Ebook Bedside cardiology: Part 1

(BQ) Part 1 book Bedside cardiology presents the following contents: Bedside cardiology - Is it evidence based, functional classification, syndrome and measurement, clinical instrument, first heart sound, palpation, blood pressure, arterial pulse, jugular venous pulse,...

Bedside Cardiology

Bedside Cardiology

Achyut Sarkar MD, D (Cardiology), DM (Cardiology)

Associate Professor of Cardiology and Incharge of

Congenital Heart Disease Program Institute of Post Graduate Medical Education and Research, Kolkata

Senior Interventionals Cardiologist

BM Birla Heart Research Center, Kolkata, West Bengal, India

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My Teachers and Students

Why another one? Why another one, when Bedside Cardiology, as a science,has been relegated in the History of Medicine and as an art, has beendescribed an art of artifact!

There is no noble intention This is only for stethoscope, for which I have

a romantic nostalgia Still, I cannot accept the image that a cardiologist isgiving round in the ward or seeing patient in his chamber, with the echoDoppler probe of his palmtop echocardiogram machine hanging from hisneck and no stethoscope!

Newer investigating tools, newer interventions are evolving almost everyday and replacing the new ones We are appreciating those Even then, are

we not thrilled when we detect an Austin Flint murmur or Graham Steellmurmur, described two centuries back? Are we not thrilled when we detect

a continuous murmur on the back of any patient?

May not be that useful, we all, still enjoy Bedside Cardiology We completelyagree to Dr Basil M RuDsky–“This is one of the few pleasures that can bederived from the ever-changing practice of medicine It stimulates acquisition

of a good doctor-patient relationship and provides a satisfying alternative tomany of the idiopathic inconsistencies and inadequacies of medical practice

It is unquestionably an art and skill that must not be allowed to succumb tothe way of the impossible dream of Don Quixote”

Achyut Sarkar For the sake of stethoscope, please read this preface!

I wish to thank Jaypee Brothers Medical Publishers for whom the creation

of this book has become possible I wish to thank Dr Saswati Sarkar for herinvaluable suggestion and inspiration I thank my father and late mother forwhom I have become a doctor I thank my daughter, Parnisha and my sonArjab They themselves are my inspiration At last, to Dr Asima Sarkar, mywife, I thank with immense gratitude She has made my house a home andhas shouldered all the responsibilities For her only, my idea has become abook

1 Bedside Cardiology: Is It Evidence-based? 1

Dyspnea 1

Jugular Venous Pressure 1

Pulse 2

Apical Impulse 2

Heart Sound 2

Murmur 3

2 Functional Classification 5

NYHA 5

Canadian Cardiovascular Society Functional Classification of Angina Pectoris 7

Specific Activity Scale 7

UCLA Congenital Heart Disease Functional Class 9

WHO Classification of Functional Status in Pulmonary Arterial Hypertension 9

The Canadian Cardiovascular Society (CCS) Severity of Atrial Fibrillation (SAF) Scale 10

Duke Activity Status Index (DASI) 10

Six-minute Walking Test 11

3 A Triad: Cardinal Symptoms in Cardiovascular System 14

Dyspnea 14

Physiologic Components of Dyspnea 14

Palpitation 18

Chest Pain 20

4 A Triad: Minor Symptoms in Cardiovascular System 25

Fatigue 25

Edema and Weight Gain 25

5 A Triad: Cardinal Symptoms in Congenital Left-to-right Shunt 28

Pulmonary Problems in Left to Right (L-R) Shunt 29

6 A Triad: Cardinal Symptoms in Congenital Cyanotic Heart Disease 31

Paroxysmal Hypoxic Spell 31

Squatting 32

Hyperviscosity Syndrome 32

Contents

7 Syndrome and Measurement 34

Syndromes 34

Measurements 43

8 Clinical Instrument 46

Stethoscope 46

Electronic (digital) Stethoscope 47

Ultrasound Stethoscope (Point-of-care echocardiography) 47

Sphygmomanometer 49

9 A Triad: Cardinal Signs in Congenital Cyanotic Heart Disease 52

Cyanosis 52

Anemia 54

Clubbing 55

10 Jugular Venous Pulse 59

Veins 59

Jugular Venous Pressure (JVP) 60

Normal Venous Pulse 65

Abnormal Venous Pulse 67

Specific Situations 70

Other Venous Pulses 74

11 Arterial Pulse 75

Origin of Pulse 75

Rate and Rhythm 77

Rate of Rise 78

Volume 79

Character: Double-peaked/double-beating pulse 79

Condition of Arterial Wall 84

Synchrony 85

12 Blood Pressure 91

Definition 91

13 Palpation 100

Apical Impulse 100

Special Clinical Conditions 109

14 First Heart Sound 111

Mechanism 111

Splitting 111

Sound Surrounding S1 114

15 Second Heart Sound 115

Mechanism 115

Splitting 115

16 Third Heart Sound 124

Physiology 124

How to Detect it 124

17 Fourth Heart Sound 127

Physiology 127

How to Detect it 127

Pressure Over Load 128

Raised End Diastolic Pressure 128

18 Ejection Sound 130

Pulmonary Valvular Click 130

19 Non-ejection Sound 134

Midsystolic Click 134

Mitral Opening Snap (OS) 135

Pericardial Sound 138

Pericardial Rub 138

Mediastinal Crunch (Hamman Sign) 139

Prosthetic Sound 139

20 Murmur 142

Systolic Murmur 144

Ejection Systolic Murmur (Midsystolic Murmur) 144

Pansystolic Murmur 149

Early Systolic Murmur 152

Late Systolic Murmur 153

Diastolic Murmur 153

Continuous Murmur 160

21 Innocent Murmur and Sound 166

22 Dynamic Auscultation 170

Prompt Sauatting 170

Standing 171

Valsalva 172

Isometric Handgrip 174

Transient Arterial Occlusion 175

Passive Leg Raising 176

Premature Beat 176

Respiration 176

Pharmacologic Agent 176

23 Is Your Patient in Heart Failure? 179

Bedside Assessment of Heart Failure 180

Clinical Aids 181

Instrumental Aids 182

Different Criteria for Heart Failure 182

24 Clinical Assessment: Pulmonary Hypertension 186

Definition 186

Clinical Classification of PH 186

Clinical Features 186

S2 188

25 Segmental Approach in Congenital Heart Disease 191

Connection and Relation 191

Segmental Approach 191

Cardiac Position 191

Situs 193

Angiographic Identification 196

Heterotaxy 198

Atrioventricular Connection 198

Loop 203

Ventriculoarterial Connection 206

Conus 210

Great Artery Spatial Relations 211

26 Clinical Approach: Congenital Cyanotic Heart Disease 214

Pathophysiological Classification 214

Tetralogy Physiology 214

Transposition Physiology 214

Eisenmenger Physiology (EP) 214

Common Mixing Physiology 215

Mixed Physiology (Effectively Two Physiologies) 215

History-onset of Cyanosis 215

Natural History Suggestive of Increased Flow 215

History 216

General Examination 216

Pulse 216

JVP 217

Palpation 217

Heart Sound 217

Murmur 218

Thus, from Clinical Examination, Initial Impression—CCHD with 219

Next Step: To look at X-ray Chest for Vascularity 219

X-ray Chest with Increased Flow 220

X-Ray Chest with Decreased Flow 222

27 Clinical Approach: Tetralogy Physiology 224

Tetralogy Physiology 224

Tetralogy Physiology: Hemodynamics 224

Tetralogy Physiology: How to Grade Severity 225

Under Umbrella of Tetralogy Physiology 226

Tetralogy Physiology: Fallot’s Tetralogy 227

Tetralogy Physiology: VSD, Pulmonary Atresia 227

X-ray Chest: VSD, Pulmonary Atresia 227

Tetralogy Physiology: DORV, PS 228

Tetralogy Physiology: CC–TGA, VSD, PS 229

Tetralogy Physiology: Univentricular Connection, PS 229

Tetralogy Physiology: Univentricular Connection, PS 229

Tetralogy Physiology: TGA, VSD, PS 230

Tetralogy Physiology: Tricuspid Atresia, VSD, PS 231

28 Clinical Approach: Eisenmenger Physiology 232

Syndrome/Complex 232

Incidence 232

Who are Clinically Susceptible 232

Incidence in Large Shunt 232

Congenital, Systemic-to-Pulmonary Shunts Associated with PAH 233

Diseases Leading to Eisenmenger Syndrome 233

Diseases Leading to Eisenmenger Syndrome 234

Onset of Eisenmenger Syndrome 234

Sex Distribution 234

Presenting Symptoms 235

Dyspnea 235

Hemoptysis 235

Squatting 235

Triad 235

Eisenmenger: Cardiac Findings 236

Eisenmenger: Palpation 236

Eisenmenger: Auscultation 236

Eisenmenger Syndrome: ASD 237

Eisenmenger Syndrome: VSD 237

Eisenmenger Syndrome: Survival 238

Eisenmenger Syndrome: PDA 238

Eisenmenger Complex 238

Eisenmenger Syndrome: Poor Prognostic Markers 239

Eisenmenger Syndrome: Cause of Death 239

How to Assess that PAH is Hyperkinetic (Reversible) or Obstructive (irreversible) 239

Index 241

Cardiac Cycle

Cardiac cycle consists of two basic phases: systole and diastole Assumingaverage heart rate as 72/minute, duration of each cardiac cycle is 0.8 secondwith ventricular systole 0.3 second and diastole 0.5 second

Fig 1: Cardiac cycle: ECG-gated relation between pressure pulses of chamber and

great vessels, jugular pressure pulse and heart sound

Fig 2: Cardiac cycle: ECG-gated heart sound

Then the atrial relaxation begins, with a pressure gradient reversal acrossthe atrioventricular valve, which floats upward before closure Now, theventricular volume is maximum This is the end-diastolic volume (EDV) orpreload Ventricular pressure, at this time is end-diastolic pressure, which is8–12 mm Hg for left and 3–6 mm Hg for right ventricle

Atrial relaxation denotes the x descent of jugular pressure pulse.

Phase 2 (Isovolumetric Contraction)

This phase begins with the QRS complex of ECG, representing ventriculardepolarization There is rapid rise of ventricular pressure, which becomesmaximal in early phase, termed maximal dp/dt As ventricular pressure crossesthe atrial pressure, AV valves start closing, resulting in S1 Mitral valve

Phase 1 (Atrial Contraction Phase)

This first phase of cardiac cycle begins with P wave of ECG, which representselectrical depolarization of atria Atrial contraction forces blood flow across

atrioventricular valve This produces a wave of atrial and jugular pressure

pulses and S4

(MC) precedes tricuspid valve closure (TC) During this phase, between AVvalve closure and semilunar valve opening, ventricular pressure rises rapidlywithout any change in volume Thus, it is named as isovolumetric contractionphase.

During this phase, there is c wave in atrial and jugular pressure pulse, due to bulging of AV leaflets into the atrium C wave is followed by ‘x’

descent

Phase 3 (Rapid Ejection Phase)

This phase begins when the ventricular pressure pulses cross that of the greatarteries Semilunar valves open up As the valve opening is wide with lowresistance, a small gradient between ventricle and great arteries is enough

in opening the semilunar valves There is rapid ejection with maximal greatarteries pressure is achieved in early phase Normal valves, during opening,

do not produce any sound Atrial pressure continues to decline, due to itsrelaxation and descent of its base, due to ventricular contraction This produces

‘x’ descent Following this, its pressure starts rising, due to inflow of venous blood, both systemic and pulmonary, and the v wave begins, until the opening

of AV valves

Fig 3: Cardiac cycle: ECG-gated relation between jugular pressure pulse and heart

sound

Phase 4 (Reduced Ejection Phase)

Ventricular repolarization, i.e T wave in ECG, begins around 200 ms afterthe onset of ventricular systole This results in reduced rate of ejection.Ventricular pressure falls below that of great arterial pressure But, ejectioncontinues due to kinetic (inertial) energy of blood

Fig 4: Cardiac cycle: Relation between pressure pulses of

ventricles, atriums and great vessels

Phase 6 (Isovolumetric Relaxation Phase)

Subsequently, great artery pressures continue to decline Due to ventricularrelaxation, its pressures fall further As both AV and semilunar valves remain

closed, ventricular volumes remain same Thus, this phase is calledisovolumetric relaxation phase As venous return continues, atrial pressureand jugular venous pressure increase further, the peak of which is denoted

by v wave.

Phase 7 (Rapid Filling Phase)

When the ventricular pressure pulses come down to atrial pressure pulses,its pressures fall below atrial pressure, thus, opening the AV valves Pressuredecline continues till full relaxation of ventricles This is followed by gradualrise of ventricular pressure, by its filling from atria AV valve opening isassociated with fall in atrial pressure and jugular venous pressure, denoted

by y descent in atrial and jugular pressure pulses.

Fig 5: Cardiac cycle: Relation between pressure pulses and heart sound

Phase 8 (Slow Filling Phase)

As ventricular filling continues, its pressures start rising, reducing ventricular pressure gradient Eventually, ventricular filling comes down,which is followed by active atrial filling, i.e., beginning of phase 1

atrio-1 Bedside Cardiology: Is

It Evidence-based?

“There is already plenty of evidence to show that we are in danger of losingour clinical heritage, and of pinning too much faith in figures thrown up bymachines Medicine must suffer if this tendency is not checked.”1Paul Wood expressed this apprehension in 1950 Since then, sixty yearshave passed And now, justifying his apprehension, bedside cardiology hasbecome a heritage science! Most importantly, evidence-based medicine isasking and demanding evidences in favor of bedside cardiology

Dyspnea

In a study2 to evaluate symptoms as predictor of heart failure or ChronicObstructive Pulmonary Disease (COPD), dyspnea on effort predicteddepressed left ventricular systolic function with a sensitivity of 100% andspecificity of 20% Orthopnea predicted heart failure with a sensitivity andspecificity of 71% and 65% and paroxysmal nocturnal dyspnea with thesensitivity and specificity of 47% and 75% respectively All these symptomshad a likehood ratio of 2 or less

Jugular Venous Pressure

In one study,3 central venous pressure was determined clinically from jugularvenous pressure and by central venous catheter The sensitivity of JVP atidentifying low (< 0 mm Hg), normal (0–7 mm Hg), or high (> 7 mm Hg)central venous pressure was 33%, 33% and 49% respectively The specificitywas 73%, 62% and 76% respectively In another study,4 clinically detectedcentral venous pressure was compared to pulmonary artery pressure bycatheter Clinical prediction was correct in 55% cases It has been shown5that a raised jugular venous pressure increases the probability, that themonitored central venous pressure will be four times higher

When the clinically measured jugular venous pressure is low, there

is least possibility (likehood ratio 0.2) of a higher monitored centralvenous pressure A normal jugular venous pressure (likehood ratio 1)

however, does not increase or decrease the probability of abnormal centralvenous pressure Hepatojugular reflux6 is a more specific test and the likehoodratio is around 6.

Pulse

“Is the pulse in atrial fibrillation irregularly irregular?”.7 In this excellentstudy, it has been shown, that nonrandom sequence of R-R interval is found

in 30% cases and pulsus alternans in 46% cases of atrial fibrillation Thus,

a particular pattern of regularity is common in atrial fibrillation, rather thanirregular irregularity

Hill sign recently has been challenged.8 Intra-arterial pressure tracinghas shown that there is no major difference between upper and lower limbpressure in aortic regurgitation and Hill sign is an sphygmomanometricartifact

Apical Impulse

In one study,9 left ventricular enlargement, as determined by the site of theimpulse and its diameter was compared with echocardiographic leftventricular enlargement Sensitivity and specificity of apical impulse outsideleft midclavicular line as an indicator of left ventricular enlargement was100% and 18% respectively with a likehood ratio of 1.2 When midsternalline was taken as reference point in place of midclavicular line, apicalimpulse situated more than 10 cm outside, indicated left ventricularenlargement with a sensitivity of 100% and specificity of 33% An increaseddiameter of apical impulse was a good indicator of left ventricularenlargement with a sensitivity of 92% and specificity of 75%

Heart Sound

A loud S2 (P2) is a strong predictor of pulmonary hypertension When P2

is audible at the apex, systolic pulmonary artery pressure may be assumedmore than 50 mm Hg.10

S3 was first described, long back, in 1856 It is taken as a hallmark ofleft ventricular dysfunction Its predictive value was studied, whichquantitated the interobserver variability of S3.11 In this study, it was foundthat if one observer heard S3, the probability that a second observer would,was between 34–38% When, on the other hand, one observer found S3, the

TABLE 1-1 Bedside cardiology has, thus following limitations

chance that a second observer would agree was between 69–79%.Auscultatory findings were verified by phonocardiogram and the positiveand negative predictive value to identify S3 was 71% and 64% respectively.When this and few other studies cast doubt about the clinical usefulness ofS3, SOLVD trial12 strongly established its usefulness In patients with heartfailure, clinical detection of S3 increased the risk of hospitalization or deathdue to pump failure by 50%

Murmur

Clinical skill to detect murmur was compared with echocardiogram in severalstudies Murmur of mitral regurgitation is detected clinically in 13–56%cases and that of tricuspid regurgitations in 28–33% cases.13, 14 Aorticstenosis murmur can be identified clinically better than other murmurs,ranging from 20–88%.15 Clinical identification of aortic regurgitation andmitral stenosis murmur are poorer Sensitivity to diagnose diastolic murmurwas only in 5–24% cases.16

Conclusion

May evidence-based medicine is casting shadow on bedside cardiology, itssurvival as a science depends upon the process of its filtration through thestringent criteria of evidence-based medicine Clinician should rememberthat the paradigm is shifting from “intuition, unsystemic clinical experiencesand patholophysiologic rationale as sufficient grounds for clinical decisionmaking” to evidence from clinical research.17

1 To identify low-frequency sound.

2 To identify murmur of low-frequency like, mitral stenosis and murmur of lower grade like aortic regurgitation.

3 To appreciate the gap between sounds (like, S2-OS, S1-EC, S1-NEC).

4 Bedside diagnosis of some common cardiac conditions such as pericardial effusion, early ventricular dysfunction, early cardiomyopathy, silent valvular disease, and mass lesions is a difficult task, but can be diagnosed comprehensively by echocardiogram.

5 Early and presymptomatic diagnosis of disease, which can alter the eventual prognosis.

3 Connors AF, McCaffree DR, Gray BA Evaluation of right heart catheterization

in the critically ill patient without acute myocardial infarction N Eng J Med 1983;308:263.

4 Eisenberg PR, Jaffe AS, Schuster DP Clinical evaluation compared to pulmonary artery catheterization in the hemodynamic assessment of critically ill patients Crit Care Med 1984;12:549.

5 Cook DJ The clinical assessment of central venous pressure Am J Med Sci 1990;299:175.

6 Cook DJ, Simel DL Does this patient have abnormal central venous pressure? JAMA 1996;275:630.

7 Rawles JM, Rowland E Is the pulse in atrial fibrillation irregularly irregular? Br Heart J 1986;56:4.

8 Kutryk M, Fitchett D: Hill’s sign in aortic regurgitation: enhanced pressure wave transmission or artifact? Can J Cardiol 1997 Mar;13(3):237.

9 Eilen SD, Crawford MH, O’Rourke RA Accuracy of precordial palpation for detecting increased left ventricular volume Ann Intern Med 1983;99:628.

10 Gaine SP, Rubin LJ: Primary pulmonary hypertension Lancet 1998;352(9129): 719.

11 Lock CE, Morgan CD, Ranganathan N The accuracy and interobserver agreement

in detecting the “gallop sound” by cardiac auscultation Chest 1998;114:128.

12 Drazner MH, Rame JE, Phil M, et al Prognostic importance of elevated jugular venous pressure and a third heart sound in patients with heart failure N Engl J Med 1983;308:263.

13 Mangione S, Nieman LZ, Gracely E The teaching and practice of cardiac auscultation during internal medicine and cardiology training Ann Intern Med 1993;119:47.

14 Attenhofer Jost CH, Turina J, Mayer K, et al Echocardiography in the evaluation

of systolic murmurs of unknown cause Am J Med 2000;108:614.

15 Spencer KT, Allen S, Anderson AS, et al Physician-performed point-of-care echocardiography using a laptop platform compared with physical examination

in the cardiovascular patient J Am Coll Cardiol 2001;37:2013.

16 Roldan CA, Shively BK, Crawford MH Value of the cardiovascular physical examination for detecting valvular heart disease in asymptomatic subjects Am

J Cardiol 1996;77:1327.

17 Evidence-based medicine working group Evidence-based medicine, a new approach to teaching the practice of medicine JAMA 1992;268:2420.

In 1928, the New York Heart Association (NYHA) published a classification

of patients with cardiac disease, based on clinical severity and prognosis.This classification has been updated in seven subsequent editions ofNomenclature and Criteria for Diagnosis of Diseases of the Heart and GreatVessels The ninth edition, revised by the Criteria Committee of the AmericanHeart Association, New York City Affiliate, was released on 1994

Changes

In the initial editions, the terms functional capacity and therapeuticclassifications were used In the subsequent editions in 1973 and 1979, theterms cardiac status and prognosis were used In the last edition, functionalclasses, which depend upon subjective symptoms, and objective assessment,based on investigations were included Anginal symptoms were also included

in the functional class, from this edition

The classifications are summarized in Table 2-1

Thus a complete diagnosis, according to this classification, is:

TABLE 2-1 NYHA functional classifications

Functional capacity Objective assessment Class I Patients with cardiac disease but without A No objective

resulting limitation of physical activity Ordinary evidence of

physical activity does not cause undue fatigue, cardiovascular

palpitation, dyspnea, or anginal pain disease.

Class II Patients with cardiac disease resulting in B Objective evidence

slight limitation of physical activity They are comfor- of minimal table at rest Ordinary physical activity results in vascular disease fatigue, palpitation, dyspnea, or anginal pain.

cardio-Class III Patients with cardiac disease resulting in C Objective evidence of

marked limitation of physical activity They are com- moderately severe fortable at rest Less than ordinary activity causes cardiovascular fatigue, palpitation, dyspnea, or anginal pain disease.

Class IV Patients with cardiac disease resulting in D Objective evidence

inability to carry on any physical activity without of severe discomfort Symptoms of heart failure or the anginal vascular disease syndrome may be present even at rest If any physical

cardio-activity is undertaken, discomfort is increased.

Uncertain Diagnosis

No Heart Disease: Predisposing Etiologic Factor

This category includes patients in whom no apparent cardiac disease, butthere is a history of etiologic factor that might cause heart disease Thesepatients need periodic follow-up

No Heart Disease: Unexplained Manifestation

This category includes patients with symptoms or signs referable to the heartbut in whom a diagnosis of cardiac disease is uncertain at the time ofexamination These patients need re-examination after a stated interval

No Heart Disease

When there is a reasonable uncertainty that the symptoms or signs are not

of cardiac origin, the diagnosis should be No heart disease.

Criticism of NYHA Classification System

1 Clinician can assess patient’s functional status very quickly by thisclassification, during the clinical assessment

2 This system assesses the patient pertaining to exercise All otherparameters, including clinical examination, ECG, X-ray and echocardio-gram are assessed in resting status This edge over other factors makesthis system a very important prognostic factor.

3 However, in an interesting study,3 “Limitations of the New York Heart Association functional classification system and self-reported walking distances in chronic heart failure”, it was shown that “54% concordance

between cardiologists even when assessing the same patient on the sameday” There was a poor agreement between “cardiologists in differentiatingbetween patients belonging to class II and class III”, which is mostimportant issue, because of the fact that to classify a patient in class I

or class IV is easy and indication of spinonolactone and Resynchronizationtherapy depend on whether patient belongs to class II or III This studyconcluded that:

4 NYHA system is poorly reproducible

5 Research papers using the NYHA classification, either as an inclusionand/or outcome measure, should record the criteria or questions used toascertain a patient’s functional class

6 Use of specific questions can markedly improve the reproducibility ofthis classification system

7 Many clinicians ask patients with heart failure, how far they can walk.Walking distance does not measure exercise capacity or correlate with

a known measure of exercise capacity Even the poor ability of patients

to estimate distance does not explain the lack of correlation withobjectively measured exercise capacity

Canadian Cardiovascular Society Functional

This classification is based on the functional class in relation to angina only(Table 2-2)

Specific activity scale denotes the activity in relation to usual daily life(Table 2-3)

Class I Activities

 Carry at least 24 pounds up 8 steps: 10 METS

TABLE 2-2 Functional class of angina

Class

Class I Ordinary physical activity does not cause angina, such as walking

and climbing stairs Angina with strenuous or rapid or prolonged exertion at work or recreation.

Class II Slight limitation of ordinary activity Walking or climbing stairs rapidly,

walking uphill, walking or stair climbing after meals, or in cold, or

in wind, or under emotional stress or only during the few hours after awakening walking more than two blocks on the level and climbing more than one flight of stairs at a normal pace and in normal condition.

Class III Marked limitation of ordinary physical activity Walking one or two

blocks on the level and climbing one flight of stairs in normal condition and at normal pace.

Class IV Inability to carry on any physical activity without discomfort; anginal

syndrome may be at rest.

 Carry objects that are at least 80 pounds: 8 METS

 Do outdoor work (shovel snow, spade soil): 7 METS

 Do recreational activities like skiing, basketball, touch football, squashhandball, etc.: 7–10 METS

 Jog or walk 5 miles an hour: 9 METS

Class II Activities

 Carry anything up a flight of 8 steps without stopping: 5.0–5.5 METS

 Have sexual intercourse without stopping: 5–5.5 METS

 Garden rake weed: 5–6 METS

 Walk at a 4-mile per hour rate on level ground: 5–6 METS

TABLE 2-3 Specific activity scales

Class I: Patient can perform to complete any activity requiring > 7 metabolic

equivalent (MET).

Class II: Patient can perform to complete any activity requiring > 5 METS but

cannot perform to complete activity requiring > 7 METS.

Class III: Patient can perform to complete any activity requiring > 2 METS but

cannot perform to complete activity requiring > 5 METS.

Class IV: Patient cannot perform to complete any activity requiring > 2 METS.

Class III Activities

 Walk down a flight of steps without stopping: 4.5–5.2 METS

 Shower without stopping: 3.6–4.2 METS

 Strip and make bed: 3.9–5 METS

This functional class, specifically deals with patient with congenital heartdisease (Table 2-4)

WHO Classification of Functional Status in

This classification, in compare to NYHA, includes syncope as a symptom,

in place of palpitation (Table 2-5)

TABLE 2-5 Functional status in PAH

• Class I: No limitation of usual physical activity.

• Class II: No symptoms at rest; mild limitation of physical activity; normal physical activity causes increased dyspnea, fatigue, chest pain, or presyncope.

• Class III: No symptoms at rest; marked limitation of physical activity; less than ordinary physical activity causes increased dyspnea, fatigue, chest pain or presyncope.

• Class IV: Unable to perform any physical activity at rest; signs of right ventricular failure; dyspnea, fatigue, chest pain, or presyncope present at rest and symptoms are increased by any physical activity.

TABLE 2-4 UCLA congenital heart disease functional classes

• Class I: Asymptomatic.

• Class II: Symptomatic, but does not interfere with normal activities.

• Class III: Symptoms interfere with some but not most activities.

• Class IV: Symptoms interfere with most if not all activities.

The Canadian Cardiovascular Society (CCS) Severity of

The Canadian Cardiovascular Society (CCS) Severity of Atrial Fibrillation(SAF) Scale is similar to the CCS Angina Funtional Class The CCS-SAFscore is calculated using three steps:

Symptoms (S): To assess the symptoms

Association (A): To decide the association of symptoms with atrial fibrillation.Functionality (F): To assess the functional status and quality of life of thepatient due to the association (Tables 2-6 and 2-7)

Is AF, when present, associated with the above-listed symptoms (A–E)?

For example: Ascertain if any of the above symptoms are present during AF and likely caused by AF (as opposed to some other cause).

A final score was calculated by the summary of giving each item a value

of 3 = ‘done without difficulty’, 2 = ‘done with difficulty’, and 1 = ‘not donebecause of health reason’ If any activity from 1 to 4 was not done because

of health reason, it was skipped to activity 5

Six-minute Walking Test

This is a reliable, inexpensive and simple objective test to assess functionalcapacity in patients with moderate to severe heart failure Various testprotocols, like 2-minute, 6-minute and 12-minute walking tests have beenused 6-minute test was first standardized by Lipkin and associates.10

1 The test is carried out in a level enclosed corridor 20 meters long

2 Each patient is instructed to cover as much ground as possible in sixminutes

3 Patient is told to walk continuously, if possible but that they could slowdown or stop, if necessary

4 The aim is that at the end of the test the patients believe that they couldnot have walked any further in the six minutes

5 The test may be repeated twice on the same day with at least three tofour hours between tests

TABLE 2-7 CCS-SAF scale

Class 0

Asymptomatic with respect to AF

Class 1

Symptoms attributable to AF have minimal effect on patient’s general QoL

• Minimal and/or infrequent symptoms, or

• Single episode of AF without syncope or heart failure.

Class 2

Symptoms attributable to AF have a minor effect on patient’s general QoL.

• Mind awareness of symptoms in patients with persistent/permanent AF, or

• Rare episodes (e.g.) less than a few per year) in patients with paroxysmal or intermittent AF.

Class 3

Symptoms attributable of AF have a moderate effect on patient’s general Qol.

• Moderate awareness of symptoms on most days in patients with persistent/ permanent AF, or

• More common episodes (e.g.) more than every few months) or more severe symptoms, or both, in patients with paroxysmal or intermittent AF.

Class 4

Symptoms attributable to AF have a severe effect on patient’s general QoL.

• Very unpleasant symptoms in patient with persistent/paroxysmal AF and/or

• Frequent and highly symptomatic episodes in patients with paroxysmal or intermittent AF and/or

• Syncope thought to be due to AF and/or

• Congestive heart failure secondary to AF.

This test may be less discriminating than the maximal or submaximalexercise test, but its simplicity and inexpensiveness are unique It can beused as serial monitoring of patients with heart failure to assess the treatment.

Evaluation of 3 functional classifications of cardiac insufficiency:

A national multicenter study National College of French Cardiologists 11

“The scope of the study is a comparison of three functional classifications:The New York Heart Association classification, the Duke Universityclassification, and the specific activity scale The NYHA classification issubjective, difficult to reproduce and poorly correlated to the functionalcapacity measured ergometrically (duration of exercise and/or VO2) A specificactivity scale adapted to national requirements appears to be the best solution.The study covered 15 successive days All patients suffering from congestiveheart failure who were examined over this period were included 700cardiologists took part in this study 2353 patients were reviewed, mean age

69 (58% male, 42% female) Heart failure was of an ichaemic origin in 37%

of cases, idiopathic in 25% and due to hypertension in 25% Symptomatologywas left sided in most cases Among NYHA class IV patients, 75% belonged

to class IV of the specific activity scale (SAS) (23% class III, 1% class II),and 88% of the Duke classification (10% class III, 1% class II) For NYHAclass III patients, 80% were SAS class III (5% class IV, 13% class II), andonly 38% (42% class IV and 16% class II) of the Duke classification.Regarding NYHA class II patients, 74% were SAS class II (21% class IIIand 4% class I), and 26% of the Duke classification (39% class I, 29% classIII and 3.6% class IV) Finally, among NYHA class I patients, 60% wereSAS class I (34% class II, 5% class III), and 74% of the Duke classification(11% class II and 13% class III)”

3 Raphael C, Briscoe C, Davies J, et al Limitations of the New York Heart Association functional classification system and self-reported walking distances in chronic heart failure Heart 2007;93;476.

4 Canadian Cardiovascular Society—functional classification severity of unstable angina circulation 1976;54:522.

5 Goldman L, Hashimoto EF, Cook EF, et al Comparative reproducibility and validity

of systems for assessing cardiovascular functional class: Advantages of a new specific activity scale Circulation 1981;64:1227.

6 Perloff JK and Child JS Congenital heart disease in adults, 2nd ed Philadelphia: WB Saunders, 1998:218.

7 McLaughlin VV, McGoon MD Pulmonary arterial hypertension Circulation 2006; 114(13):1417.

8 Dorian P, Cvitkovic SS, Kerr CR, et al A novel, simple scale for assessing the symptom severity of atrial fibrillation at the bedside: The CCS SAF Scale Can J Cardiol 2006;22:383-6.

9 Alonso J, Permanyer-Miraldaf G, Cascantf P, et al Measuring functional status of

chronic coronary patients Reliability, validity and responsiveness to clinical change

of the reduced version of the Duke Activity Status Index (DASI) Eur Heart J 1997; 18:414.

10 Lipkin DP, Scriven AJ, Crake T Six minute walking test for assessing exercise capacity

in chronic heart failure Br Med J 1986;292:653.

11 Gibelin P, Poncelet P, Gallois H, et al Evaluation of three functional classifications

of cardiac insufficiency: a national multicenter study National College of French Cardiologists Ann Cardiol Angeiol 1995; 44(6):304.

A Triad: Cardinal Symptoms in Cardiovascular System

Dyspnea, palpitation and chest pain are the most important cardinal symptoms

of one’s own breathing

Physiologic Components of Dyspnea

 Mechanoreceptors (respiratory muscles)

 Hypoxia (carotid and aortic bodies)

 Changes in PCO2/pH (medullary center)

 Medullary center (afferent input and efferent output)

 Cortical function (sense of effort)

Basic Mechanism

Length-Tension Afferent Dissociation

Inappropriateness/Neuromechanical/Efferent-This theory states that dyspnea results from mismatch between centralrespiratory motoractivity and incoming afferent information from receptors

in theairways, lungs, and chest wall structures The afferentfeedback fromperipheral sensory receptors may allow the brainto assess the effectiveness

of the motor commands issued to the ventilatory muscles, i.e theappropriateness of the responsein terms of flow and volume for the command.When changes in respiratorypressure, airflow, or movement of the lungs andchest wall arenot appropriate for the outgoing motor command, the intensity

of dyspnea is heightened Thus, any dissociation betweenthe motor commandand the mechanical response of the respiratorysystem may produce a sensation

of respiratory discomfort, dyspnea

Dyspnea in Heart Failure

Muscle Hypothesis

According to this hypothesis, skeletal muscle, both respiratory and peripheral,plays the key role in the pathophysiology of exercise intolerance in heartfailure Heart failure leads to systemic inflammatory response along with animbalance between anabolic and catabolic factor There is muscle catabolismleading to respiratory muscle myopathy causing dyspnea, and peripheralmyopathy causing fatigue

Skeletal muscle abnormality leads, also, to increase in the ergoreflex, amuscle reflex stimulated by work done, through the ergoreceptors Stimulation

of the ergoreflex leads to greater ventilatory response to exercise than normal.This results in the sensation of dyspnea At the same time, this reflex leads

to greater sympathetic activation, another feature common during exercise,

in heart failure

Heart failure also results in increased level of proinflammatory cytokinines,interlukin-1 and interferon in skeletal muscles Those cytokinines increasethe level of nitric oxide synthase Intracellular nitric oxide level shoots up

to a high level and inhibits mitochondrial oxidative phosphorylation Exercisetraining reduces inflammation and inflammatory markers and increasesmitochondrial volumes in skeletal muscle Thus, muscle fatigue is reducedand exercise tolerance is improved in heart failure

Lung Hypothesis

This is the time-old concept of explanation of exercise intolerance in heartfailure, which leads to pulmonary venous hypertension and capillarycongestion with interstitial edema Lung becomes stiffer with reducedcompliance Increased tissue pressure leads to earlier closure of dependentairways with air trapping These factors altogether behave as restrictiveventilatory defect Work of breathing is increased to distend the stiff lungs.Tidal capacity is reduced and respiratory rate is increased as compensation.Both engorged blood vessels and peribronchiolar cuffing may causebronchoconstriction with increased airway resistance There is also ventilation-perfusion mismatch, increased alveolar-arterial oxygen difference andincreased ratio of dead space to tidal volume

Formal Measurement of Dyspnea

Modified Borg scale is a reliable assessment tool for dyspnea Patients use

to find that the language in this scale adequately expressed their dyspnea(Table 3-2)

Ventilatory capacity ismeasured prior to exercise, ventilation is measuredduring exercise,and these are related to the intensity of dyspnea rated usingVisual Analogue Scale (VAS) which consists of a line, usually 100 mm inlength, placed either horizontally or vertically upon a page, with anchors toindicate extremes of a sensation Theanchors on the scale have not beenstandardized, but “not breathlessat all” to “extremely breathless” and “noshortness ofbreath” to “shortness of breath as bad as can be” are frequentlyused Scoring is accomplished by measuring the distance from thebottom ofthe scale (or left side if oriented horizontally) tothe level indicated by thesubject The reliability and validityof the VAS as a measure of dyspnea hasbeen reported (Fig 3-1)

TABLE 3-1 Severity scale of dyspnea

Grade Degree Characteristics

0 None Only with strenuous activity

1 Slight When hurrying on level ground or climbing a slight incline

2 Moderate Needs to walk more slowly than others of the same age or

has to stop for breath when walking at own pace on level ground

3 Severe Stops for breath after 100 yards or after a few minutes

4 Very severe Housebound or dyspnea when dressing or undressing

Fig 3-1: Visual analog scale

Orthopnea

It is defined as dyspnea during recumbency In the horizontal position, there

is redistribution of blood volume from the lower extremities and splanchnicbeds to the lungs In normal individuals, this has little effect, but in patients

in whom the left ventricle, because of disease, cannot pump the additionalvolume out, there is a significant reduction in vital capacity and pulmonarycompliance with resultant shortness of breath

Besides, in heart failure, there may be reabsorption of edema fluid frompreviously dependent parts of the body, overloading the congestedpulmonary circulation Pulmonary congestion decreases when the patientassumes a more erect position, and this is accompanied by an improvement

Paroxysmal Nocturnal Dyspnea

In a typical episode, patient is suddenly awakened 2 to 3 hours after going

to sleep, gasping for air He quickly sits up and puts his feet over the side

of the bed, coughing, wheezing and sweating He gets relief only after sittingfor 10 to 15 minutes

Pathophysiology is similar to that for orthopnea The failing left ventricle

is suddenly unable to match the output of a more normally functioning rightventricle; this results in pulmonary congestion Other mechanisms includedecreased responsiveness of the respiratory center in the brain, decreasedadrenergic activity in the myocardium during sleep and nocturnal arrhythmia

Commonest diseases are mitral stenosis, other valvular heart diseases,

ischemic heart disease and dilated cardiomyopathy

Noncardiac causes of nocturnal dyspnea are nocturnal asthma, COPD,

pulmonary embolism, obstructive sleep apnea, anxiety and hyperventilation

A patient symptomatic with PND is classified as NYHA class 3

Trepopnea

May occur with asymmetric lung disease when the patient lies with the moreaffected lung down because of gravitational redistribution of blood flow.Left atrial myxoma, by obstructing mitral inflow in lateral decubitus cancause trepopnea

Platypnea

Upright posture causes increased wasted ventilation ratio and dyspnea inCOPD Platypnea in association with orthodeoxia (arterial deoxygenation inthe upright position) has been reported, occasionally in cyanotic congenitalheart disease Probable explanation is slight decrease in systemic bloodpressure in the upright position, resulting in increased right-to-left shunting

Palpitation

Palpitation can be defined as uncomfortable awareness of one’s own heartbeat Patient describes the feeling as skipped or missed beat and a poundingsensation in chest Most common causes of palpitation are arrhythmia andanxiety Though, occasionally it may indicate life-threatening arrhythmia,most often it is a benign symptom

 Cardiac cause: 45% (Arrhythmia: 40%; other cardiac causes: 5% cases)

 Anxiety or panic disorder: 30% cases

 Medications: 5% cases

 Other noncardiac causes: 5% cases

 No specific causes: 15% cases

Cardiac Arrhythmias

Bradycardia and tachycardia, premature ventricular and atrial contractions,sick sinus syndrome, advanced arteriovenous block, or ventricular tachycardiacan cause palpitation Arrhythmia, most often, does not cause palpitation.Episodes of ventricular tachycardia and supraventricular tachycardia may beperceived as palpitations but also can be asymptomatic or lead to syncope

Anxiety or Panic Disorder

It is characterized by recurrent unexpected panic attack, more common inrelatively younger women who somatize more frequently However, oneshould not over diagnose anxiety and should do a total evaluation, asarrhythmia can coexist with anxiety Anxiety causes catecholamine surgeand may induce ventricular tachycardia

Nonarrhythmic Cardiac Cause

Rugurgitant lesions, like aortic and mitral regurgitation and lesions, whichcause volume-overload, like ASD and VSD are important causes of palpitation

associated giddiness, syncope, angina or dyspnea should be evaluated.Examiner himself can demonstrate or the patient may be asked to tap outthe rhythm.

Symptoms

 Flip-flopping in chest: Suggestive of atrial or ventricular ectopic

 Fluttering in chest: Suggestive of atrial or ventricular tachyarrhythmia

 Vibrating neck: Suggestive of tachyarrhythmia, where atria are contractingagainst closed AV valves, producing large cannon waves Patient feelsrapid regular vibrating or pounding sensation in neck and a bulging can

be seen, called frog sign Most common cause is AV nodal reentranttachycardia

Circumstances

Palpitation and syncope: Palpitation turns in an ominous symptom when

palpitation is associated with dizziness, presyncope or syncope Ventriculartachycardia is a strong probability Supraventricular tachycardia canoccasionally cause syncope, immediately after the onset Rapid heart ratewith low cardiac output and acute vasodilatation are the mechanism ofsyncope

Palpitation and dyspnea: Usually indicate arrhythmia associated with

ventricular dysfunction, aortic stenosis, HCM mitral stenosis and ischemicheart disease

Palpitation and posture: AVNRT may be initiated by standing posture from

bending over and may be terminated after lying down Patient with regurgitantlesion feels the pounding sensation more in lying or left lateral decubitus

Palpitation and catecholamine excess: Exercised induced disproportionate

rapid palpitation may be due to catecholamine induced idiopathic ventriculartachycardia, atrial fibrillation or supraventricular arrhythmia Postexercisepalpitation may occur due to vagal induced atrial fibrillation Mild exertion

or emotional stress can cause palpitation in young female patient due tohypersensitivity of beta-adrenergic stimulation It is called inappropriatesinus tachycardia

Chest Pain

Chest pain is the commonest symptom in regard to cardiovascular system

It is the important task for the clinician to establish whether the chest pain

is cardiac or noncardiac In an outpatient set up, less than 25% patient withchest pain will have cardiac cause and in an emergency set up, around 70%patient will have cardiac cause of chest pain (Table 3-3).

TABLE 3-3 Common causes of chest pain

Cardiac Chest Pain

Angina

One should determine three factors:

1 Substernal chest pain

2 Provoked by effort

3 Relieved by nitroglycerine

When all the three characteristics are present, it is typical anginal chestpain, which bears a high risk for coronary artery disease (CAD) in all agegroup When two features are present, it is atypical angina, which bearsintermediate risk for CAD in all men and in women older than 50 years.When only one feature is present, it is nonanginal chest pain and it carriesintermediate risk for CAD in men older than 40 years and women older than

60 years

Acute Myocardial Infarction (AMI)

In an acute chest pain presentation, 3% patient diagnosed as having noncardiacchest pain may suffer AMI or death within one month Thus, in acute chestpain setting, patients presented with atypical chest pain, but having cardiacrisk factors, should be followed-up carefully Rouan decision rule bears a

Diagnosis Percentage of patient

considerable predictive value regarding acute myocardial infarction in acutechest pain with a nonspecific ECG (Table 3-4).

Pericardial Pain

Major part of pericardium is pain insensitive Pain due to pericarditis is due

to adjacent pleural involvement Pain may radiate to neck, shoulder or back.Most commonly, it is retrosternal, aggravated by coughing, deep breathingand change in posture, all of which cause pleural movement Sitting uprightand leaning forward relieve pain

Pulmonary Embolism

Chest pain, due to pulmonary embolism is due to dilatation of pulmonaryartery or pulmonary infarction leading to pleural involvement One canfollow the Well model for clinical diagnosis (Table 3-5)

Aortic Dissection

At the very beginning, pain reaches at peak, front and back of the chest and

is described as ripping, tearing, severe sharp pain There may be absence ofpulse in one or both arms, CVA or paraplegia or aortic regurgitation

TABLE 3-4 Rouan decision rule for myocardial infarction

Pain described as pressure.

Pain radiating to arm, shoulder, neck, or jaw.

TABLE 3-5 Well model for pulmonary embolism (PE)

Clinical findings Points

Chest Wall Pain

History of osteoarthritis, rheumatoid arthritis and finding of local tendernessincrease the likelihood of chest wall pain Costochondral and costosternalsyndrome are the common causes of chest wall pain Tietze’s syndrome,tenderness, swelling and redness of costocnondritis is an infrequent finding.Chest wall pain distributed along a dermatome can be due to cervical rootdisease, intercostal muscle cramp and herpes zoster

Gastrointestinal Diseases

Esophageal pain due to acid reflux is a retrosternal burning pain, precipitated

by some specific foods, more on lying down, early morning and relieved by reducing agent Chest pain due to esophageal spasm is compressive in nature,may radiate down arms and sometimes, is relieved by antianginal medications.Pain due to peptic ulcer disease, gallbladder disease and pancreatitis canradiate to lower chest wall

acid-Clinical Approach

A thorough history and clinical examination can diagnose most of the chestpain causes:

1 Mode of onset, duration and frequency

2 Site of pain and radiation

3 Character of pain

4 Aggravating and relieving factors

5 Associated symptoms

Further Reading

1 Abbott AV Diagnostic approach to palpitation Am Fam Physician 2005;71(4):743.

2 American Thoracic Society (Dyspnea (Mechanisms, assessment, and management)

A consensus statement Am J Respir Crit Care Med 1999;159:321.

3 Capewell S and McMurray J "Chest pain? Please admit": is there an alternative? BMJ 2000;320:951.

4 Coats A JS, Clark AL, Piepoli M, et al Symptoms and quality of heart failure: The muscle hypothesis Heart 1994;72;S36.

5 Hlatky MA Evaluation of chest pain in the emergency department N Engl J Med 1997;337:1687.

6 Manning HL and Schwartzstein RM Pathophysiology of dyspnoea N Engl J Med 1995;333:1547.

7 Pickett CC, Zimetbaum PJ Palpitations: A proper evaluation and approach to effective medical therapy Curr Cardiol Rep 2005;7:362.

8 Piepoli M, Clark AL, Volterrani M, et al Contribution of muscle afferents to the hemodynamic, autonomic, and ventilatory responses to exercise in patients with chronic heart failure: Effects of physical training Circulation 1996;93:940.

9 Swap CJ, Nagurney JT Value and limitations of chest pain history in the evaluation

of patients with suspected acute coronary syndromes JAMA 2005;294:2623.

10 Wang CS, FitzGerald JM, Schulzer M, et al Does this dyspnoeic patient in the emergency department have congestive heart failure? JAMA 2005;294(15):1944.

11 Weber BE, Kapoor WN Evaluation and outcomes of patients with palpitations.

Am J Med 1996;100:138.

12 Zimetbaum P, Josephson ME Evaluation of patients with palpitation N Engl J Med 1998;338:1369.