CHAPTER 11: THE HISTORY, PHYSICAL EXAMINATION, AND CARDIAC AUSCULTATION

The history and physical examination have always been the cornerstone of the evaluation of the patient with known or suspected cardiovascular disease. In the past five decades, there has been an unprecedented development and implementation of cardiovascular diagnostic modalities, which provide high-resolution, real-time images of cardiac structure and measurements of cardiac function. The new generation of cardiovascular specialists is now relying more and more on the results of these tests to make clinical decisions, with decreasing emphasis on teaching and performing a proper history and physical examination. However, optimal patient care should use cardiovascular testing to confirm and supplement the clinical impression based on the history and examination—not replace it.

The initial interview with the patient is a necessity that has not changed over the decades. A properly taken history not only provides the richest source of clinical information regarding a patient’s illness, but is key to understanding the effect of the illness on the patient and family as well as individual needs and preferences. This knowledge, as well as the compassion and empathy that the physician can extend to the patient and family during this initial interaction, is of great importance not only in the clinical decision making but also in forming a trustful patient-physician relationship. It is important to always listen to patients. There are frequently subtle clues to the diagnosis that may be revealed by careful interrogation, but many times other clues are spontaneously brought forth by patients themselves. Finally, patients now present with multiple medical problems in addition to the cardiovascular problem, and a thorough history will provide insight into any contribution of noncardiac causes to the new onset or exacerbation of symptoms.

With the widespread availability of cardiac imaging, there has been an evolution in the detail and focus of the physical examination. It is no longer necessary to be able to obtain all the necessary information from the examination, because the imaging modalities will provide diagnostic and hemodynamic results with a greater degree of certainty and accuracy than even a master clinician can achieve. For instance, maneuvers performed on a patient with a diastolic rumble to differentiate mitral stenosis from an Austin-Flint murmur are no longer relevant; the question is easily answered from a comprehensive two-dimensional and Doppler echocardiogram. The severity of mitral stenosis is much more accurately obtained from a transmitral Doppler gradient as opposed to the subjective assessment of the A2-opening snap interval on the examination.

However, a well-performed physical examination is necessary to provide an initial clinical impression of the type and severity of cardiac disease as well as its effect on the patient. The subsequent diagnostic studies should then be used to confirm or refute this initial impression, and the final diagnosis can only be made if there is a concordance of the two. No test is 100% reliable, and many results are dependent on the performance of the test and interpretation of the data. The history and examination should be used to determine a “pretest probability” to which the results of the test can be applied.² For instance, a patient with symptoms and physical examination findings consistent with severe aortic stenosis but a low gradient on Doppler echocardiography represents discordant data. The clinician must be aware of the limitations of echocardiography, such as when a Doppler beam is not well aligned with the velocity jet, resulting in underestimation of the severity of stenosis. In this case, the results from the echocardiogram should be questioned, and further testing with either transesophageal echocardiography or cardiac catheterization is required. Alternatively, a patient with a nonischemic cardiomyopathy may have the diagnosis of severe mitral regurgitation due to a large jet of mitral regurgitation on color flow imaging, but a barely audible apical murmur on physical examination will refute this diagnosis.

Several books dedicated to physical examination have been published, and our intent is not to replicate their work. We wish to present an approach to the physical examination of correlating relevant findings on examination with key findings from our newer diagnostic modalities. It is essential to understand the underlying pathophysiology of the cardiac disease to guide optimal patient care. The findings on a well-performed physical examination provide not only diagnostic information but are also a window to normal and abnormal hemodynamics. The components of the examination, when coupled with direct hemodynamic assessment by either Doppler echocardiography or cardiac catheterization, provide the clinician with a tremendous overview of the hemodynamic effect of the disease on the cardiovascular system. When one hears a third heart sound at the bedside in a patient with heart failure, automatically a high E velocity on a transmitral Doppler velocity curve or a rapid filling wave on left ventricular invasive catheterization hemodynamic tracings should be expected. The paradoxical splitting of the second heart sound in a patient with hypertrophic cardiomyopathy should match the marked prolongation of ejection time produced by a pressure overload on the left ventricle from the dynamic obstruction. Only with a multimodality approach combined with clinical observations can correlations between concordant/discordant clinical/imaging findings be made to provide the optimal patient care.³ Our goal in this chapter is to provide a practical, contemporary approach to history taking and physical examination, correlating the findings to hemodynamic and imaging data from echocardiography and cardiac catheterization.

Overview

The clinical history is the cornerstone of the evaluation of patients with cardiovascular disease. However, like any other skill, taking a proper history requires practice and a methodology. Several things should be avoided. First, patients should always to be allowed to speak. Clinicians tend to interrupt their patients only minutes into the interview; this limits the amount of information a patient can provide and compromises the patient-provider relationship. Secondly, open-ended questions should be used initially (“how would you describe your chest pain?” versus “is the pain sharp?”) and then directed questions used afterward to avoid influencing the patient’s response. Thirdly, the examiner must confirm interpretation of the patient’s description of symptoms. For example, angina pectoris due to myocardial ischemia can have multiple descriptions, such as pain, pressure, tightness, ache, burning, shortness of breath, or even an “uncomfortable feeling.” The basic characteristics of each symptom should also be recorded: quality; location; severity; tempo (onset and progression); and aggravating or alleviating factors, including response to medications. Lastly, watch for gestures or body language to provide ancillary data; a classic example is the Levine sign—the clinched fist over the precordium suggesting angina as the cause of the chest pain.

We will briefly review the approach to the cardiac history. However, a comprehensive history should include past medical history, prior surgeries (extremely important in patients with valvular or congenital heart disease), social history (smoking, illicit drugs, and alcohol use), and family history (familial cardiomyopathies, sudden death, aortopathies, and aortic dissection). An important pertinent aspect of a patient’s history should include the status of dental care, especially in patients being considered for intervention using prosthetic valves or material. Finally, it is of great importance to determine patients’ emotional and physical reaction to their cardiac disease and how it is affecting their lives and their family’s lives.

Specific Symptoms

Chest Pain

Assessment of the etiology of chest pain is one of the most difficult tasks in the practice of cardiology. Given the adverse cardiovascular events associated with coronary artery disease, the main concern of a clinician is to rule in or rule out myocardial ischemia as the underlying cause. If details regarding the patient’s pain (or discomfort) are not properly gathered, overtesting is frequently performed (biomarkers, exercise tests, or even coronary angiography) or other equally life-threatening entities might be missed (such as pulmonary embolus or aortic dissection). Not uncommonly, clinicians forego the description of patient symptoms, essentially jumping from the chief complaint (“chest pain”) to the laboratory testing and imaging.

The duration of the symptoms is important in patients with chest pain. Angina typically lasts less than 5 minutes and will improve after exertion is discontinued or nitroglycerin taken; symptoms should not last more than 30 minutes unless coronary thrombosis with myocardial infarction has occurred. The chest pain in these patients with stable exertional angina occurs in response to an increase in myocardial oxygen demand; so it is precipitated by exertion, emotion, cold temperature and is worse after heavy meals. Rarely, patients will report that angina improves with continued exercise (ie, walk-through angina). Chest pain lasting hours and days without signs of myocardial injury/ischemia (troponin elevation or electrographic changes) significantly argues against angina. There is usually a progression in patients with coronary artery disease, with gradually increasing frequency of angina pectoris brought on by less and less exertion. However, plaque rupture will occur on top of hemodynamically insignificant lesions,⁴ with the abrupt onset of rest discomfort in the absence of a recent progression of symptoms or even in the absence of a prior history of angina or cardiac disease.

Forrester and Diamond⁵ categorized chest pain into typical angina (all three criteria were present), atypical angina (two criteria), and noncardiac chest pain (only one criterion). They based this classification on whether the pain (1) was substernal and pressure-like, (2) was precipitated by exertion or emotional stress and (3) was relieved by rest or nitroglycerin and lasted less than 30 minutes. In certain patient populations (eg, elderly men), this approach yielded such a high pretest probability of coronary artery disease that stress testing was unnecessary for the diagnosis of coronary atherosclerosis. This continues to be of value in clinical practice, particularly for male patients. It is commonly stated that women often present with atypical symptoms and the diagnosis of myocardial ischemia may be missed using these classic criteria. However, data suggest that anginal symptoms might be similar in men and women and that the concept of females frequently presenting with atypical symptoms might be misleading.⁶ There are other etiologies of chest pain that require urgent diagnosis and intervention. These include, but are not limited to, aortic dissection, penetrating aortic ulcers, and pulmonary embolism. Table 11–1 provides specific characteristics of chest pain history according to the different etiologies; these are generalizations and may not apply to an individual patient, but application of these criteria is helpful in forming an initial impression of the etiology of the pain and can then direct the clinician to further targeted testing.

Dyspnea

The onset, progression, and triggers of dyspnea or breathlessness should be recorded. Shortness of breath that is cardiac in nature is usually exertional, and continuous dyspnea at rest is usually noncardiac unless there are signs on physical examination of severe fluid overload. Patients may describe a need to take deep breaths at rest; that symptom is rarely cardiac in origin. Pulmonary symptoms such as cough, wheezing, and sputum production suggest a noncardiac etiology. This is also suggested by very intermittent worsening or oscillating in symptoms (“good days and bad days”). However, fluid congestion from a cardiac etiology can result in features of bronchospasm as the initial manifestation.

Positional changes are important to document; orthopnea and paroxysmal nocturnal dyspnea suggest heart failure as the cause of the patient’s dyspnea. True paroxysmal nocturnal dyspnea occurs several hours after a patient lays down, because there is redistribution of fluid from the venous capacitance vessels into the central circulation. Patients will feel agitated, need to sit up, and seek cold fresh air, with the dyspnea taking 10 to 15 minutes to subside. Patients who wake up at night feeling short of breath but are better within seconds after a few deep breaths do not have paroxysmal nocturnal dyspnea. Platypnea-orthodeoxia⁷ (worsening dyspnea and hypoxia in the sitting position) can be seen in patients with intracardiac shunting (either through an atrial septal defect or patent foramen ovale⁸) or in hepatopulmonary syndrome.

Syncope

A thorough history is vital in the evaluation of patients with syncope and, perhaps, the best diagnostic tool for the evaluation of those patients. The circumstance of the syncopal spell (how the patient was feeling earlier that day or the day before) as well as warning and/or postictal symptoms should be noted. The combination of diaphoresis, nausea, prolonging standing, and exposure to warm places suggests a vasovagal etiology. Situational causes of syncope should be sought, such as micturition or bowel movements. Positional changes, in particular orthostatic changes, leading to syncope are important and suggest orthostatic hypotension as the underlying cause; this is particularly important in elderly. Exertional syncope is usually due to a structural abnormality with obstruction to outflow (aortic stenosis, hypertrophic cardiomyopathy), especially when the syncope occurs just after the cessation of exertion. Exertional syncope in pulmonary hypertension is rare, but it is a very ominous sign, typically seen in young females. Syncopal spells without any warning unrelated to exertion are particularly concerning for a cardiac arrhythmia and are of high concern in patients with diseases, such as hypertrophic cardiomyopathy, in which there is an underlying substrate for ventricular arrhythmias.

Palpitations

The duration, onset and offset, and associated symptoms (presyncope, chest discomfort) should be recorded. Concomitant neck pulsations are classic for atrioventricular reentrant tachycardia. Potential triggers such as caffeine, alcohol, or dehydration are important for diagnosis and management. It is helpful to ask patient to reproduce the cadence by tapping their fingers. A fast irregular pattern suggests atrial fibrillation, whereas single forceful taps suggest ectopic beats. It is important to remember that in patients with underlying structural heart disease, the onset of arrhythmias usually portends progressive hemodynamic deterioration.

Other Symptoms

Lower extremity edema is a common complaint in patients with heart disease. The distinction between edema from right heart failure and venous insufficiency can be difficult to establish by history, and both may coexist; edema occurring only at the end of the day suggests a primary venous etiology. Abdominal swelling due to ascites might be present in patients with severe heart failure, severe tricuspid regurgitation, or constrictive pericarditis, but needs to be differentiated from primary liver disease, which may be a result of right heart failure. Ascites and edema are the most prominent symptoms of patients with constrictive pericarditis.

Fatigue and weakness are nonspecific symptoms and can be secondary to either cardiac or noncardiac issues; therefore, ascertaining that fatigue is a manifestation of a cardiac etiology is challenging. Fatigue as a cardiac symptom is common in patients with right ventricular failure or severe tricuspid regurgitation and constrictive pericarditis. Polypharmacy is common in cardiac and elderly patients, and fatigue might be a medication side effect (such as from beta-blockers) or a sign of medication-induced hypotension.

Systemic symptoms such as fever, chills, and malaise might be seen in the setting of infective endocarditis. Rarely, hoarseness and dysphagia are caused by compression of contiguous structures in the setting of aortic aneurysm or severe left atrial enlargement (as in advanced mitral stenosis).

Functional Capacity

Assessment of functional capacity should be documented for management and follow-up purposes. The Canadian Cardiovascular Society⁹ (Table 11–2) and the New York Heart Association¹⁰ scales (Table 11–3) are widely used tools. In our experience, even a simple 1 (bedridden) to 10 (no physical limitations) Likert scale is helpful in the longitudinal assessment of patients and tends to correlate well with objective exercise capacity (exercise maximal oxygen consumption). In some diseases, there is such a gradual hemodynamic impairment that patients may not perceive a functional limitation; they will slowly decrease their activity level. Information obtained from a spouse or other close observer regarding activity level over years may be of value.

With the aging population, it is important to assess the presence and extent of frailty in patients being considered for interventions. The ability to perform activities of daily living is a necessary component of the frailty assessment. The degree of independence and interaction with family will be useful information for decision making regarding interventions in the elderly frail patient.

General Examination and Inspection

A thorough general examination, including a funduscopic examination, should always be performed and signs of other comorbidities (such as cirrhosis, obstructive lung disease, or stroke) sought. Attention to patient’s dentition is of major importance—in particular in patients with valve disease or for those undergoing preoperative evaluation. Visible pulsations should be noted, with respect to location and origin (arterial versus venous). Details regarding the noncardiovascular and eye examinations are, however, beyond the scope of this chapter.

Our patient population is aging, and frailty assessment should also be included as part of the physical examination. Gait speed (15-feet walk), handgrip strength, and muscle wasting should be recorded; multiple scores^11,12 have also been developed. This assessment should be a standard part of clinical evaluation and should be performed in patients undergoing catheter-based interventions or surgical treatment.

Several syndromes have been associated with cardiovascular disease, including aortopathies, congenital heart disease, or even cardiac tumors. Careful inspection of the facies, body habitus, and extremities are necessary in order to suspect the presence of a syndrome. Although these syndromes are rare, their identification can lead to the initial suspicion of the cardiac diagnosis, which may have life-saving implications for patients and their families. Some of those findings are illustrated in the Table 11–4.

Blood Pressure Measurement

Blood Pressure: Technique

Although vital signs are frequently recorded by the ancillary staff prior to the encounter with the provider, we recommend that the measurements be repeated during physical examination by the clinician. This prevents abnormalities from being “missed” due to time constraints and also forces the examiner to certify that all the necessary steps for the measurement of blood pressure have been done (eg, that both arms are checked); this is particularly important during the patient’s initial evaluation.

Blood pressure should be measured at rest (a common mistake is to measure it immediately after the patients have just walked into the room) and the appropriate cuff size used (the width of the inflatable bladder should correspond to 40% of the arm circumference). Smoking and caffeine should be avoided prior to measurement of the blood pressure. During initial assessment, blood pressure should be measured in both arms; differences in systolic blood pressure between arms are typically less than or equal to 20 mm Hg (usually higher in the right arm). This is a mandatory step prior to bypass surgery and in patients with internal mammary grafts who present with angina; a simple blood pressure check might be sufficient to diagnose subclavian stenosis.

Additional steps should be taken according to the clinical scenario. In patients complaining of syncope or presyncope, measurements in the supine, sitting, and standing positions must be performed. Systolic blood pressure should not fall more than 20 mm Hg on standing; diastolic blood pressure typically rises. Mild reflex tachycardia is common, but rates above 100 beats/min should not be expected. Newly hypertensive patients or patients with known bicuspid valve should have blood pressures measured in the lower extremity since coarctation of the aorta might be present. A large cuff should be applied to the patient’s thigh and the popliteal artery auscultated. Alternatively, a smaller cuff can be applied to calf and the stethoscope applied to the dorsalis pedis artery. Normally, the lower extremity blood pressure tends to be 10 to 20 mm Hg higher than in the upper extremities.

Digital blood pressures cuffs have been shown to be reliable and accurate in most situations; however, major abnormalities might be missed if manual blood pressure measurement is not performed. Digital blood pressure cuffs may not be accurate in assessing pulse pressure in patients with aortic regurgitation or high output states; the digital cuffs will not be able to determine the presence of a pulsus paradox or pulsus alternans. Therefore, we recommend that manual blood pressure measurement should always be performed. With the stethoscope’s diaphragm applied to the brachial artery, the ipsilateral radial pulse is palpated and the cuff inflated to 20 to 30 mm Hg above the level required to obliterate the pulse; the cuff should be then deflated slowly. Systolic blood pressure corresponds to the appearance of Korotkoff sounds (phase I) and diastolic blood pressure to the level where the Korotkoff sounds entirely disappear (phase V). In some patients, the Korotkoff sounds might disappear and became audible again at lower pressures (ie, the auscultatory gap). This is a common finding in elderly patients, and simultaneous palpation of the radial artery while the cuff is inflated prevents underestimation of the blood pressure. In hypotensive patients, Korotkoff sounds might not be audible; blood pressure should be determined by palpation of the radial artery.

Heart rate and the cardiac rhythm (regular, regularly irregular, or irregularly irregular) should also be recorded. Other vital signs (temperature and respiratory rate) and their abnormalities should be noted.

Blood Pressure Abnormalities

Pulse pressure (the difference between systolic and diastolic blood pressure levels) should be noted. A narrow pulse pressure is seen in shock and hypotension; the arterial pulse usually shows low amplitude. A wide pulse pressure is seen in hypertension (commonly in the elderly, due to noncompliant arteries), severe aortic regurgitation (secondary to lower diastolic blood pressure) or arteriovenous shunting (such as patent ductus arteriosus or dialysis fistula).

Pulsus alternans (Fig. 11–1) corresponds to beat-to-beat changes in systolic blood pressure (or the intensity of Korotkoff sounds themselves); this can detected both by auscultation and by palpation, during which time the patient should be instructed to breathe calmly. Pulsus alternans is a sign of severe left ventricular systolic dysfunction.

Pulsus paradoxus (Fig. 11–2) corresponds to respirophasic changes in blood pressure. “Paradox” is a misnomer because minor drops in blood pressure with inspiration are normal. In pathologic situations, there is an exaggeration of this phenomenon. Normally, systolic blood pressure should not fall more than 10 mm Hg on inspiration. The presence of “pulsus” is a subtle finding and requires that proper technique is applied. The examiner should inflate the blood pressure cuff 15 to 20 mm Hg above the systolic blood pressure (determined by palpation and auscultation). The cuff should then be slowly deflated and the Korotkoff sounds auscultated while the patient breathes normally; the sounds will show respirophasic changes, decreasing or disappearing with inspiration. Eventually, those respirophasic changes will not be noticeable, and expiratory and inspiratory Korotkoff sounds will have similar intensities. The “pulsus” will be the difference between the peak systolic blood pressure levels measured during expiration and inspiration, and more than 10 mm Hg is abnormal. Pulsus paradoxus is classically described as a sign of cardiac tamponade or constrictive pericarditis due to the enhancement ventricular interdependence seen on those two entities (with inspiration right ventricular stroke volumes increases while left ventricular stroke volume falls; this is secondary to pericardial restraint). Pulsus paradoxus can also be seen in morbid obesity and in lung disease, as a result of major changes in intrathoracic pressures.

Percussion

In the past, some authors recommended the use of percussion for the determination of cardiac position (levocardia vs dextrocardia) and its relation to abdominal viscera (situs solitus or inversus, based on gastric tympanic sounds). Today, this can be easily determined with chest radiography and echocardiography. Thus, cardiac percussion is not necessary in current practice.

Palpation

Palpation is perhaps the most underemphasized part of the cardiovascular examination, both in medical education and bedside assessment. Proper technique includes palpation of the left and right ventricles as well as palpation of the cardiac base (great vessels). Via “simple” palpation, assessments of ventricular size, cardiac valve function, diastolic function (when third or fourth sounds are palpable), and pulmonary hypertension can be suspected. Masters of physical examination advocate that auscultation “merely” serves to confirm inspection and palpation findings.

Palpation of the great vessels is part of a comprehensive cardiovascular physical examination and should be performed over the second right intercostal space (aortic area) and left intercostal space (pulmonic area), best felt in the sitting position. A detectable pulsation represents palpable, and therefore, increased, aortic (A2) or pulmonic (P2) components of the second heart sound. A palpable A2 component is rare. A palpable P2, however, is a critical finding because it suggests severe pulmonary hypertension, which can either be due to etiologies associated with increased pulmonary vascular resistance or left-sided diseases.

Attention should be turned to the presence of thrills, palpable murmurs which have a marked increase in the degree of turbulence. Thrills can be present at the apex, left lower sternal border, cardiac base, suprasternal notch/neck, and the posterior chest. When present, the location, timing, and radiation of a thrill should be described. Diastolic thrills are very rare. In current practice, the most common source of a thrill is a ventricular septal defect, which manifests as a systolic thrill at the left lower sternal border. It should be emphasized that the presence of a thrill is not diagnostic of a specific cardiac lesion, and the diagnosis should be made on the basis of the constellation of findings observed on examination.

Cardiac palpation should proceed with evaluation of the apical impulse. We recommend the term apical impulse instead of point of maximal impulse because patients with significantly enlarged right ventricles might have parasternal lifts that are more prominent than the left ventricular apical impulse. The apical impulse might be visible, facilitating its localization; therefore, inspection should precede palpation. In addition, some of other palpable abnormities may also be visible (eg, a rapid filling wave that corresponds to a third heart sound). Palpation (and auscultation) must be performed directly over the skin. Thus, patients should always be offered an examination gown and a sheet used to preserve patient’s privacy. Examination of the patient in his or her clothes compromises the quality of the examination and is discouraged.

With the patient in the supine position, if not visible, the examiner should look for the apical impulse using the entire right hand starting at the inframammary area. In patients with large breasts, the examiner’s left hand should be used to mobilize the breast to locate the apex. Once a palpable pulsation is identified, the finger pads should be then used for analysis (Fig. 11–3). If the apical impulse cannot be palpated, the patient should be positioned in the left lateral decubitus position and asked to place his or her left hand underneath the pillow; slight elevation the head of the bed (30 degrees) might also be helpful. Both maneuvers facilitate expansion of the thorax, increasing the space between the ribs. Held expiration may also facilitate cardiac palpation. The apical impulse should be palpable in the majority of patients, even in individuals with normal hearts.

Once the apical impulse is identified, the examiner should assess its location, size, and quality/contour. The apical impulse is usually located at the fifth intercostal space in the midclavicular line. With left ventricular enlargement, the apical impulse is deviated laterally and inferiorly while right ventricular enlargement displaces the apex laterally. Moving the patients from supine to a left lateral decubitus position only shifts the apical impulse laterally by 2 to 3 cm and should not be responsible for marked apical displacement.

When the left ventricular size is normal, the apical impulse occupies an area of 3 cm or less in diameter; the size of the apical impulse should be described in centimeters rather than fingerbreadths because it is more precise. Increase in the area occupied by the apical impulse suggests left ventricular dilatation, described as a diffuse apical impulse (as opposed to localized). Isolated left ventricular hypertrophy typically does not cause enlargement of the apical impulse; hypertrophy is associated with a sustained impulse. An enlarged apical impulse suggests an enlarged left ventricle due to a myopathic process or volume overload as seen in severe aortic or mitral regurgitation.

The contour of the apical impulse should be also be determined. Isovolumic contraction moves the apex closer to chest wall, allowing its palpation; as a consequence, the impulse is usually only palpable during the first two-thirds of ventricular systole (Fig. 11–4). Although simultaneous auscultation can help quantifying the duration of apical impulse, in practical terms the determination of a normal versus prolonged (described as sustained) apical impulse comes with experience. It is extremely important, therefore, for the clinician to perform cardiac palpation in every patient, including the ones with known normal hearts, so a sense of normality can be developed.

A sustained apical impulse can be found when ventricular mass is increased (ventricular hypertrophy or dilation) or when there is obstruction to left ventricular ejection (as observed in aortic stenosis or hypertrophy cardiomyopathy). Not only duration, but also the amplitude should be noted. In hypertrophy and obstruction to flow, the apical impulse is rather forceful, “pushing” the examiner’s hands. Conversely, in patients with severe left ventricular dysfunction, the impulse can be quite feeble. In sinus tachycardia (eg, after exercise or related to infection), the apical impulse can be hyperdynamic. In patients with mitral stenosis and a pliable mitral valve, apical palpation results in a unique tactile (shock-like) sensation due to a prominent first heart sound—so-called tapping apical impulse—which is essentially pathognomic for rheumatic mitral stenosis. Patients with hypertrophic obstructive cardiomyopathy might also have a classic apical impulse—the so-called “triple ripple” (see Fig. 11–4). This corresponds to the presence of palpable systolic impulse in early and midsystole, separated by withdrawal of the apical impulse related to dynamic outflow obstruction; a palpable atrial contraction corresponds to the third impulse.

A palpable third or fourth heart sound may be suspected by inspection (sometimes placing the tip of a pen over the apical impulse and watching the motion of the pen itself can be helpful). A palpable fourth heart sound follows atrial contraction and will be felt as a presystolic palpable impulse (preceding the rise of the apical impulse); the fourth heart sound tends to be more easily palpated than auscultated. A palpable third heart sound corresponds to the ventricular diastolic rapid filling phase and will occur in early diastolic; it can be felt as the apical impulse retracts. The third heart sound is usually more easily auscultated than palpated. Although systolic clicks and some diastolic sounds can be palpable, they are rarely felt.

Given its anterior position within the chest, an enlarged right ventricle can be palpated as a parasternal lift (or heave). It should be noted that in thin patients or patients with abnormalities of the sternum (such as pectus excavatum), a parasternal lift can be present in the setting of a normal right ventricular size. Palpation of the right ventricle can be accomplished several different ways (Fig. 11–5), being performed with patient in the supine position. The examiner should gently place his or her thenar/hypothenar surfaces on the patient’s left lower sternal border. The right ventricle can also be palpated by placing the examiner’s index, middle, and fourth fingers over the third, fourth, and fifth intercostal spaces, respectively, at the left parasternal line. A third form of palpation is to place the right hand in the subxiphoid area. This maneuver is particularly helpful in patients with obstructive lung disease. Abnormalities in the contour of the right ventricular impulse can be appreciated but are much less prominent than apical ones. Pulmonary stenosis can give rise to a sustained parasternal lift; presystolic and early diastolic waves can be also be appreciated on occasion.

Arterial Pulse Examination

Technique

Analysis of the arterial pulse can be accomplished by palpation of the carotid and/or the brachial arteries. We encourage the examiner to be familiar with palpation of the brachial arteries, which can be particularly helpful in patients with increased neck circumference, previous cervical radiation, or in the presence of carotid disease. Palpation of the brachial arteries can be achieved by resting the patient’s elbow on the examiner’s right palm with palpation of the vessel being exerted with right thumb; the brachial pulse is usually deeper than others. The examiner’s left hand should gently extend/flex the patient’s arm in order to improve palpation of the vessel. Alternatively, palpation can also be performed directly by the examiner’s left finger pads with the right fingers being used for extra pressure, if needed. Palpation of the carotid arteries should be performed with the right finger pads; the sternocleidomastoid muscle should be mobilized laterally to optimize palpation of the vessel. Once the artery has been properly identified, attention should to paid to the amplitude and contour of the arterial pulse (Fig. 11–6), as will be described below. Palpation of the other upper and lower extremity pulses is part of a comprehensive cardiovascular examination and should always be performed, particularly with simultaneous palpation of the radial and femoral pulse in patients with suspected coarctation of the aorta.

Abnormalities of Arterial Pulse

The classic arterial pulse contour described in severe aortic stenosis is tardus (slurred upstroke and delayed peak) and parvus (reduced in amplitude) (see Fig. 11–6). The degree of tardus (graded as 1+ to 4+) is a measure of the severity of the stenosis and reflected in the late peaking continuous wave velocity contour on Doppler echocardiography as well as the delayed upstroke on the central aortic pressure at cardiac catheterization (Fig. 11–7). Although frequently described in textbooks as one single pattern, one of the two components might prevail (more tardus than parvus), and they should be graded separately. Typically found in valvular aortic stenosis, it should be noted that the parvus and tardus pulse also accompany other forms of fixed left ventricular outflow obstruction (eg, supravalvular aortic stenosis). In this case, however, a normal aortic component of the second heart sound will indicate the aortic valve is spared. In dynamic left ventricular outflow obstruction (hypertrophic cardiomyopathy), the arterial pulse is usually of normal amplitude but has brisk upstroke, secondary to an unopposed forceful contraction in early systole (before obstruction develops) by the hypertrophied ventricle. Hypertrophic cardiomyopathy with obstruction is a cause of a bifid pulse, caused by the occurrence of obstruction starting in mid-systole. This is seen as a spike-and-dome pattern on aortic pressure (see Fig. 11–6) tracings, but the presence of this finding on examination is uncommon.

In severe aortic regurgitation, the associated volume overload and left ventricular dilatation cause an increase in stroke volume. The combination of increased stroke volume and the regurgitation itself gives rise to an arterial pulse that is increased in amplitude—“bounding”—which also collapses very quickly (see Fig. 11–6). This is so-called water hammer pulse, typical of severe isolated aortic regurgitation. This phenomenon is not only palpable but might also be manifested as visible arterial pulsations (carotids and brachial arteries, most commonly). When mixed aortic valve disease is present and the aortic regurgitation is the predominant lesion, an arterial contour with increased amplitude and two palpable systolic peaks can be present—the bisferiens pulse.

Other described abnormalities of the arterial contours include the anacrotic pulse of aortic stenosis, where a positive inscription can be palpated on the ascending limb of the aortic contour, or the dicrotic pulse, when there is an exaggeration of the dicrotic notch (palpated on descending limb of the aortic pulse), typically seen in shock and severe peripheral vasoconstriction. Hypotension and narrow pulse pressure are also usually present (see Fig. 11–6). In patients with severe left ventricular systolic dysfunction, pulsus alternans might be present, where the amplitude of the arterial pulse will vary with every heart beat; sometimes the amplitude might be so diminished that only every other beat can be palpated. As opposed to pulsus paradoxus (previously described in the vital signs section), those variations in amplitude are not respirophasic. The presence of pulsus alternans is an ominous sign suggesting very profound severe ventricular systolic dysfunction. These abnormalities can be easily noted invasively by arterial pulse recording or an ascending aortic pressure (see Figs. 11–1 and 11–2).

The examiner should also assess the amplitude of the arterial pulse as an indirect measurement of cardiac output; arterial pulse amplitude tends to be proportional to stroke volume. The presence of a low amplitude pulse in the absence of aortic stenosis should suggest reduced cardiac output, such as with severe left ventricular systolic dysfunction, severe mitral stenosis, or constrictive pericarditis. Conversely, the combination of bounding pulses, left ventricular enlargement, and heart failure should suggest high-output failure, patent ductus arteriosus, or other arteriovenous fistulae. In shock, the arterial pulse is of decreased amplitude but also hyperdynamic as the result of accompanying tachycardia.

Venous Pulse Examination

Inspection

The first step in analyzing the venous pressure and the venous waveform contour is ascertaining that the visible pulsation is indeed venous. A carotid arterial pulsation seen below the angle of the jaw might be mistaken for severe elevation in venous pressure. Inspection of the internal, instead of the external, jugular vein has been traditionally preferred to determine the contour of the venous pulsations. Because it emanates from a low-pressure system, venous pulsations should disappear when light pressure is applied proximally (eg, above the clavicle), whereas arterial pulsation cannot be compressed and should “push” the examiner’s fingers. In normal circumstances, the venous contour has two upstrokes and the arterial waveform has a single one. This feature, however, should not be used in isolation, because rhythm abnormalities (such as atrial fibrillation with loss of the a wave) or severe tricuspid regurgitation will lose the double venous upstroke. Lastly, venous waveforms show respirophasic changes with its waveforms becoming more prominent on inspiration, although the venous pressure itself might drop slightly or remain unchanged.

Estimation of Venous Pressure

The proper technique used in the estimation of central venous pressure is often confusing to the novice examiner. Estimation of central venous pressure is a crucial part of the physical examination; not only cardiologists, but all clinicians should to be very familiar with the method. Its importance in the diagnosis and management of patients is clearly stated in the American College of Cardiology/American Heart Association heart failure guidelines.¹³ An elevated venous pressure is the equivalent of a dilated inferior vena cava on echocardiography, which does not collapse with inspiration and is the first clue to hemodynamic decompensation.

Estimated central venous pressure is measured in centimeters of water (H₂O) because it represents the height of a column of fluid. Thus, the venous pressure in cm of H₂O does not equal the right atrial measured in mm Hg at catheterization (1 cm of H₂O = 0.74 mm Hg). Central venous pressure is recognized on physical examination as the vertical distance from the highest point of the visible jugular venous pulsation to the right atrium. The internal jugular vein is typically the one analyzed. The sternal angle, or angle of Louis, which corresponds to the manubriosternal junction has been shown to lay 5 cm above the level of the mid–right atrium (Fig. 11–8). Therefore, estimated central venous pressure equals the vertical distance of the maximum visible jugular venous pulse to the angle of Louis plus 5 cm. The head of the bed should be adjusted in order to optimize analysis of the venous pulsations so that the highest point where venous pulsations can be identified is to be used as the reference point.

In patients with very elevated central venous pressures such as seen in constrictive pericarditis, the top of venous pulse might not be seen until the patient is standing. Conversely, in patients with low central venous pressures, the patient might be almost supine until venous pulsations can be appreciated. Thus, failure to perform inspection of the neck in different positions might lead to misinterpretation of central venous pressure.

There are two simple and practical ways that estimating central venous pressures can be done at the beginning of the physical examination while the patient is sitting at 45 degrees. The lack of a visible pulsation corresponds to a normal venous pressure of less than 8 cm of H₂O. A visible venous pulsation at the level of the clavicle corresponds to 10 cm of H₂O, midneck 15 cm of H₂O, and angle of jaw 20 cm of H₂O. Another method is to simply report out the height of the venous pulsation (in cm) above the angle of Louis at 45 degrees. In the normal patient without cardiac disease, the venous pressure is less than 3 cm above the angle of Louis. If pulsations cannot be visualized, the venous pressure is most likely normal, but it is necessary to lower the head of the bed until a pulsation is seen to ensure that the venous pressure is not so high that pulsations cannot be seen.

Although the terms jugular venous distention and elevated central venous pressure are frequently used interchangeably, the central venous pressure should always be quantitated objectively. Jugular venous distention might be seen in primary venous disorders (eg, in superior vena cava syndrome).

Normal Venous Pulse

After central venous pressure has been estimated, the examiner then should focus on the venous contour. Similar to the technique used for the estimation of venous pressure, the head of bed should be adjusted to provide optimal visualization of the venous pulsations. The normal jugular venous contour has two upstrokes—a and v waves—and two downstrokes—x and y descents (Fig. 11–9). A third positive wave—the c wave—is seen on right atrial pressure tracings but is not usually visualized on the neck veins.

Positive waves are typically more easily appreciated on inspection than the descents. The a wave corresponds to atrial systole and is followed by x descent, which is the result of two phenomena—atrial diastole and apical displacement of tricuspid annulus during ventricular systole. The origin of the c wave had been controversial, but it appears that the inflection seen on the jugular wave recordings results from the contiguous carotid pulsations rather than tricuspid valve closure. The v wave represents venous return, whereas the y descent occurs with opening of the tricuspid valve and early diastolic filling of the right ventricle. In normal subjects, right atrial a wave is larger than the v wave.

In order to analyze the waveforms themselves, it is necessary for each wave to be accurately identified. Proper timing can be achieved by simultaneous palpation of the patient’s left (or contralateral) carotid with the examiner’s right hand or simultaneous auscultation of the precordium. The a wave precedes the carotid upstroke and the first heart sound; once the a wave has been identified, the second positive deflection should be v wave. When a single venous upstroke is present (as in atrial fibrillation), only a positive wave (v wave) following carotid upstroke will be noted. The radial pulse should not be used as the pulse reference because there is a small delay between the radial and carotid upstroke, which can lead to inaccurate conclusions, especially when tachycardia is present.

Jugular venous wave recording was readily available in the past but the technique has essentially disappeared with widespread use of echocardiography. In the current era, hepatic vein pulsed-wave Doppler provides an objective corresponding image of the jugular wave contour (S wave = x descent; D wave = y descent) (Fig. 11–10). Cardiac catheterization also provides the opportunity for the examiner to compare his or her noninvasive and invasive data with direct measurement of right atrial pressure. We would recommend that clinicians estimate right atrial pressure and waveforms prior to sending patients to the catheterization laboratory for hemodynamic assessment. This process will result in “calibration” of the examiner’s physical examination skills and more accurate appreciation of the findings.

Abnormal Venous Pulse

Abnormalities of the a Wave

Abnormalities of the a wave can result from primary right-sided valvular disease, hemodynamic abnormalities of the right ventricle or heart rhythm abnormalities. An increase in the amplitude of the a wave is seen in situations where there is increased contribution of atrial contraction to ventricular diastolic filling. An elevated atrial reversal velocity on the hepatic vein Doppler tracing corresponds to a large a wave. This can occur in the setting of right ventricular diastolic dysfunction and is typically seen in pulmonary hypertension, pulmonary stenosis, or less frequently in restrictive cardiomyopathies. Classically described in rheumatic tricuspid stenosis, very enlarged a waves—giant a waves—will be present secondary to atrial contraction against a stenotic tricuspid valve (Fig. 11–11). The occurrence of very large a waves (as opposed to large v wave) is primarily encountered in patients being evaluated for tricuspid prosthesis obstruction with an elevated diastolic gradient.

Atrial fibrillation is characterized by the absence of organized atrial contraction; thus, in patients with atrial fibrillation, the a wave will be absent (Fig. 11–12). In atrial flutter, small, regular flutter waves can be seen instead of a waves. Initially described as a delay between a and v waves on the jugular venous pulse, the diagnosis of first-degree atrioventricular block or Wenckebach phenomenon features on neck veins is of historical interest. The presence of brisk, extremely prominent a waves, the so-called cannon a waves, are still valuable in clinical practice. These are the result of atrial contraction against a closed tricuspid valve. Variable cannon a waves suggest the diagnosis of complete heart block in patients with new-onset bradycardia, and its occurrence in wide complex tachycardia is diagnostic of ventricular tachycardia rather than aberrancy.

Abnormalities of the x Descent

The most common abnormality observed in clinical practice is the blunting of x descent that is seen in atrial fibrillation. Atrial fibrillation results in a loss of atrial contraction, as well as atrial relaxation, leading to this abnormality. The corresponding finding is a reduced or absent systolic forward flow (S wave) on the hepatic vein Doppler tracing (see Fig. 11–12). In patients with myopathic diseases, annular motion can be markedly reduced as evidenced by low tissue Doppler velocities, and thus the x descent will be blunted (see Fig. 11–9). Lastly, in patients with tricuspid regurgitation, a positive v wave will take the place of the x descent. Increased amplitude of x descents—“deep x descents”—are classically seen in constrictive pericarditis (see Fig. 11–6), as the result of both enhanced annular descent and preserved atrial relaxation.

Abnormalities of the v Wave

In severe tricuspid regurgitation, right atrial pressure rises as the tricuspid regurgitant volume enters the right atrium. This leads to two abnormalities of the v wave—an increase in its amplitude and a more premature inscription of its upstroke (see Fig. 11–12). The large v wave occurs throughout systole and, thus, should be timed with the carotid pulsation. The most extreme exemplification of this phenomenon is the occurrence of a single, large positive v wave, described as ventricularization of right atrial pressure tracings. This will manifest as a systolic reversal of flow on the hepatic vein Doppler tracing.

Abnormalities of the y Descent

Increased amplitude of the y descent can be seen in any disease that leads to prominent rapid filling of the right ventricle in early diastole. This can be seen in tricuspid regurgitation with or without elevation in right heart filling pressures, but also in abnormalities of right ventricular diastolic function, such as restrictive cardiomyopathy or constrictive pericarditis (see Fig. 11–9). The early rapid filling is seen as a prominent early diastolic forward flow on the hepatic vein Doppler velocity curve with a high initial E velocity and short deceleration time on the tricuspid inflow velocity curve.

Conversely, in cardiac tamponade there is blunting of the y descent given the impaired ventricular filling due to elevated intrapericardial pressures preventing early rapid filling (see Fig. 11–8). Reduction in amplitude and slope of the y descent is seen in tricuspid valve native or prosthetic stenosis.

Kussmaul Sign

The Kussmaul sign is characterized by an increase in jugular venous pressure associated with inspiration as opposed to usual drop that is seen in normal individuals (Fig. 11–13). Although described in constrictive pericarditis, the sign can be present in any disease associated with severe elevation in right-sided filling pressures.

Abdominojugular Reflux

Also known as hepatojugular reflux, the term abdominojugular reflux better describes the maneuver, when the examiner applies gentle pressure to the center of the patient’s abdomen (around the umbilicus). As abdominal pressure is applied, there is a transient, minor increase in jugular (central) venous pressure and an accentuation of jugular venous waveforms. The patient should be made aware of the maneuver in order to avoid sudden abdominal muscle tensioning and an elevation of intrathoracic pressures (similar to the ones seen with Valsalva maneuver). Normally, these changes will only last a few beats (around 5 seconds) despite continued pressure and the venous pressure will return to baseline. A sustained response (lasting more than 10–15 seconds)¹⁴ (Fig. 11–14) suggests elevated right-sided filling pressures.

Technique

Proper technique must be reviewed prior to discussing auscultatory findings; this involves patient positioning, areas of auscultation, and the stethoscope itself. In order to avoid missing subtle findings, cardiac auscultation must be performed with the patient in three different positions: these positions include sitting, supine, and left lateral decubitus. The sitting position is important for auscultation of sounds emanating from the base of heart and great vessels as well as pericardial rubs and some tricuspid murmurs. Although most standard cardiac auscultation is performed with the patient supine, auscultation over the apex with the patient in the left lateral decubitus position brings out mitral murmurs and low-pitched cardiac sounds that might not be otherwise appreciated.

Five areas of auscultation have been classically described (Fig. 11–15)—mitral (over the apical impulse), tricuspid (fifth intercostal space at the left parasternal line), pulmonic (second intercostal space at the left parasternal line), aortic (second intercostal space at the right parasternal line) and accessory aortic area (third intercostal space at the left parasternal line); however, the stethoscope should not “jump” from one area to the other. Instead, the examiner should march the stethoscope from the apex toward the sternum, then up along the parasternal line, ending at the right parasternal area at the level of the second intercostal space. With the patient sitting, the opposite is then performed, using the right upper border at the starting point. This meticulous process ensures that abnormal auscultatory findings, heard over a very localized area, will not be missed as they might if only the five main areas are auscultated. When indicated, auscultation should also be extended to areas where murmurs typically radiate, such as the left axilla, neck, suprasternal notch, right infraclavicular area, and back. In each area, careful attention must be paid to each heart sound, systole, and diastole.

The examiner should always take full advantage of the two parts of the stethoscope—the bell and diaphragm. The bell is designed for auscultation of low-pitched sounds (third and fourth heart sounds, diastolic rumble, vascular bruits), whereas the diaphragm should be used for most heart sounds and murmurs. The bell should be gently applied to the bare chest; if excessive pressure is exerted, the bell works as a diaphragm. The examiner, however, should also use this property in his or her favor—for example, in a patient with mitral stenosis, variable stethoscope pressure should be used to focus on the rumble (bell) or the opening snap (diaphragm).

First Heart Sound

Normal First Heart Sound

The first heart sound (S1) corresponds to closure of the atrioventricular valves and, therefore, marks the end of diastole. It has two components—mitral (M1) and tricuspid (T1), with the latter following the former in normal circumstances. In most patients, M1 overshadows T1 and S1 is heard as a single sound. Sometimes, however, both components can be heard over the left lower sternal border, causing splitting of S1; this is a normal finding. Both components should have the same pitch and intensity and should be easily differentiated from a right-sided fourth heart sound (lower pitched) and an early systolic click (higher pitched and usually auscultated in a much wider area). Splitting of S1 might be slightly more prominent in patients with a right bundle branch block.

Abnormalities of the First Heart Sound

An increase in the intensity of the S1 can be encountered in situations where the PR interval is short, such as preexcitation or tachycardia. Sinus tachycardia associated with a hyperdynamic left ventricle is the most common cause of a loud S1 in clinical practice.

Mitral stenosis can lead to both increase and decrease in the intensity of S1, depending on degree of calcification and mobility of the valve leaflets. When mitral leaflets are pliable, the intensity of S1 is increased and this might be the only sign of rheumatic involvement of the mitral valve. The finding of a loud S1 also has therapeutic implications because it suggests that the patient is likely a good candidate for percutaneous balloon valvuloplasty. In cases where the leaflets are calcific and immobile, the first heart sound becomes soft.

A decrease in the intensity of S1 is recognized in patients with prolonged PR interval or after long R-R intervals (diastolic periods) in patients with atrial fibrillation. Given the wide variability of R-R intervals in atrial fibrillation, S1 usually has variable intensity. Decreased S1 amplitude is also recognized in myopathic processes and in patients with severe reduction in systolic function due to a poorly contractile ventricle. Lastly, a soft S1 might also be observed in acute aortic regurgitation due to marked elevation in left ventricular diastolic pressures and early closure of the mitral valve.

Most clinical abnormalities alter intensity of the M1 component of the first heart sound. An exception is the patient with Ebstein anomaly when the large, sail-like anterior tricuspid leaflet gives rise to a loud T1 component.

Second Heart Sound

Normal Second Heart Sound

The second heart sound (S2) corresponds to closure of the semilunar valves and has an aortic (A2) and a pulmonary (P2) component. The S2 sound is high pitched and best heard with the diaphragm. As opposed to S1, its two components are audible in the majority of patients. The S2 intensity and timing carry very valuable diagnostic information.

In order for the examiner to describe specific abnormalities of A2 and P2 (or to ensure that normality is indeed present), it is mandatory that both components are simultaneously auscultated and actively sought. P2 is typically audible in a limited area over the second left intercostal space and is sometimes only appreciated with the patient sitting. Therefore, one can only state that a single S2 is present if appropriate auscultatory maneuvers are taken and a single component remains audible. In normal circumstances, both A2 and P2 should have similar intensities when auscultated simultaneously in the pulmonic position. A P2 should not be audible at other positions unless pulmonary hypertension is present.

Physiologic Splitting of S2

During normal inspiration, there is enhanced venous return to right-sided cardiac chambers, as well as increased capacitance in pulmonary vasculature. The combination of these two phenomena leads to an increase in right ventricular ejection time with inspiration and delay in closure of the pulmonary valve following inspiration. The normal lack of significant respirophasic change in left ventricular ejection time results in a single audible S2 during expiration (P2 occurring simultaneously with A2) and two distinct components on inspiration (with P2 following A2), so called physiologic splitting of S2 (Fig. 11–16).

Abnormal Splitting of S2

Nonphysiologic splitting of S2 can be categorized as paradoxical, persistent, or fixed (see Fig. 11–16). The abnormalities can be secondary to hemodynamic or conduction derangements. In paradoxical splitting of S2, there is a delay in aortic valve closure, with P2 preceding A2. S2 is split during expiration and becomes single during inspiration as P2 becomes closer to A2; hence the paradox (ie, the opposite of normal). This delay in A2 is secondary to a prolongation of left ventricular ejection time, which can be due to increase in afterload or nonuniform contraction of left ventricle (conduction abnormalities). The long ejection time can be measured from the duration of flow through the left ventricular outflow tract or across the aortic valve by Doppler echocardiography; it usually exceeds 300 milliseconds in these instances.

Although classically described in valvular aortic stenosis, paradoxical splitting of the S2 is more common in obstructive hypertrophic cardiomyopathy, suggesting severe dynamic left ventricular outflow obstruction. In severe aortic stenosis, the A2 component is either absent or diminished, and splitting of S2 is rarely appreciated. In left bundle branch block, activation of left ventricular lateral wall is delayed, also prolonging ejection period. This is a sign of left ventricular dyssynchrony and, in our experience, patients with decreased left ventricular systolic function and paradoxical splitting of S2 appear to respond favorably to cardiac resynchronization therapy. Right ventricular pacing also promotes delayed activation of the left ventricle and paradoxical spitting of S2.

In persistent splitting, S2 is widely split at baseline (both A2 and P2 can be heard) but with inspiration the A2-P2 interval becomes longer. This is secondary to an underlying delay in the occurrence of P2. Wide splitting of S2, therefore, reflects abnormal right ventricular ejection hemodynamics. The most common cause in clinical practice is right bundle branch block, although severe increase afterload resulting from pulmonary hypertension can also lead to wide splitting of S2.

Fixed splitting of S2 is classically found in ostium secundum atrial septal defect, where wide splitting of S2 is present at baseline with minimal or no change in A2-P2 interval during inspiration. The wide S2 splitting on expiration is related to increased pulmonary vascular capacitance associated with increase pulmonary blood flow, delaying the P2 component. As a result of the interatrial communication, the decrease in venous return during expiration is compensated by an increase in left-to-right shunt without changes in right ventricular preload. The lack of significant respirophasic changes in both preload and afterload results in no change in right ventricular ejection period and, therefore, a fixed A2-P2 interval.

Abnormalities of S2 Components

A loud P2 is a sign of pulmonary arterial hypertension; in severe cases of pulmonary hypertension, P2 is palpable. P2 is generally heard over a small area in the left upper chest; a P2 component that can be auscultated at other areas is a clue that P2 is increased. In general, a P2 heard at the left lower sternal border indicates moderate pulmonary hypertension and if audible at the apex indicates severe pulmonary hypertension.

A diminished P2 is noted in patients with increased anteroposterior thoracic distance. The opposite is also true; patients with diminished anteroposterior thoracic dimension, such as patients with pectus excavatum, can have an abnormally loud P2. In patients with obstructive lung disease, increased lung volume contributes to decrease in P2, this being the most common cause for a single S2 in practice. A diminished or absent P2 is also noted in patients with severe valvular pulmonary stenosis. Lastly, a single S2 is a characteristic clinical finding in patients with congenitally corrected transposition, where the posterior location of the pulmonary valve prevents auscultation of P2 component.

A loud A2 is expected in patients with severe systemic arterial hypertension. A very loud A2—tambour like—was also described in syphilitic aortitis, but the disease is almost rarely encountered nowadays.

A diminished A2 is a classic finding of valvular calcific aortic stenosis and is also an important marker of disease severity, especially when the A2 component is absent. The presence of a normal A2 component in a patient with “severe aortic stenosis” and echo-Doppler findings of fixed obstruction should prompt investigation for subaortic or supravalvular obstruction.

Fourth Heart Sound

In the early phases of diastolic dysfunction, abnormal (prolonged) ventricular relaxation impairs early diastolic ventricular filling, decreasing the amount of filling in early diastole with a compensatory enhanced atrial contribution of diastolic filling.¹⁵ An audible left heart fourth heart sound (S4) represents this prominent, forceful left atrial contraction into a noncompliant left ventricle. It occurs, therefore, in late diastole (presystole) and is never present in atrial fibrillation. A left-sided S4 is a low-pitched sound, typically only heard at the apex with the bell and easily missed if auscultation in the left lateral decubitus position is not performed.

Doppler echocardiographic findings that correlate to the presence of an audible S4 are that of an abnormal relaxation pattern (grade I pattern) (Fig. 11–17) on the transmitral flow velocity curve include a low E:A ratio and a prolonged deceleration time with a shortened duration of the a wave. There are also increased atrial reversal velocities on pulmonary vein echo-Doppler profiles. Left ventricular tracings will show a slow rate of fall of left ventricular pressure during isovolumic relaxation (reduced negative dP/dt), lack of rapid filling waves, and prominent a waves. Patients with impaired ventricular relaxation typically have normal mean left atrial pressures and thus are not in heart failure at rest but will develop shortness of breath with exertion as the diastolic filling period shortens. These patients rely on atrial contraction for diastolic filling, and thus loss of organized atrial contraction is generally poorly tolerated.

Abnormal ventricular relaxation occurs most frequently with left ventricular hypertrophy due to aortic stenosis, hypertrophic cardiomyopathy, and systemic hypertension. It also occurs with ongoing myocardial ischemia and is frequently observed as part of aging. Thus, an audible S4 is expected in all those entities, but should not be observed in young adults, since myocardial relaxation is normal in that age group.

A right-sided S4 is usually associated with right ventricular pressure overload as seen in pulmonary hypertension, pulmonary stenosis, or early phases of restrictive cardiomyopathy. A right-sided S4 is usually heard at the left lower sternal border and increases with inspiration.

Third Heart Sound

A third heart sound (S3) will occur when there is prominent early rapid ventricular filling during diastole. It is a low-pitched sound heard in early diastole, most likely due to tensing of the chordae as the left ventricle rapidly expands from the early filling. An S3 is best heard at the apex with the bell lightly placed and the patient in a left lateral decubitus position. It occurs 100 to 150 milliseconds after S2. This sound correlates with a high initial E velocity, an increased E:A ratio, and short deceleration time on the transmitral flow velocity curve.

There are a number of different etiologies for the generation of an S3. The most common is in a patient with an abnormal stiffness of the myocardium coupled with high filling pressures. The high left atrial pressure produces high driving pressure across the mitral valve to account for the early rapid filling, which is followed by a rapid increase in left ventricular diastolic pressure.¹⁵ This is manifested as a steep rapid filling wave on left ventricular pressures tracing and large left atrial v waves (reflecting the pressure rise as pulmonary venous blood enters an overloaded left atrium). An S3 can be a dynamic finding and usually dependent on the volume status of the patient. If there is severe elevation of left atrial pressure, there will be an S3 on auscultation with a restrictive pattern on the transmitral flow velocity curve (high E:A ratio and short deceleration time) (see Fig. 11–17). However, with diuresis and lowering of the left atrial pressure, the transmitral flow pattern will change from restrictive (grade III pattern) to pseudonormal (grade II pattern) and even delayed relaxation (grade I pattern) with disappearance of the S3 on examination. A persistent S3 despite treatment indicates the end stage of diastolic dysfunction (stage IV pattern) caused by severe irreversible fibrosis of the myocardium.

There are other etiologies for a S3 on examination, all of which reflect rapid early diastolic filling. Rapid early diastolic filling occurs in young healthy hearts due to vigorous ventricular relaxation, which “sucks” the blood in from left atrium to left ventricle in early diastole, allowing for a higher preload while maintaining low to normal pressures. The transmitral Doppler velocity curve will have the same appearance as a restrictive filling pattern (high E:A ratio and short deceleration time). However the mitral annular motion will be enhanced, seen as a high e′ velocity on the Doppler tissue velocity curve. Thus, S3s are often noted in young individuals, athletes, and pregnant patients. Conversely, they are rarely observed in patients older than 40 years; the presence of an S3 in patients older than age 40 suggests organic heart disease.

Constrictive pericarditis is also a form of severe diastolic heart failure, where the scarred, inelastic pericardium significantly impairs ventricular diastolic filling. Rapid filling waves on right and left ventricular hemodynamic tracings were some of the earliest hemodynamic signs of constrictive pericarditis described by cardiac catheterization. This prominent early diastolic filling is responsible for the pericardial knock heard in constrictive pericarditis. The knock tends to happen slightly earlier than the typical S3 and tends to have a higher pitch.

High E wave velocities and rapid filling waves on ventricular tracings can also be seen in severe mitral regurgitation. These are secondary to the large volume of blood rapidly returning from left atrium to left ventricle in early diastole. This increased rapid early diastolic filling can produce a low-pitched “filling sound” in mitral regurgitation and is a key marker of severe mitral regurgitation.

Although the findings described so far are related to left-sided etiologies (except for the pericardial knock, which is most likely originated from the right ventricle), the same rationale can be applied to right-sided lesions. A right-sided S3 can be heard in severe right ventricular diastolic dysfunction, such as severe right-sided heart failure and restrictive cardiomyopathy. Filling sounds can also be heard in severe tricuspid regurgitation and may be the only finding on auscultation; the systolic murmur may be barely audible due to equalization of the right atrial and right ventricular pressures during systole. Inspiration will enhance the intensity of a right-sided S3 and S4.

Gallops

When tachycardia is present in conjunction with an S3 or an S4, a gallop rhythm is said to be present. If both are present and diastolic periods are markedly diminished (due to faster heart rates), S3 and S4 will occur that same time—a summation gallop. This physical finding is analogous to the presence of fused E and A waves on mitral inflow echo-Doppler.

Opening Snap of Mitral Stenosis

The opening snap of rheumatic mitral stenosis is an early diastolic, high-pitched sound originating from sudden tensing of abnormal leaflets and subvalvular apparatus during valve opening (equivalent of the “hockey stick deformity” on two-dimensional echocardiography). The finding of an opening snap has important clinical implications and deserves meticulous assessment. Because of its high pitch, the opening snap has a much wider area of radiation than the associated diastolic rumble of mitral stenosis; it can be heard at the left sternal border and even at the base of the heart in the aortic position. An opening snap has a much higher pitch than an S3, which is low pitched and heard only at the apex. It may be difficult to differentiate an opening snap from a loud P2, but a P2 should not be heard at the aortic position unless there are systemic levels of pulmonary hypertension.

The presence of a crisp opening snap suggests that the mitral leaflets are mobile and pliable and hence amenable to percutaneous balloon valvotomy. With more severe calcification and immobility of the leaflets, the opening snap becomes softer or disappears. The opening snap also allows the assessment of left atrial pressures and severity of the mitral stenosis. The mitral valve will open when left ventricular pressure drops below left atrial pressure. With mild degrees of stenosis, left atrial pressure is not severely elevated and mitral valve opening occurs late. The result is a long A2 (aortic valve closure) to opening snap (mitral valve opening) interval. With severe mitral stenosis, there is an elevated left atrial pressure with earlier opening of the mitral valve, generating a short A2-OS interval. Intervals of less than 70 milliseconds suggest severe mitral stenosis, whereas intervals greater than 100 milliseconds are compatible with mild obstruction.

Systolic Clicks

Systolic clicks can arise from valvular and nonvalvular structures (eg, the great arteries). The two most common (and more relevant) clicks are the ones heard in bicuspid aortic valve and mitral valve prolapse. Although the former is typically described as an ejection click and the latter a nonejection click, a description based on timing is more appropriate.

The click of a bicuspid aortic valve (and sometimes of other congenitally abnormal aortic valves such as unicuspid valves) is secondary to the doming of the valve cusps in early systole as the aortic valve opens. The sound is high pitched (higher than S1) and sometimes quite loud; it should not be confused with a loud split S1 (two components of same pitch and intensity) or an S4 (low-pitched sound that vanishes if the bell is firmly pressed against the skin).

Doming of the cusps is also seen in valvular pulmonary stenosis, and an early systolic click is also typical. As in bicuspid aortic valve, the click of pulmonary stenosis introduces the systolic murmur. However, the click noted in pulmonary stenosis has a unique and important characteristic—it decreases in intensity with inspiration and moves closer to S1. This is the only right-sided auscultatory finding that diminishes with inspiration. As a result of increased venous return and increased right ventricular filling on inspiration, the pulmonary cusps acquire a more cephalad configuration. There is less cusp excursion during systole and a softer click.

Early systolic clicks can also arise from dilated great vessels (aorta or pulmonary artery). These are difficult to discern from the clicks associated with dysplastic or congenitally abnormal semilunar valves at the bedside. Another rare source of systolic clicks is an atrial septal aneurysm, arising from the motion of a very redundant valve of the fossa ovalis. These less common abnormalities should also be looked for when echocardiography studies are ordered for the evaluation of systolic clicks.

The systolic click(s) associated with mitral valve prolapse usually occurs in mid-to-late systole, when there is full excursion of the prolapsed mitral leaflet(s) into the left atrium. The click can be single or multiple (salvo of clicks). The timing of the click of mitral valve prolapse occurring later in systole helps to differentiate it from clicks arising from semilunar valves. With increased preload (squatting, supine) the click occurs later in systole, whereas decreased preload (Valsalva maneuver, standing) has the opposite effect.

Miscellaneous

Pericardial rubs may have three components, one systolic and two diastolic. Systolic and presystolic sounds are most commonly present. The pericardial rubs are described as “scratchy,” with a high pitch. Although the presence of pericardial rubs can be intermittent, the practitioner should optimize the patient’s position in order to better detect the rub. Pericardial rubs are generally best heard with the patient sitting, leaning forward with held expiration.

There are extracardiac sounds that can be heard on auscultation of the heart. A mediastinal “crunch” is caused by inflammation or air in the mediastinum that is of high pitch and has a rhythm that corresponds to the cardiac contraction within this mediastinum; this sound is markedly enhanced during inspiration. Pleural rubs may be mistaken for cardiac sounds, particularly in the patient who has tachypnea, and auscultation during held respiration is required to differentiate this sound from a cardiac etiology. Pacemaker wires can produce clicks and high-pitched “squeaks” resulting from excessive motion of the wires during the cardiac cycle.

Prosthetic Heart Valves

Auscultation of prosthetic heart valves is an important component of the physical examination. All mechanical valves should produce a crisp, high-pitched sound during valve closure, irrespective of the type of valve. The older generation valves, such as a ball–cage prosthesis and some of the tilting disk prostheses, will produce a click during valve opening; however, the newer generation floating disk and bileaflet valves are usually silent with valve opening. There is always an intrinsic degree of obstruction with any prosthesis, which produces a short systolic ejection murmur in the aortic or pulmonic position, and may produce a diastolic rumble in the mitral or tricuspid valve position. However, murmurs of prosthetic valve regurgitation indicate pathology.

Murmurs are the auscultatory equivalents of nonlaminar flow through an anatomic structure (eg, a cardiac valve or intracardiac shunt). When similar sounds originate from peripheral vessels, by convention, a bruit is described. In echocardiography, nonlaminar flow is manifest by turbulent high velocity flow and assessed by continuous-wave Doppler echocardiography. Although other factors play a role (eg, the size of an interventricular communication, the effective orifice area in a regurgitant atrioventricular valve or blood viscosity), murmurs tend to reflect the pressure difference between structures from which the murmur originates. The diastolic murmur from a stenotic atrioventricular valve (mitral or tricuspid) tends to be low-pitched and quiet, because atrial and ventricular diastolic pressures are typically low. The murmur of aortic regurgitation is a high-pitched “cooing” sound resulting from the high pressure difference between the aorta and left ventricular pressures during diastole.

When a murmur is identified, several characteristics need to be analyzed and described; these include timing (systolic, diastolic, or continuous), pitch, intensity (“loudness”), contour (or shape, eg, crescendo vs decrescendo), and radiation. Dynamic changes, such as respirophasic or postextrasystolic changes and response to maneuvers should also be noted. The murmur intensity should be graded from I to VI (Table 11–5).

“Drawing” physical examination findings used to be part of clinical documentation, perhaps best exemplified in Paul Wood’s legendary index cards. Although electronic clinical notes do not allow these features to be incorporated into patients’ charts, we recommend trainees go through the exercise of drawing murmurs. These exercises force the examiner to critically review the auscultatory findings, which include the timing of onset and cessation of the murmur, the contour of the murmur, and its relationship to normal and abnormal heart sounds.

Systolic Murmurs

General Principles

The most commonly encountered systolic murmurs originate from regurgitant atrioventricular valves or from accelerated flow across semilunar valves. The shapes of those murmurs will reflect the differences in hemodynamics as well as dynamic changes in the valvular and subvalvular apparatus. These differences in timing of onset and cessation are reflected in the continuous-wave Doppler traces of the atrioventricular valve regurgitation and semilunar valve obstruction.

In typical atrioventricular regurgitation, the murmur starts at mitral valve closure and extends to the mitral valve opening (Fig. 11–18). As a result, the murmur will have its onset immediately after the first heart sound and will extend through the S2—holosystolic. Given the high pressure differences between ventricles and atria throughout systole, the murmur is high pitched and does not change in contour: hence the term plateau. An analogous process happens in ventricular septal defects, where the pressure gradient between left and right ventricles also extends from mitral valve closure (S1) to mitral valve opening.

Semilunar valves open when the ventricular pressure exceeds the pressure in the great vessels. Thus, these murmurs will start after S1 occurs (see Fig. 11–18). The shape of these murmurs will reflect the changes in ejection hemodynamics throughout systole, giving rise to its diamond shape, where the murmur increases and then decreases in intensity (crescendo-decrescendo). These systolic ejection murmurs have a harsher quality than the regurgitant murmurs.

Atrioventricular Valve Regurgitation: Holosystolic Murmurs

Mitral regurgitation murmurs are typically best heard over the cardiac apex, but radiation will vary depending on the underlying disease. When the mitral regurgitation jet is anteriorly directed (toward the aorta), as noted in patients with prolapse or a flail segment of the posterior mitral leaflet, the murmur radiates to the left sternal border. In posteriorly directed mitral regurgitation jets caused by prolapse or flail of the anterior mitral leaflet, the murmur radiates to the left axilla, back, and thoracic spine.

Although typically described as holosystolic and plateau in quality, mitral regurgitation murmurs will vary according to the underlying pathology. In regurgitation resulting from rheumatic mitral valve or flail mitral leaflet, the murmur will be holosystolic. In mitral valve prolapse with an intact chordal apparatus, the regurgitation starts after the leaflet has prolapsed into the left atrium; a gap between S1 and the murmur is then present, which frequently starts after a midsystolic click. The late occurrence of a murmur in mitral valve prolapse is of great diagnostic importance. First, it suggests that the tendinous cords are intact and no flail segment is present. Secondly, it suggests that the regurgitation is not severe; late (ie, nonholosystolic) murmurs are rarely severe. Doppler echocardiography will clearly demonstrate the difference between a holosystolic murmur and a late systolic regurgitation both on color flow imaging and continuous-wave Doppler velocity curves (Fig. 11–19).

In secondary mitral regurgitation (the mitral regurgitation results from a disease of the ventricle and not the valve), the murmur can be soft and underwhelming despite the presence of severe regurgitation; this is likely due to a combination of reduced ventricular contraction and a large regurgitant orifice. If the mechanism is annular dilation, the murmur tends to be holosystolic, whereas in ischemic mitral regurgitation the murmur may be late peaking. Ischemic mitral regurgitation can also be dynamic, with variation in the physical examination findings depending on the presence or absence of ischemia.

In acute severe mitral regurgitation secondary to papillary muscle rupture or mitral valve dehiscence, the left atrium is not accustomed to the severe volume overload. A very large v wave is generated because of lack of atrial compliance, and left ventricular and left atrial pressures essentially equalize in systole (Fig. 11–20). The auscultatory result is a very short, early systolic murmur or even absence of a murmur. Accordingly, color-flow and continuous-wave Doppler findings are also often very brief, making the diagnosis of acute mitral regurgitation challenging. Thus, a high clinical index of suspicion is needed. Patients with acute severe mitral regurgitation are in frank pulmonary edema and therefore sitting upright, whereas patients with ventricular septal defect can tolerate the supine position.

Tricuspid regurgitation is usually secondary to dilatation of the tricuspid valve annulus and manifested as a holosystolic murmur, best heard at the left lower sternal border. The murmur can be very subtle, rarely greater than a grade II in intensity. Although described as a classic sign in tricuspid regurgitation, an increase in the intensity of the holosystolic murmur (Carvallo sign) is not a sensitive sign. The clinical suspicion of severe tricuspid regurgitation is made more on the basis of a large v wave in the jugular venous contour rather than the presence of a murmur.

Ventricular septal defects, most often muscular, can also present as holosystolic murmurs. Small ventricular septal defects are usually associated with a loud murmur, frequent accompanied by a thrill, and best heard at the left lower sternal border. If there is a large septal defect, the murmur can be soft or even absent, particularly when an Eisenmenger’s physiology is present.

Systolic Ejection Murmurs

In aortic stenosis, a diamond-shaped murmur can be auscultated at the third left intercostal space, second right intercostal space, or supraclavicular region, usually radiating to the carotids. In young patients with bicuspid valve–related aortic stenosis, the murmur is often quieter over the precordium and best heard toward the suprasternal notch. The murmur of aortic stenosis can radiate and, in fact, increase in intensity, toward the apex—the Gallavardin phenomenon.¹⁶ As the disease progresses; the peak of murmur occurs later in systole; it has an early systolic peak in mild and moderate aortic stenosis and late peak in severe aortic stenosis (Fig. 11–21). The duration of the murmur becomes longer as the severity increases, so that in severe aortic stenosis the murmur extends to the second heart sound. The pitch of the murmur also tends to change with more severe stages, when the murmur acquires a high-pitched, musical characteristic. The severity of aortic stenosis based on the quality of the murmur is reflected in the continuous-wave Doppler velocity curves, with early peaking velocities in mild stenosis and mid-to-late peak (longer acceleration time) in more severe aortic stenosis.¹⁷ The more severe the stenosis, the longer the ejection time on the continuous-wave Doppler tracing.

Pulmonic stenosis is less common than aortic stenosis. There will be a systolic ejection murmur heard best in the pulmonic position at the left sternal border and radiate to the left clavicle. Early ejection clicks and abnormalities of S2 are frequently present, as described previously.

In obstructive hypertrophic cardiomyopathy, two distinct systolic murmurs are audible. The harsh murmur related to subaortic obstruction is generally best heard at the left sternal border and will have crescendo-decrescendo contour with a midsystolic peak. A separate, murmur is heard best at the apex and starts in midsystole. It is caused by the secondary mitral regurgitation from distortion of the mitral valve apparatus related to systolic anterior motion of the mitral valve. This is of clinical importance because relief of the outflow obstruction will also reduce the mitral regurgitation. Both murmurs will increase in intensity during the strain phase of the Valsalva maneuver, on standing and post–premature ventricular beats. Both murmurs will also decrease with squatting. It is also important to note the dynamic changes in the apical murmur (in addition to the murmur associated with the left outflow tract obstruction) during maneuvers, particularly with squatting. If the apical murmur does not change, a primary mitral valve problem should be suspected.

Pathologic murmurs should be differentiated from innocent or benign murmurs. Benign murmurs arise from increased flow through a semilunar valve and thus have a diamond-shape. However, they typically peak in early systole, and are usually grades II or less in intensity, and end before S2. Innocent murmurs change according to position, being more prominent in the supine compared to sitting position. In childhood, an innocent murmur is usually caused by increased flow across the pulmonic valve and is heard best in the pulmonic position at the upper left sternal border. In older age, aortic valve sclerosis occurs because of mild thickening of the aortic valve cusps, and a soft ejection murmur is heard at the aortic position in the upper right sternal border. In both of these cases, a normal carotid upstroke and normal components of S2 are used to help in differentiating these from pathological murmurs. Functional murmurs result from increased forward flow across a normally functioning semilunar valve. These murmurs can be observed in pregnancy, high-output state, or anemia. The high-output state associated with an arteriovenous fistula in patients with chronic renal failure is commonly associated with a loud functional murmur, which will decrease in intensity with temporary occlusion of the fistula.

Diastolic Murmurs

General Principles

Diastolic murmurs can arise from atrioventricular valve stenosis and semilunar valve regurgitation. The timing and quality of the murmurs are based on the pressure differences across the abnormal valves, which are reflected in the continuous-wave Doppler velocity curves of these valve abnormalities. It is primarily the pitch and location of diastolic murmurs that define the etiology.

Diastolic Rumbles

The rumble of mitral stenosis is a subtle, low-pitched murmur, best heard over the apex; occasionally the murmur is heard only with the patient in left lateral decubitus. The bell should be placed very lightly over the apex and the examiner should concentrate on listening during diastole. The duration of the murmur (early-mid to holodiastolic) tends to be directly proportional to the diastolic gradient and severity of stenosis. If sinus rhythm is present, the murmur increases during atrial contraction—presystolic accentuation. Because diastolic mean gradients are also directly related to heart rate, maneuvers that increase heart rate (sit-ups or phantom bike) facilitate detection of the murmur. Tricuspid stenosis is rare and usually occurs in conjunction with mitral stenosis. Faint diastolic rumbles are often noted in patients with prosthetic mitral or tricuspid tissue prostheses; however, the presence of a loud diastolic murmur in a patient with a mitral or tricuspid prosthesis should raise concern for dysfunction or thrombosis.

Functional diastolic rumbles can occur with increased forward flow across the atrioventricular valves (eg, in a patient with an atrial septal defect); a flow rumble is noted due to increased flow across the tricuspid valve related to the left-to-right shunt. A diastolic flow murmur is also heard in patients with severe mitral or tricuspid regurgitation caused by increased return flow across the valve. A middiastolic rumble—the Austin-Flint murmur—may be heard in aortic regurgitation when an eccentric jet hits the anterior leaflet of mitral valve, causing it to reverberate and generating the apical rumble.

Diastolic Decrescendo Murmurs

The murmur of aortic regurgitation is a diastolic decrescendo, high-pitched blowing murmur, usually heard best at the left intercostal border. It is best heard using the diaphragm placed firmly in the sitting position. To hear a soft murmur, the patient should lean forward with a breath held. The duration as well as the intensity of the murmur are generally related to the severity of the regurgitation. In mild regurgitation, the murmur is early diastolic, whereas a holodiastolic murmur suggests more severe regurgitation. However, it is the peripheral signs of a wide pulse pressure that are most indicative of severe aortic regurgitation. Aortic regurgitation murmurs heard over the second right intercostal space result from annular dilatation, whereas murmurs heard over the third left intercostal space result from a valvular process.

The murmur associated with pulmonary regurgitation is typically heard over the second left intercostal space, has a low pitch, and can be difficult to hear. The bell of the stethoscope is generally used. The murmur typically increases with inspiration, allowing its differentiation from aortic regurgitation. In very severe cases of pulmonary regurgitation, there is equalization of right ventricular and pulmonary artery diastolic pressures in early-to-mid diastole, rendering a rather short murmur. Functional pulmonary regurgitation can also be present when there is severe pulmonary hypertension—the Graham-Steel murmur. This murmur has a high pitch compared to primary pulmonary regurgitation and follows a loud pulmonary component of the second heart sound, suggesting the underlying association.

Continuous Murmurs

The continuous murmur is characterized by a “to-and-fro” sound with no interruption between systole and diastole. The pitch should be similar but the intensity can vary throughout the cardiac cycle. By definition, the continuous murmur envelops the heart sounds. This is distinctly different than a systolic and diastolic murmur, as noted in mixed aortic valve disease. In that case, one will hear a harsh, diamond-shaped systolic murmur, a second heart second (which might be single), and a diastolic murmur. These murmurs will have two distinctly different pitches.

The most common continuous murmur seen in current practice is secondary to iatrogenic arteriovenous fistulas (for hemodialysis), which is generally appreciated in the region of the clavicle on the respective side. Other causes of continuous murmurs are rare and include patent ductus arteriosus (best heard over the left infraclavicular area), ruptured sinus of Valsalva aneurysm, coronary fistula, intrathoracic arteriovenous fistulae, severe coarctation of the aorta, and a surgically created shunt (eg, Blalock-Taussig, Potts, Waterston).

The venous hum is a continuous murmur heard on auscultation of the neck. It results from a high flow in the internal jugular vein, which most likely causes a vibration of the venous wall. It is most commonly heard in young, otherwise healthy individuals and is not associated with pathology. The venous hum will disappear with the supine position or with compression of the vein itself.

Dynamic Auscultation

Dynamic auscultation should play an integral role in differentiating the etiology of systolic murmurs. It should also be performed during examination of young individuals engaged in competitive sports, in whom a latent obstruction from obstructive hypertrophic cardiomyopathy could be missed if maneuvers are not performed. Dynamic auscultation includes respirophasic changes and changes in murmur intensity on postectopic beats, as well as changes induced by specific maneuvers as well.

Inspiration increases venous return to the right cardiac chambers, augmenting right-sided murmurs and diastolic sounds. The exception to the rule is the systolic click of pulmonary stenosis, which diminishes with inspiration. Typically described as a classic sign of tricuspid regurgitation (versus other systolic murmurs) is the Carvallo sign: an increase in the intensity of the murmur with inspiration. Negative intrathoracic pressures generated by inspiration lead to an increase in left ventricular afterload; therefore, the dynamic left ventricular outflow tract systolic murmur of hypertrophic cardiomyopathy will decrease on inspiration (Fig. 11–22).

In patients with systolic murmur, attention should be paid to the change in intensity of the murmur on the postectopic beats. There is an increase in ventricular contractility and a decrease in afterload on the postectopic beat; thus, there will be an increase in the intensity of the murmur with both fixed (aortic stenosis) and dynamic (hypertrophic cardiomyopathy) left ventricular outflow tract obstruction. This response is much more striking in the setting of obstructive hypertrophic cardiomyopathy because there is also an increase in the degree of obstruction (Fig. 11–23). Alternatively, in patients with mitral regurgitation, there is no change in the intensity of the murmur on the postectopic beat due to the decrease in afterload.

The Valsalva maneuver consists of expiration against a closed glottis, generating in an increase in intrathoracic pressures of 30 to 40 mm Hg for a least 10 seconds. It is a method by which systolic murmurs may be differentiated. A simple way of performing the maneuver is by placing the examiner’s hand over the patient’s abdomen and asking the patient to push against it. The normal response to the maneuver consists of four phases¹⁸: phase I, a transient increase in systemic blood pressure during the strain phase secondary to the elevation in intrathoracic pressures; phase II, a decrease in pulse pressure and stroke volume to decreased venous return, which results in reflex tachycardia (the so-called active phase); phase III, further decrease in blood pressure due to the initial release of the straining phase; and phase IV, an overshot of blood pressure levels over the ones observed at baseline. Each of these phases is associated with changes in heart rate; the most important ones are the reflex tachycardia observed in phase II and reflex bradycardia in phase IV as blood pressures increases (Fig. 11–24).

Given the reduction in stroke volume occurring during phase II of the maneuver, most systolic murmurs will decrease during that phase; the exceptions are the murmurs of mitral valve prolapse and hypertrophic cardiomyopathy. In mitral valve prolapse, there is further atrial displacement of the leaflets during phase II, resulting in an earlier click and longer and typically louder murmur. In hypertrophic cardiomyopathy, the smaller ventricular cavity will lead to more severe subaortic obstruction and a louder murmur. Of note, these changes tend to be more pronounced if the patient is sitting or upright. It is important to document the change in intensity of the murmur only after at least six to eight beats during the strain phase, because this is the time period during which the change in blood volume must circulate through the pulmonary circulation to reach the left side of the heart. The examiner should also note the changes in heart rate through the phase II of the maneuver. If there is not a tachycardia during phase II, there is autonomic dysfunction, autonomic blockade (eg, beta-blockers), or high filling pressures (Fig. 11–25). In these cases, the response of a murmur will not be useful. During phase 4, all murmurs usually increase, except with hypertrophic cardiomyopathy.

The stand-to-squat-to-stand maneuver is particularly helpful in patients with hypertrophic cardiomyopathy and mitral valve prolapse. Squatting increases both preload and afterload. As a result, squatting significantly diminishes (or even abolishes) the intensity of the murmur of obstructive cardiomyopathy. This is also true for mitral regurgitation that is secondary to systolic anterior motion of the mitral valve. In mitral valve prolapse, the systolic click occurs later in systole and the murmur becomes shorter (Fig. 11–26). All other murmurs will have either an increase in intensity or no change in intensity with squatting. On standing, there is an immediate decrease in afterload followed by a decrease in venous return after several beats. Thus, there will be an immediate and then progressive increase in the intensity of the dynamic outflow murmur of hypertrophic cardiomyopathy.

In instances where there are very soft murmurs out of proportion to the presenting symptoms, a reexamination after exercise may reveal a significant change in the intensity and characteristic of the murmur. This is important in patients with hypertrophic cardiomyopathy and a labile outflow tract obstruction, or in patients with mitral stenosis. Exercise can involve sit-ups on the examining table, step-ups on the bench, or even walking up and down hallways and stairwells. These exercise maneuvers are also useful to bring out an S3 if absent at rest. Handgrip isometric exercise to increase afterload and amyl nitrate to decrease afterload are maneuvers that have been used to differentiate the rumble of mitral stenosis from an Austin-Flint murmur, but they are no longer necessary with the advent of echocardiography.

Each clinician needs to develop his or her own stepwise approach to the cardiovascular examination. We wish to present our own approach (Table 11–6), which we apply in a general fashion to the majority of patients presenting with cardiovascular disease, understanding that the examination is always then focused on an individual patient’s problem. We feel that the initial history should be taken with the patient fully dressed to allow a one-to-one relationship to be built. However, for a comprehensive physical examination, it is necessary for the patient to be undressed with an appropriate gown or cover-up. An examination should never be done placing the stethoscope under a shirt or blouse, and full inspection of the chest and extremities is always necessary.

The initial approach that we take is to approach the patient in the sitting position, looking at the overall appearance to determine if there are unusual features that may suggest a syndrome. Shaking the hands will help in a frailty assessment as well as determining tissue perfusion. Palpating the radial pulse in both wrists will provide the heart rate and rhythm and any blood pressure differences in the two upper extremities. Looking at the nail beds is important for the presence of clubbing, cyanosis, or high pulse pressures. Then taking the blood pressure by cuff in both arms should be performed.

Inspection of the rest of the chest and extremities will identify skin lesions, skin infections, or prior surgical scars that may influence the diagnosis and decision making. Examining the venous pulsations in the sitting position will provide an initial clue as to whether there is elevation of venous pressure. Palpation of the carotid and brachial arteries is then performed, listening first for bruits. Palpation of the chest for thrills and palpable heart sounds is done next, followed by auscultation of the lungs.

Auscultation of heart sounds in the sitting position should be performed using the diaphragm starting at the base of the heart, inching across to the left sternal border, and then inferiorly to the lower left sternal border and then to the apex. In each position one should listen to S1, S2, systole and diastole. In particular, the splitting of S2 should be evaluated in the sitting position. Aortic and pulmonary outflow murmurs should be evaluated. Aortic and pulmonic regurgitant murmurs should be sought with the patient leaning over with breath held at end expiration. Pericardial rubs are best heard in this position.

Following the auscultation in the sitting position, an examination of the venous pressure and venous contour should be done, with a gradual change in the position of the patient from sitting at 90 degrees down to the supine position until the venous pulsations are visible in the internal jugular vein. Once the top of the pulsations is established, the height of the venous pressure is estimated, usually at 45 degrees or less.

The patient is then placed in the supine position and palpation is then performed again, primarily to feel any parasternal lift and the position of the apical impulse. Auscultation is then performed starting from the apex to the left sternal border up to the base of the heart. Again, S1, S2, systole and diastole are listened to at each position.

The patient is then placed in the left lateral decubitus position. The apical impulse is palpated, this time to determine the contour of the impulse, whether localized or enlarged, sustained or hyperdynamic or feeble, and to feel for and palpable S4 or S3. Auscultation is then performed with the bell at the apex, specifically to listen for diastolic filling sounds and diastolic rumbles.

Finally, examination of the abdomen is performed, palpating for the liver and aorta, and listening for abdominal bruits. Examination of the lower extremities for edema, lesions, and palpation of all pulses should be done, always feeling the radial and femoral pulses simultaneously.

Additional focused parts of the examination should be performed depending on the clinical scenario. In patients with suspected constrictive pericarditis, a more detailed evaluation of the venous pressure and contour is required. In patients who present with exertional dyspnea and no significant findings on initial examination, repeating auscultation during exercise may elicit an S3 or diastolic rumble. Patients with hypertrophic cardiomyopathy should always undergo further dynamic auscultation with the Valsalva maneuver, stand-to-squat-to-stand, and even exercise to further evaluate a dynamic obstruction. Table 11–7 outlines the important physical findings for each individual cardiac lesion that aid in diagnosis and determination of severity.