Cardiology Board Review E-Book

Ramdas G. Pai

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 894

Veröffentlichungsjahr: 2023

Beschreibung

Multiple choice question-and-answer book for cardiologists at all levels, now updated to include 100 new questions covering additional topics

Cardiology Board Review, Second Edition is a multiple-choice question-and-answer study aid that is written for the primary purpose of helping candidates prepare for the American Board of Internal Medicine (ABIM) subspecialty certification. The questions address all areas of cardiology, some of which include: physical examination, ECG section with high resolution images, non-invasive and invasive imaging, myocardial diseases, and more.

Each of the 1,400 questions is followed by four answers to choose from and the discussions address not only the rationale behind picking the right choice, but also fills in information around the topic so that important key concepts are clearly laid out. This helps candidates to prepare for the test, while also developing a clear understanding of various aspects of cardiology, including diagnosis and management.

Written by two highly experienced authors in the field of healthcare, Cardiology Board Review, Second Edition covers topics such as:

• History and physical examinations, electrocardiography, chest x-rays in cardiology, stress testing and risk stratification of asymptomatic subjects, and echocardiography
• Cardiac magnetic resonance imaging, cardiac computed tomography, cardiac catheterization, acute coronary syndromes, and chronic coronary artery disease
• Heart failure, transplant, left ventricular assist devices, pulmonary hypertension, cardiomyopathies, hypertension, and diabetes mellitus
• Lipids, valvular heart disease, adult congenital heart disease, pericardial diseases, aortic diseases, and cardiac arrhythmias
• Pacemakers and defibrillators, cardiac masses, systemic disorders affecting the heart, and heart disease and pregnancy

Providing comprehensive coverage of all relevant subjects and offering the easy-to-understand "why" behind the answer to each question, this second edition of Cardiology Board Review is an essential study resource for fellows in training, practicing cardiologists, and those preparing for ABIM subspecialty board in cardiology.

Leseprobe

Table of Contents

Cover

Title Page

Copyright Page

List of Contributors

Preface

1 History and Physical Examination

Answers

2 Electrocardiography

Answers

3 Chest X‐Ray in Cardiology

Answers

4 Stress Testing and Risk Stratification of Asymptomatic Subjects

Answers

References

5 Echocardiography

Answers

References

6 Cardiac Magnetic Resonance Imaging

Answers

7 Cardiac Computed Tomography

Answers

Further Reading

8 Cardiac Catheterization

Answers

9 Acute Coronary Syndromes

Answers

References

10 Chronic Coronary Artery Disease

Answers

References

11 Heart Failure, Transplant, Left Ventricular Assist Devices, Pulmonary Hypertension

Answers

References

12 Cardiomyopathies

Answers

References

Further Reading

13 Hypertension

Answers

References

14 Diabetes Mellitus

Answers

References

15 Lipids

Answers

References

16 Valvular Heart Disease

Answers

References

17 Adult Congenital Heart Disease

Answers

References

18 Pericardial Diseases

Answers

References

Further Reading

19 Aortic Diseases

Answers

References

20 Carotid and Vertebral Artery Disease

Answers

References

21 Peripheral Vascular Disease

Answers

References

Suggested Reading

22 Cardiac Arrhythmias

Answers

Reference

23 Pacemakers and Defibrillators

Answers

24 Cardiac Masses

Answers

25 Systematic Disorders Affecting the Heart

Answers

26 Interdisciplinary Consultative Cardiology

Answers

Reference

27 Heart Disease and Pregnancy

Answers

References

28 Racial and Gender Disparities

Answers

29 Pharmacologic Principles of Cardiac Drugs

Answers

30 Anticoagulation

Answers

References

31 Aspirin and Antiplatelet Therapy

Answers

32 Statistical Concepts

Answers

Reference

33 Genetics

Answers

References

34 Cardiac Emergencies and Resuscitation

Answers

Index

End User License Agreement

List of Tables

Chapter 19

Table 19.1

Table 19.2

Table 19.3

Chapter 20

Table 20.1 Society for Radiologists in Ultrasound (SRU) Consensus Criteria ...

Chapter 21

Table 21.9a Fontaine stages.

Table 21.9b Rutherford.

Table 21.9c TASC II classification of superficial femoral artery occlusion....

Table 21.22 Classification of acute limb ischemia.

List of Illustrations

Chapter 1

Figures 1.26–1.31

Figures 1.32–1.37

Figures 1.38–1.45

Chapter 2

Figure 2.1

Figure 2.2

Figure 2.3

Figure 2.4

Figure 2.5

Figure 2.6

Figure 2.7

Figure 2.8

Figure 2.9

Figure 2.10

Figure 2.11

Figure 2.12

Figure 2.13

Figure 2.14

Figure 2.15

Figure 2.16

Figure 2.17

Figure 2.18

Figure 2.19

Figure 2.20

Figure 2.21

Figure 2.22

Figure 2.23

Figure 2.24

Figure 2.25

Figure 2.26

Figure 2.27

Figure 2.28

Figure 2.29

Figure 2.30

Figure 2.31

Figure 2.32

Figure 2.33

Figure 2.34

Figure 2.35

Figure 2.36

Figure 2.37

Figure 2.38

Figure 2.39

Figure 2.40

Figure 2.41

Figure 2.42

Figure 2.43

Figure 2.44

Figure 2.45

Figure 2.46

Figure 2.47

Figure 2.48

Figure 2.49

Figure 2.50

Figure 2.51

Figure 2.52

Figure 2.53

Figure 2.54

Figure 2.55

Figure 2.56

Figure 2.57

Figure 2.58

Figure 2.59

Figure 2.60

Figure 2.61

Figure 2.62

Figure 2.63

Figure 2.64

Figure 2.65

Figure 2.66

Figure 2.67

Chapter 3

Figure 3.1a

Figure 3.2a

Figure 3.3a

Figure 3.4a

Figure 3.5a

Figure 3.6a

Figure 3.7

Figure 3.8a

Figure 3.10a

Figure 3.11a

Figure 3.12a

Figure 3.13

Figure 3.14

Figure 3.15a

Figure 3.17

Figure 3.18

Figure 3.19a

Figure 3.20

Figure 3.21

Figure 3.22a

Figure 3.23

Figure 3.24

Figure 3.25a

Figure 3.26a

Figure 3.27a

Figure 3.1b

Figure 3.2b

Figure 3.2c

Figure 3.3b

Figure 3.3c

Figure 3.4b

Figure 3.5b

Figure 3.6b

Figure 3.8b

Figure 3.10b

Figure 3.11b

Figure 3.12b

Figure 3.15b

Figure 3.19b

Figure 3.22b

Figure 3.25b

Figure 3.26b

Figure 3.27b

Chapter 4

Figure 4.21

Figure 4.22

Figure 4.23

Figure 4.24

Figure 4.25

Figure 4.26

Figure 4.27

Figure 4.28

Figure 4.29

Figure 4.30

Figure 4.31

Chapter 5

Figure 5.11

Figure 5.13

Figure 5.14

Figure 5.15

Figure 5.16

Figure 5.17

Figure 5.18

Figure 5.20

Figure 5.21

Figure 5.22

Figure 5.23

Figure 5.24

Figure 5.25

Figure 5.26

Figure 5.27

Figure 5.28

Figure 5.29

Figure 5.30

Figure 5.31

Figure 5.32

Figure 5.33

Figure 5.34

Figure 5.35

Figure 5.36

Figure 5.37

Figure 5.38

Figure 5.39

Figure 5.40

Figure 5.41

Figure 5.42

Figure 5.43

Figure 5.44

Figure 5.45

Figure 5.46

Figure 5.47

Figure 5.48

Figure 5.49

Figure 5.50

Figure 5.51

Figure 5.52

Figure 5.53

Figure 5.54

Figure 5.55

Figure 5.56

Figure 5.58

Figure 5.59

Figure 5.60

Figure 5.61

Figure 5.62

Figure 5.63

Figure 5.64

Figure 5.65

Figure 5.66

Figure 5.67

Figure 5.68

Figure 5.69

Figure 5.70

Figure 5.71

Figure 5.72

Figure 5.73

Figure 5.74

Figure 5.75

Figure 5.76

Figure 5.77

Figure 5.78

Figure 5.79

Figure 5.80

Figure 5.81

Figure 5.82

Figure 5.83

Figure 5.84

Chapter 6

Figure 6.8

Figure 6.9

Figure 6.10

Figure 6.11

Figure 6.12

Figure 6.13

Figure 6.14

Figure 6.15

Figure 6.16

Figure 6.17

Figure 6.18

Figure 6.19

Figure 6.20

Figure 6.21

Figure 6.22

Figure 6.23

Figure 6.24

Figure 6.25

Figure 6.26a

Figure 6.27a

Figure 6.28a

Figure 6.29a

Figure 6.30

Figure 6.31

Figure 6.32

Figure 6.33

Figure 6.34

Figure 6.35

Figure 6.36

Figure 6.26b

Figure 6.27b

Figure 6.28b

Figure 6.29b

Chapter 7

Figure 7.31

Figure 7.32

Figure 7.33

Figure 7.34

Figure 7.35

Figure 7.36

Figure 7.37

Figure 7.38

Figure 7.39

Figure 7.40

Figure 7.41

Figure 7.42

Figure 7.43

Figure 7.44

Figure 7.45

Figure 7.46

Figure 7.47

Figure 7.48

Figure 7.49

Figure 7.52

Figure 7.53

Figure 7.54

Figure 7.57a

Figure 7.58

Figure 7.59

Figure 7.60

Figure 7.61a

Figure 7.63a

Figure 7.64

Figure 7.57b

Figure 7.61b

Figure 7.63b

Figure B7.1

Chapter 8

Figure 8.1

Figure 8.3

Figure 8.6

Figure 8.14

Figure 8.15a

Figure 8.17

Figure 8.18

Figure 8.19

Figure 8.20

Figure 8.21

Figure 8.22

Figure 8.23

Figure 8.24

Figure 8.25

Figure 8.26

Figure 8.27

Figure 8.28

Figure 8.29

Figure 8.30

Figure 8.31

Figure 8.15b

Chapter 11

Figure 11.77

Figure 11.78

Figure 11.79

Chapter 12

Figure 12.24

Figure 12.27

Figure 12.28

Figure 12.29

Figure 12.30

Figure 12.31

Figure 12.32

Figure 12.33

Figure 12.34

Figure 12.35

Chapter 15

Figure 15.1 Major recommendations for statin therapy for ASCVD prevention....

Figure 15.2 Treatment algorithm – the chronic disease management model for p...

Chapter 16

Figure 16.42

Figure 16.43

Figure 16.44

Figure 16.45

Figure 16.46

Figure 16.47

Figure 16.48

Figure 16.49

Figure 16.50

Figure 16.51

Figure 16.52

Figure 16.53

Figure 16.54

Figure 16.55

Figure 16.56

Figure 16.57

Figure 16.58

Figure 16.59

Figure 16.60

Figure 16.61

Figure 16.62

Figure 16.15 Indications for AVR in patients with AS (ETT: exercise toleranc...

Figure 16.20 Indications for AVR for chronic AR.

Figure 16.22 Indications for intervention for rheumatic MS (AF: atrial fibri...

Figure 16.25 Indications for surgery for MR (CAD: coronary heart disease; CR...

Figure 16.29 Indications for surgery for TR (PHTN: pulmonary hypertension; R...

Figure 16.32 Anticoagulation for prosthetic valves (ASA: aspirin; LMWH: low ...

Figure 16.39 Imaging studies in

native valve endocarditis

(

NVE

) and

prosthet

...

Figure 16.40 Diagnosis and treatment of IE (ICD: implantable cardioverter de...

Figure 16.41 Anticoagulation of pregnant patients with mechanical valves (aP...

Chapter 17

Figure 17.15

Figure 17.60

Figure 17.61

Figure 17.62

Figure 17.63

Figure 17.64

Figure 17.65

Figure 17.66

Figure 17.67a

Figure 17.68

Figure 17.69

Figure 17.70a

Figure 17.71

Figure 17.72

Figure 17.73

Figure 17.92

Figure 17.93

Figure 17.67b

Figure 17.67c

Figure 17.70b

Chapter 18

Figure 18.36

Figure 18.37

Chapter 19

Figure 19.7

Figure 19.9

Figure 19.10

Figure 19.12

Figure 19.22a

Figure 19.23a

Figure 19.30

Figure 19.31a

Figure 19.22b

Figure 19.23b

Figure 19.31b

Chapter 20

Figure 20.1a

Figure 20.12

Figure 20.16

Figure 20.1b

Figure 20.2

Chapter 21

Figure 21.40a

Figure 21.7 All‐cause mortality as a function of baseline ABI.

Figure 21.12a Total occlusion of the infrarenal aorta.

Figure 21.12b Bilateral superficial femoral arteries filling via collaterals...

Figure 21.25

Figure 21.29 Bilateral RAS.

Figure 21.40b

Figure 21.40c

Chapter 22

Figure 22.10

Figure 22.27

Figure 22.31

Figure 22.32

Figure 22.33

Figure 22.34a

Figure 22.35a

Figure 22.36

Figure 22.37a

Figure 22.38a

Figure 22.39a

Figure 22.40

Figure 22.41

Figure 22.42

Figure 22.43

Figure 22.44

Figure 22.45

Figure 22.46

Figure 22.47

Figure 22.48

Figure 22.49

Figure 22.50

Figure 22.51

Figure 22.52

Figure 22.34b

Figure 22.35b

Figure 22.37b

Figure 22.38b

Figure 22.39b

Chapter 24

Figure 24.1

Figure 24.3

Figure 24.5

Figure 24.7a

Figure 24.8a

Figure 24.9a

Figure 24.10a

Figure 24.12a

Figure 24.13a

Figure 24.15a

Figure 24.16a

Figure 24.17a

Figure 24.18a

Figure 24.19a

Figure 24.20a

Figure 24.22a

Figure 24.23a

Figure 24.24a

Figure 24.25a

Figure 24.26a

Figure 24.28a

Figure 24.29

Figure 24.30

Figure 24.31a

Figure 24.32a

Figure 24.33a

Figure 24.34a

Figure 24.34b

Figure 24.6

Figure 24.7b

Figure 24.8b

Figure 24.9b

Figure 24.10b

Figure 24.11 Left: Spindled tumor cells surrounding vessel. Right: Spindled ...

Figure 24.12b

Figure 24.13b

Figure 24.15b

Figure 24.16b

Figure 24.17b

Figure 24.18b

Figure 24.19

Figure 24.20b

Figure 24.22b

Figure 24.23b

Figure 24.24b

Figure 24.25b

Figure 24.26b

Figure 24.28b

Figure 24.31b

Figure 24.32b

Figure 24.33b

Figure 24.34c

Chapter 32

Figure 32.4

Figure 32.1

Figure 32.3

Figure 32.13

Guide

Cover Page

Title Page

Copyright Page

List of Contributors

Preface

Table of Contents

Begin Reading

Index

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Cardiology Board Review

Second Edition

Ramdas G. Pai, MD, FRCP (Edin), FACC

University of California Riverside School of Medicine

Riverside, CA, USA

Padmini Varadarajan, MD, FACC

University of California Riverside School of Medicine

Riverside, CA, USA

With contributions from Patrick Bagdasaryan, Percy Genyk, Chris Hauschild, Gagan Kaur, Ashis Mukherjee, Balaji Natarajan, Chirag Patel, Mandira Patel, Prashant Patel, Ravi Rao, Prabhdeep Sethi, Jarmanjeet Singh, Vrinda Vyas

This edition first published 2023© 2023 John Wiley & Sons Ltd

Edition HistoryWiley‐Blackwell (1e, 2018)

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by law. Advice on how to obtain permission to reuse material from this title is available at http://www.wiley.com/go/permissions.

The right of Ramdas G. Pai and Padmini Varadarajan to be identified as the authors of this work has been asserted in accordance with law.

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List of Contributors

Patrick Baghdasaryan, MDCardiology FellowUniversity of California Riverside School of MedicineCA, USA

Percy GenykCardiology FellowUniversity of California Riverside School of MedicineCA, USA

Christopher Hauschild, MDDepartment of PharmacyLoma Linda University Medical CenterLoma LindaCA, USA

Gagan Kaur, MDCardiology FellowUniversity of California Riverside School of MedicineCA, USA

Ashish Mukherjee, MD, FACC, FSCAIClinical Professor, Health SciencesProgram Director, Interventional CardiologyPulse CardiologyUniversity of California Riverside School of MedicineCA, USA

Balaji Natarajan, MDInterventional Cardiology FellowUniversity of California Riverside School of MedicineCA, USA

Ramdas G. Pai, MD, FRCP(Edin), FACCProfessor and Chairman of MedicineChair of Clinical SciencesDirector of Cardiovascular Fellowship ProgramUniversity of California Riverside School of MedicineRiversideCA, USA

Chirag Patel, MDCardiology FellowUniversity of California Riverside School of MedicineCA, USA

Mandira Patel, MDCardiology FellowUniversity of California Riverside School of MedicineCA, USA

Prashanth Patel, MD, FACCInterventional cardiologyPulse Cardiology, San BernardinoCA, USA

Ravi Rao, MDCardiology FellowUniversity of California Riverside School of MedicineCA, USA

Prabhdeep S. Sethi, MDAssociate Clinical Professor, Health SciencesPulse CardiologyUniversity of California Riverside School of MedicineCA, USA

Jarmanjeet Singh, MDCardiology FellowUniversity of California Riverside School of MedicineCA, USA

Padmini Varadarajan, MD, FACCProfessor of MedicineChief of CardiologyVice Chair of Internal MedicineAssociate Program Director of Cardiology Fellowship and Internal Medicine Residency ProgramsUniversity of California Riverside School of MedicineCA, USA

Vrinda Vyas, MDCardiology FellowUniversity of California Riverside School of MedicineCA, USA

Lily Yam, PharmDDepartment of PharmacyLoma Linda University Medical CenterLoma LindaCA, USA

Preface

The second edition of the Cardiology Board Review has been revised and updated and is a comprehensive review of major topics in Cardiology. This book will be very useful for those preparing for initial and recertification exams in Cardiology. It has been edited by Internationally acclaimed teaching physicians with an expertise in major topics in Cardiology.

The book is divided into chapters organized in a question‐and‐answer format making it easy to prepare for the Board examination. The answers are explained in detail, accompanied by references to major trials and some clinical pearls. The book also highlights a special section on electrocardiograms which are of high resolution. Sections on various imaging modalities like Chest X‐Ray, echocardiography, cardiac computed tomography, and cardiac magnetic resonance imaging are also included. Questions not typically encountered in other board review books such as racial disparities in medicine and cardiac emergencies are provided to aid with detailed preparation. Finally, the book also facilitates comprehensive and critical review of cardiovascular medicine to enhance one's diagnostic and therapeutic skills.

1History and Physical Examination

1.1.

A 25‐year‐old woman presents for routine follow up. She has a 2/6 ejection systolic murmur best heard in the second left intercostal space with normal S1. The S2 is split during inspiration only, and P2 intensity is normal. No apical or parasternal heave. The murmur diminishes during expiration and standing up. What is the likely cause of the murmur?

Physiological or normal

Atrial septal defect

(

ASD

)

Bicuspid aortic valve

Hypertrophic obstructive cardiomyopathy

(

HOCM

)

1.2.

A 29‐year‐old pregnant woman was found to have a systolic murmur best heard in the second left intercostal space. It is rough and there was a palpable thrill in the same area and in the suprasternal notch. Patient is asymptomatic and has normal exercise tolerance. What is the likely explanation for the murmur?

Pulmonary stenosis

(

PS

)

Normal flow murmur due to increased cardiac output

Posterior mitral leaflet prolapse causing an anteriorly directed jet

Mammary soufflé

1.3.

A 22‐year‐old patient has a hypoplastic radial side of the forearm and fingerized thumb. What might this be associated with?

ASD

Tetralogy of Fallot

Coarctation of aorta

Ebstein's anomaly

1.4.

A 28‐year‐old man presented with a history of shortness of breath on exertion. On examination, the pulse rate was 76 bpm and

blood pressure

(

BP

) 126/80 mmHg. The left ventricular apex was prominent and forceful. The S1 and S2 were normal, but there was a 2/6 ejection systolic murmur best heard in the third right intercostal space. There was no appreciable variation with respiration, but there was an increase in intensity with the Valsalva maneuver and on standing up. It seemed to be less prominent on squatting. There was no audible click. This patient is likely to have?

Valvular aortic stenosis

Hypertrophic obstructive cardiomyopathy

(

HOCM

)

Mitral valve prolapse

(

MVP

)

Innocent murmur

1.5.

A 36‐year‐old asymptomatic woman was found to have a systolic murmur best heard in the apex, but also in the aortic area. It was mid to late systolic and was associated with a sharp systolic sound. What is the likely cause of the murmur?

Posterior mitral leaflet prolapse

Anterior mitral leaflet prolapse

Valvular aortic stenosis

Aortic subvalvular membrane

1.6.

A 78‐year‐old man with hypertension and diabetes mellitus presented with exertional shortness of breath of 6months' duration. Examination revealed a 4/6 crescendo‐decrescendo or ejection systolic murmur best heard in the second right intercostal space. The first component of the second sound was soft. The murmur was also heard along the right carotid artery. What is this patient likely to have?

Mild aortic stenosis

Moderate or severe aortic stenosis

Pulmonary stenosis

MR

1.7.

A thrill and a continuous machinery murmur in the left infraclavicular area is indicative of what?

Patent ductus arteriosus

(

PDA

)

Increased flow due to left arm arteriovenous (AV) fistula for dialysis

Venous hum

Pulmonary AV fistula

1.8.

Which of the following is not a feature of aortic coarctation?

A continuous murmur on the back

Lower blood pressure in the legs compared with an arm

Radiofemoral delay

Pistol shot sounds on femoral arteries

1.9.

A 22‐year‐old newly immigrant woman was referred to the high‐risk pregnancy clinic because of clubbing and cyanosis. Examination in addition revealed a parasternal heave, 4/6 ejection systolic murmur in the third left intercostal space, normal

jugular venous pressure

(

JVP

), and oxygen saturation of 75%. What will you recommend after confirmation of the diagnosis?

Continue pregnancy with sodium restriction

Continue pregnancy, but deliver at 28 weeks

Advise termination of pregnancy

Perform percutaneous ASD closure and continue pregnancy

1.10.

What is the cause of murmur in ASD?

Continuous due to flow across the defect

Ejection systolic due to increased flow across the pulmonary valve

Mid‐diastolic due to increased flow across the tricuspid valve

Continuous murmur over lung fields due to increased flow in lungs

1.11.

What is a systolic click that disappears on inspiration likely to be due to?

Pulmonary valvular stenosis

Bicuspid aortic valve

MVP

Pulmonary hypertension

1.12.

A 36‐year‐old woman presented with an 8‐month history of progressive exertional dyspnea. Physical examination revealed a heart rate of 74 bpm, regular, BP 126/78 mmHg, with no pedal edema. JVP and carotid upstroke were normal. Cardiac auscultation revealed normal S1, an accentuated P2 with narrow splitting of S2, an ejection click, and a 2/6 ejection systolic murmur. What is the likely diagnosis?

Pulmonary hypertension

PS

Aortic stenosis

ASD

1.13.

Causes of prominent “a” wave in jugular venous pulsations include all of the following except which option?

PS

Pulmonary hypertension

Tricuspid stenosis

Aortic stenosis

ASD

1.14.

What is a 6‐year‐old Amish boy in Pennsylvania with short stature, polydactyly, short limbs, absent upper incisor teeth with dysplasia of other teeth, and a systolic murmur most likely to have?

ASD

Ventricular septal defect

Aortic coarctation

PS

1.15

Which of the following describes a ventricular septal defect murmur?

Holosystolic

Ejection systolic

Systolic‐diastolic

None of the above

1.16.

Clubbing and cyanosis in lower limbs, but not upper limbs, is indicative of which of the following?

PDA with coarctation of the aorta

PDA with pulmonary hypertension

Ventricular septal defect Eisenmenger's

ASD Eisenmenger's with coarctation of aorta

1.17.

A 46‐year‐old man presented with progressive fatigue and leg swelling. He had no significant past medical history except a front‐on collision in a car he was driving. Examination revealed 2+ edema, raised JVP, and an enlarged liver, which seemed to expand during systole. What is the likely diagnosis?

Severe tricuspid stenosis

Severe

tricuspid regurgitation

(

TR

)

Constrictive pericarditis

Restrictive cardiomyopathy

1.18.

A 23‐year‐old has a mid‐diastolic rumble and sharp early diastolic sound. What is the likely explanation?

Mitral stenosis

Constrictive pericarditis

Restrictive cardiomyopathy

Bicuspid aortic valve

1.19.

A 28‐year‐old man has history of progressive fatigue and exertional shortness of breath over the previous 6 months. Examination revealed a raised JVP that seemed to increase with inspiration and a sharp precordial sound in early diastole. What is the most likely diagnosis?

Right ventricular infarct

Tricuspid stenosis

Constrictive pericarditis

Restrictive cardiomyopathy

1.20.

A 66‐year‐old woman with left breast cancer post mastectomy, radiation, and chemotherapy was admitted with shortness of breath, heart rate of 120 bpm, and BP of 90/60 mmHg. On slow cuff deflation during BP measurement, Korotkoff's sounds started at 90 mmHg during expiration only and throughout the respiratory cycle at a cuff pressure of 70 mmHg. An echocardiogram was obtained. What is this likely to show?

Akinesis of the left anterior descending area

Thick pericardium

Large pericardial effusion

Large, globally hypokinetic left ventricle.

1.21.

Features of restrictive cardiomyopathy may include all of the following except?

Raised JVP

Loud S3

Kussmaul's sign

A diastolic knock in the pulmonary area

1.22.

Pulsus paradoxus despite tamponade may not be present in which of the following?

ASD

Aortic stenosis

Mitral stenosis

Old age

1.23.

Pulsus paradoxus may occur in all of the following except?

Tamponade

Status asthmaticus

Pulmonary embolism

Aortic stenosis

1.24.

A Square sign during Valsalva maneuver occurs in which of the following?

HOCM

MVP

Aortic stenosis

Congestive heart failure

1.25.

An abnormal Schamroth's test may be found in all of the following except?

Tetralogy of Fallot

Subacute bacterial endocarditis

Left atrial myxoma

Aortic stenosis

1.26–1.31.

For the jugular vein or RA pressure tracings shown in

Figures 1.26–1.31

, match with an appropriate clinical scenario from the following choices:

Normal

Pericardial constriction

Restrictive cardiomyopathy

ASD

Tricuspid stenosis

TR

Cardiac tamponade

Superior vena cava syndrome

Heart failure

PS

Figures 1.26–1.31

1.32–1.37.

For the jugular vein or RA pressure tracings shown in

Figures 1.32–1.37

, match with an appropriate clinical scenario from the following choices:

Normal

Pericardial constriction

Restrictive cardiomyopathy

ASD

Tricuspid stenosis

TR

Cardiac tamponade

Superior vena cava syndrome

Heart failure

PS

Complete heart block

Figures 1.32–1.37

1.38–1.45.

For the carotid pulse or arterial pressure tracings shown in

Figures 1.38–1.45

, match with an appropriate clinical scenario from the following choices:

Normal

Constriction

Aortic stenosis

AR

Mitral stenosis

Mixed aortic stenosis and AR

Cardiac tamponade

HOCM

Heart failure

Complete heart block

MR

Premature ventricular contraction

(

PVC

)

Figures 1.38–1.45

Answers

1.1.

A. Physiological or normal.

The murmur is <3/6 in intensity and diminishes with standing, when venous return is less, indicating a flow murmur. S2 split during inspiration only is physiological. During inspiration, increased venous return and pulmonary flow prolongs right ventricular (RV) ejection. This delays P2. The S2 split will be fixed with a similar gap during both inspiration and expiration. Characteristics of a physiological systolic murmur include being 2/6 in intensity or less, diminution during standing and normal physiological split.

1.2.

A.

Pulmonary stenosis

(

PS

).

A murmur associated with a thrill indicates it is pathological and not just due to increased cardiac output. A thrill in the suprasternal notch is pathognomonic of PS. Valvular PS would be associated with an ejection click which diminishes with inspiration. Left parasternal heave would be indicative of RV hypertrophy (RVH) secondary to pressure overload on the RV imposed by PS. Murmur because of posterior mitral leaflet prolapse may be heard in the aortic area as the mitral regurgitation jet may hug the ascending aorta and the murmur may be transmitted along that. Mammary soufflé occurs in lactating women because of increased blood flow to the breast and the murmur is continuous.

1.3.

A. ASD.

The features are suggestive of Holt‐Oram syndrome. They can also have unequal arm length, various other deformities of the hand, VSD and varying degrees of atrioventricular conduction disturbances. Cardiac anomalies are present in 75% of patients with Holt‐Oram syndrome which is a genetic defect.

1.4.

B. HOCM.

In HOCM, the left ventricular (LV) outflow obstruction is dynamic and is increased by an increase in LV contractility or a reduction in LV size. Standing, Valsalva maneuver, and amyl nitrite inhalation reduce venous return, reduce LV filling, reduce LV size and increase systolic anterior motion of the anterior mitral leaflet (SAM), resulting in increased LV outflow tract (LVOT) obstruction. Squatting kinks the leg arteries, raising peripheral resistance and hence an increase in LV volume through an increase in afterload. This increase in LV size reduces SAM and LV outflow obstruction. Valvular aortic stenosis murmur intensity is flow dependent, and hence reduction in venous return with standing or Valsalva maneuver as well as an increase in peripheral resistance with squatting would diminish the murmur. In mitral valve prolapse (MVP), an increase in LV volume would reduce prolapse, and a reduction in LV volume would lengthen the murmur by producing earlier prolapse. MVP is generally associated with a mid‐systolic click.

1.5.

A. Posterior mitral leaflet prolapse.

The systolic click and late systolic murmur indicate MVP. In anterior leaflet prolapse, the mitral regurgitation (MR) jet is directed posteriorly and murmur may be conducted to the axilla. In posterior leaflet prolapse, the jet is anterior wall hugging, along the aortic root, which facilitates its conduction to the aortic area.

1.6.

B. Moderate or severe aortic stenosis.

This is a classic aortic stenosis murmur with carotid conduction. Soft A2 (first component of S2 indicates significant aortic stenosis). Features of severe aortic stenosis are late‐peaking murmur, absent A2, paradoxic splitting of S2, (i.e. split during expiration instead of inspiration), and a slow‐rising carotid pulse (pulsus parvus et tardus).

1.7.

A.

Patent ductus arteriosus

(

PDA

).

Though the other conditions can produce continuous murmurs, they are not associated with a thrill or machinery character. Pulmonary AV fistula results in a continuous murmur over the lung fields. The venous hum is due to flow in the jugular veins and gets less by assuming the supine position. The murmur due to AV fistula created for hemodialysis is heard on the side of the fistula in the clavicular area due to increased venous flow – this can be temporarily silenced by transient pressure over the fistula.

1.8.

D. Pistol shot sounds on femoral arteries.

Pistol shot sounds occur in severe aortic regurgitation (AR). Others are features of aortic coarctation. Continuous murmur on the back is due to chest wall arterial collaterals bypassing aortic coarctation. Radiofemoral delay and lower BP in the leg are due to obstruction in the aorta and collateral dependent flow in the lower extremities. In severe coarctation, the flow in the abdominal aorta would be nonpulsatile and continuous.

1.9.

C. Advise termination of pregnancy.

The findings are typical of tetralogy of Fallot, and the murmur is due to PS. Murmur of ASD is due to flow and softer and not associated with clubbing or cyanosis unless associated with Eisenmenger's syndrome. Tetralogy of Fallot is associated with extremely high risk, and the pregnancy should be terminated. Other very high‐risk cardiac conditions include severe pulmonary hypertension, severe LV dysfunction or prior history of peripartum cardiomyopathy, and severe left‐sided obstructive valvular diseases.

1.10.

B. Ejection systolic due to increased flow across the pulmonary valve.

Flow across the defect and the lungs does not produce murmurs. The gradient across ASD is less than 1 mmHg and does not produce turbulence to produce a murmur. It takes a torrential shunt to produce a mid‐diastolic flow murmur across the tricuspid valve as the tricuspid aortic valve area of 7–8 cm2 (compared to 5 cm2 for the mitral valve and about 3.5 cm2 for pulmonary and aortic valves). Flow murmurs are generated across smaller valves.

1.11.

A. Pulmonary valvular stenosis.

In severe PS, due to low pulmonary artery (PA) pressure, an increase in venous return to right ventricle during inspiration may open the pulmonary valve before systole, eliminating the ejection click.

1.12.

A. Pulmonary hypertension.

This is suggested by loud P2. In pulmonary hypertension, P2 moves closer to A2 due to higher pulmonary valve closure pressure, and S2 may be single when PA pressure approaches systemic pressure. Ejection click and soft ejection systolic murmur may occur because of PA dilation. Other features of pulmonary hypertension may include a palpable PA in the second left intercostal space, a palpable P2 or diastolic knock, parasternal heave due to RVH and a prominent “a” wave in jugular venous pulsation due to RVH resulting in accentuated right atrial (RA) systole. PS results in a louder murmur and diminished P2. ASD results in wide, fixed, splitting of S2.

1.13.

E. ASD.

A prominent “a” wave occurs due to forceful right atrial systole against some resistance, and this can occur against stenotic tricuspid valve, hypertrophied RV (PS and pulmonary hypertension) or hypertrophied ventricular septum (aortic stenosis, hypertrophic cardiomyopathy, or hypertension). In ASD, a defect in the atrial septum would not allow a prominent “a” wave, even in the presence of pulmonary hypertension, as the right atrium would decompress into the left atrium during atrial systole.

1.14.

A. ASD.

ASD, or common atrium as part of Ellis‐van Creveld syndrome (EVC) or mesoectodermal or chondroectodermal dysplasia, is an autosomal recessive inheritance disorder that occurs in the old‐order Amish population. The EVC gene is on chromosome number 4, short arm. It is a form of ciliopathy. Other ciliopathies that result in abnormal organogenesis include Bardet‐Biedl syndrome, polycystic kidney and liver disease, Alstrom syndrome, Meckel‐Gruber syndrome, and some forms of retinal degeneration, and so on.

1.15.

A. Holosystolic as the pressure gradient between LV and RV is throughout LV isovolumic contraction, ejection and isovolumic relaxation. On echo‐Doppler, there may also be a presystolic left‐to‐right flow associated with left atrial systole.

1.16.

B. PDA with pulmonary hypertension.

In PDA Eisenmenger's, the shunt reversal through PDA causes desaturation in the lower part of the body only, resulting in central cyanosis and clubbing in lower extremities and not upper extremities (differential cyanosis). In ASD and VSD, Eisenmengers, cyanosis and clubbing involve both the upper and lower extremities. In PDA without suprasystemic pulmonary hypertension, the flow will be from the aorta to pulmonary artery only and no desaturated blood comes to the aorta.

1.17.

B. Severe tricuspid regurgitation (TR).

Liver that is pulsatile (expansile) in systole is indicative of a powerful right atrial “V” wave, and this suggests severe TR. This can also be seen in the jugular venous pulsation. Sternal compression during the motor vehicle accident likely caused a flail tricuspid valve and severe TR. Liver pulsation in tricuspid stenosis is presystolic. Liver pulsations are not seen in constriction or restriction.

1.18.

A. Mitral stenosis.

This is typical mitral stenosis with pliable leaflets, which causes opening snap (OS). The A2–OS interval is a good measure of mitral stenosis severity. Normally, 70–100 ms (same as isovolumetric relaxation time). Less than 70 ms indicates high left atrial pressure, suggesting severe mitral stenosis. In constrictive pericarditis, you can get a pericardial knock which is a sharp protodiastolic sound that occurs a little later. Restrictive cardiomyopathy produces S3 due to high left atrial pressure and is generally later and is a dull sound like a thud and best heard with the bell of the stethoscope. S3 is due to rapid deceleration of the early passive filling wave across the mitral valve.

1.19.

C. Constrictive pericarditis.

A rise in JVP is paradoxical (Kussmaul's sign), and sharp protodiastolic sound is a pericardial knock – classic features of constriction. Kussmaul's sign occurs due to lack of transmission of negative intrathoracic pressure to the right atrium through the rigid pericardium. Hence, the increased venous return during inspiration causes a rise in RA pressure. In tricuspid stenosis, inspiratory increase in venous return may not readily empty into the right ventricle, causing a paradoxical rise in JVP with inspiration. Kussmaul's sign can occur in an RV infarct but occurs in the setting of inferior myocardial infarction. Restrictive cardiomyopathy may be associated with S3, which is less sharp (a thud), but no venous paradox.

1.20.

C. Large pericardial effusion.

This is typical cardiac tamponade with classic paradoxic pulse, hypotension, and tachycardia. Constriction causes venous paradox.

1.21.

C. Kussmaul's sign.

As the pericardium is normal in restrictive cardiomyopathy, inspiratory negative intrathoracic pressure is transmitted to the pericardial space and cardiac chambers, and hence the venous paradox does not occur. Diastolic knock is palpable with loud P2; a feature of pulmonary hypertension that it is common in restrictive LV physiology.

1.22.

A. ASD.

Pulsus paradoxus may not be present when LV filling is not affected by phase of inspiration due to lack of interventricular dependence, as in ASD, or LV filling from other sources, such as severe AR or MR.

1.23.

D. Aortic stenosis.

1.24.

D. Congestive heart failure.

See the explanation in Box 1.1 Clinical Pearls. This is because though a Valsalva maneuver reduces left‐sided venous return, it does not affect LV stroke volume as it is already well filled and beyond the peak of Starling's curve. An increase in intrathoracic pressure is transmitted to the aorta, causing an increase in aortic pressure.

1.25.

D. Aortic stenosis.

This test is named after a South African cardiologist for diagnosis of clubbing. In clubbing, the angle between the nail and nail fold is >165° and when nails of the fingers from both sides are apposed, the gap between them disappears. Clubbing is seen in cardiac conditions (in addition to a variety of pulmonary diseases), in subacute bacterial endocarditis, congenital cyanotic heart diseases, and left atrial myxoma.

1.26.

A. Normal.

Note the mean RA pressure of <5 mmHg and the “a” wave due to atrial systole is slightly higher than the “V” wave, which occurs because of RA filling on the closed tricuspid valve. A smaller “V” wave indicates a compliant right atrium. The sharp “C” wave that coincides with the QRS complex of the electrocardiogram is due to a combination of tricuspid valve closure and transmitted carotid impulse.

1.27.

E. Tricuspid stenosis.

Note the large “a” wave as the RA contracts against a stenosed tricuspid valve; the gradient is reflected as a large “a” wave. Note the mean RA pressure is also slightly elevated commensurate with trans tricuspid gradient. In conditions causing RVH (pulmonary hypertension, PS, aortic stenosis with septal hypertrophy), the “a” wave may be prominent due to noncompliant RV (RV fourth heart sound), but mean RA pressure may not be high unless there is heart failure.

1.28.

B. Pericardial constriction.

Note the elevated RA pressure with rapid “Y” descent.

1.29.

D. ASD.

In ASD, the “a” and “V” waves would be of similar height because the defect leads to equilibration of the LA and RA pressures.

1.30.

F. TR.

The large “V” wave is due to TR filling up the RA during systole. When the “V” wave pressure is about 25–30 mmHg, it may become palpable to the examining finger and associated with an expansile liver.

1.31.

B. Pericardial constriction.

The increasing mean RA pressure with inspiration is the venous paradox or Kussmaul's sign. This is due to dissociation between intrathoracic and intrapericardial pressures because of a thick pericardium. During inspiration, the intrathoracic pressure drops, increasing venous return to the right atrium, but the intrapericardial and intra‐RA pressure does not drop and returning blood increases the pressure further. Kussmaul's sign can occur even in acute pericarditis and RV infarcts; the latter invoking pericardial restraint.

1.32.

J. PS.

Note a large “a” wave with near‐normal mean RA pressure. Contrast this with tricuspid stenosis.

1.33.

G. Cardiac tamponade.

Note the raised RA pressure with prominent “X” and “Y” troughs.

1.34.

K. Complete heart block.

The intermittent large waves are “cannon a” waves when atria and ventricles happen to contract simultaneously due to AV dissociation.

1.35.

A. Normal.

The RA pressure is <5 mmHg and drops with inspiration.

1.36.

H. Superior vena cava syndrome.

Note the high JVP which does not drop on inspiration as the superior vena cava is blocked and the jugular vein is not in communication with right atrial hemodynamics or pulsatile changes. In contrast to constriction, the JVP in superior vena cava syndrome is nonpulsatile. It would be high in both.

1.37.

I. Heart failure.

High JVP that drops with inspiration.

1.38.

A. Normal.

This is the typical normal tracing. Note the fairly rapid upstroke, pulse pressure of about 40 mmHg, dicrotic notch and dicrotic wave.

1.39.

C. Aortic stenosis.

Note the very slow rise, attributable to high blood flow velocity across the valve which converts pressure to kinetic energy.

1.40.

D. AR.

Note the rapid upstroke, rapid downstroke (water‐hammer pulse), wide pulse pressure, and low diastolic pressure due to peripheral vasodilation. This can also occur in PDA and large AV fistulae.

1.41.

F. Mixed aortic stenosis and AR.

This is called pulsus bisferiens or double pulse. Can also occur in HOCM.

1.42.

I. Heart failure.

This is pulsus alternans. Alternating strong and weak pulse with regular RR interval due to alternating stronger and weaker myocardial contraction with every other beat attributable to altered calcium handling by contractile proteins. It is a sign of severe systolic dysfunction.

1.43.

G. Cardiac tamponade.

A BP drop with inspiration is called pulsus paradoxus. An inspiratory drop of >10 mmHg may indicate tamponade.

1.44.

L. Premature ventricular contraction (PVC).

With appropriate increase in pulse pressure in the post PVC beat, because of a combination of increased preload due to a long filling period and increased contractility due to the force‐frequency relationship.

1.45.

H. HOCM.

In this patient, after PVC, instead of an augmented pulse there is a smaller pulse volume. This is due to the fact that increased contractility in the post‐PVC beat increases dynamic LVOT obstruction and reduces stroke volume. This is called Brockenbrough phenomenon on cardiac catheterization. This contrasts with valvular aortic stenosis, where pulse pressure increases after a PVC.

Box 1.1Clinical Pearls

Loud S1 occurs when the mitral valve closes forcefully from an open position against the transmitral gradient or prematurely and occurs in mitral stenosis, short pulmonary regurgitation (PR) interval, and hyperdynamic circulation.

S1 is soft in MR, with a long PR interval, and severe AR. In severe AR, the mitral valve may move toward closure in presystole.

P2 can be loud in pulmonary hypertension (higher pulmonary valve closure sound) and dilated PA (better P2 transmission).

S2 may be paradoxically split when aortic valve closure is delayed and comes after P2 as in left bundle branch block, severe aortic stenosis, severe LV dysfunction, and PDA (increased transaortic flow). S2 is split in expiration and not in inspiration when RV filling and ejection time are increased.

The only right‐sided sound/murmur is attenuated by inspiration is pulmonary ejection click of valvular PS as an inspiratory increase in venous return to the right ventricle in the presence of RVH may cause an increase on RV end diastolic pressure high enough to open the pulmonary valve as the PA pressure is lower.

A Carey Coombs murmur is a mid‐diastolic mitral murmur due to mitral valvulitis in rheumatic fever.

An Austin Flint murmur is a mitral mid‐diastolic murmur heard in severe AR. Potential explanations include: AR jet causing an anterior mitral leaflet vibration, or mitral/AR jet interaction or an AR jet causing a partial diastolic closure of anterior mitral leaflet.

A Graham Steel murmur is an early diastolic murmur of PR that occurs in severe pulmonary hypertension. A higher PA diastolic pressure causes turbulence of the PR jet and the murmur.

A mid‐diastolic murmur of mitral stenosis is best heard with the bell without much pressure as it is a low‐frequency murmur and better heard in the left lateral position. Presystolic accentuation indicates atrial contraction.

A tapping apex typically occurs in mitral stenosis and it is palpable S1.

Maneuvers are helpful in evaluating murmurs. Inspiration increases right‐sided venous return and augments right‐sided murmurs. Standing reduces venous return and, after three or four beats, LV filling as well reducing its size. This may augment an HOCM murmur and lengthen an MR murmur of MVP. Squatting kinks limb arteries and increases afterload. This may reduce murmurs of valvular aortic stenosis through reduced stroke volume and an HOCM murmur through an increase in LV volume and shorten a murmur of MVP through increasing LV volume and reducing prolapse.

The Valsalva maneuver involves expiration against a closed glottis, increasing the intrathoracic pressure. There are four phases of heart rate and BP response. The normal response includes the following:

Phase 1. Early during the Valsalva maneuver, pressure on the intrathoracic aorta and pulmonary veins emptying into left heart transiently increases filling, stroke volume, and BP with reflex slowing of heart.

Phase 2. With a continued Valsalva maneuver, LV filling diminishes and lowers stroke volume and BP, resulting in compensatory tachycardia. Reflex peripheral vasoconstriction slowly increases BP and lowers the heart rate.

Phase 3. With release of the Valsalva maneuver, pressure on the aorta drops, and BP drops with some increase in heart rate.

Phase 4. The left ventricle fills, with an increase in stroke volume with continued peripheral vasoconstriction causing BP to overshoot the baseline value. This will reflexively reduce the heart rate below the baseline.

Phase 2 is used in dynamic auscultation.

In HOCM, the Valsalva maneuver results in a smaller left ventricle size causing increased LVOT obstruction and an increase in murmur intensity.

In MVP, reduced LV volume with phase 2 Valsalva results in earlier and greater prolapse and the MR murmur lengthens.

A heaving apex denotes LV hypertrophy; forceful apical lift signifies LV volume overload, tapping apex loud S1, and bifid apex with presystolic lift LV occurs due to a combination of LVH with a forceful atrial kick causing S4 as it occurs in hypertrophic cardiomyopathy.

Left parasternal or precordial bulge indicates RVH occurring before the rib cage ossifies (young age), and parasternal lift or heave indicates RVH starting after childhood.

A downward tug on the larynx held up with fingers after deglutition indicates aortic arch aneurysm. Also called tracheal tug or Oliver's sign, this occurs with every heartbeat.

A large, sharp systolic wave in jugular venous pulsation during systole is the cannon wave. This occurs when the right atrium contracts over a closed tricuspid valve, as in complete heart block (intermittent) or junctional or idioventricular rhythm with retrograde ventriculoatrial conduction.

2Electrocardiography

ECG diagnostic criteria are listed in Box 2.1.

For the tracings in the questions/figures in this section, please analyze carefully and list the important findings and possible clinical setting. Answers are found at the end of the chapter.

Figure 2.1

Figure 2.2

Figure 2.3

Figure 2.4

Figure 2.5

Figure 2.6

Figure 2.7

Figure 2.8

Figure 2.9

Figure 2.10

Figure 2.11

Figure 2.12

Figure 2.13

Figure 2.14

Figure 2.15

Figure 2.16

Figure 2.17

Figure 2.18

Figure 2.19

Figure 2.20

Figure 2.21

Figure 2.22

Figure 2.23

Figure 2.24

Figure 2.25

Figure 2.26

Figure 2.27

Figure 2.28

Figure 2.29

Figure 2.30

Figure 2.31

Figure 2.32

Figure 2.33

Figure 2.34

Figure 2.35

Figure 2.36

Figure 2.37

Figure 2.38

Figure 2.39

Figure 2.40

Figure 2.41

Figure 2.42

Figure 2.43

Figure 2.44

Figure 2.45

Figure 2.46

Figure 2.47

Figure 2.48

Figure 2.49

Figure 2.50

Figure 2.51

Figure 2.52

Figure 2.53

Figure 2.54

Figure 2.55

Figure 2.56

Figure 2.57

Figure 2.58

Figure 2.59

Figure 2.60

Figure 2.61

Figure 2.62

Figure 2.63

Figure 2.64

Figure 2.65

Figure 2.66

Figure 2.67

Answers

2.1.

Second‐degree atrioventricular (AV) block, Mobitz type I (AV Wenckebach). Note increasing PR interval and PR interval being the shortest after a dropped beat. Also, note that the patient has

intraventricular conduction delay

(

IVCD

) and lateral T‐wave inversion. Despite IVCD, it is less likely to be trifascicular block as AV Wenckebach is generally a nodal rather than infra‐Hisian phenomenon.

2.2.

Right ventricular (RV) hypertrophy (RVH) with strain and biatrial enlargement. R in V1

>

5 mm with right axis deviation and ST–T changes in right chest leads support RVH. P wave amplitude

>

3 mm supports right atrial enlargement and P‐terminale in V1

>

1 × 1 box supports left atrial enlargement.

2.3.

Sinus rhythm with bifascicular block. Note the

right bundle branch block

(

RBBB

) and left axis deviation with mean QRS axis less than −30° suggesting

left anterior fascicular block

(

LAHB

). Also note the peak of R wave is earliest in III, followed by II, and then I, indicating late activation of left ventricular (LV) lateral wall supplied by anterior fascicle. The inferior wall is supplied by posterior fascicle and R wave peaks early in these leads.

2.4.

Sinus arrhythmia with short PR interval suggesting Lown‐Ganong‐Levine syndrome. Note that there is no delta wave or QRS prolongation indicating

Wolff‐Parkinson‐White

(

WPW

) syndrome. In Lown‐Ganong‐Levine syndrome, the accessory pathway is atrio‐Hisian, shortening the PR interval. In WPW syndrome, AV preexcitation of a portion of ventricular myocardium results in delta wave and QRS prolongation.

2.5.

Atrial fibrillation. Note the absence of P wave and irregularly irregular ventricular response. Also note the low QRS voltage (

<

5 mm in limb and

<

10 mm in chest leads), which should raise the suspicion of chronic obstructive pulmonary disease, pericardial effusion, or diffuse myocardial disease.

2.6.

Acute anterior

ST elevation myocardial infarction

(

STEMI

). Note hyperacute, tombstone ST elevation in V2 and V3.

2.7.

Hyperkalemia. Note the peaked, tall T waves in V2 and V3.

2.8.

Junctional tachycardia. P waves are inverted in inferior leads with superior axis indicating junctional or low atrial origin.

2.9.

RVH. qR in V1 with right axis deviation and strain pattern in right chest leads is suggestive of RVH.

2.10.

WPW syndrome (? Posteroseptal).

2.11.

Seven beats of accelerated idioventricular rhythm, followed by a fusion beat and then accelerated junctional rhythm. This is suggestive of digoxin toxicity.

2.12.

Atrial flutter with 2 : 1 conduction. Flutter waves are clearly visible in inferior leads.

2.13.

Posterior myocardial infarction. Note the tall R waves in V1 and V2 with upright T wave associated with Q waves inferolaterally. In RVH, one would expect to see strain pattern in right chest leads.

2.14.

Ventricular tachycardia. Broad complexed tachycardia with RBBB morphology with left rabbit ear, QRS duration of 200 ms and indeterminate axis – all suggestive of

ventricular tachycardia

(

VT

) rather that

supraventricular tachycardia

(

SVT

) with aberrancy.

2.15.

Atypical atrial flutter with 3 : 1 conduction, intermittent RV pacing (third and last three beats) and one fusion complex (fifth beat).

2.16.

Acute anterior STEMI. Note Q waves and ST elevation of 3–4 mm in V1 and V2.

2.17.

Sinus rhythm with low QRS voltage (

<

5 mm in limb leads or

<

10 mm in chest leads). Consider pericardial effusion, emphysema.

2.18.