Section I INTR INTRODUCTIONODUCTION

Chapter 1The History and Physical Examination . . . . . . . . . 2

Chapter 2Coronary Atherosclerosis . . . . . . . . . . . . . . . . . . . 18

Chapter 3Electrocardiography . . . . . . . . . . . . . . . . . . . . . . . 29

Chapter 4Noninvasive Cardiac Imaging . . . . . . . . . . . . . . . 42

Chapter 5Diagnostic Coronary Angiography . . . . . . . . . . . 53

Chapter 6Use of Diagnostic Testing . . . . . . . . . . . . . . . . . . 64

Section IINTRINTRODUCTIONODUCTION

THE CONCEPT OF PRIORPROBABILITY

The history and physical examination shouldenable the clinician to establish the prior proba-bility of heart disease: that is, the likelihood thatthe symptoms reported by the patient result fromheart disease. A reasonable goal is to establish apatient’s risk of heart disease as “low,” “interme-diate,” or “high.” One demonstration of this prin-ciple in clinical medicine is the assessment ofpatients with chest pain, in which the power ofexercise stress testing to accurately diagnosecoronary heart disease (CHD) depends on theprior probability of disease. In patients with verylow risk of CHD based on clinical findings, exer-cise stress testing resulted in a large number offalse-positive test results. Because 15% or less ofexercise stress tests produce positive results inindividuals without CHD, use of this test in a low-risk population can result in an adverse ratio offalse-positive:true-positive test results and unnec-essary cardiac catheterizations. Conversely, inpatients with a very high risk of CHD based onclinical findings, exercise stress testing can resultin false-negative test results—an equally undesir-able outcome because patients with significantcoronary artery disease (CAD) and their physi-cians may be falsely reassured that no furtherevaluation or treatment is necessary.

INTRODUCTION

Emphasis is increasing on quantifying priorprobability to an even greater degree using vari-ous mathematical models. This is a usefulapproach in teaching and may be clinically fea-sible in some diseases. However, for the majori-ty of patients with suspected heart disease, cat-egorizing risk as low, intermediate, and high isappropriate, reproducible, and feasible in a busyclinical practice. Therefore, obtaining the historyand physical examination represents a key stepbefore any testing, to minimize use of inappro-priate diagnostic procedures.

THE HISTORYA wealth of information is available to clini-

cians who perform a careful assessment of thepatient’s history. Key components are assess-ment of the chief complaint; careful questioningfor related, often subtle, symptoms that may fur-ther define the chief complaint; and determina-tion of other factors that help categorize the like-lihood of disease. Major symptoms of heartpatients include chest discomfort, dyspnea, pal-pitations, and syncope or presyncope.

Chest DiscomfortDetermining whether chest discomfort results

from a cardiac cause is often a challenge. Themost common cause of chest discomfort is

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The ability to determine whether disease is present or absent—and how that patient should be treated—is the ultimate goal for clinicians evaluating patients with suspected heart disease. Despite the num-ber of diagnostic tests available, never has the importance of a careful history and physical examina-tion been greater. Selection of the most appropriate test and therapeutic approach for each patientcan only result from establishing the prior probability of disease, an assessment based on a skillfullyperformed history and physical examination. Opportunities for error in this judgment are abundant.Screening patients for coronary risk using a broad and unfocused panel of laboratory and noninva-sive tests instead of a history and physical examination is inappropriate. While entire texts have beenwritten on cardiac history and physical examination, this chapter specifically focuses on features ofthe cardiac history and the cardiovascular physical examination that help discern the presence orabsence of heart disease.

Marschall S. Runge and E. Magnus Ohman

Chapter 1

The History and PhysicalExamination

INTRODUCTION

THE HISTORY AND PHYSICAL EXAMINATION

myocardial ischemia, which produces anginapectoris. Many causes of angina exist, and thedifferential diagnosis for chest discomfort isextensive (Table 1-1). Angina that is repro-ducible and constant in frequency and severityis often referred to as stable angina. For the pur-poses of this chapter, stable angina is a condi-tion that occurs when CAD is present and coro-nary blood flow cannot be increased toaccommodate for increased myocardial de-mand. However, as discussed in chapters 7through 9, there are many causes of myocardialischemia, including fixed coronary arterystenoses and endothelial dysfunction, whichleads to reduced vasodilatory capacity.

A description of chest discomfort can helpestablish whether the pain is angina or of anotherorigin. First, a description of the quality and loca-tion of the discomfort is essential (Fig. 1-1). Chestdiscomfort because of myocardial ischemia maybe described as pain, a tightness, a heaviness, orsimply an uncomfortable and difficult-to-describefeeling. The discomfort can be localized to themid chest or epigastric area or may be charac-terized as pain in related areas, including the leftarm, both arms, the left jaw, or the back. Theradiation of chest discomfort to any of theseareas increases the likelihood of the discomfortbeing angina. Second, the duration of the dis-comfort is important because chest discomfortdue to cardiac causes generally lasts minutes.Therefore, pain of very short duration (“sec-onds” or “moments”), regardless of how typicalit may be of angina, is less likely to be of cardiacorigin. Likewise, pain that lasts for hours, onmany occasions, in the absence of objective evi-dence of myocardial infarction (MI), is not likelyto be of coronary origin. Third, the presence ofaccompanying symptoms should be consid-ered. Chest discomfort may be accompanied byother symptoms (including dyspnea, diaphore-sis, or nausea), any of which increase the likeli-hood that the pain is cardiac in origin. However,the presence of accompanying symptoms is notneeded to define the discomfort as angina. Inaddition, factors that precipitate or relieve thediscomfort should be evaluated. Angina typical-ly occurs during physical exertion, during emo-tional stress, or in other circumstances ofincreased myocardial oxygen demand. When

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Table 1-1 Differential Diagnosis of Chest Discomfort

Cardiovascular

Ischemic• Coronary atherosclerosis (angina pectoris)

Stable coronary disease• Unstable coronary syndrome• Aortic stenosis• Hypertrophic cardiomyopathy• Aortic regurgitation• Mitral regurgitation• Severe systemic hypertension• Severe RV/pulmonary hypertension• Severe anemia/hypoxia

Nonischemic• Aortic dissection• Pericarditis• Mitral valve prolapse syndrome: autonomic

dysfunction

Gastrointestinal

• Gastroesophageal reflux disease (GERD)• Esophageal spasm• Esophageal rupture• Hiatal hernia• Cholecystitis

Pulmonary

• Pulmonary embolus• Pneumothorax• Pneumonia• COPD• Pleurisy

Neuromusculoskeletal

• Thoracic outlet syndrome• Degenerative joint disease of the cervical or

thoracic spine• Costochondritis• Herpes zoster

Psychogenic

• Anxiety• Depression• Cardiac psychosis• Self-gain

RV indicates right ventricular.

Pain of Myocardial Ischemia

Chiefly retrosternaland intense

Most commonly radiatesto left shoulder and/orulnar aspect of left armand hand

May also radiate toneck, jaw, teeth, back,abdomen, or right arm

Commondescriptions of pain

Othermanifestationsof myocardialischemia

Viselike Constricting Crushing weight and/or pressure

FearPerspiration

Shortnessof breath Nausea,

vomiting

Weakness, collapse, coma

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Figure 1-1

INTRODUCTION


exercise precipitates chest discomfort, reliefafter cessation of exercise substantiates thediagnosis of angina. Sublingual nitroglycerinalso relieves angina, generally over a period ofminutes. Instant relief or relief after longer peri-ods lessens the likelihood that the chest discom-fort was angina.

Although an exercise history is important inassessing CHD risk, individuals, especially seden-tary ones, may have anginalike symptoms thatare not related to exertion. These include post-prandial and nocturnal angina or angina thatoccurs while the individual is at rest. Asdescribed herein, “rest-induced angina,” or thenew onset of angina, connotes a different patho-physiology than effort-induced angina. Anginacan also occur in persons with fixed CAD andincreased myocardial oxygen demand due toanemia, hyperthyroidism, or similar conditions(Table 1-2). Angina occurring at rest, or with min-imal exertion, may denote a different pathophys-iology, one involving platelet aggregation andclinically termed “unstable angina” or an “acutecoronary syndrome” (see chapter 8).

Patients with heart disease need not presentwith chest pain at all. Anginal equivalentsinclude dyspnea during exertion, abdominal dis-comfort, fatigue, or decreased exercise toler-ance. Clinicians must be alert to and specificallyask about these symptoms. Often, a patient’sfamily member or spouse notices subtlechanges in endurance in the patient or that theindividual no longer performs functions thatrequire substantial physical effort. Sometimespatients may be unable to exert themselves dueto comorbidities. For instance, the symptoms ofmyocardial ischemia may be absent in patientswith severe peripheral vascular disease whohave limiting claudication. One should also beattuned to subtle or absent symptoms in individ-uals with diabetes mellitus (including type I andtype II diabetes), a “coronary risk equivalent” asdefined by the Framingham Risk Calculator.

When considering the likelihood that CHDaccounts for a patient presenting with chest dis-comfort or any of the aforementioned variants,assessment of the cardiac risk factor profile isimportant. The Framingham Study first codifiedthe concept of cardiac risk factors. Although cli-nicians had long thought these were important

factors, their quantification has become increas-ingly important. Cardiac risk factors determinedby the Framingham Study include a history ofcigarette smoking, diabetes mellitus, hyperten-sion, or hypercholesterolemia; a family historyof CHD (including MI, sudden cardiac death,and first-degree relatives having undergonecoronary revascularization); age; and sex (male).Although an attempt has been made to rankthese risk factors, all are important, with a histo-ry of diabetes mellitus being perhaps the singlemost important factor. Subsequently, a muchlonger list of potential predictors of cardiac riskhas been made (Table 1-3). An excellent, easy touse model for predicting risk is the FraminghamRisk Calculator, as described in the Adult Treat-ment Panel III (ATP III) guidelines.

Symptoms suggestive of vascular diseaserequire special attention. Peripheral vascular dis-ease may mask CHD because the individualmay not be able to exercise sufficiently to pro-voke angina. A history of stroke, transientischemic attack, or atheroembolism in any vas-cular distribution is usually evidence of signifi-cant vascular disease. Sexual dysfunction in menis not an uncommon presentation of peripheralvascular disease. Raynaud’s-type symptomsshould also be elicited, since the presence ofsuch symptoms is suggestive of abnormal vas-cular tone and function, and increases the riskthat coronary heart disease is present.

Determining whether the patient has stable orunstable angina is as important as making thediagnosis of angina. Stable angina is important

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Table 1-2Conditions That Cause IncreasedMyocardial Oxygen Demand

• Hyperthyroidism• Tachycardia of various etiologies• Hypertension• Pulmonary embolism• Pregnancy• Psychogenic • Central nervous system stimulants• Exercise• Psychological stress• Fever

to evaluate and treat, but does not necessitateemergent intervention. The diagnosis of unsta-ble angina, or acute coronary syndrome, carriesa significant risk of MI or death in the immediatefuture. The type of symptoms reported bypatients with stable and unstable angina differlittle, and the risk factors for both are identical.Indeed, the severity of symptoms is not neces-sarily greater in patients with unstable angina,just as a lack of chest discomfort does not ruleout significant CHD. The important distinctionbetween stable and unstable coronary syndromesrests in whether the onset is new or recent and/orprogressive. The initial presentation of angina is,by definition, unstable angina. Although for a highpercentage of individuals this may merely repre-sent the first recognizable episode of angina. Forthose with unstable angina, the risk of MI in thenear future is markedly increased. Likewise, whenthe patient experiences angina in response todecreased levels of exertion or when exertionalangina has begun to occur at rest, these urgent cir-cumstances require immediate therapy. The treat-ment of stable angina and acute coronary syn-dromes is discussed in chapters 7 and 8. TheCanadian Cardiovascular Society Functional Clas-sification of Angina Pectoris is a useful guide foreveryday patient assessment (Table 1-4). Catego-rizing patients according to their class of symp-toms is rapid and precise and can be used in fol-low-up. Class IV describes the typical patient with

INTRODUCTION


acute coronary syndrome.Finally, it is important to distinguish those

patients who have noncoronary causes of chestdiscomfort from those with CHD. Patients withgastroesophageal reflux disease (GERD) oftenpresent with symptoms that are impossible to dis-tinguish from angina. In numerous studies, GERDis the most common diagnosis in patients whoundergo diagnostic testing for angina and arefound not to have CHD. The characteristics of thepain can be identical. Because exercise canincrease intraabdominal pressure, GERD may beexacerbated with exercise, especially after meals.Symptoms from GERD can also be relieved withuse of sublingual nitroglycerin. GERD can alsoresult in early morning awakening (as can unsta-ble angina) but tends to awaken individuals 2 to 4hours after going to sleep, rather than 1 to 2 hoursbefore arising, as is the case with unstable angina.Other causes (Table 1-1) of anginalike pain can bebenign, or suggestive of other high-risk syn-dromes, such as aortic dissection. Many of these“coronary mimics” can be ruled out by patient his-tory, but others, such as valvular aortic stenosis,can be confirmed or excluded by physical exami-

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Table 1-3Cardiac Risk Factors

• Diabetes• Smoking• High BP• High cholesterol• Hyperlipidemia• Sedentary lifestyle• High-fat diet• Stress• “Metabolic syndrome” • Family history of CHD (including history of MI,

sudden cardiac death, and first-degree relativeswho underwent coronary revascularization)

• Age • Male sex

CHD indicates coronary heart disease; MI, myocardial infarction.

Table 1-4Canadian Cardiovascular Society Classification of Angina Pectoris

I Ordinary physical activity, for example, walking orclimbing stairs, does not cause angina; anginaoccurs with strenuous, rapid, or prolongedexertion at work or recreation.

II Slight limitation of ordinary activity; for example,angina occurs when walking or stair climbing aftermeals, in cold, in wind, under emotional stress oronly during the few hours after awakening, whenwalking more than two blocks on the level, or whenclimbing more than one flight of ordinary stairs at anormal pace and during normal conditions.

III Marked limitation of ordinary activity; for example,angina occurs when walking one or two blocks onthe level or when climbing one flight of stairs duringnormal conditions and at a normal pace.

IV Inability to carry on any physical activity withoutdiscomfort; angina syndrome may be present at rest.comfort; angina syndrome may be present at rest.

From Campeau L. Grading. F angina pectoris. Circulation1976;54:522.

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nation. The goal of taking the history is to alert theclinician to entities that can be confirmed orexcluded by physical examination, or that neces-sitate further diagnostic testing.

Dyspnea, Edema, and AscitesDyspnea can accompany angina pectoris or it

can be an anginal equivalent. Dyspnea can alsoreflect congestive heart failure (CHF) or occurbecause of noncardiac causes. The key tounderstanding the etiology of dyspnea is a clearpatient history, which is then confirmed by a tar-geted physical examination.

Dyspnea during exertion that quickly resolvesat rest or with use of nitroglycerin may be aresult of myocardial ischemia. It is important toestablish the amount of activity necessary toprovoke dyspnea, the reproducibility of thesesymptoms, and the duration of recovery. As withangina, dyspnea as an anginal equivalent or anaccompanying symptom tends to occur at agiven workload or stress level—dyspnea occur-ring one day at low levels of exertion, but notprompted by vigorous exertion on another dayis less likely to be an anginal equivalent.

In patients with CHF, dyspnea reflects left ven-tricular (LV) dysfunction (Fig. 1-2). Althoughmost commonly LV systolic dysfunction is thecause of the dyspnea, dyspnea also occurs inindividuals with preserved LV systolic functionand severe diastolic dysfunction. These two enti-ties present differently, however, and physicalexamination can distinguish them. With LV sys-tolic dysfunction, dyspnea tends to graduallyworsen, and its exacerbation is more variablethan that of exertional dyspnea resulting frommyocardial ischemia, although both are due tofluctuations in pulmonary arterial volume andleft atrial filling pressures. Typically, patients withLV systolic dysfunction do not recover immedi-ately after exercise cessation or use of sublin-gual nitroglycerin, and the dyspnea may lingerfor longer periods. Orthopnea, the occurrenceof dyspnea when recumbent, or paroxysmalnocturnal edema provides further support for apresumptive diagnosis of LV systolic dysfunc-tion. Patients with LV diastolic dysfunction tendto present abruptly with severe dyspnea thatresolves more rapidly in response to diuretictherapy than does dyspnea caused by LV sys-

tolic dysfunction. The New York Heart Associa-tion (NYHA) Classification for CHF (Table 1-5) isextremely useful in following patients with CHFand provides a simple and rapid means for lon-gitudinal assessment. The NYHA Classificationalso correlates well with prognosis. Patients whoare NYHA Class I have a low risk of death or hos-pital admission within the following year. In con-trast, the annual mortality rate of those withNYHA Class IV symptoms exceeds 30%.

As with chest discomfort, the differential diag-nosis of dyspnea is broad, encompassing manycardiac and noncardiac causes (Table 1-6). Con-genital heart disease, with or without pulmonaryhypertension, can cause exertional dyspnea.Patients with significant intra- or extracardiacshunts and irreversible pulmonary hypertension(Eisenmenger’s syndrome) are dyspneic duringminimal exertion and often at rest. It is also possi-ble to have dyspnea because of acquired valvularheart disease, usually from aortic or mitral valvestenosis or regurgitation. All of these causesshould be easily distinguished from CHD or CHFby physical examination. Primary pulmonarycauses of dyspnea must be considered, withCOPD and reactive airways disease (asthma)being most common. Again, a careful history forthe risk factors (e.g., cigarette smoking, industrial

Table 1-5New York Heart Association Classification of CHF

Class I Patients with no limitation of activities;they have no symptoms after ordinaryactivities.

Class II Patients with slight, mild limitation ofactivity; they are comfortable at rest orduring mild exertion.

Class III Patients with marked limitation of activity;they are comfortable only at rest.

Class IV Patients who should be at complete rest,confined to a bed or a chair; any physicalactivity brings on discomfort andsymptoms occur at rest.

From the Criteria Committee of the New York Heart Association. Dis-eases of the Heart and Blood Vessels: Nomenclature and Criteria forDiagnosis. Boston. Brown; 1964.

Cyanosis of lips and nail beds may be present if the patient is hypoxic.

Chest auscultation reveals bilateral rales and pleural effusions (when CHF is chronic).

Cardiac auscultation for third heart sounds (S3) and murmurs should be performed in standard positions, including that with the patient sitting forward.

Patients with left-sided CHF may be uncomfortable lying down.

S3S2Systolic murmur

S1

Physical ExaminationLeft-Sided Cardiac Heart Failure

Figure 1-2

exposure, allergens) associated with these enti-ties and an accurate physical examinationshould distinguish primary pulmonary causesfrom dyspnea due to CHD or CHF.

Peripheral edema and ascites are physicalexamination findings consistent with right ven-tricular (RV) failure. These findings are includedin the history because they may be part of thepresentation. Although patients often commenton peripheral edema, with careful questioning,they may also identify increasing abdominalgirth consistent with ascites. Important ques-

INTRODUCTION


tions on lower extremity edema include deter-mination of whether the edema is symmetric(unilateral edema suggests alternate diagnoses)and whether the edema improves or resolveswith elevation of the lower extremities. The find-ing of “no resolution overnight” argues againstRV failure as an etiology. In addition, for periph-eral edema and ascites, it is important to askquestions directed toward determining the pres-ence of anemia, hypoproteinemia, or othercauses. The differential diagnosis of edema isbroad and beyond the scope of this chapter.

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9

Palpitations and SyncopeIt is normal to be aware of the sensation of the

heart beating, particularly during or immediatelyafter exertion or emotional stress. Palpitationsrefer to an increased awareness of the heartbeating. Patients use many different descriptions,including a “pounding or racing of the heart,” thefeeling that their heart is “jumping” or “thump-ing” in their chest, the feeling that the heart “skipsbeats” or “races,” or countless other descriptions.A history showing that palpitations have begunto occur during or immediately after exertion,and not at other times, raises the concern that

these sensations reflect ventricular ectopy asso-ciated with myocardial ischemia. It is more diffi-cult to assess the significance of palpitationsoccurring at other times. Supraventricular andventricular ectopy may occur at any time andmay be benign or morbid. As discussed in chap-ters 20, 22, and 23, ventricular ectopy is worri-some in patients with a history of MI or car-diomyopathy. Lacking this information, cliniciansshould be most concerned if lightheadedness orpresyncope accompanies palpitations.

Syncope generally indicates an increased riskfor sudden cardiac death and is usually a result ofcardiovascular disease and arrhythmias. If a syn-copal episode is a presenting complaint, thepatient should be admitted for further assess-ment. In approximately 85% of patients, thecause of syncope is cardiovascular. In patientswith syncope, one must assess for CHD, car-diomyopathy, and congenital or valvular heartdisease. In addition, neurocardiogenic causesrepresent a relatively common and importantpossible etiology for syncope. Table 1-7 showsthe differential diagnosis for syncope. It is criticalto determine whether syncope really occurred. Awitness to the episode and documentation of anintervening period are very helpful. In addition,with true syncope, injuries related to the suddenloss of consciousness are common. However, anindividual who reports recurrent syncope (wit-nessed or unwitnessed) but has never injuredhim- or herself may not be experiencing syncope.This is not to lessen the concern that a seriousunderlying medical condition exists, but rather toreaffirm that the symptoms fall short of syncope,with its need for immediate evaluation.

THE PHYSICAL EXAMINATIONThere are several advantages to obtaining

patient history before the physical examination.First, the information gained in the history directsthe clinician to pay special attention to aspects ofthe physical examination. For instance, a historyconsistent with CHD necessitates careful inspec-tion for signs of vascular disease; a history sug-gestive of CHF should make the clinician pay par-ticular attention to the presence of a third heartsound. Second, the history allows the clinician toestablish a rapport with patients, to assurepatients that he or she is interested in their well-

Table 1-6 Differential Diagnosis of Dyspnea

Pulmonary

• Reactive airways disease (asthma)• COPD• Emphysema• Pulmonary edema• Pulmonary hypertension• Lung transplant rejection• Infection • Interstitial lung disease• Pleural disease• Pulmonary embolism• Respiratory muscle failure• Exercise intolerance

Cardiac

• Ischemic heart disease/angina pectoris• Right-sided heart failure• Aortic stenosis or regurgitation• Arrhythmias• Dilated cardiomyopathy• Hypertrophic cardiomyopathy• CHF• Mitral regurgitation or stenosis• Mediastinal abnormalities• Pericardial tuberculosis• Transposition of the great arteries

Other

• Blood transfusion reaction• Measles

CHF indicates congestive heart failure.

being, and that the physical examination is animportant part of a complete evaluation. In thislight, the therapeutic value of the physicalexamination to the patient should not beunderestimated. In spite of the emphasis ontechnology today, even the most sophisticatedpatients expect to be examined, to have theirhearts listened to, and to be told whether wor-risome findings exist or the examination resultswere normal.

General Inspection and Vital SignsMuch useful information can be gained by an

initial “head-to-toe” inspection and assessmentof vital signs. For instance, truncal obesity maysignal the presence of type II diabetes or themetabolic syndrome. Cyanosis of the lips andnail beds may indicate underlying cyanotic heartdisease. Hairless, dry-skinned lower extremitiesor distal ulceration may indicate peripheral vas-cular disease. Other findings are more specific

INTRODUCTION


(Fig. 1-3). Abnormalities of the digits are found inatrial septal defect; typical findings of Down’ssyndrome indicate an increased incidence ofventricular septal defect or more complex con-genital heart disease; hyperextensible skin andlax joints are suggestive of Ehlers-Danlos syn-drome; and tall individuals with arachnodactyly,lax joints, pectus excavatum, and an increasedarm–height ratio may have Marfan’s syndrome.These represent some of the more commonmorphologic phenotypes in individuals withheart disease. Vital signs can also be helpful.Although normal vital signs do not rule outCHD, marked hypertension may signal cardiacrisk, whereas tachycardia, tachypnea, and/orhypotension at rest suggest CHF.

Important Componentsof the Cardiovascular Examination

The clinician should focus efforts on thosesites that offer a window into the heart and vas-culature. Palpation and careful inspection of theskin for secondary changes because of vasculardisease or diabetes is important. Lips, nail beds,and fingertips should be examined for cyanosis(including clubbing of the fingernails) and, whenindicated, for signs of embolism. Examination ofthe retina using an ophthalmoscope can revealevidence of longstanding hypertension, dia-betes, or atheroembolism, denoting underlyingvascular disease. Careful examination of thechest, including auscultation, can help to differ-entiate causes of dyspnea. The presence ofdependent rales is consistent with left-sidedheart failure. Pleural effusions can result fromlongstanding LV dysfunction or noncardiaccauses, and can be present with predominantlyright-sided heart failure, representing transuda-tion of ascites into the pleural space. Hyperex-pansion with or without wheezing suggests aprimary pulmonary cause of dyspnea, such asCOPD or reactive airways disease. The pres-ence of wheezing rather than rales does not ruleout left-sided heart failure. It is not uncommonto hear wheezing with left-sided CHF. Mostcommonly, wheezing from left-sided CHF is pri-marily expiratory. Inspiratory and expiratorywheezing, particularly with a prolonged inspira-tory:expiratory ratio is more likely to be causedby intrinsic lung disease.

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Table 1-7 Causes of Syncope

Cardiogenic

• MechanicalOutflow tract obstructionPulmonary hypertensionCongenital heart diseaseMyocardial disease—low output states

• ElectricalBradyarrhythmiasTachyarrhythmias

• NeurocardiogenicVasovagal (vasodepression)Orthostatic hypotension

Other

• Peripheral neuropathy• Medications• Primary autonomic insufficiency• Intravascular volume depletion• Reflex• Cough• Micturition• Acute pain states• Carotid sinus hypersensitivity

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“Simian“ crease on the palm

Hyperextensibility of thumbs and fingers

Easy splitting of the skin (so-called cigarette paper scars) over bony prominences, hyperelastic auricles

Hyperextensibility of elbows

Hyperelasticity of skin

Upper body segm

entLow

er body segment

Walker-Murdoch wrist sign. Because of long fingers and thin forearm, thumb and little finger overlap when patient grasps wrist.

Typical facies seen in Down’s syndrome

Upward slanting eyes contrasting with ethnic group

Small mouth with protruding tongue

Wide gap between the first and second toes

Ehlers-Danlos syndrome

Marfan’s syndrome

Down’s syndrome

Physical Examination: General InspectionFigure 1-3

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Careful auscultation of the abdomen can reveal bruits from vessels such as aorta and renal arteries.

Diminished or absent peripheral pulses indicate peripheral vascular disease.

Dilatation of the abdominal portion of the aorta can be recognized by palpation.

Cardiac apical impulse(palpation of the precordium)

S1 S2 S1 S2 S1 S2

Normal Hyperdynamic impulse (hypertrophic cardiomyopathy)

Diffuse and sustained (left ventricular dysfunction)

Normal

Phono

Carotidpulse

ECG ECG

Phono

Carotidpulse

ECG

Phono

Carotidpulse

ECG

S1 S2 S2S1

S1 S2

S1 S2 Diastolic murmur

S1 S2

S1 S2SM S1 S2SM

S3S3

a

a a

c

xv

v v

y

y y

h

SM

S1 S2a

v

yc

x

Hypertrophic cardiomyopathy(Bisferiens pulse)

Phono

Jugularpulse

Normal

ECG

Phono

Jugularpulse

Tricuspid regurgitation

ECG

Phono

Jugularpulse

Pulmonary hypertensionsecondary to mitral stenosis

Aortic regurgitation(Corrigan’s pulse)

Important Components of Cardiac Examination

Examples of carotid pulses and the entities with which they are associated

Examples of venous pulses and the entities with which they are associated

Figure 1-4

INTRODUCTION


The vascular examination is an important com-ponent of a complete evaluation. The quality ofthe pulses, in particular the carotid and thefemoral pulses, can identify underlying disease(Fig. 1-4). Diminished or absent distal pulsesindicate peripheral vascular disease. The exam-iner should also auscultate for bruits over bothcarotids, over the femoral arteries, and in theabdomen. Abdominal auscultation should beperformed, carefully listening for aortic or renalbruits, in the mid abdominal area before abdom-inal palpation, which can stimulate increasedbowel sounds. Distinguishing bruits from trans-mitted murmurs in the carotid and abdominalareas can be challenging. When this is a con-cern, carefully marching out from the heartusing the stethoscope can be helpful. If theintensity of the murmur or bruit continuallydiminishes farther from the heart, it becomesmore likely that this sound originates from theheart, rather than from a stenosis in the periph-eral vasculature. Much information is availableabout the peripheral vascular examination, butby following the simple steps outlined herein,the examiner can gather the majority of theaccessible clinical information.

Examination of the jugular venous pulsationsis a commonly forgotten step. Jugular venouspressure, which correlates with right atrial pres-sure and RV diastolic pressure, should be esti-mated initially with the patient lying with theupper trunk elevated 30°. In this position, at nor-mal jugular venous pressure, no pulsations arevisible. This correlates roughly to a jugularvenous pressure less than 6 to 10 cm. Theabsence of jugular vein pulsations with thepatient in this position can be confirmed byoccluding venous return by placing a fingertipparallel to the clavicle in the area of the stern-ocleidomastoid muscle. The internal and exter-nal jugular veins should partially fill. Althoughwith normal jugular venous pressure examina-tion of the waveforms is less important, the headof the examination table can be lowered untilthe jugular venous pulsations are evident. Whenthe jugular venous pulsations are visible at 30°,the examiner should note the waveforms. It ispossible to observe and time the a and v wavesby simultaneously timing the cardiac apicalimpulse or the carotid impulse on the contralat-

eral side. An exaggerated a wave is consistentwith increased atrial filling pressures because oftricuspid valve stenosis or increased RV diastolicpressure. A large v wave generally indicates tri-cuspid valve regurgitation, a finding easily con-firmed by auscultation.

Finally, before cardiac auscultation, it is impor-tant to palpate the precordium. This is the easi-est way to identify dextrocardia. Characteristicsof the cardiac impulse can also yield importantclues about underlying disease. Palpation of theprecordium is best performed from the patient’sright side with the patient lying flat. The cardiacapical impulse is normally located in the fifthintercostal space along the midclavicular line.Most examiners use the fingertips to palpate theapical impulse. It is often possible to palpatemotion corresponding to a third or fourth heartsound. Use of the fingertips offers fine detail onthe size and character of the apical impulse. Adiffuse and sustained apical impulse is consis-tent with LV systolic dysfunction. Patients withhypertrophic cardiomyopathy, in contrast, oftenhave a hyperdynamic apical impulse. Thrills, pal-pable vibrations from loud murmurs or bruits,can also be palpated.

The RV impulse, if identifiable, is located alongthe left sternal border. Many clinicians prefer topalpate the RV impulse with the base of thehand, lifting the fingertips off the chest wall. InRV hypertrophy a sustained impulse can be pal-pated and the fingertips then can be placed atthe LV impulse to confirm that the two are dis-tinct. In patients with a sustained RV impulse,the examiner should again look for prominent aand v waves in the jugular venous pulsations.

Cardiac AuscultationHearing and accurately describing heart

sounds is arguably the most difficult part of thephysical examination. For this reason andbecause of the commonplace use of echocar-diography, many clinicians perform a cursoryexamination. The strongest arguments for per-forming cardiac auscultation carefully are todetermine whether further diagnostic testing isnecessary; to correlate findings of echocardiog-raphy with the clinical examination so that, inlongitudinal follow-up, the clinician can deter-mine progression of disease without repeating

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echocardiography at each visit; and because themore a clinician makes these correlations, thebetter his or her skills in auscultation willbecome and the better his or her patients will beserved. It should also be noted that, with normalgeneral cardiac physical examination results, theabsence of abnormal heart sounds, and a nor-mal electrocardiogram, the use of echocardiog-raphy for evaluation of valvular or congenitalheart disease is not indicated. Furthermore, ifthere are no symptoms of CHF or evidence ofhemodynamic compromise, echocardiographyis not indicated for assessment of LV function.Practice guidelines from cardiologists and gen-eralists agree on this point, as do third-partyinsurers. It is neither appropriate nor feasible toreplace a careful cardiovascular examinationusing auscultation with more expensive testing.

However, echocardiography has revolution-ized the quantitative assessment of cardiovascu-lar hemodynamics: that is, the severity of valvu-lar and congenital heart disease. No longer is itnecessary for the clinician to make an absolutejudgment on whether invasive assessment (car-diac catheterization) is needed to further definehemodynamic status or whether the condition istoo advanced to allow surgical intervention.Therefore, cardiac auscultation is an extremelyimportant screening technique for significanthemodynamic abnormalities and an importantmeans by which the physician can longitudinal-ly follow patients with known disease.

There are several keys to excellence in auscul-tation. Foremost is the ability to perform a com-plete general cardiac physical examination, asdescribed previously. The findings help the exam-iner focus on certain auscultatory features. Sec-ond, it is important to use a high-quality stetho-scope. Largely dictated by individual preference,clinicians should select a stethoscope that hasbell and diaphragm capacity both (for optimalappreciation of low- and high-frequency sounds,respectively) and that fits the ears comfortablyand is well insulated so that external sounds areminimized. Third, it is important to perform aus-cultation in a quiet environment. Particularly asskills in auscultation are developing, trying tohone these in the hall of a busy emergency roomor on rounds while others are speaking is timespent poorly. Additionally, taking the time to

return to see a patient with interesting findingsdetected during auscultation, and repetition, arekeys to becoming competent in auscultation.

The patient should be examined while he orshe is in several positions: while recumbent,while in the left lateral decubitus position, andwhile sitting forward. Every patient is differentand, using all three positions, the examiner canoptimize the chance that soft heart sounds canbe heard. Likewise, it is important to listen care-fully at the standard four positions on the chestwall (Fig. 1-5), as well as over the apical impulseand RV impulse (if present). It is also best to iso-late different parts of the examination in time.Regardless of the intensity of various sounds, itis best to always perform the examination in thesame order so that the presence of a loud mur-mur, for instance, does not result in failure to lis-ten to the other heart sounds.

Listen for S1 (the first heart sound) first. As withjugular venous pulsations, the heart sounds canbe timed by simultaneously palpating the car-diac apical impulse or the carotid upstroke. Eventhe most experienced clinician occasionallyneeds to time the heart sounds. Is a single soundpresent, or is the first heart sound split? Is asound heard before S1, indicating an S4? Next,listen to the second heart sound. Normally thefirst component (A2, the aortic valve closingsound) is louder than the second component(P2, the pulmonic valve closing sound). A loudersecond component may indicate increased pul-monary pressure. A more subtle finding is areversal of A2 and P2 timing that occurs with leftbundle branch block and in some other circum-stances. Additionally, it is important to assesswhether A2 and P2 are normally split or whetherthey are widely split with no respiratory varia-tion—a finding suggestive of an atrial septaldefect. The examiner should then listen careful-ly for a third heart sound. An S3 is often bestheard over the tricuspid or mitral areas and is alow-frequency sound. It is heard best with thebell and is often not heard with the diaphragm.

After characterizing these heart sounds, it istime to listen carefully for murmurs. Murmursare classified according to their intensity, theirduration, their location, and their auscultatorycharacteristics: crescendo, decrescendo, blow-ing, among others. It is also important to note

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Innocent murmur Innocent murmur with widely split S2

Systolic murmur from increased pulmonic flow followed by fixed, widely split S2 (Atrial septal defect)

Systolic murmur followed by widely split S2

Murmur and ejection click (pulmonary hypertension)

Holosystolic murmur (acute mitral regurgitation)

Systolic murmur (chronic mitral regurgitation) with S3 and S4 (dilated cardiomyopathy)

Holosystolic murmur (IVSD or mitral or tricuspid regurgitation)

Late systolic murmur following midsystolic click (mitral prolapse)

Ejection sound followed by a murmur that extends through A2 with widely split S2 and the presence of S4 (moderate pulmonary stenosis)

Continuous murmur (patent ductus arteriosus)

Diastolic murmur (aortic or pulmonary regurgitation)

Long diastolic murmur following opening snap (mitral stenosis)

EC

P2A2S1

S4

S2S1S1 S1

S2 S2 OS

S1

S1

S1

S1 S1S2 S2

S2

S2 P2

Click

A2S3S4

EC

S1 S1 S1 S1S2 A2

A2 A2P2 P2 P2ES

Aortic area

Mitral area

12

3

4

5

6

7

Tricuspid area

Tricuspid area

Mitral valve

Aortic valve

Pulmonic valve

Valves

Pulmonic area

Cardiac AuscultationPrecordial areas of auscultation

Diagrams of murmurs

Figure 1-5

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Vascular resistance and venous return are altered by maneuvers used to modify auscultatory findings of many different etiologies. Mitral valve prolapse is used here to exemplify the use of some of these maneuvers.

Ejection clicks, such as those of a stenotic aortic valve, can be differentiated from nonejection clicks, such as the click commonly auscultated in mitral valve prolapse. The "mobility" of the click as response to changes in the left ventricular volume provoked by the maneuvers points to a nonejection click, in this case of mitral valve prolapse.

S1 Midsystolic click

S2

Systolic murmur

SquattingIncreases peripheral vascular resistance and ventricular volume

StandingDecreases ventricular volume

Valsalva’sIn the second stage of Valsalva’s maneuver diminishment of venous return and decrease of ventricular volume occurs. The click is less intense and moves near S1. The murmur is less audible as well.

S2

Isometric exerciseHandgrip also increases peripheral vascular resistance and ventricular volume, retarding the midsystolic click that moves near S2.

S2S1 Systolic click near S2

S2S1 Systolic click near S2

Accentuated systolic murmur

S1 Click Murmur

S2S1 Click

Murmur

ManeuversFigure 1-6

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the site where the murmur is loudest andwhether the murmur radiates to another area ofthe precordium or to the carotids. All of thesefeatures contribute to determining the origin ofthe murmur, the likelihood that it represents anacute or chronic process, and how it affects thediagnostic and therapeutic approaches. Mostimportantly, it is necessary for clinicians to judgewhether a murmur represents cardiac disease oris innocent. Innocent murmurs, also termed“flow murmurs,” are common in children. Morethan 60% of children have innocent murmurs.Innocent murmurs become less common inadults; however, an innocent murmur can still befound into the fourth decade of life. Alterations inhemodynamics induced by pregnancy, anemia,fever, hyperthyroidism, or any state of increasedcardiac output can produce an innocent mur-mur. These murmurs are generally midsystolicand heard over the tricuspid or pulmonic areasand do not radiate extensively. They are oftenloudest in thin individuals. Innocent murmurs donot cause alterations in the carotid pulse and donot coexist with abnormal cardiac impulses orwith other abnormalities, such as extra heartsounds (S3 and S4), in adults. In elderly individu-als, a common finding is a systolic murmur thatshares auditory characteristics with the murmurof aortic stenosis; however, carotid upstrokes arenormal. This finding, aortic sclerosis, may neces-sitate confirmation by echocardiography. It rep-resents sclerosis of the aortic leaflets, but withoutsignificant hemodynamic consequence.

The characteristics of the most common andhemodynamically important murmurs are shownin Figure 1-5. As noted previously, the murmur isdefined not only by its auditory characteristics,but also by the company it keeps. Often the keyto excellence in auscultation is being thorough inall aspects of the cardiovascular examination.

ManeuversNo discussion of cardiac auscultation would

be complete without the use of maneuvers toaccentuate auscultatory findings. As shown inFigure 1-6, patient positioning can alter periph-eral vascular resistance or venous return, accen-tuating murmurs that are modulated by thesechanges. Murmurs associated with fixed valvu-lar lesions change little with changes in position

or the maneuvers illustrated in Figure 1-6. Thus,these maneuvers are most useful for diagnosingentities in which hemodynamic status affectsmurmurs. The two classic examples are the clickand murmur of mitral valve prolapse, as shownhere, and the aortic outflow murmur of hyper-trophic cardiomyopathy (not shown).

FUTURE DIRECTIONSHandheld echocardiography machines can be

carried on the shoulder and have a small transduc-er that can obtain echocardiographic images ofsufficient quality to quantify murmurs and assessLV dysfunction. Although these portable echocar-diographic machines have advantages and havebeen incorporated in medical school curricula atmany institutions, they have not yet replaced thestethoscope, nor are they likely to do so.

The roles of cardiac history and physical exami-nation have changed. Before the noninvasivetesting of today, astute clinicians were the arbitersof whether invasive diagnostic testing was need-ed, based largely on examination findings alone.Today, it is believed that the role of the clinician isto use physical examination findings to establishthe prior probability of cardiovascular disease,whether CHD, valvular heart disease, or congeni-tal heart disease, thereby determining the needfor further testing. In the continual quest forimproved noninvasive testing, it is likely that aclinician’s skill will continue to evolve as the inter-play between history taking, physical examina-tion, and diagnostic testing further develops.

REFERENCESAmerican College of Cardiology Foundation. Clinical State-

ments/Guidelines. Available at: http://www.acc.org/clini-cal/statements.htm.

American Heart Association. Heart Profilers. Available at:http://www.americanheart.org/presenter.jhtml?identifier=3000416.

Diamond GA, Forrester JS. Analysis of probability as an aidin the clinical diagnosis of coronary–artery disease. N EnglJ Med 1979;300:1350–1358.

European Society of Cardiology. Available at:http://www.escardio.org.

Harvey WP. Cardiac Pearls [videorecording]. Atlanta: EmoryMedical Television Network; 1981.

Hurst JW, Morris DC. Chest Pain. Futura Publishing; 2001.National Heart, Lung and Blood Institute. Third Report of the

Expert Panel on Detection, Evaluation, and Treatment ofHigh Blood Cholesterol in Adults (Adult Treatment PanelIII). Available at: http://www.nhlbi.nih.gov/guidelines/cholesterol/index.htm.

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