfunction comprises a range of clinical scenarios. The most common ECG
manifestations are sinus bradycardia, sinus pauses, and chronotropic incompetence. In this patient,
the combination of atrial tachycardia termination with delayed recovery of sinus node activity
resulted in asystolic pauses with sufficient drop in cerebral blood flow to cause near-syncope.
Presumably, had the patient been upright as he was while shopping, a frank syncope may have
occurred.

16 u Section 2: Conduction Disturbances

Disclosure
This work was supported in part by a grant from the Dr. Earl E. Bakken Family in support of HeartBrain research.

References
1. Short DS. The syndrome of alternating bradycardia and tachycardia. Br Heart J. 1954;16:208–214.
2. Benditt DG, Milstein S, Goldstein MA, et al. Sinus node dysfunction: Pathophysiology, clinical features, evaluation
and treatment. In Cardiac Electrophysiology: From Cell to Bedside. 2nd ed. Zipes DP, Jalife J, Eds. Philadelphia, PA:
WB Saunders Company. 1990:1215–1247.

Case 2.4 u 17

CASE

2.5

Alan Cheng, MD
Jane E. Crosson, MD

Patient History
A 64-year-old male presented with new-onset exertional dyspnea. The baseline ECG is shown
(Figure 2.5.1). During stage II of the Bruce protocol, his heart rate increased to 113 bpm (Figure
2.5.2) but suddenly dropped to 75 bpm (Figure 2.5.3) while exercising.

Question
What is the reason for this change in heart rate?

Figure 2.5.1

18 u Section 2: Conduction Disturbances

Figure 2.5.2

Figure 2.5.3

Discussion
This a case of exercise-induced heart block. In Figure 2.5.1 at rest, the patient exhibits sinus
rhythm with right bundle branch conduction delay/block. As he exercises, there is appropriate
augmentation of his sinus rate and atrioventricular (AV) conduction. However, as the heart rate
increases with adrenergic stimulation, a 2:1 block (red arrows denoting P waves buried in T waves)

Case 2.5 u 19

is observed. Exercise-induced heart block suggests disease that is below the AV node, which has a
higher risk for progression to complete heart block. With AV nodal disease, AV conduction is
expected to improve with catecholamine stimulation and vagal withdrawal in response to exercise.
Given the worsening AV conduction exhibited in the setting of increased adrenergic stimulation,
this case illustrates an individual who has progressive infranodal conduction system disease and
would likely benefit from pacemaker implantation.1

Reference
1. Hemann BA, Jezior MR, Atwood JE. Exercise-induced atrioventricular block: a report of 2 cases and review of the
literature. J Cardiopulm Rehabil. 2006;26(5):314–318.

20 u Section 2: Conduction Disturbances

Sanoj Chacko, MD, PhD
Benedict M. Glover, MD
Adrian Baranchuk, MD

CASE

2.6

Patient History
A 76-year-old male patient with a history of hypertension lasting 10 years was admitted due to a
syncopal episode associated with bradycardia. No history of ischemic heart disease. The patient was
not receiving any atrioventricular node (AVN) blocking agents. His initial ECG rhythm strip
obtained at a different center is shown in Figure 2.6.1.

Figure 2.6.1 A. ECG strip showing Wenckebach periods of alternate beats. There is a special relationship between P waves and
R waves. The arrows are pointing to the P waves to facilitate analysis. The first P wave conducts with a PR interval of 260 ms, the second
P wave is blocked in the lower AV node; the third P wave conducts with a PR interval of 524 ms. The fourth P wave is blocked in the lower
AV node (L-AVN) and the fifth P wave is also blocked but in the upper AV node (U-AVN), completing a Wenckebach series. The sixth P wave
conducts with a PR interval of 260 ms reinitiating the sequence. See text for details. B. Ladder diagram of the rhythm strip showing the
conduction abnormalities and the level of block. A, atrium; U-AVN, Upper atrioventricular node; L-AVN, Lower atrioventricular node;
V, Ventricle.

Question
What is the mechanism?
1.
2.
3.
4.

Complete heart block
Wenckebach heart block
Mobitz II AV block
Wenckebach periods of alternate beats
Case 2.6 u 21

Discussion, Interpretation, and Answer
The ECG findings are consistent with two levels of block in the AVN with an atrial rate of 115 bpm
and a ventricular rate of 35–40 bpm. The superior aspect of the AVN conducts with Wenckebach
phenomenon and the inferior aspect with a Mobitz type-II AVN block. We have inserted arrows
and numbered the P waves (Figure 2.6.1A) and added a ladder diagram (Figure 2.6.1B), to facilitate
the analysis. The first P wave conducted to the ventricle with a PR interval of 260 ms (possibly in
the superior aspect of the AVN), the second P wave is blocked (possibly in the inferior aspect of the
AVN); the third P wave conducted again with a PR interval of 524 ms depicting Wenckebach
phenomenon (superior aspect of AVN). The fourth P wave is blocked (inferior aspect of the AVN)
and the fifth P wave is blocked in the superior aspect of the AVN completing the Wenckebach series
(3:2 in the superior aspect of the AVN). The sixth P wave conducted at a PR interval of 260 ms
re-initiating the same pattern. This ECG demonstrates 5:2 AV block with Wenckebach Periods of
Alternate Beats (WPAB), a phenomenon that was described as associated with transversal
dissociation of the AV node-His. However, as the QRS morphology is wide, Wenckebach in the
infrahisian region cannot be completely ruled out. Transverse dissociation of the AVN-His bundle
into two horizontal levels “connected in series” usually manifests with 2:1 (or higher) block in the
“distal” level and Wenckebach periods in the “proximal” level.1
Compared to the classical AVN Wenckebach which shows gradual prolongation of the PR
interval followed by a single dropped P wave, WPAB ends with or begins from two consecutive
blocked P waves and invariably involves infranodal conduction system.2 WPAB may be a
consequence of a single lesion or two independent lesions, one of which causes classical Wenckebach
while the other causes Mobitz II block. In a series of five clinical cases of WPAB, marked
prolongation of refractoriness within the intraventricular conduction system was found leading to
four of them progressing into complete heart block.2 One more recent case report of a patient with
an acute coronary syndrome presented with WPAB evolving into complete heart block.3
WPAB is an uncommon electrocardiographic phenomenon representing advanced nodal and
distal conduction disease. These cases usually require permanent pacing. Careful interpretation of
the ECG provides information about the underlying electrophysiological mechanism.

References
1. Elencwajg B, Zaman L, Rozanski JJ, Myerburg RJ, Castellanos A. Transverse dissociation of the human His bundle.
Pacing Clin Electrophysiol. 1982; 5(3):323–328.
2. Halpern MS, Nau GJ, Levi RJ, Elizari MV, Rosenbaum M. Wenckebach periods of alternate beats clinical and
experimental observations. Circulation. 1973;48:41–49.
3. Sclarovsky S, García-Niebla J. Current role of electrocardiography in acute coronary syndrome. Is it an outdated
technique? Rev Esp Cardiol. 2009;62:451–463.

22 u Section 2: Conduction Disturbances

Pieter Koopman, MD
Hein Heidbuchel, MD, PhD

CASE

2.7

Patient History
An 80-year-old female is admitted to the emergency department (ED) in a state of severe confusion.
She suffered a mild myocardial infarction 10 years before, for which she underwent successful
percutaneous coronary intervention. She presents with an asymptomatic irregular heartbeat,
despite already being treated with beta-blockers.

Figure 2.7.1

Questions
1. What is the explanation for the wide QRS complexes (Figure 2.7.1)?
2. How should this patient be treated?

Case 2.7 u 23

Discussion

Figure 2.7.2

As the ladder diagram illustrates (Figure 2.7.2), the ECG shows a sinus rhythm with seconddegree atrioventricular (AV) block. The PR interval is prolonged for the conducting beats, so the AV
block is most likely supranodal. Every second P wave is blocked (2:1 A-V conduction), which is
evident on the far right side of the tracing. With the exception of the P wave following the black
single arrow in the tracing, every third P wave is also blocked. That block is due to ventricular
refractoriness following forgoing ventricular extrasystoles. Moreover, the premature beats are not
extremely broad, and have a right bundle branch block morphology and left axis, pointing to an
origin in the left posterior fascicle. The coupling intervals of these ectopic beats are variable (double
arrows), but intervals in between ectopic beats are similar. This behavior is typical for ventricular
parasystole due to an automatic focus with entrance block from the ventricle. The parasystolic focus
itself was not able to induce a ventricular complex at the timing of the single black arrow, because of
ventricular refractoriness due to the prior sinus beat.
Parasystole is caused by a secondary pacemaker site in the heart, firing at a fixed rate
independently from the sinus discharge rate. Normally, subsidiary pacemakers are prematurely
discharged by impulses from the sinus node, but in the case of parasystole, this independent
pacemaker site is “protected” by the presence of “entrance block” (sinus impulses fail to depolarize
the latent pacemaker secondary to block in the surrounding tissue). A block must be unidirectional,
so impulses from the parasystolic focus can exit. Therefore, parasystolic ectopic beats will wander
through the sinus beats with varying coupling intervals, but with fixed inter-ectopic intervals (or
sometimes multiples of a common denominator). Features of abnormal automaticity and
unidirectional block can be found in Purkinje fibers that survive in regions of transmural
24 u Section 2: Conduction Disturbances

myocardial infarction. Parasystole is more commonly found in cardiac patients than in healthy
individuals, but the arrhythmia itself is benign. Parasystole is often refractory to various antiarrhythmic agents and is therefore difficult to treat. As this patient also exhibited a symptomatic
second-degree AV block, pacemaker implantation should be considered, especially if the AV block
persisted after cessation of beta-blocker therapy.

Reference
1. Courtemanche M, Glass L, Rosengarten MD. Modeling ventricular parasystole. Ann N Y Acad Sci. 1990;591:178–
189.

Case 2.7 u 25

CASE

2.8

Nishant Verma, MD, MPH
Bradley P. Knight, MD

Patient History
This ECG (Figure 2.8.1) was recorded on a 26-year-old female with Marfan syndrome, complicated
by severe aortic insufficiency, dilated cardiomyopathy, and New York Heart Association Class IV
heart failure. She had previously undergone orthotopic heart transplantation (OHT). There is a
concern for an atrial arrhythmia and need for cardioversion.

Question
What is the diagnosis?

Figure 2.8.1 Rhythm strip in a patient with a recent OHT. For explanation, see discussion.

Discussion
During OHT, the three methods to anastomose the donor and recipient tissue are the classic
biatrial (Shumway-Lower) technique,1 bicaval approach,2 and total heart transplantation.3 Currently,
the bicaval anastomosis is the most favored method due to anatomic and hemodynamic
favorability.4 Total heart transplantation is technically more difficult,5 and the biatrial technique
has been associated with an increased rate of bradycardia and need for permanent pacemaker.6 In
the bicaval approach, the vena cavae are connected to the donor heart and no native (recipient) right
atrial tissue remains. However, with biatrial anastomosis, a significant portion of the native right
atrial tissue remains, including the native sinus node. This may often lead to interesting and
confusing ECG patterns, especially if the surgical technique that was used is not known during
rhythm analysis. Although the bicaval approach is used in most cases, there are still surgeons who
perform the classic biatrial approach in some situations.
26 u Section 2: Conduction Disturbances

In this case, the patient underwent biatrial OHT, and the electrophysiology service was
consulted due to concern for atrial arrhythmia and need for cardioversion. In fact, two independent
atrial rhythms are seen, one from the native heart and the other from the donor heart. The ECG
(Figure 2.8.1) shows sinus rhythm with 2:1 atrioventricular (AV) block and atrial parasystole
mimicking an atrial tachycardia (AT). The donor heart rhythm was determined to be sinus
tachycardia at a rate of approximately 115 bpm with 2:1 AV block. The native sinus rhythm had a
rate similar to the donor heart; however, it remained dissociated from the rest of the rhythm. Due
to persistent AV block, the patient required treatment for her bradycardia rather than a tachycardia,
and underwent implantation of a dual-chamber permanent pacemaker.
This patient underwent an OHT via a classic biatrial anastomosis; therefore the native and
recipient sinus nodes remained in place. Confusion regarding the ECG rhythm arose due to the
existence of two independent atrial rhythms, one from the donor and another from the
recipient. The donor atrial rhythm (*) has a rate of approximately 115 bpm and shows 2:1 AV
block (I–* denotes blocked beats). The native atrial rhythm (x) is dissociated and continues
independently at a similar rate.

References
1. Lower RR and Shumway NE. Studies on orthotopic homotransplantation of the canine heart. Surg Forum.
1960;11:18–19.
2. Sarsam MA, Campbell CS, Yonan NA, Deiraniya AK, Rahman AN. An alternative surgical technique in orthotopic
cardiac transplantation. J Card Surg. 1993;8(3):344–349.
3. Dreyfus G, Jebara V, Mihaileanu S, Carpentier AF. Total orthotopic heart transplantation: An alternative to the
standard technique. Ann Thorac Surg. 1991;52(5):1181–1184.
4. Jacob S, Sellke F. Is bicaval orthotopic heart transplantation superior to the biatrial technique? Interact Cardiovasc
Thorac Surg. 2009;9(2):333–342.
5. Schnoor M, Schäfer T, Lühmann D, Sievers HH. Bicaval versus standard technique in orthotopic heart
transplantation: A systematic review and meta-analysis. J Thorac Cardiovasc Surg. 2007;134(5):1322–1331.
6. Deleuze PH, Benvenuti C, Mazzucotelli JP, et al. Orthotopic cardiac transplantation with direct caval anastomosis:
Is it the optimal procedure? J Thorac Cardiovasc Surg. 1995;109(4):731–737.

Case 2.8 u 27

CASE

2.9

Christian Steinberg, MD
Andrew D. Krahn, MD

Patient History
A 65-year-old male patient was evaluated for suspicion of unstable angina. His past medical history
was unremarkable and he was on no medication prior to his admission. His initial ECG on arrival
showed normal sinus rhythm with a narrow QRS with no significant ST-T changes. While awaiting
his coronary angiogram, another ECG with intermittent wide QRS complex tachycardia was
recorded (Figure 2.9.1). The patient was asymptomatic during the ECG recording.

Figure 2.9.1 Atrial tachycardia with alternating bundle-branch block aberrancy. The ECG shows three different types of QRS morphology
(*) best seen in the rhythm strip of lead V1. The baseline QRS complex is narrow and regular (black arrows) at a rate of 81 bpm. There
are intermittent regular wide QRS complexes with an alternating typical right bundle branch block (RBBB; blue arrows) and left bundle
branch block (LBBB; red arrows) pattern. The rate of the RBBB complexes is 158 bpm, whereas the rate of the LBBB is 150 bpm. At the
atrial level there are regular monomorphic P waves at a cycle length of 340 ms (heart rate of 176 bpm). The PR relationship is 2:1 for
most of the recording, but there is intermittent 1:1 AV conduction that is associated with an alternating RBBB/LBBB pattern (dashed
arrows). The PR relationship and atrial activation pattern suggest an underlying atrial tachycardia or atypical atrial flutter. There is
alternating AV-conduction from 2:1 to 1:1 as a result of Wenckebach conduction in the AV node. The wide QRS complexes are the result
of alternating bundle branch block aberrancy during 1:1 AV conduction, which explains the typical RBBB and LBBB morphology. The likely
mechanisms for the RBBB and LBBB aberrancy include phase 3 block and linking phenomenon (retrograde concealed penetration into the
bundle branches).

Interpretation
Atrial tachycardia (AT) with predominant 2:1 AV conduction is present. Intermittent 1:1 AV
conduction is associated with alternating bundle branch block (right and left bundle branch block
aberrancy). The likely mechanisms of the aberrant conduction include phase 3 block and linking
phenomenon.
The P-wave morphology suggests an origin from the superolateral left atrium, possibly from the
left superior pulmonary vein.
28 u Section 2: Conduction Disturbances

Discussion
Aberrant conduction is characterized by prolongation of the QRS duration in response to
premature supraventricular impulse propagation with functional delay or block through parts of the
His-Purkinje system (HPS). A unique feature of the HPS is the variation of the refractory period in
response to the preceding cycle length,1 which is also the basis for aberrant conduction. Four
different mechanisms of aberrancy have been described: (1) phase 3 block, (2) acceleration
dependent aberrancy, (3) phase 4 block, and (4) aberrancy due to retrograde concealed penetration
of an antegrade blocked bundle branch (linking phenomenon).2–7 Aberrant conduction caused by
phase 3 block is also referred to as Ashman’s phenomenon and was first described in atrial
fibrillation.2 It is typically observed after abrupt cycle length changes with a long–short pattern.1,2
In the present case, aberrant conduction is repetitively induced during an intermittent change from
2:1 to 1:1 AV conduction of the underlying atrial tachycardia. Perpetuation of aberrancy and
alternating functional bundle branch blocks are typically explained by the linking phenomenon.3–5
The understanding of aberrancy is of clinical importance because aberrancy is typically a
benign phenomenon that must be differentiated from ventricular arrhythmia. Aberrant conduction
can occur in individuals with a healthy HPS and do not reflect the need for a pacemaker.4

References
1. Denker S, Shenasa M, Gilbert CJ, et al. Effects of abrupt changes in cycle length on refractoriness of the HisPurkinje system in man. Circulation. 1983;67(1):60–68.
2. Gouaux JL, Ashman R. Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia. Am
Heart J. 1947;34(3):366–373.
3. Wellens HJ, Durrer D. Supraventricular tachycardia with left aberrant conduction due to retrograde invasion into
the left bundle branch. Circulation. 1968;38(3):474–479.
4. Stark S, Farshidi A. Mechanism of alternating bundle branch aberrancy with atrial bigeminy: Electrocardiographicelectrophysiologic correlates. J Am Coll Cardiol. 1985;5(6):1491–1495.
5. Luzza F, Oreto G, Donato A, et al. Supernormal conduction in the left bundle branch unmasked by the linking
phenomenon. Pacing Clin Electrophysiol. 1992;15(9):1248–1252.
6. Oreto G, Smeets JL, Rodriguez LM, et al. Supernormal conduction in the left bundle branch. J Cardiovasc
Electrophysiol. 1994;5(4):345–349.
7. Luzza F, Consolo A, Oreto G. Bundle branch block in alternate beats: The role of supernormal and concealed
bundle branch conduction. Heart Lung. 1995;24(4):312–314.

Case 2.9 u 29

CASE

2.10

Yuji Nakazato, MD, PhD

Patient History
A 72-year-old female was admitted with presyncope. She had no specific heart disease except
hypertension. She had been taking enalapril (5 mg/day) for 10 years.

Figure 2.10.1

Figure 2.10.2

30 u Section 2: Conduction Disturbances

Questions
1. What is the diagnosis of this ECG?
2. What is the reason for the right bundle branch block (RBBB)?

Discussion
In Figure 2.10.1, 3 individual channel ECG strips are displayed. Figure 2.10.2 clearly demonstrates
narrow QRS escape beats (E) and wide QRS (RBBB) capture beats (C). An escape beat is usually
generated from just below the blocked site. Therefore, if the blocked site was infrahisian bundle
lesion, it should be a wide QRS. However, in this case, the escape beats are narrow QRS.
Nevertheless, the captured beats show RBBB.

Question
What is the mechanism of this phenomenon?

Figure 2.10.3

Case 2.10 u 31

Figure 2.10.4

Discussion
This phenomenon is a longitudinal dissociation of His bundle inducing RBBB. These unusual
mechanisms are demonstrated in Figure 2.10.3. If there were eccentrically complete conduction
disturbances in the His bundle, cardiac impulse would conduct through the incompletely damaged
fiber with delay. In addition, there is usually a depressed transverse conduction of the His bundle.
Therefore, it causes delayed RBB excitation and results in RBBB pattern QRS configuration on
captured beats (Figure 2.10.3A). On the other hand, escape beats are narrow QRS (Figure 2.10.3B).
Thus, bundle branch block on the ECG does not always mean the existence of true bundle branch
conduction disturbance. To confirm this phenomenon, His bundle recording was done. Split His
potential (H, H′) revealed intra His block and H-V interval (35 ms). The escape beat was identical
with spike-V interval (35 ms) by His bundle pacing (Figures 2.10.3C and 2.10.4). It could also prove
the RBB conduction is intact.

References
1. El-Sherif N, Amay-Y-Leon F, Schonfield C, et al. Normalization of bundle branch block patterns by distal His bundle
pacing. Clinical and experimental evidence of longitudinal dissociation in the pathologic His bundle. Circulation.
1978;57:473–483.
2. Narula OS. Longitudinal dissociation in the His bundle. Bundle branch block due to asynchronous conduction
within the His bundle in man. Circulation. 1977;56:996–1006.

32 u Section 2: Conduction Disturbances

SECTION 3
Miscellaneous Phenomena: Concealed Conduction,
Superabnormalities, Aberrancy Conduction, Premature Atrial
and Ventricular Contractions (PACs and PVCs)

CASE

David J. Callans, MD

3.1

Patient History
A 46-year-old male with no structural heart disease with palpitations secondary to frequent
premature ventricular complexes (PVCs) as shown in Figure 3.1.1. An ablation attempt at an
outside hospital was unsuccessful and resulted in right bundle branch block (RBBB).

Figure 3.1.1

ECG Masters’ Collection: Favorite ECGs from Master Teachers Around the World, Vol. 2 © 2018 Mohammad Shenasa, Mark E. Josephson,
N.A. Mark Estes III, Ezra A. Amsterdam, Melvin Scheinman. Cardiotext Publishing, ISBN: 978-1-942909-20-0.

33

Question
Which of the following sites is the most likely origin of the PVCs?
A. Posterior medial papillary muscle
B. Parahisian location approached from the right ventricle
C. Parahisian location approached from the left ventricle
D. Anterior interventricular vein/great cardiac vein junction

Discussion
The PVC morphology is quite similar to the QRS in conducted sinus rhythm, including being
similarly narrow. Despite the RBBB morphology, the PVC was ablated just proximal to the His
electrogram recorded in the right ventricle. The parahisian location of the PVC focus conducted
with a RBB morphology because of the destruction of the right bundle with the prior ablation
attempt.

Reference
1. Ban JE, Chen YL, Park HC, et al. Idiopathic ventricular arrhythmia originating from the para-Hisian area:
Prevalence, electrocardiographic and electrophysiological characteristics. J Arrhythm. 2014;30:48–54.

34 u Section 3: Miscellaneous Phenomena

CASE

3.2

Alan Cheng, MD
Jane E. Crosson, MD

Patient History
A 69-year-old male presenting for an annual physical was noted to have skipped beats on
auscultation. An ECG was performed as shown in Figure 3.2.1.

Figure 3.2.1

Discussion
This ECG reveals occasional narrow complex beats that at a first glance appear to be secondary to
conducted premature atrial contractions with a compensatory pause. Upon closer inspection, these
extra beats are not premature atrial complexes, but rather His extrasystoles.1 Looking closely at the
rhythm strip for lead V1 at the bottom of the ECG, one can clearly see the P waves preceding most
of the QRS complexes. The extra beat (green arrow) does not appear to be preceded by a premature
atrial event as the T-wave morphology is identical to other beats that are not followed by a
premature QRS. Additionally, the sinus cadence is unperturbed, suggesting no premature atrial
event present to reset the sinus cadence.

Reference
1. Marriot HJ, Nizet PM. Main-stem extrasystoles with aberrant ventricular conduction mimicking ventricular
extrasystoles. Am J Cardiol. 1967;19:755–757.

Case 3.2 u 35

CASE

3.3

Marc Dubuc, MD
Jason Andrade, BSc, MD

Patient History
A 53-year-old male presented for evaluation after experiencing a long history of intermittent
palpitations.

Figure 3.3.1

Question
What abnormality is demonstrated in the figure, and where does this abnormality originate?

Discusssion
This ECG (Figure 3.3.1) demonstrates sinus rhythm with frequent monomorphic premature
ventricular complexes (PVCs) (*). The PVCs are initially occurring in a bigeminal pattern, and later
as ventricular trigeminy. The PVCs are followed by a compensatory pause (retrograde atrial
conduction via the atrioventricular node can be seen within the T wave—arrow). Morphologic
analysis localizes the PVC to the left ventricular outflow tract region (high to low axis with R wave
duration in leads V1 and V2 is > 50% of the QRS duration, the V2 R:S ratio is ≥1, and the PVC QRS
transition is earlier than in sinus rhythm).

References
1. Bazan V, Gerstenfeld EP, Garcia FC, et al. Site-specific twelve-lead ECG features to identify an epicardial origin for
left ventricular tachycardia in the absence of myocardial infarction. Heart Rhythm. 2007;4:1403–1410.
2. Hachiya H, Aonuma K, Yamauchi Y, et al. How to diagnose, locate, and ablate coronary cusp ventricular
tachycardia. J Cardiovasc Electrophysiol. 2002;13(6):551–556.

36 u Section 3: Miscellaneous Phenomena

CASE

N.A. Mark Estes, III, MD

3.4

Patient History
Figure 3.4.1 shows an ECG of a 40-year-old female with cardiac arrest with sustained
monomorphic left bundle branch block (LBBB) morphology and ventricular tachycardia while
running.

Figure 3.4.1

Question
What is the ECG abnormality?

Discussion
The ECG demonstrates q waves in the inferior and anterior leads with a first-degree atrioventricular
block. Cardiac echocardiogram and magnetic resonance imaging with gadolinium were normal, as
was an evaluation for pulmonary or systemic sarcoidosis. Despite the extremely abnormal ECG and
cardiac arrest, no underlying structural heart disease has been identified. Genetic testing for
hypertrophic and dilated cardiomyopathy was negative.

Case 3.4 u 37

CASE

3.5

Massimo Santini, MD

Patient History
confermato
A 55-year-old female patient with medically managed hypertension for 5Nonyears
presented to the
emergency department (ED) with atypical chest pain for 3 hours. Her ECG is shown in Figure 3.5.1.

Figure 3.5.1

Question
Is it possible to diagnose the site of ectopic atrial rhythm by ECG analysis?

Discussion, Interpretation, and Answer
The origin of this rhythm is clearly not from the sinus node as the P waves have a different axis
from that of the sinus wave; therefore, it appears to be an ectopic atrial rhythm. However, ectopic
atrial rhythms may arise from different loci in both atria. The P waves have a different morphology
depending on where the ectopic focus is. Here, the PR interval is normal, but the P waves are
negative in leads aVF, II, and III as well as leads V3 to V6. Moreover, the P wave in lead V1 is slightly
positive and clearly positive in aVL. In this case, the ectopic atrial rhythm is usually called a
coronary sinus rhythm or low atrial rhythm since the impulse is assumed to originate from the
ostium of the coronary sinus.

38 u Section 3: Miscellaneous Phenomena

SECTION 4
Preexcitation Syndromes

CASE

Bernard Belhassen, MD

4.1

Patient History
Electrophysiologic study was performed in a 40-year-old woman with a history of palpitations. The
patient developed a short-lasting, irregular tachyarrhythmia with left bundle branch block (LBBB)
complexes during manipulation of a diagnostic electrode catheter in the right atrium (Figure 4.1.1).

Question
What is the explanation for the LBBB complexes?

Figure 4.1.1

ECG Masters’ Collection: Favorite ECGs from Master Teachers Around the World, Vol. 2 © 2018 Mohammad Shenasa, Mark E. Josephson,
N.A. Mark Estes III, Ezra A. Amsterdam, Melvin Scheinman. Cardiotext Publishing, ISBN: 978-1-942909-20-0.

39

Discussion
The tachyarrhythmia is due to an atrial tachyarrhythmia (fibrillation or flutter). All QRS complexes
during the tachyarrhythmia have a LBBB pattern. However, various morphologic types of LBBB are
present. Taking into account that none of the LBBB complexes have a ventricular origin (such as
catheter-induced for example), there are three possible diagnoses for explaining the LBBB
complexes: (1) classical LBBB; (2) right ventricular preexcitation due to an anterolateral
atrioventricular accessory pathway; or (3) antegrade conduction over an atriofascicular or nodoventricular pathway. The actual diagnosis ascertained by the electrophysiology study was antegrade
conduction over a right anterolateral atriofascicular Mahaim fiber that was subsequently
successfully ablated with radiofrequency at the tricuspid annulus. The various morphologic
patterns of LBBB present during tachyarrhythmia suggest the existence of an antegrade
preexcitation, rather than classical LBBB. However, the prolonged PR interval associated with the
lack of preexcitation during sinus rhythm after termination of the AF makes the possibility of
antegrade conduction over an anterolateral atrioventricular accessory pathway very unlikely.

40 u Section 4: Preexcitation Syndromes

Alan Cheng, MD
Jane E. Crosson, MD

CASE

4.2

Patient History
A 22-year-old man with double inlet left ventricle, intermittent episodes of ventricular
preexcitation, and complaints of palpitations underwent 24-hour Holter monitoring.
A baseline ECG (Figure 4.2.1) revealed sinus rhythm with first-degree atrioventricular (AV)
delay. This tracing was recorded while the patient was asleep. Sinus rhythm was present with firstdegree AV conduction delay and no evidence of ventricular preexcitation. By the fourth sinus beat
(green arrow), there is evidence of slowing and subsequent conduction block to the ventricle,
presumably through a transient increase in vagal tone. AV conduction resumes with the next sinus
beat (red arrow), but conduction to the ventricle is now seen to occur predominantly through an
accessory pathway.

Question
What is accounting for this change in AV conduction?

Figure 4.2.1

Discussion
Double inlet left ventricle is one of the most common forms of univentricular heart syndromes, the
others being double inlet right ventricle, single ventricle heterotaxy, and unbalanced common
atrioventricular canal defects.1 These patients have a high predilection for heart block2 and
development of sustained atrial arrhythmias, the latter most commonly after palliative surgery.
Figure 4.2.1 illustrates a classic example of the linking phenomenon. During the initial portion
of the tracing, sinus conduction occurs across the AV node. As the ventricle is depolarized,
ventricular depolarization results in retrograde penetration of the accessory pathway, thereby
resulting in antegrade block for the next sinus beat. Antegrade conduction across the accessory
pathway is blocked and this is perpetuated with subsequent sinus beats. With increasing vagal tone
and block across the AV node (green arrow), there is no subsequent retrograde penetration of the
accessory pathway. Hence, by the time the next sinus beat is delivered (red arrow), the accessory

Case 4.2 u 41

pathway has recovered and is now able to support antegrade conduction. As antegrade conduction
across the accessory pathway continues, retrograde penetration of the AV node occurs and
perpetuates AV node conduction block and persistence of ventricular preexcitation (i.e., linking).

References
1. Khairy P, Poirier N, Mercier LA. Congenital heart disease for the adult cardiologist. Circulation. 2007;115:800–812.
2. Davachi F, Moller JH. The electrocardiogram and vectorcardiogram in single ventricle: Anatomic correlations. Am J
Cardiol. 2969;23:19–31.

42 u Section 4: Preexcitation Syndromes

CASE

Robert Frank, MD

4.3

Patient History
A 30-year-old female was hospitalized after an episode of abrupt syncope, followed by a long postsyncopal period of dizziness. She had no significant past medical history, a normal clinical
examination and cardiac echocardiography, but a wide QRS (Figure 4.3.1).

Figure 4.3.1 First ECG in sinus rhythm. C1 to C6 is the same as V1 to V6.

Case 4.3 u 43

Question
What is the diagnosis?

Answer
A short PR interval with wide QRS with a slow onset (called delta wave) is characteristic of Wolff–
Parkinson–White (WPW) syndrome (ventricular preexcitation).

Question
Where is the site of preexcitation?

Answer
A wide, preexcited negative QRS in leads V1 and V2 is always right sided, and an inferior frontal axis
≥60° reflects an anteroseptal localization. A preexcited QRS positive in leads V1 and V2 is left sided,
and a preexcited QRS negative in lead V1 and positive in lead V2 is in a septal location.
A transesophageal incremental atrial pacing study was performed and the shortest 1/1
conducted atrioventricular cycle was of 300 ms (Figure 4.3.2).

Figure 4.3.2 Incremental transoesophageal atrial pacing just above the shortest 300 ms 1/1 conducted cycle.

Question
What is the most likely cause of syncope in this case?

44 u Section 4: Preexcitation Syndromes

Answer
Tachyarryhmias with very short ventricular cycles are the most probable mechanism in syncopal
WPW patients. However, this is encountered with ventricular cycles below 250 ms (mostly below
200 ms). Therefore, the potential mechanism of tachyarrhythmias with short ventricular cycles did
not apply to this case as the accessory pathway was blocked below 300 ms. An electroencephalogram
suggested some kind of epilepsy. However, she had a new syncopal episode, which was recorded.
The surprise was a complete atrioventricular (AV) block, and a pacemaker was implanted
(Figure 4.3.3).

Figure 4.3.3 A few weeks later after the most recent syncopal episode with sudden Mobitz type 2, third-degree AV block.

Discussion
In some patients with preexcited ECGs, the Kent Bundle may be the only conduction pathway. The risk
of inducing a complete AV block must be taken in account in patients before the decision to ablate an
accessory pathway in a patient without reentrant tachycardia and no conduction through the AV node
when the accessory pathway is blocked. Occurrence of high grade AV block in a young person brings
up the possibility of an inherited genetic disorder. In this case, a PRAKG2 mutation must be excluded.

References
1. Seipel L, Both A, Breithardt G, et al. His bundle recordings in a case of complete atrioventricular block combined
with pre-excitation syndrome. Am Heart J. 1976;92(5):623–629.
2. Dinckal MH, Davutoglu V, Bayata S, et al. Masked complete atrioventricular block in a patient with ventricular
preexcitation. J Interv Card Electrophysiol. 2004;11(1):33–35.

Case 4.3 u 45

CASE

4.4

Henry H. Hsia, MD

Patient History
A 34-year-old female with paroxysmal symptomatic palpitations. An echocardiogram demonstrated
apical displacement of the tricuspid valve with tethering of the septal leaflet, suggestive of Ebstein’s
anomaly. No evidence of structural heart disease or other valvular pathology was noted. Despite
antiarrhythmic therapy, her symptoms persisted with severe dizziness and near syncope.

Question
What is the diagnosis?

Figure 4.4.1

The 12-lead ECG showed a sinus rhythm with normal intervals and a leftward axis (Figure
4.4.1). There is no evidence of ventricular preexcitation, premature atrial or ventricular ectopy, or
repolarization abnormalities. A 12-lead ECG obtained during symptomatic palpitations showed a
wide QRS complex tachycardia at ~185 bpm (Figure 4.4.2).

46 u Section 4: Preexcitation Syndromes

Figure 4.4.2

Discussion and Interpretation
The wide complex tachycardia had a left bundle branch block (LBBB)-like QRS pattern, with a leftsuperior frontal axis and a late precordial transition (between leads V5 and V6) (Figure 4.4.2). The
presence of a sharp septal R wave with a relatively rapid QRS onset suggests rapid ventricular
activations, perhaps utilizing the His-Purkinje system. This raises the possibility of a
supraventricular tachycardia (SVT) with aberrant conduction, in the absence of scar-based
myocardial substrate.
Although there was no evidence of ventricular preexcitation during baseline sinus rhythm with
normal intervals, a characteristic “rS” pattern was noted at lead III (Figure 4.4.1). This raises the
suspicion of an atriofascicular tract with decremental antegrade conduction property. Sternick, et al
found an incidence of “rS” pattern in lead III in 60% of their cohorts with atriofascicular tract and
tachycardia, compared to only 6% in matched controls.
The QRS pattern during the wide complex tachycardia is also consistent with the diagnosis of
an atriofascicular tachycardia with a LBBB/left superior QRS axis and poor R-wave progression in
the precordial leads. The electrocardiographic clues suggesting an antidromic tachycardia using a
atriofascicular tract include (1) LBBB QRS morphology tachycardia, (2) QRS axis of 0° to -75° (left
axis deviation), (3) QRS duration less than 150 ms, and (4) late precordial transition after lead V4.

Case 4.4 u 47

Figure 4.4.3. Post-ablation ECG.

The patient underwent a successful catheter ablation of a right atriofascicular tract. The postablation ECG showed a right bundle branch block (RBBB) pattern in sinus rhythm (Figure 4.4.3).
The presence of RBBB is consistent with the patient’s underlying diagnosis of Ebstein’s anomaly and
right ventricular conduction delay. The presence of a right-side antegrade conducting accessory
pathway (atriofascicular) preexcited the right ventricle and masked the underlying RBBB.

References
1. Sternick EB, Timmermans C, Sosa E, et. al. The electrocardiogram during sinus rhythm and tachycardia in patients
with Mahaim fibers: The importance of an “rS” pattern in lead III. J Am Coll Cardiol. 2004;44:1626–1635.
2. Bardy GH, Fedor JM, German LD, Packer DL, Gallagher JJ. Surface electrocardiographic clues suggesting presence
of a nodofascicular Mahaim fiber. J Am Coll Cardiol. 1984;3:1161–1168.

48 u Section 4: Preexcitation Syndromes

Begüm Yetiş Sayın, MD
Sercan Okutucu, MD
Ali Oto, MD

CASE

4.5

Patient History
A 64-year-old woman admitted to the emergency department (ED) with palpitations and dizziness
for 2 hours. Her ECG on admittance is shown below (Figure 4.5.1).

Figure 4.5.1

Question
What is the diagnosis of this ECG?

Discussion
Despite antiarrhythmic medication, sinus rhythm could not be achieved. She was converted to sinus
rhythm by DC cardioversion. There was short PR interval and (+) delta waves on inferior leads
(Figure 4.5.2, arrows). An electrophysiologic study revealed left lateral accessory pathway and
tachycardia was diagnosed as preexcited atrial fibrillation. ECGs (Figure 4.5.2) before (A) and after
ablation (B).
Features of preexcited atrial fibrillation include tachycardia (usually greater than 200 bpm), an
irregular rhythm, absence of P waves and a wide QRS due to abnormal ventricular depolarization
via accessory pathway.1

Case 4.5 u 49

Figure 4.5.2

Reference
1. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With
Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task
Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2016;67(13):e27–e115.

50 u Section 4: Preexcitation Syndromes

CASE

Philip Podrid, MD

4.6

Patient History
A 35-year-old male with a history of Wolff–Parkinson–White (WPW) undergoes an ablation
because of documented atrioventricular reentrant tachycardia (AVRT). His preablation ECG is
shown (Figure 4.6.1). Two years after the ablation he complains of recurrent palpitations. An ECG
is obtained (Figure 4.6.2). Several weeks later, he presents to the emergency department (ED)
because of an episode of palpitations (Figure 4.6.3).

Figure 4.6.1

Case 4.6 u 51

Figure 4.6.2

Figure 4.6.3

Questions
1. Figure 4.6.1 shows a WPW pattern. What is the location of the accessory pathway?
2. What does Figure 4.6.2 indicate?
3. What is the etiology for the tachycardia in Figure 4.6.3?

52 u Section 4: Preexcitation Syndromes

Diagnosis
Figure 4.6.1 shows sinus bradycardia, left atrial abnormality, WPW pattern (left-sided posteroseptal
bypass tract).
Figure 4.6.2 shows sinus bradycardia, left atrial abnormality, premature atrial complex with
preexcitation.
Figure 4.6.3 shows long RP tachycardia, orthodromic AVRT with rate-related intraventricular
conduction delay.

Discussion
In Figure 4.6.1, there is a regular rhythm with a rate of 52 bpm. There is a P wave before each QRS
complex (+) with a constant PR interval (0.16 seconds). The P wave is positive in leads I, II, aVF, and
V4 –V6. This is a sinus bradycardia. The P wave is broad and prominently notched in several leads,
consistent with a left atrial abnormality or left atrial hypertrophy. While the PR interval is normal,
there is no PR segment. As the PR interval includes the P wave as well as the PR segment, the
normal PR interval in this patient is due to the broad P wave. The short/absent PR interval means
that there is enhanced AV conduction. The QRS complex duration at the base is prolonged (0.12
seconds) as a result of a slurred upstroke (↑); this is a delta wave. The peak of the QRS complex is
narrow. The presence of a short PR segment and a delta wave is diagnostic of a WPW pattern. The
WPW complex is the result of fusion, with early and direct myocardial activation via the accessory
pathway (i.e., preexcitation), which then fuses with impulse conduction via the normal AV node and
His-Purkinje system. This accounts for the wide base of the QRS complex and the narrow peak of
the QRS complex. The delta wave is positive in lead V1, meaning that the initial impulse originates
in the left ventricle and is directed toward the right ventricle. There are Q waves in leads II, III, and
aVF (^), which is consistent with a posteroseptal bypass tract. The Q waves are termed a pseudo
inferior wall myocardial infarction. Since there is initial direct myocardial activation, abnormalities
affecting the ventricles cannot be reliably diagnosed, including infarction patterns. There is positive
concordance (tall R waves) across the precordium (←), which is also consistent with a WPW
pattern. This is a pattern seen when there is direct myocardial activation, such as what occurs with
WPW pattern or a ventricular complex. The axis is extremely leftward between -30° and -90°
(positive QRS complex in lead I and negative in leads II and aVF). The two etiologies for an extreme
left axis include a left anterior fascicular block (rS QRS morphology in leads II and aVF), or an
inferior wall myocardial infarction (deep Q waves in leads II and aVF). In this case there is a pseudo
inferior wall infarction pattern. This is the etiology for the left axis. The QT/QTc intervals are
normal (440/410 ms and 420/390 ms when corrected for the prolonged QRS duration).
In Figure 4.6.2, there is a regular rhythm at a rate of 52 bpm. There is a P wave before each QRS
complex (+), and the P wave is positive in leads I, II, aVF, and V4 –V6. The PR interval is constant
(0.16 seconds) and there is a prominent PR segment. This is a sinus bradycardia. The P-wave
morphology is the same as in Figure 4.6.1, and there is evidence for a left atrial abnormality or
hypertrophy. The QRS complex duration is normal (0.08 seconds) and there is a normal axis
betwee