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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.
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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.
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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).
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Normal First Heart Sound
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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.
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Abnormalities of the First Heart Sound
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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.
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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.
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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.
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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.
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Normal Second Heart Sound
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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.
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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.
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Physiologic Splitting of S2
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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).
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Abnormal Splitting of S2
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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.
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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.
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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.
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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.
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Abnormalities of S2 Components
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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Opening Snap of Mitral Stenosis
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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.
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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.
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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.
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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).
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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.
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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.
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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.
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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.
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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.
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Prosthetic Heart Valves
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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.