Cardiology Board Review E-Book

Ramdas G. Pai

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch
• Veröffentlichungsjahr: 2017

Seitenzahl: 705

Beschreibung

This compact but comprehensive board review includes everything you need to successfully prepare for the ABIM Cardiology Board Review examination. * Features over 1200 questions with answers and clear explanations * Includes over 400 accompanying images * Covers all key areas of cardiology practice, from history/physicial examination through all major diseases/disorders, along with special topics, e.g. consultative cardiology, covered on the exam * Complements standard textbook reading * Written by an internationally-recognized, well-respected and well-published senior cardiologist, expert in valvular heart disease and cardiovascular imaging

Leseprobe

Cardiology Board Review

Ramdas G. Pai

University of California Riverside School of Medicine California, USA

Padmini Varadarajan

Loma Linda University Medical Center California, USA

Sudha M. Pai

Loma Linda University Medical Center California, USA

This edition first published 2018

© 2018 John Wiley & Sons Ltd

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Library of Congress Cataloging-in-Publication Data:

Names: Pai, Ramdas G., author. | Varadarajan, Padmini, author. | Pai, Sudha

 M., 1958- author.

Title: Cardiology board review / by Ramdas G. Pai, Padmini Varadarajan, Sudha

 M. Pai.

Description: Hoboken, NJ : Wiley, 2017. | Includes index. |

Identifiers: LCCN 2017026562 (print) | LCCN 2017028086 (ebook) | ISBN

 9781118699003 (pdf) | ISBN 9781118699010 (epub) | ISBN 9781118699027 (pbk.)

Subjects: | MESH: Heart Diseases | Examination Questions

Classification: LCC RC669.2 (ebook) | LCC RC669.2 (print) | NLM WG 18.2 | DDC

 616.1/20076--dc23

LC record available at https://lccn.loc.gov/2017026562

Cover images: inset – © RichHobson/Gettyimages; main – © asiseeit/Gettyimages

Cover design by Wiley

Contents

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

21 Peripheral Vascular Disease

Answers

References

Suggested Reading

22 Cardiac Arrhythmias

Answers

Reference

23 Pacemakers and Defibrillators

Answers

24 Cardiac Masses

Answers

25 Systemic 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 Pharmacological Principles of Cardiac Drugs

Answers

30 Anticoagulation

Answers

References

31 Aspirin and Antiplatelet Therapy

Answers

32 Statistical Concepts

Answers

Reference

33 Genetics

Answers

Reference

34 Cardiac Emergencies and Resuscitation

Answers

Index

EULA

List of Tables

19

Table 19.13

Table 19.15

20

Table 20.7

21

Table 21.9a

Table 21.9b

Table 21.9c

Table 21.22

List of Illustrations

1

Figures 1.26–1.31

Figures 1.32–1.37

Figures 1.38–1.45

2

Question/Figure 2.1

Question/Figure 2.2

Question/Figure 2.3

Question/Figure 2.4

Question/Figure 2.5

Question/Figure 2.6

Question/Figure 2.7

Question/Figure 2.8

Question/Figure 2.9

Question/Figure 2.10

Question/Figure 2.11

Question/Figure 2.12

Question/Figure 2.13

Question/Figure 2.14

Question/Figure 2.15

Question/Figure 2.16

Question/Figure 2.17

Question/Figure 2.18

Question/Figure 2.19

Question/Figure 2.20

Question/Figure 2.21

Question/Figure 2.22

Question/Figure 2.23

Question/Figure 2.24

Question/Figure 2.25

Question/Figure 2.26

Question/Figure 2.27

Question/Figure 2.28

Question/Figure 2.29

Question/Figure 2.30

Question/Figure 2.31

Question/Figure 2.32

Question/Figure 2.33

Question/Figure 2.34

Question/Figure 2.35

Question/Figure 2.36

Question/Figure 2.37

Question/Figure 2.38

Question/Figure 2.39

Question/Figure 2.40

Question/Figure 2.41

Question/Figure 2.42

Question/Figure 2.43

Question/Figure 2.44

Question/Figure 2.45

Question/Figure 2.46

Question/Figure 2.47

Question/Figure 2.48

Question/Figure 2.49

Question/Figure 2.50

Question/Figure 2.51

Question/Figure 2.52

Question/Figure 2.53

Question/Figure 2.54

Question/Figure 2.55

Question/Figure 2.56

Question/Figure 2.57

Question/Figure 2.58

Question/Figure 2.59

Question/Figure 2.60

Question/Figure 2.61

Question/Figure 2.62

Question/Figure 2.63

Question/Figure 2.64

Question/Figure 2.65

Question/Figure 2.66

Question/Figure 2.67

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

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

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

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

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 7.57b

Figure 7.61b

Figure 7.63b

Figure B7.1

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 8.15b

11

Figure 11.77

Figure 11.78

Figure 11.79

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

15

Figure 15.1

Major recommendations for statin therapy for ASCVD prevention.

Source:

adapted from Jensen

et al.

(2013).

Figure 15.2

Treatment algorithm—the chronic disease management model for primary care of patients with overweight and obesity.

Source

: adapted from Jensen

et al.

(2013).

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 tolerance test).

Source:

adapted from Nishimura

et al.

(2014).

Figure 16.20

Indications for AVR for chronic AR.

Source:

adapted from Nishimura

et al.

(2014).

Figure 16.22

Indications for intervention for rheumatic MS (AF: atrial fibrillation; LA: left atrium; NYHA: New York Heart Association; PCWP: pulmonary capillary wedge pressure; PMBC: percutaneous mitral balloon commissurotomy).

Source:

adapted from Nishimura

et al.

(2014).

Figure 16.25

Indications for surgery for MR (CAD: coronary heart disease; CRT: cardiac resynchronization therapy; HF: heart failure; Rx: treatment).

Source:

adapted from Nishimura

et al.

(2014).

Figure 16.29

Indications for surgery for TR (PHTN: pulmonary hypertension; RV: right ventricle; TA: tricuspid annular; TVR: TV replacement).

Source:

adapted from Nishimura

et al.

(2014).

Figure 16.32

Anticoagulation for prosthetic valves (ASA: aspirin; LMWH: low molecular weight heparin; MVR: mitral valve replacement; SC: subcutaneous; UFH: unfractionated heparin; VKA: vitamin K antagonist).

Source:

adapted from Nishimura

et al.

(2014).

Figure 16.39

Imaging studies in native valve endocarditis (NVE) and prosthetic valve endocarditis (PVE).

Source:

adapted from Nishimura

et al.

(2014).

Figure 16.40

Diagnosis and treatment of IE (ICD: implantable cardioverter defibrillator).

Source:

adapted from Nishimura

et al.

(2014).

Figure 16.41

Anticoagulation of pregnant patients with mechanical valves (aPTT: activated PTT).

Source:

adapted from Nishimura

et al.

(2014).

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 17.67b

Figure 17.67c

Figure 17.70b

18

Figure 18.36

Figure 18.37

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

20

Figure 20.1a

Figure 20.12

Figure 20.16

Figure 20.1b

Figure 20.2

21

Figure 21.40a

Figure 21.7

All-cause mortality as a function of baseline ABI.

Source:

adapted from Resnick

et al.

(2004).

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

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

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

Source:

reproduced with permission of Dr Natesa G. Pandian.

Figure 24.20a

Figure 24.22a

Figure 24.23a

Figure 24.24a

Figure 24.25a

Figure 24.26a

Figure 24.28a

Figure 24.29

Source:

reproduced with permission of Dr Natesa G. Pandian.

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 and round cells with occasional mitosis.

Figure 24.12b

Figure 24.13b

Figure 24.15b

Figure 24.16b

Figure 24.17b

Source:

reproduced with permission of Dr Natesa G. Pandian.

Figure 24.18b

Figure 24.19b

Figure 24.20b

Figure 24.22b

Figure 24.23b

Figure 24.24b

Figure 24.25b

Source:

reproduced with permission of Dr Natesa G. Pandian.

Figure 24.26b

Figure 24.28b

Figure 24.31b

Figure 24.32b

Figure 24.33b

Figure 24.34c

32

Figure 32.4

Figure 32.1

Figure 32.3

Figure 32.13

Guide

Cover

Table of Contents

Preface

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Preface

This book is a very comprehensive review of all major topics in cardiology with an intention to help those preparing for initial and recertification exams in cardiology and those who want to review cardiology in an easy-to-do fashion. It is a compilation of over 1300 questions encompassing all the topics in cardiology. This has been edited by an internationally acclaimed teaching physician with an expertise in all aspects of cardiology. The book is organized in a question-and-answer format and is divided into easy-to-follow chapters related to different areas of cardiovascular medicine. The answers are explained in detail and are accompanied by references to major trials in cardiology and guidelines, and some clinical pearls where applicable. The explanations are clear and evidence based. The book highlights a special section on electrocardiograms which are of high resolution. The answers to the questions are given in depth, which will allow the examinees to prepare for this section and take the exam with greater confidence as this section is scored separately from the main exam. The chapters on imaging have questions relating to chest X-ray, cardiac computed tomography, echo, stress echo, cardiac magnetic resonance imaging, nuclear stress testing, and so on. The book also deals with questions relating to topics not usually encountered in similar books: for example, racial disparities in medicine, cardiac emergencies, and so on. The book also facilitates critical review of cardiovascular medicine to enhance one's diagnostic and therapeutic skills.

1History and Physical Examination

A 25-year-old woman has a 2/6 ejection systolic murmur best heard in the second left intercostal space with normal S1. The S2 is split during inspiration, and P2 intensity is normal. No apical or parasternal heave. The murmur diminishes during expiration and standing up. What is the murmur likely due to?

Physiological or normalAtrial septal defect (ASD)Bicuspid aortic valveHypertrophic obstructive cardiomyopathy (HOCM)

A 29-year-old pregnant woman was found to a 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 of the murmur?

Pulmonary stenosis (PS)Normal flow murmur due to increased cardiac outputPosterior mitral leaflet prolapse causing an interiorly directed jetMammary soufflé

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

ASDTetralogy of FallotCoarctation of aortaEbstein's anomaly

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 standing up. It seemed to be less prominent on squatting. There was no audible click. What is the murmur likely due to?

Valvular aortic stenosisHOCMMitral valve prolapse (MVP)Innocent murmur

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 prolapseAnterior mitral leaflet prolapseValvular aortic stenosisAortic subvalvular membrane

A 78-year-old man with hypertension and diabetes mellitus presented with exertional shortness of breath of 6 months’ duration. Examination revealed a 4/6 crescendo–decrescendo 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 stenosisModerate or severe aortic stenosisPulmonary stenosisMR

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 dialysisVenous humPulmonary AV fistula

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

A continuous murmur on the backLower blood pressure in legs compared with armRadiofemoral delayPistol shot sounds on femoral arteries

A 22-year-old newly immigrant woman was referred to 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 restrictionContinue pregnancy, but deliver at 28 weeksAdvise termination of pregnancyPerform percutaneous ASD closure and continue pregnancy

What is the murmur of ASD?

Continuous due to flow across the defectEjection systolic due to increased flow across the pulmonary valveMid-diastolic due to increased flow across the tricuspid valveContinuous over lung fields due to increased flow in lungs

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

Pulmonary valvular stenosisBicuspid aortic valveMVPPulmonary hypertension

A 36-year-old woman presented with an 8-month history of progressive exertional dyspnea. Physical examination revealed heart rate of 74 bpm, regular, BP 126/78 mmHg, 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 hypertensionPSAortic stenosisASD

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

PSPulmonary hypertensionTricuspid stenosisAortic stenosisASD

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?

ASDVentricular septal defectAortic coarctationPS

Which of the following describes ventricular septal defect murmur?

HolosystolicEjection systolicSystolico-diastolicNone of the above

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

PDA with coarctation of aortaPDA with pulmonary hypertensionVentricular septal defect Eisenmenger'sASD Eisenmenger's with coarctation of aorta

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 stenosisSevere tricuspid regurgitation (TR)Constrictive pericarditisRestrictive cardiomyopathy

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

Mitral stenosisConstrictionRestrictionBicuspid aortic valve

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

Right ventricular infarctTricuspid stenosisConstrictive pericarditisRestrictive cardiomyopathy

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 left anterior descending areaThick pericardiumLarge pericardial effusionLarge, globally hypokinetic left ventricle.

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

Raised JVPLoud S3Kussmaul's signA diastolic knock in pulmonary area

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

ASDAortic stenosisMitral stenosisOld age

Pulsus paradoxus may occur in all of the following except which option?

TamponadeStatus asthmaticusPulmonary embolismAortic stenosis

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

HOCMMVPAortic stenosisCongestive heart failure

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

Tetralogy of FallotSubacute bacterial endocarditisLeft atrial myxomaAortic 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:

Figures 1.26–1.31

NormalPericardial constrictionRestrictive cardiomyopathyASDTricuspid stenosisTRCardiac tamponadeSuperior vena cava syndromeHeart failurePS

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:

Figures 1.32–1.37

NormalPericardial constrictionRestrictive cardiomyopathyASDTricuspid stenosisTRCardiac tamponadeSuperior vena cava syndromeHeart failurePSComplete heart block

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:

Figures 1.38–1.45

NormalConstrictionAortic stenosisARMitral stenosisMixed aortic stenosis and ARCardiac tamponadeHOCMHeart failureComplete heart blockMRPremature ventricular contraction (PVC)

Answers

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.

A. Pulmonary stenosis (PS).

A murmur associated with a thrill indicates that 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).

A. ASD.

The features are suggestive of Holt–Oram syndrome.

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 reduce venous return, reduce LV filling, and increase systolic anterior motion of the anterior mitral leaflet (SAM), resulting in increased LV outflow tract (LVOT) obstruction. Squatting kinks leg arteries, raising peripheral resistance and hence an increase in LV volume. This 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 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.

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.

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 slow-rising carotid pulse (pulsus parvus et tardus).

A. Patent ductus arteriosus (PDA).

Though the other conditions can produce continuous murmurs, they are not associated with a thrill or machinery character.

D. Pistol shot sounds on femoral arteries.

Pistol shot sounds occur in severe aortic regurgitation (AR). Others are features of aortic coarctation.

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 pregnancy should be terminated.

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

Flow across the defect and the lungs does not produce murmurs. It takes a torrential shunt to produce a mid-diastolic flow murmur across the tricuspid valve.

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.

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 second left intercostal space, a palpable P2 or diastolic knock, parasternal heave due to RVH and 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.

E. ASD.

Prominent “a” wave occurs due to forceful RA systole, 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, 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.

A. ASD.

ASD or common atrium as part of Ellis–van Creveld syndrome or mesoectodermal or chondroectodermal dysplasia is an autosomal recessive inheritance disorder that occurs in 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.

A. Holosystolic.

B. PDA with pulmonary hypertension.

In PDA Eisenmenger's, the shunt reversal through PDA causes desaturation in lower part of the body only, resulting in central cyanosis and clubbing in lower extremities and not upper extremities.

B. Severe tricuspid regurgitation (TR).

Liver that is pulsatile (expansile) in systole is indicative of a powerful RA “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 pre-systolic. Liver pulsations are not seen in constriction or restriction.

A. Mitral stenosis.

This is typical mitral stenosis with pliable leaflets, which causes opening snap. 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.

C. Constrictive pericarditis.

Rise in JVP is paradoxical (Kussmaul's sign), and sharp protodiastolic sound is pericardial knock – classic features of constriction. Kussmaul's sign occurs because of lack of transmission of negative intrathoracic pressure to the right atrium through the rigid pericardium. Hence, increased venous return during inspiration causes a rise in RA pressure. In tricuspid stenosis, inspiratory increase in venous return may not readily empty into right ventricle, causing a paradoxical rise in JVP with inspiration. Kussmaul's sign can occur in 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.

C. Large pericardial effusion.

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

C. Kussmaul's sign.

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

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.

D. Aortic stenosis.

D. Congestive heart failure.

See 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. Increase in intrathoracic pressure is transmitted to the aorta, causing an increase in aortic pressure.

D. Aortic stenosis.

This test is named after South African cardiologist for diagnosis of clubbing. In clubbing, the angle between the nail and nail fold is >165° and when nails of fingers from two 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.

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.

E. Tricuspid stenosis.

Note the large “a” wave as the RA contracts against a stenosed tricuspid valve; the gradient is reflected as large “a” wave. Note that the mean RA pressure is slightly elevated as well commensurate with transtricuspid 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.

B. Pericardial constriction.

Note elevated RA pressure with rapid “Y” descent.

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.

F. TR.

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

B. Pericardial constriction.

The increasing mean RA pressure with inspiration is the venous paradox or Kussmaul's sign. This is because of dissociation between intrathoracic and intrapericardial pressures because of 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.

J. PS.

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

G. Cardiac tamponade.

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

K. Complete heart block.

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

A. Normal.

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

H. Superior vena cava syndrome.

Note the high JVP which does not drop on inspiration as superior vena cava is blocked and 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.

I. Heart failure.

High JVP that drops with inspiration.

A. Normal.

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

C. Aortic stenosis.

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

D. AR.

Note 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.

F. Mixed aortic stenosis and AR.

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

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.

G. Cardiac tamponade.

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

L. Premature ventricular contraction (PVC).

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

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 1.1 Clinical Pearls

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

S1 is soft in MR, long PR interval, and severe AR. In severe AR, 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, PDA (increased transaortic flow). S2 is split in expiration and not in inspiration when RV filling and ejection time are increased.

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

Carey Coombs murmur is mid-diastolic mitral murmur due to mitral valvulitis in rheumatic fever.

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

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

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 left lateral position. Presystolic accentuation indicates atrial contraction.

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 reduces its size. This may augment HOCM murmur and lengthen MR murmur of MVP. Squatting kinks limb arteries and increases afterload. This may reduce murmurs of valvular aortic stenosis through reduced stroke volume and HOCM murmur through an increase in LV volume and shorten 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. 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 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. Left ventricle fills, with increase in stroke volume with continued peripheral vasoconstriction causing BP to overshoot the baseline value. This will reflexly reduce heart rate below baseline.

Phase 2 is used in dynamic auscultation.

In HOCM, the Valsalva maneuver results in 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.

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 ossified (young age), and parasternal lift or heave indicates RVH starting after childhood.

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

Question/Figure 2.1

Question/Figure 2.2

Question/Figure 2.3

Question/Figure 2.4

Question/Figure 2.5

Question/Figure 2.6

Question/Figure 2.7

Question/Figure 2.8

Question/Figure 2.9

Question/Figure 2.10

Question/Figure 2.11

Question/Figure 2.12

Question/Figure 2.13

Question/Figure 2.14

Question/Figure 2.15

Question/Figure 2.16

Question/Figure 2.17

Question/Figure 2.18

Question/Figure 2.19

Question/Figure 2.20

Question/Figure 2.21

Question/Figure 2.22

Question/Figure 2.23

Question/Figure 2.24

Question/Figure 2.25

Question/Figure 2.26

Question/Figure 2.27

Question/Figure 2.28

Question/Figure 2.29

Question/Figure 2.30

Question/Figure 2.31

Question/Figure 2.32

Question/Figure 2.33

Question/Figure 2.34

Question/Figure 2.35

Question/Figure 2.36

Question/Figure 2.37

Question/Figure 2.38

Question/Figure 2.39

Question/Figure 2.40

Question/Figure 2.41

Question/Figure 2.42

Question/Figure 2.43

Question/Figure 2.44

Question/Figure 2.45

Question/Figure 2.46

Question/Figure 2.47

Question/Figure 2.48

Question/Figure 2.49

Question/Figure 2.50

Question/Figure 2.51

Question/Figure 2.52

Question/Figure 2.53

Question/Figure 2.54

Question/Figure 2.55

Question/Figure 2.56

Question/Figure 2.57

Question/Figure 2.58

Question/Figure 2.59

Question/Figure 2.60

Question/Figure 2.61

Question/Figure 2.62

Question/Figure 2.63

Question/Figure 2.64

Question/Figure 2.65

Question/Figure 2.66

Question/Figure 2.67

Answers

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.

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.

Sinus rhythm with bifascicular block. Note right bundle branch block (RBBB) and left axis deviation with mean QRS axis less than −30° suggesting left anterior fascicular block (LAHB). Also note that 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. Inferior wall is supplied by posterior fascicle and R wave peaks early in these leads.

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.

Atrial fibrillation. Note absence of P wave and irregularly irregular ventricular response. Also note 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.

Acute anterior ST elevation myocardial infarction (STEMI). Note hyperacute, tombstone ST elevation in V2 and V3.

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

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

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

WPW syndrome (? posteroseptal).

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

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

Posterior myocardial infarction. Note 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.

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.

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

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

Sinus rhythm with low QRS voltage (<5 mm in limb leads or <10 mm in chest leads). Consider pericardial effusion, emphysema.

Nonconducted P (second from right) followed by a P associated with a ventricular escape beat showing T wave inversion. Consistent with Mobitz type II AV block. Also note anterior Q wave, RBBB and LAFB – a substrate for trifascicular block.

Atrial fibrillation with rapid ventricular response. Also note low QRS voltage and diffuse ST elevation, suggesting pericarditis with effusion which may result in atrial fibrillation through atrial irritation.

Acute pericarditis. Note diffuse concave-up ST elevation and PR segment depression in most of the leads and reciprocal PR segment elevation and ST depression in aVR.

Episodes of complete heart block. Note >1 nonconducted P in a row. Note old inferior and acute anterior STEMI and mechanism of heart block is likely to be infra-Hisian with high risk of lack of escape rhythm.

Premature ventricular contractions (PVCs), three-beat VT (beats 2–4), accelerated idiojunctional rhythm (fairly regular narrow complex with no preceding P at a rate of 65 bpm, beats 9–12), Afib (lack of a P wave), short QT interval. These are highly indicative of digoxin toxicity. Digoxin toxicity blocks AV node and promotes subsidiary pacemakers at a faster rate.

Junctional rhythm with ventricular bigeminy.

Junctional rhythm with RBBB (beats 1, 4, and 5) with intermittent V-pacing (beats 2, 3, 6, and 7). Note a small pacer spike, changed QRS morphology upright in I, and different T wave morphology with paced beats.

Dual-chamber pacing.

Ventricular bigeminy.

Atrial pacing, ventricular tracking with ventricular pseudofusion. The V-spike before QRS is coincidental and QRS has normal conducted morphology. Lengthening AV delay will conserve the battery.

Dual-chamber pacing with ventricular couplet (beats 7 and 8).

Atrial flutter with 2 : 1 conduction and intermittent V-pacing.

WPW syndrome.

Dual-chamber pacer with atrial sensing and V-pacing producing slightly fused complex. Only very initial part of QRS is slightly slurred, indicating pacer-induced depolarization and rest of the QRS is normally conducted. Note LAFB as well.

High-grade AV block. The P waves are numbered. The atrial rate is about 86 bpm, and between 1 and 2 (rate 43) a P wave is dropped, indicating 2 : 1 sino-atrial block (produced by a nonconducted premature atrial contraction (PAC) between 1 and 2 through concealed retrograde conduction. The PAC is deforming the ST segment). Then there is 2 : 1 A : V block till 7 followed by two successive Ps being dropped (complete AV block) with a ventricular escape beat at 9 burying a P wave.

Narrow complex regular tachycardia at a rate of 150 .bpm without a discernible P wave. Likely paroxysmal SVT and possible atrioventricular nodal reentry tachycardia.

Broad complex tachycardia at a rate of 140 bpm, suggestive of VT. Note negative concordance in chest leads, superior axis, QRS duration of >200 ms, and slow upstroke of QRS complex – all suggestive of VT.

Atrial flutter with 2 : 1 conduction. Note clear flutter waves in lead II. There is a single PVC.

Atrial paced rhythm with normal AV conduction and normal QRS.

Atrial sensed and ventricular paced rhythm. Note that QRS is upright in V1, suggesting probable LV rather than RV pacing. Patient has a biventricular (BiV) pacer.

WPW syndrome. Note the delta waves in V4 and V5.

Dual-chamber pacer with atrial tracking and V-pacing producing fusion QRS complexes with initial portion due to pacing and remainder being conducted.

VOO pacing with pacer competing with junctional rhythm producing fully paced beat (1), fusion complex (2), pseudofusion (3), and lack of sensing (5–9). Also note QT prolongation. T wave inversion can occur because of repolarization memory secondary to V-pacing.

Dual-chamber pacing.

WPW syndrome, probably posteroseptal pathway because of inferior Q waves, positive delta waves in anterolateral leads, and rapid transition from V1 to V2.

BiV pacer with atrial and LV pacing. Note that QRS is negative in lateral leads and positive in V1, indicating LV pacing.

Broad complex tachycardia at a rate of 140 bpm with QRS duration of 160 ms, RBBB pattern with right rabbit ear and right axis deviation and rapid upstroke of initial part of QRS (in V5/V6) with broadening of latter part suggesting SVT with aberrancy. Note that the PVC did not reset the rhythm.

Broad complex tachycardia with monophasic RBBB pattern in V1, right axis deviation, and QRS duration of 160 ms. No P waves seen. Note rapid rise of QRS voltage in V5 and V6. The patient had SVT with aberrancy.

Atrial fibrillation for the first five beats, then V-pacing for a beat followed by sinus rhythm with first-degree AV block and lack of V-sensing in last three beats. Also note acute anterior STEMI.

BiV pacer. Patient is paced in atrium and left ventricle, producing RBBB QRS morphology.

Blocked PACs. The pauses are due to nonconducted PACs which occurred on the T wave and during refractory period of AV node. This does not signify AV nodal disease. When there are pauses, always look for nonconducted PACs. Also note QT prolongation.

Acute inferolateral STEMI. Note reciprocal ST depression in aVR; in pericarditis, there is reciprocal ST and PR segment elevation in aVR.

BiV hypertrophy. R in V1 is >5 mm and R/S in V1 is 1, suggesting RVH. R in V5 plus S in V2 is 35 mm, and ST depression in V5 and V6 suggests LV hypertrophy (LVH).

Normal electrocardiogram.

Acute inferior STEMI with near-complete ST segment resolution and inferior Q waves.

Acute inferolateral STEMI.

Multifocal atrial tachycardia. Note three different P wave morphologies and average rate >100 bpm.

Sinus tachycardia.

Intermittent dropped QRSs without progressive PR prologation suggesting second-degree Mobitz type II AV block. Also note that patient has left bundle branch block (LBBB), further supporting that the mechanism of AV block is likely infra-Hisian rather than intranodal. High risk of complete heart block.

Bifascicular block. Patient has RBBB and right axis deviation, suggesting left posterior fascicular block. Note the peaks of R wave in leads II and III follow lead I, suggesting activation spreading from lateral to inferior wall, the region of posterior fascicle.

Dual-chamber pacing, but QRS is native rather than paced. The V-spike comes before QRS, but QRS is narrow and has near-normal morphology.

Inferior myocardial infarction, age undetermined, possibly recent (slight ST elevation in leads III and aVF.

Bifascicular block with RBBB and LAFB. Also note absence of r in leads V1 to V4, indicating anterior myocardial infarction. Hence, the likely mechanism is diffuse conduction system disease through ischemia and signifies high risk because of infra-Hisian mechanism and extent of myocardial involvement.

Severe hyperkalemia with near sine wave appearance: Note peaked T waves, QRS prolongation, and absent P waves.

Atrial flutter with 2 : 1 conduction. The atrial rate is 240 bpm and ventricular rate is 120 bpm.

Marked respiratory sinus arrhythmia. Note that the P wave morphology is constant and cyclical changes in P–P intervals are consistent with frequency of respiration. It is a marker of vagotonia and seems to be more marked in the young and at slow heart rates.

Atrial tachycardia with variable block.

Paroxysmal atrial fibrillation with rapid ventricular response.

Atypical atrial flutter with variable block and IVCD of LBBB morphology.

Atrial tachycardia with 3 : 1 conduction. Atrial rate is about 225 bpm, and this could also be slow flutter because of antiarrhythmic therapy.

Box 2.1 ECG Diagnostic Criteria

Normal sinus P wave

P wave duration <120 ms

Amplitude ≤2.5 mm

P wave axis between 45° and 75° in frontal plane

Criteria for left atrial enlargement

P wave duration >120 ms in lead II

Notched P wave in lead II with inter-notch distance >40 ms (P-mitrale)

P-terminale in V1 >0.04 mm

P wave axis between +45° and −30° in frontal plane (left axis deviation)

Criteria for right atrial enlargement

P wave amplitude >2.5 mm in lead II (P-pulmonale)

Area under initial positive part of P wave in V1 >0.06 mm