Official reprint from UpToDate® www.uptodate.com ©2019 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Auscultation of heart sounds Author: Theo E Meyer, MD, PhD Section Editor: Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC Deputy Editor: Susan B Yeon, MD, JD, FACC All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Mar 2019. | This topic last updated: Dec 12, 2018. INTRODUCTION The cardiovascular physical examination includes auscultation and palpation of the heart, as well as examination of the arterial and venous pulses. The purpose of auscultation of the heart is to characterize heart sounds and murmurs. (See "Examination of the precordial pulsation" and "Examination of the arterial pulse" and "Examination of the jugular venous pulse".) This topic will review the auscultation of heart sounds. The auscultation of cardiac murmurs is discussed separately. (See "Auscultation of cardiac murmurs in adults".) STETHOSCOPES A variety of stethoscopes are available for auscultation of heart sounds. Many stethoscopes have a separate bell and diaphragm. The bell is most effective at transmitting lower frequency sounds, while the diaphragm is most effective at transmitting higher frequency sounds. Some stethoscopes combine these functions into a single surface such that the intensity of pressure of the stethoscope against the skin determines whether the stethoscope functions as a bell or a diaphragm. In addition, pressing the bell more firmly against the skin alters the frequencies that are loudest towards those of a diaphragm, such that higher frequency sounds become louder and lower frequency sounds become softer. Acoustic as well as electronic stethoscopes are used for cardiac auscultation. There is limited evidence comparing these devices [1­3]. Electronic auscultatory devices utilize advanced acoustic sensor­based digital signal processing with a wide range of frequency response modes to enhance sound acquisition [4]. Electronic devices offer bell or diaphragm modes, similar to acoustic stethoscopes, although the acoustic characteristics of these devices differ [5]. Since an electronic stethoscope is sensitive to ambient and friction noise, various electronic stethoscope models offer technology for noise reduction. An electronic device enables shared auscultation for teaching purposes and also enables direct digital recording of heart sounds for review and analysis. CLASSIFICATION OF HEART SOUNDS Heart sounds are broadly classified into high­ and low­frequency sounds [6]. High­frequency sounds arise from closing or opening valves, including mitral and tricuspid valve closing sounds (M1 and T1), non­ejection sounds, opening snaps, aortic and pulmonary valve closure sounds (A2 and P2), and early valvular ejection sounds. Prosthetic valve sounds are also high frequency. (See 'First heart sound (S1)' below and 'Second heart sound (S2)' below and 'Ejection sounds' below and 'Non­ejection systolic sounds' below and 'Early diastolic high­frequency sounds' below and 'Prosthetic valve sounds' below.) Low­frequency sounds include the third heart sound (S3, which may be physiologic or pathologic), associated with early ventricular filling, and the fourth heart sound (S4), associated with the atrial contribution to ventricular filling in late diastole. (See 'Third (S3) and fourth (S4) heart sounds' below.) FIRST HEART SOUND (S1) Genesis, timing, and location of S1 — The classic hypothesis for the genesis of the first heart sound (S1), for which there is much support, relates the high­frequency components of S1 to mitral and tricuspid valve closure. The first component of S1 is attributed to mitral valve closure (M1) and the second to closure of the tricuspid valve (T1) [7­10]. More detailed examination of closure sounds also suggest that the peak tension on the chordae tendineae and leaflets themselves appear to contribute to the production of M1 and T1 [11,12]. A second hypothesis suggests that the principal high­frequency elements of S1 are related to movement and acceleration of blood in early systole, and are influenced by the peak rate of rise of left ventricular (LV) systolic pressure (dP/dt), which is a measure of contractility and ejection of blood into the root of the aorta [13]. S1 occurs just before or is coincident with the upstroke of the carotid pulse. M1 precedes the upstroke of the carotid pulse because it occurs before LV ejection begins. However, the delay between M1 and the upstroke of the carotid pulse normally is too short to be appreciated at the bedside. T1 normally coincides with the upstroke of the carotid pulse. S1 normally is louder than the second heart sound (S2) over the apex and along the lower left sternal border; intensity is reduced if S1 is softer than S2 over these areas. S1 intensity is likely to be accentuated if S1 is much louder than S2 over the left or right second interspace. The M1 sound is much louder than the T1 sound due to higher pressures in the left side of the heart; thus, M1 radiates to all precordial areas (loudest at the apex), and T1 is usually only heard at the left lower sternal border. This makes the M1 sound the main component of S1, and is best heard with the diaphragm of the stethoscope. Intensity of S1 — The following factors influence the intensity of S1: ● Mitral valve position at the onset of systole (wide versus partially open). ● Rate of M1 and T1. ● Mobility and structural integrity of the atrioventricular (AV) valves (eg, fibrosis, commissural fusion of the leaflets, tethering of the posterior mitral leaflet, etc). ● The PR interval, the timing of atrial contraction (a determinant of mitral valve position) as it relates to the onset of LV contraction. ● Force of ventricular systolic contraction. Some of these factors, such as the rate of M1 and the strength of ventricular systole, are interrelated; more than one factor may contribute to altered S1 intensity. ● Increased intensity of S1 – The following factors contribute to the position of mitral valve (distance to closure) and velocity of closure (table 1): • Increased transvalvular gradient, especially at end­diastole (mitral or tricuspid valve obstruction as in mitral stenosis (movie 1), tricuspid stenosis, or atrial myxoma). • Increased transvalvular flow (left­to­right shunt in patent ductus arteriosus, ventricular septal defect, and high output state). • Short diastole (tachycardia). • Short PR intervals (preexcitation syndrome) The relative contribution of the distance of travel and the velocity of M1 to increased S1 intensity is difficult to determine; both factors are likely to play a role. When M1 occurs on the steeper part of the LV pressure development, the intensity of S1 increases; this phenomenon may also contribute to an accentuated S1 observed in patients with extremely short PR intervals, mitral stenosis, and left atrial myxoma (figure 1)[14]. Similarly, S1 is normal or even accentuated in patients with mitral valve prolapse with late systolic regurgitation. Increased intensity of S1 in some patients with mitral valve prolapse syndrome may be caused by an increased strength of ventricular systole (hyperkinetic). The increased intensity of T1 in atrial septal defect and tricuspid valve obstruction (eg, tricuspid stenosis, right atrial myxoma) can also be explained by the same phenomenon. The tricuspid valve is held open by increased transvalvular flow and the transvalvular gradient until final closure with increased velocity occurs with right ventricular (RV) systole. ● Decreased intensity of S1 – A soft S1 is mostly related to decreased mobility or due to a semi­ closed position of the leaflets prior to systole. Thus, S1 is soft when the mitral valve is immobile due to calcification and fibrosis, despite a significant transvalvular gradient. S1 may also be reduced when the leaflets are semi­closed prior to the onset of systole or when the velocity of closure is reduced, as can occur with LV dysfunction. These situations are illustrated by the following examples (table 1): • S1 is very soft or absent when mitral regurgitation (MR) results from fibrosis and destruction of the valve leaflets (as in patients with rheumatic valve disease), which prevent effective M1. In contrast, MR due to perforation of the valve leaflets from bacterial endocarditis may not be associated with a reduced intensity of S1. • Reduced S1 intensity occurs when the mitral valve remains in the semi­closed position before the onset of ventricular systole, and the velocity of valve closure is decreased. S1 is usually soft when the PR interval is prolonged (exceeding 0.2 seconds) since semi­closure of the mitral valve occurs following atrial systole and before ventricular systole begins. Premature closure of the mitral valve can occur in patients with severe acute aortic regurgitation due to a rapid rise in LV diastolic pressure; the mitral valve may be virtually closed at the onset of systole, resulting in a markedly decreased intensity of or even absent S1 [15]. (See "Acute aortic regurgitation in adults", section on 'Cardiac auscultation'.) • S1 is soft in some patients with left bundle branch block without any other obvious abnormality; the mechanism is unclear. Decreased valve closure velocity due to myocardial dysfunction is possible. • Hemodynamically significant aortic stenosis may be associated with a soft S1; this can occur in the absence of spreading calcification to the mitral valve and in the presence of a normal PR interval [14]. Semi­closure of the mitral valve due to a powerful atrial contraction and an abnormally elevated LV diastolic pressure before the onset of ventricular systole is the most likely explanation. • S1 is frequently soft in patients with dilated cardiomyopathy, even in the absence of a prolonged PR interval or bundle branch block. The decreased S1 is almost invariably associated with a significantly reduced LV ejection fraction (LVEF) and elevated pulmonary capillary wedge pressure. The mechanism for a soft S1 in these patients remains unclear; semi­closure of the mitral valve due to an elevated LV diastolic pressure and decreased velocity of valve closure due to myocardial dysfunction may contribute. • Decreased conduction of sounds through the chest wall reduces the intensity of S1 in patients with chronic obstructive pulmonary disease, obesity, and pericardial effusion. ● Variation in the intensity of S1 may be evident in the following situations: • It is a common feature of atrial fibrillation; the mechanism appears to be a variation in the velocity of valve closure related to changes in the RR cycle length. • The intensity of S1 varies in the presence of premature beats. • Changing intensity of S1 occurs in AV dissociation, whether the heart rate is slow or fast (eg, in complete heart block or ventricular tachycardia). The changing intensity is due to random variation of the PR interval; the short PR interval is associated with an increased intensity and the long PR interval with a decreased intensity. The pulse is regular in AV dissociation; thus, the varying intensity of S1 in a patient with a regular pulse almost always suggests AV dissociation. • Auscultatory alternans, in which S1 is soft and loud with alternate beats, is a rare finding in severe cardiac tamponade; it is almost always associated with electrical alternans and pulsus paradoxus. Although the pulse is regular, changes in the intensity of S1 occur regularly with the alternate beats and not randomly as in AV dissociation. Splitting of S1 — There are normally two components of S1: The mitral component precedes the carotid pulse upstroke, and the tricuspid component occurs later. The interval between M1 and T1 is 0.02 to 0.03 seconds, and can be appreciated with the diaphragm of the stethoscope along the lower left sternal border [7]. The mitral component is much louder than the tricuspid component and is normally heard more widely across the precordium; the tricuspid component is of low intensity and is best heard over the left third and fourth interspaces close to the sternal border. Abnormal splitting of S1 can result from conduction disturbances (eg, complete right bundle branch block), and/or hemodynamic causes (eg, atrial septal defect with large left to right shunt). Wide splitting of S1 is a feature of Ebstein anomaly which is associated with right bundle branch block [16]. The extra early systolic sound around S1 is also referred to as the "sail sound." This auscultatory finding in patients with Ebstein anomaly appears not simply as a closing sound of the tricuspid valve, but as a complex closing sound that includes a sudden stopping sound after the anterior and/or other tricuspid leaflets balloon out in systole [17]. (See "Clinical manifestations and diagnosis of Ebstein anomaly".) SECOND HEART SOUND (S2) Genesis, timing, and location — The S2 consists of two components: aortic and pulmonary valve closure sounds, traditionally designated as A2 and P2, respectively [7]. Simultaneous M­mode echocardiograms and external phonocardiograms in healthy subjects showed that the onset of A2 was synchronous with the coaptation of the aortic valve cusps and a sharp vibration on the aortic wall. The closed valve oscillated for 30 to 45 ms after the coaptation of the cusps. Magnified echocardiographic studies of the interventricular septum revealed a consistent, momentary quiver across the septal myocardium a mean of 4 ms after the onset of S2 [18]. The same mechanism can be inferred for the P2 component of S2. The onset of A2 occurs with the dicrotic notch of the aortic root pressure pulse [19,20]. S2 occurs after the peak of the carotid pulse and coincides with its downslope. The two components of S2 are best heard with the diaphragm of the stethoscope and over the left second interspace, close to the sternal border. A2 is widely transmitted to the right second interspace, along the left and right sternal border, and to the cardiac apex. P2 is normally best heard and recorded over the upper left sternal border and is poorly transmitted. S2 is best heard when patients are semi­recumbent (30 to 40 degrees upright) with quiet inspiration. Factors determining the intensity of S2 — The major determinants of A2 intensity (and therefore the major determinants of S2) include (table 2): ● ● ● ● Aortic pressure, a major determinant of the velocity of valve closure Relative proximity of the aorta to the chest wall Size of the aortic root Mobility and structural integrity of the aortic valve The intensity of P2 is determined by: ● Pulmonary arterial pressure, particularly the diastolic pressure ● Size of the pulmonary artery ● Mobility and structural integrity of the pulmonary valve The intensity of P2 is determined by comparing its intensity with A2. An increased P2 intensity is suggested when it is louder over the left second interspace or when there is transmission to the cardiac apex. ● Increased intensity of A2 often occurs in: • Systemic hypertension. • Coarctation of the aorta. • Ascending aortic aneurysm; a "tambour" quality of A2 is commonly heard (table 2). • When the aortic root is relatively anterior and closer to the anterior chest wall, as in tetralogy of Fallot and transposition of the great arteries. ● Increased intensity of P2 often occurs in: • Pulmonary arterial hypertension of any etiology (most common, even with pulmonary regurgitation) [21]. • Idiopathic pulmonary artery dilation. • Atrial septal defect (ASD); P2 is increased considerably and frequently greater than A2 over the left second interspace. A2 is soft in patients with mitral regurgitation (MR), and P2 may appear to be increased. In these circumstances, one cannot rely on the relative intensity of P2 for the diagnosis of pulmonary hypertension (PH). ● Decreased intensity of A2 occurs in: • Conditions that affect the mobility and integrity of the aortic valve • Severe aortic regurgitation (AR) or stenosis • Hypotension ● Decreased intensity of P2 occurs in: • Conditions that affect the mobility and integrity of the pulmonary valve. • Pulmonary stenosis and regurgitation. • Significant RV outflow obstruction associated with a soft and delayed P2. The low pulmonary artery pressures also play a role in attenuating P2. Splitting of S2 — Under normal physiologic conditions, the A2 and P2 components of S2 vary with inspiration. A2 and P2 are usually fused during the expiratory phase of continuous respiration, but during the inspiratory phase, separation of A2 and P2 occurs; the degree of splitting varies from 0.02 to 0.06 seconds (movie 2) [22]. The underlying mechanism for the normal splitting of S2 during inspiration relates to longer RV ejection during inspiration compared with the LV, which is correlated with increased right­sided and decreased left­sided filling. The width and order of splitting of S2 are altered in a variety of clinical settings. ● Wide splitting of S2 occurs in the following conditions: • Electromechanical delay of the RV (table 2 and figure 2): - Right bundle branch block (RBBB) (movie 3), artificial pacing from the LV, and Wolff­ Parkinson­White (WPW) syndrome with LV preexcitation. - Premature beats and an idioventricular rhythm of LV origin (QRS complex of RBBB morphology) are also associated with wide splitting. • Hemodynamic causes: - Increased resistance to RV ejection and prolongation of RV ejection time are other important causes of wide expiratory splitting of S2 as seen in pulmonary valve, infundibular, supravalvular, or pulmonary branch stenosis, and pulmonary arterial hypertension. In patients with pulmonary valve and infundibular stenosis, wide splitting of S2 is associated with reduced intensity of P2, while P2 is accentuated in PH and pulmonary branch stenosis. In pulmonary valve stenosis, the degree of expiratory splitting of S2 (the A2­P2 interval) is directly related to the severity of stenosis and RV systolic hypertension [23]. Further splitting of S2 during inspiration usually occurs in these conditions, but wide splitting of S1 is not observed. - Isolated reduction of the LV ejection time may also cause wide splitting of S2, due to the early occurrence of A2. Examples of this hemodynamic abnormality include severe MR when forward stroke volume decreases with increases in regurgitant volume [24]. In constrictive pericarditis, differential filling of the ventricles occurs during inspiration, resulting in a lower LV stroke volume [25]. ● Wide and fixed splitting of S2 – Fixed splitting of S2 has been defined as ≤20 ms of variation in the A2­P2 interval between the inspiratory and expiratory phases of respiration [26]. However, such limitation in variation of splitting may be difficult to discern clinically, so wide and variable splitting may be difficult to distinguish from wide and fixed splitting. One common cause of wide and fixed splitting of S2 is a large interatrial communication (ASD, common atrium) and left­to­right or bidirectional shunt; abnormally wide splitting of S2 occurs, and respiratory variations of the A2­P2 intervals are minimal or absent (movie 4). (See "Clinical manifestations and diagnosis of atrial septal defects in adults", section on 'Heart sounds'.) The mechanism of wide expiratory splitting of S2 in ASD appears to result from two physiological mechanisms. First, P2 is delayed due to a marked increase in RV stroke volume (left­to­right shunt), which prolongs right­sided ejection. Second, when the right and left atria become a near common chamber, differential filling that normally occurs between the RV and LV during inspiration no longer exists (table 2) [26,27]. The other cause of fixed splitting of S2 is RV failure, when the RV is unable to vary its stroke volume during inspiration, and inspiratory prolongation of its ejection time and delay of P2 does not occur. Therefore, any condition that induces severe RV failure, such as RV outflow obstruction, PH, and primary RV dysfunction, can be associated with fixed splitting (table 2). ● Reversed (paradoxical) splitting of S2 – Paradoxical splitting occurs when A2 follows P2 during the expiratory phase of respiration. The splitting of S2 is then maximal during expiration, and the splitting is less or S2 becomes single during inspiration with the normal inspiratory delay of P2 [7,28]. Reversed splitting of S2 may result from either conduction disturbances or hemodynamic causes (table 2). • Electromechanical delay Left bundle branch block, artificial RV pacing, preexcitation of the RV (WPW syndrome), and premature beats of RV origin are examples of conduction disturbances associated with delayed activation of the LV, and consequently delayed completion of LV ejection causes a delayed A2 and reversed splitting of S2. • Hemodynamic factors: - A markedly prolonged LV ejection time may delay A2 sufficiently to cause reversed splitting of S2. With fixed LV outflow tract obstruction, as in patients with aortic valve stenosis, LV ejection time is lengthened, and reversed splitting of S2 usually indicates hemodynamically significant outflow obstruction (movie 5). However, P2 may be inaudible due to the long ejection systolic murmur of aortic stenosis, making it difficult to recognize the reversed splitting. - A prolonged LV ejection time and reversed splitting of S2 can occur with myocardial dysfunction, as in myocardial ischemia, or in patients with long­standing severe AR [29]. However, reversed splitting is rarely observed with severe heart failure (HF) because of the concomitant decrease in stroke volume, which is an important determinant of LV ejection time. The distinction between hypertrophic cardiomyopathy (HCM) and MR or ventricular septal defect (VSD), conditions in which the character and locations of the systolic murmur may appear similar on auscultation, is facilitated by recognizing the character of S2 splitting. Reversed splitting suggests HCM, while physiologic splitting favors MR or VSD. Single S2 — A single S2 may result from the absence of either of the two components of S2 or from the fusion of A2 and P2 without inspiratory splitting (table 2). ● Absence of A2 is occasionally observed in severe calcific aortic stenosis with an immobile aortic valve. A2 may be absent in some patients with severe AR due to destruction of the valve leaflets. (See "Clinical manifestations and diagnosis of aortic stenosis in adults", section on 'Cardiac auscultation' and "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults", section on 'Cardiac auscultation'.) ● P2 is absent with congenital absence of the pulmonary valve, pulmonary atresia, or truncus arteriosus. In severe pulmonary valve stenosis or in tetralogy of Fallot, P2 may be markedly attenuated and escape recognition by auscultation. (See "Clinical manifestations and diagnosis of pulmonic stenosis in adults", section on 'Clinical manifestations' and "Pathophysiology, clinical features, and diagnosis of tetralogy of Fallot", section on 'Cardiac auscultation'.) ● A2 is delayed and may be fused with P2 with aortic stenosis (movie 6). Fusion of A2 and P2 without inspiratory splitting occurs in Eisenmenger syndrome with VSD and in patients with a single ventricle. (See "Clinical manifestations and diagnosis of aortic stenosis in adults", section on 'Cardiac auscultation' and "Evaluation and prognosis of Eisenmenger syndrome", section on 'Physical examination'.) However, a truly single S2 is rare. An apparently single S2 usually results from the inability to hear or record P2 due to emphysema, obesity, or pericardial effusion. THIRD (S3) AND FOURTH (S4) HEART SOUNDS Genesis, timing, and location of S3 and S4 — S3 and S4 are low­frequency diastolic sounds that appear to originate in the ventricles. The precise mechanism of the genesis of S3 and S4 has not been identified with certainty [30]. It is generally agreed that both sounds, occasionally termed "ventricular filling sounds," are associated with ventricular filling and an increase in ventricular dimensions. They are heard during the rapid filling and atrial filling phases of ventricular diastole, respectively. ● S3 occurs as the rapid filling phase of diastole is completed [31]. It appears to be related to a sudden limitation of the movement during ventricular filling along its long axis [32], and it coincides with the y descent of the atrial pressure pulse, occurring usually 0.14 to 0.16 seconds after the second heart sound (S2). ● S4 occurs during the atrial filling phase after the P wave on the electrocardiogram (ECG) and coincides with atrial systole and a waves of the atrial pressure pulse, and with the apical impulse. S3 and S4 are best heard with the bell of the stethoscope. Auscultation over the cardiac apex in the left lateral decubitus position is preferable for identification of LV S3 and S4. RV S3 and S4 are best heard along the lower left sternal border; occasionally, right­sided filling sounds are also heard over the lower right sternal border and over the epigastrium. The intensity of S3 and S4 of RV origin usually increases during inspiration, while that of LV origin remains unchanged. S3 is closer to S2, and S4 occurs prior to the first heart sound (S1). An abnormal S3 or S4 tends to be louder and of higher pitch (sharper) and is frequently referred to as a "gallop." S3 is the ventricular gallop, and S4 is the atrial gallop. S3 and S4 can be fused during tachycardia to produce a loud diastolic filling sound, termed a "summation gallop" [33]. At the bedside, carotid massage can cause separation of S3 and S4 as the heart rate slows. S3 and S4 may occasionally be intensified or precipitated by exercise or by sustained hand grip. Gallops can sometimes be seen and palpated. (See "Examination of the precordial pulsation".) It is often difficult to distinguish between gallop sounds of RV and LV origin at the bedside when they are present in the same patient. However, if one follows the "inching" method of auscultation (eg, auscultation starting over the cardiac apex and then gradually moving the stethoscope inch by inch to the left lower sternal border), the decreasing intensity of gallops of LV origin and the increasing intensity of gallops of RV origin can be appreciated. Furthermore, the intensity of the right­sided gallop sound increases during inspiration. LV gallops Clinical significance of S3 — Although an S3 can be heard in healthy young children and adults (movie 7), it is usually abnormal in patients over the age of 40 years, suggesting an enlarged ventricular chamber. An S3 gallop is an important and common early finding of HF associated with dilated cardiomyopathy and may also be heard in patients with diastolic HF (although less frequently than with systolic HF), aortic valve disease, and coronary artery disease (CAD) (movie 8) [34]. In such patients, an S3 gallop is usually associated with left atrial pressures exceeding 20 mmHg, increased LV end­diastolic pressures (>15 mmHg), and elevated serum brain natriuretic peptide (BNP) concentrations [35­37]. (See "Evaluation of the patient with suspected heart failure", section on 'Heart sounds'.) An S3 gallop is almost always present in patients with hemodynamically significant chronic mitral regurgitation (MR); the absence of S3 is an important finding to exclude severe chronic MR. An S3 gallop in patients with chronic aortic regurgitation (AR) is frequently associated with a decreased LVEF and increased diastolic volume; its recognition should prompt further evaluation [38]. The diagnostic test characteristics of the S3 and S4 for detection of LV dysfunction were evaluated in a phonocardiographic study of patients who were undergoing cardiac catheterization [37]. These sounds were not very sensitive (40 to 50 percent) for the detection of an elevated LV end­diastolic pressure or a reduced LVEF; however, the S3 was highly specific (90 percent) for these parameters and for an elevated serum BNP concentration. An additional problem is appreciable interobserver variability in the ability to detect an S3 on cardiac auscultation that cannot be solely explained by the experience of the observer [39,40]. The presence of an S3 gallop also has prognostic significance, being associated with a higher risk of progression to symptomatic HF in those with asymptomatic LV dysfunction, and a higher risk of hospitalization for HF or death from pump failure in patients with overt HF [41,42]. One limitation to these observations is the operator dependence for the detection of this physical finding. An S3 often occurs in high­output states such as thyrotoxicosis or pregnancy. It can also be appreciated in athletes with slow heart rates and increased filling volumes [43]. In these settings, it does not necessarily indicate LV dysfunction [44]. Clinical significance of S4 — An audible S4 is generally abnormal in young adults and children. Effective atrial contraction and ventricular filling are both required for production of atrial gallop sounds. Thus, this sound is usually absent in atrial fibrillation and in significant AV valve stenosis. S4 can be heard in many healthy older adults without any other cardiac abnormality, due to decreased ventricular compliance with age. An S4 is always abnormal when it is palpable, regardless of patient age. S4 may become audible in otherwise healthy subjects with a prolonged PR interval due to the separation of S4 from S1. In patients with complete AV block, S4 is heard at a faster rate than S1 and S2 and may not indicate any hemodynamic abnormality. An abnormal S4 is most frequently observed in patients with decreased LV distensibility (movie 9) [45]. Thus, S4 is common in hypertensive heart disease, aortic stenosis, and HCM. LV hypertrophy, which is present in all these conditions, contributes to decreased LV distensibility. In aortic stenosis, the presence of an S4 has been reported to indicate hemodynamically significant LV outflow obstruction, with a peak transvalvular gradient ≥70 mmHg and an elevated LV end­diastolic pressure [46]. However, in patients over 40 years of age, S4 can occur due to myocardial disease in the absence of significant aortic stenosis. Thus, in elderly patients, the presence of an S4 cannot be used to assess the severity of aortic stenosis. Associated CAD may also cause an S4 in patients with mild to moderate aortic stenosis. An S4 is heard in the vast majority of patients during the acute phase of myocardial infarction (MI) [47]. Although pulmonary venous pressure may also be elevated, there is a poor correlation between the presence and absence of an S4 and hemodynamic abnormalities. Thus, S4 is a poor guide to assess the severity of LV dysfunction in patients with acute MI. Audible and/or palpable atrial gallops are a frequent finding in chronic LV aneurysm and are usually found with LV dyskinesia associated with elevated end­diastolic pressures. In patients with chronic CAD, the transient appearance of an S4, particularly during chest pain, is a strong indication of transient myocardial ischemia. A loud S4 that is also usually palpable is a frequent finding in patients with acute and severe MR or AR. It is almost always associated with an increased LV end­diastolic pressure (>15 mmHg) [48]. The predictive value is increased in the presence of both S3 and S4 gallops [35]. (See "Examination of the precordial pulsation".) Right ventricular gallops — An S3 gallop of RV origin frequently occurs in patients with significant tricuspid regurgitation, whether it is primary or secondary to pulmonary hypertension and RV failure. An S3 gallop is also heard in RV failure in the absence of tricuspid regurgitation. An S4 of RV origin is most commonly heard in patients with RV outflow obstruction (pulmonary valve stenosis) and pulmonary arterial hypertension [49]. It likely denotes decreased RV distensibility due to hypertrophy. Differential diagnosis — An S3 and S4 may be confused with a split S2 and split S1, respectively. When split, the two parts of S1 or S2 typically have a similar pitch, while S3 and S4 are lower pitched sounds than S2 and S1. This difference in pitch can be brought out by listening with the bell and the diaphragm of the stethoscope. The lower­pitched S3 and S4 will be more pronounced when listening gently with the bell, while the higher­pitched split S1 and S2 will be more pronounced when listening with the diaphragm or when applying the bell more firmly to the skin. (See 'Stethoscopes' above.) Auscultation to distinguish S3 and S4 from a splitting of S2 and S1 is best performed in the 45­degree left lateral decubitus position (ie, with the chest rotated toward the examination table). The location of the sound is useful in distinguishing an S4 from a split S1. The LV S4 is usually localized over the cardiac apex, and becomes softer as the bell of the stethoscope is moved gradually to the left sternal border. PERICARDIAL KNOCK Ventricular filling is confined to early diastole in constrictive pericarditis and terminates with a sharp S3; this is termed a "pericardial knock." Its timing is earlier than a normal S3 and typically occurs 0.10 to 0.12 seconds after an S2. It is a common finding in constrictive pericarditis and can occur with or without pericardial calcification [50]. It is occasionally heard only during inspiration and along the lower right sternal border, suggesting an early manifestation of RV constriction. (See "Constrictive pericarditis".) EJECTION SOUNDS An ejection sound is a high­frequency "clicky," early systolic sound. When aortic or pulmonary ejection sounds occur in the presence of normal semilunar valves, the origin may be the proximal aortic or pulmonary artery segments. Thus, the term "vascular ejection sound" has been suggested. These sounds generally tend to occur later and are not associated with "doming" of the semilunar valves, which is characteristic of a valvular ejection sound. The mechanism of the vascular ejection sound remains unclear. Aortic ejection sound — The aortic ejection sound is usually recorded 0.12 to 0.14 seconds after the Q wave on the ECG. It is best heard with the diaphragm of the stethoscope and is widely transmitted, heard at the cardiac apex and also over the right second interspace. Its intensity does not vary with respiration. Aortic ejection sounds occur in association with a deformed but mobile aortic valve and with aortic root dilation. Thus, it is present in aortic valve stenosis, bicuspid aortic valve, aortic regurgitation, and with aneurysm of the ascending aorta. An aortic ejection sound is also heard in some patients with systemic hypertension, probably due to associated aortic root dilation. Aortic ejection sounds are heard frequently in patients with mild to moderate aortic valve stenosis; they may be absent in severe calcific aortic stenosis, presumably due to the loss of valve mobility [51]. Since ejection sounds are usually absent in subvalvular and supravalvular aortic stenosis, the presence of an ejection sound helps to identify the site of obstruction at the level of the aortic valve. An ejection sound also does not favor the diagnosis of HCM. Identification of the aortic ejection sound is the most important and consistent bedside clue for the diagnosis of an uncomplicated bicuspid aortic valve [52]. In patients with coarctation of the aorta, an aortic ejection sound usually signifies the presence of an associated bicuspid aortic valve. Pulmonary ejection sound — A pulmonary ejection sound occurs earlier than an aortic ejection sound and is recorded 0.09 to 0.11 seconds after the Q wave on the ECG, beginning at the time of maximal opening of the pulmonary valve. It is also a "clicky" sound of high frequency and is best heard with the diaphragm of the stethoscope. In contrast to the aortic ejection sound, it is not widely transmitted and is usually best heard at the left second interspace and along the left sternal border; it is not usually heard over the cardiac apex or right second interspace. The most helpful distinguishing feature of a pulmonary ejection sound is its decreased intensity, or even its disappearance during the inspiratory phase of respiration. During expiration, the valve opens rapidly from its fully closed position; sudden "halting" of this rapid opening movement is associated with a maximal intensity of the ejection sound. With inspiration, the increased venous return to the RV augments the effect of right atrial systole and causes partial opening of the pulmonary valve prior to ventricular systole. The lack of a sharp opening movement of the pulmonary valve explains the decreased intensity of the pulmonary ejection sound during inspiration. The tricuspid closure sound should not be confused with the pulmonary ejection sound. The intensity of tricuspid closure sound tends to increase rather than decrease during inspiration. Pulmonary ejection sounds tend to be present in clinical conditions associated with a deformed pulmonary valve and pulmonary artery dilation, including pulmonary valve stenosis, idiopathic dilation of the pulmonary artery, and chronic pulmonary arterial hypertension of any etiology [53­56]. The interval between the S1 and the pulmonary ejection sound is directly related to the RV isovolumic contraction time, which usually is prolonged in PH, explaining a relatively late occurrence of the ejection sound in these patients. With increasing severity of pulmonary valve stenosis, the isovolumic systolic interval shortens, and the pulmonary ejection sound therefore tends to occur soon after the S1. In patients with very severe pulmonary valve stenosis, the ejection sound can fuse with the S1 and may not be recognized. NON­EJECTION SYSTOLIC SOUNDS The non­ejection systolic sounds are also high­frequency sounds that occur much later after the first heart sound (S1) and are best heard with the diaphragm of the stethoscope. These sounds are not widely transmitted and not usually heard over the right or left second interspace. Midsystolic click — Prolapse of the mitral valve is the most common cause for a non­ejection midsystolic click; the timing coincides with maximal prolapse of the mitral valve into the left atrium. It may or may not be associated with a late systolic murmur (movie 10 and movie 11) [57­60]. (See "Definition and diagnosis of mitral valve prolapse".) When the click occurs early in systole, it can be confused with the ejection sound or the second component of a widely split S1. A number of bedside maneuvers can be performed to confirm the presence of a midsystolic click. These maneuvers are based upon the fact that the systolic dimension or volume at which mitral valve prolapse and the click occur tend to remain fixed in the same patient [61]. Thus, whenever the "click" volume or dimension is reached following the onset of ventricular ejection (corresponding roughly to the S1), a midsystolic click occurs. The S1­click interval, then, can vary according to the preejection (end­diastolic) ventricular volume and the rate of ejection. ● The S1­click interval will increase, producing a late mid­systolic click whenever there is an increase in end­diastolic volume (eg, supine position, squatting, hand grip) (movie 11). ● The S1­click interval usually shortens, and the click tends to occur earlier when there is a reduction in end­diastolic volume (eg, standing, phase 2 Valsalva maneuver, amyl nitrite) or when there is an increased rate of ejection, as occurs after an ectopic beat as a result of post­ectopic potentiation (movie 10). It is important to identify the other cardiovascular anomalies that may accompany mitral valve prolapse, including Marfan syndrome, atrial septal defect (secundum or primum), musculoskeletal abnormalities, systemic lupus erythematosus, and HCM. When there is no associated anomaly, isolated mitral valve prolapse is identified [57]. (See "Definition and diagnosis of mitral valve prolapse", section on 'Clinical manifestations'.) Tricuspid valve prolapse also produces high­frequency midsystolic, "clicky" sounds; these are best heard with the diaphragm of the stethoscope over the lower left sternal border and occasionally over the lower right sternal border. The interval between S1 and the tricuspid valve click tends to increase following inspiration and after raising the legs and other maneuvers that increase RV volume. Isolated tricuspid valve prolapse occurs only rarely, and in most instances it accompanies mitral valve prolapse. Tricuspid valve prolapse, however, may occur in the absence of mitral valve prolapse in patients with Ebstein anomaly. Precordial honk — The systolic "whoop" or "precordial honk" are short musical systolic murmurs often preceded by a click and occurring in mid or late systole. These sounds can be transient, occur only in certain positions, or may be precipitated by exercise. Mitral valve prolapse is the cause for the "whoop" or "honk" in most cases [62,63]. Pseudo­ejection sound — A nonejection sound has been observed in some patients with HCM associated with systolic anterior motion of the anterior mitral leaflet. This sound has been termed a "pseudo­ejection sound" [64]. Unlike the ejection click of aortic stenosis, this sound begins considerably after the upstroke of the carotid pulse. The precise mechanism of the pseudo­ejection sound in HCM remains unclear. It may either result from contact of the anterior leaflet with the septum or from the deceleration of blood flow in the LV outflow tract. EARLY DIASTOLIC HIGH­FREQUENCY SOUNDS The most common causes for sounds occurring in diastole include the opening snap of the mitral or tricuspid valve or a tumor plop associated with an atrial myxoma (table 3). Opening snap — The opening snap is a high­frequency, early diastolic sound associated with mitral or tricuspid valve opening (movie 1). This opening of the AV valves, which is normally silent, becomes audible in the presence of pathologic conditions. The opening snap results from rapid opening of the mitral valve to its maximal open position; thus, mobility of the valve contributes to its genesis. It is absent when the mitral valve is heavily calcified and immobile. However, the opening snap is heard in the vast majority of patients with mitral stenosis, and along with an accentuated first heart sound (S1), frequently provides the first clue to the diagnosis. Mitral valve — Mitral stenosis is the most frequent and important cause of an opening snap. It can occur rarely in patients with pure mitral regurgitation (MR) [48,65]. The opening snap is best heard with the diaphragm of the stethoscope, medial to the cardiac apex. It is usually widely transmitted and can be easily heard over the left second interspace and along the left sternal border. The opening snap coincides with the full opening of the mitral valve and occurs 0.04 to 0.12 seconds after the second heart sound (S2) (movie 1) [66]. The opening snap can easily be confused with a split S2 since it is frequently transmitted to the left second interspace. However, careful auscultation over the left second interspace in the supine position and during both phases of respiration reveals three high­frequency sounds in close proximity to each other during inspiration; the initial two are the two components of S2, and the third is the opening snap. The recognition of these three sounds during inspiration helps to differentiate mitral stenosis, as seen in mitral valve obstruction, from atrial septal defect (ASD), which may also be associated with a mid­diastolic rumble. In ASD, only the two components of the S2 are heard during expiration and inspiration. The severity of mitral stenosis can be assessed at the bedside by noting the interval between the aortic component of S2 and the opening snap. The S2­opening snap interval is related to the difference in pressures at the time of aortic valve closure and the opening of the mitral valve, which occurs during the isovolumic relaxation phase when the LV pressure falls below the left atrial pressure. When mitral stenosis is severe, left atrial pressure is higher, and the pressure crossover point between the LV and left atrium is closer to S2, which reduces the S2­opening snap interval. At the bedside, the shorter S2­opening snap interval sounds like a widely split S2. However, the S2­ opening snap interval is not only related to the height of the left atrial pressure, but also to aortic valve closing pressure. Thus, with a higher aortic valve closing pressure (systemic hypertension) and earlier closure of the aortic valve, the S2­opening snap interval may be longer with the same degree of elevation of left atrial pressure. Similarly, when the aortic valve closing pressure is lower (aortic regurgitation and aortic stenosis), aortic valve closure is later, and the S2­opening snap interval becomes shorter with the same degree of mitral stenosis. The S2­opening snap interval also becomes shorter when mitral stenosis is associated with MR with a large V wave. Furthermore, tachycardia decreases the S2­opening snap interval as the left atrial pressure increases with increasing heart rate in mitral stenosis. Thus, assessment of the severity of mitral stenosis by estimating the S2­opening snap interval alone should be done with caution in the presence of tachycardia, hypertension, MR, and aortic valve disease. (See "Clinical manifestations and diagnosis of rheumatic mitral stenosis".) Tricuspid valve — Tricuspid valve stenosis may be associated with a tricuspid valve opening snap that is not widely transmitted and is heard best over the lower left sternal border. The tricuspid opening snap can also be heard in some patients with an ASD and a large left­to­right shunt [26]. Tumor plop — Early diastolic sounds (tumor "plop") are occasionally heard in atrial myxoma. These sounds appear to occur when tumors move into the ventricle and come to a sudden halt [67]. (See "Cardiac tumors".) Vegetation plop — Vegetation plop is an early diastolic sound that is occasionally heard in bacterial endocarditis. It appears that this sound is produced when a large vegetation attached to the mitral valve leaflet enters the LV during early diastole [68]. Other causes — A high­frequency, diastolic sound can be heard in other conditions and should be differentiated from the opening snap or tumor plop. ● In some patients with mitral valve prolapse, a high­frequency sound is heard in early diastole that appears to be related to the rapid inward movement of the prolapsed mitral valve toward the LV cavity before the opening of the mitral valve [69]. This early diastolic sound should not be confused with an opening snap due to mitral stenosis. ● In some patients with HCM who have a small LV cavity size, early diastolic high­frequency sounds are heard coinciding with the time of contact of the anterior leaflet of the mitral valve to the interventricular septum [70]. ● High­frequency early diastolic sounds, similar to the opening snap, can be heard in some patients with severe MR due to ruptured chordae. PROSTHETIC VALVE SOUNDS The various types of prosthetic and tissue valves that are in use for valve replacement may produce both opening and closing sounds. The relative intensity of the opening and closing sounds vary according to the type and design of the prosthetic valve used (table 4). The artificial valve sounds are of high frequency, are much louder than normal valve sounds, and are of a "clicky" character. The opening or closing sound may consist of multiple clicks, which do not necessarily indicate valve malfunction. ● The closing sound is generally louder than the opening sound with a disk valve ● Both the opening and closing sounds are loud with the ball­and­cage type of valve ● The closing sounds of the porcine valve are much louder than the opening sounds Valve malfunction — Changes in the normal sounds produced by the prosthetic valve may indicate valve malfunction. However, malfunction of an artificial valve can exist despite a normal intensity or character of the opening or closing sounds. Doppler echocardiography and cardiac catheterization are usually necessary to establish this diagnosis. (See "Diagnosis of mechanical prosthetic valve thrombosis or obstruction" and "Overview of the management of patients with prosthetic heart valves".) ● The closing sound is usually louder than the opening sound, regardless of the type of prosthetic valve used. A decreased intensity of the closing sound should raise the possibility of malfunction of the artificial valve. ● The absence of an opening click has been found in dehiscence of a mitral valve prosthesis [71]. ● Obstruction of a prosthetic valve in the mitral position may be associated with a markedly decreased S2­opening sound interval. A marked variation in the S2­mitral prosthesis opening sound may indicate malfunction of a mechanical mitral prosthesis. The variation in this interval usually does not exceed 25 ms with a normally functioning prosthesis [72]. Ball variance — "Ball variance" is a term used to describe certain physical changes in a ball­and­ cage valve and is associated with changes in the intensity of opening and closing sounds [73]. Ball variance is related to a specific model of the caged ball type of prosthetic valve, which is rarely used at the present time. PERICARDIAL FRICTION RUB AND OTHER ADVENTITIOUS SOUNDS A pericardial rub is generated by the friction of two inflamed layers of the pericardium and occurs during the maximal movement of the heart within its pericardial sac. Thus, the rub can be heard during atrial systole, ventricular systole, and the rapid­filling phase of the ventricle (three­component rub) (movie 12). However, the rub may be present only during one (one component) or two phases (two components) of the cardiac cycle. In myopericarditis following transmural MI, a one­component rub, usually during ventricular systole, is more frequent than two­ or three­component rubs. Pericardial rubs are of scratching or grating quality and appear superficial. They are best heard with the diaphragm of the stethoscope. The intensity frequently increases after application of firm pressure with the diaphragm, during held inspiration, and with the patient leaning forward. The rub may be localized or widespread, but usually is heard over the left sternal border. (See "Acute pericarditis: Clinical presentation and diagnostic evaluation".) Pericardial rubs should be distinguished from the other superficial "scratchy" sounds. ● In patients with thyrotoxicosis, a to­and­fro, high­pitched sound may be heard over the left second interspace, known as a Means­Lerman scratch; it may simulate a pericardial friction rub. (See "Overview of the clinical manifestations of hyperthyroidism in adults".) ● Acute mediastinal emphysema, usually a benign, relatively common complication of open heart surgery, may be associated with a "crunching" noise over the precordium that is coincident with ventricular systole (mediastinal crunch). ● In patients with Ebstein anomaly, the sail sound may be of a scratchy quality and simulate a pericardial friction rub. ● The movement of the balloon flotation catheter or the transvenous pacing catheter across the tricuspid valve can cause an early systolic superficial scratchy sound that may also simulate a soft, one­component friction rub. These sounds frequently disappear with the alteration of patient position. ● A pleuropericardial rub results from the friction between the inflamed pleura and the parietal pericardium; it can be heard only during the inspiratory phase of respiration. ● Twitching of the intercostal muscles or of the diaphragm during artificial pacing may cause a superficial, scratchy, and high­frequency sound unrelated to the cardiac cycle. This sound is called "pacemaker heart sound." The twitching of the intercostal muscles results from stimulation of the adjacent intercostal nerves by the pacemaker stimulus [74]. ● Inadvertent entry of air into the RV cavity via the systemic venous system may occur during placement of catheters or pacemakers in the right side of the heart or as a complication of needle aspiration biopsy of the lungs. The movement of air in the right ventricular cavity with systole and diastole may produce a peculiar "slushing" or crunching sound ("mill wheel" murmur) over the entire precordium, which can occasionally resemble pericardial friction rub [75]. ● Swallowing sounds – These sounds are produced during swallowing and can be confused with heart sounds. It is postulated that these sounds are produced by vibrations of the vocal cords during swallowing [76]. SUMMARY AND RECOMMENDATIONS ● Heart sounds are broadly classified into high­ and low­frequency sounds. (See 'Classification of heart sounds' above.) • High­frequency sounds arise from closing or opening valves including mitral and tricuspid valve closing sounds (M1 and T1), and aortic and pulmonary valve closure sounds (A2 and P2). • Low­frequency sounds include the third heart sound (S3, which may be physiologic or pathologic), associated with early ventricular filling and the fourth heart sound (S4), associated with the atrial contribution to ventricular filling in late diastole. (See 'Classification of heart sounds' above.) ● The intensity of the first heart sound (S1) can be helpful in assessing left ventricular (LV) function and hemodynamics. (See 'Intensity of S1' above.) • A loud S1 in the absence of a short PR interval indicates increased peak rate of rise of LV systolic pressure (dP/dt), as seen in patients with increased transatrioventricular valve gradients (mitral or tricuspid stenosis). • A soft S1 in the absence of a prolonged PR interval usually indicates increased LV end­ diastolic pressure (LVEDP) and decreased peak dP/dt or reduced mobility of the atrioventricular valves (calcified mitral stenosis). ● Fixed wide splitting of the second heart sound (S2) is highly suggestive of an atrial septal defect. (See 'Splitting of S2' above.) ● Paradoxical splitting of S2 in the absence of left bundle branch block suggests LV outflow obstruction or impaired contractile function. (See 'Splitting of S2' above.) ● An S3 gallop in adults in the absence of mitral regurgitation usually indicates elevated LVEDP and increased brain natriuretic peptide levels. (See 'Clinical significance of S3' above and "Evaluation of the patient with suspected heart failure", section on 'Heart sounds'.) ● An abnormal S4 is most frequently observed in patients with decreased LV distensibility (eg, acute myocardial ischemia, LV hypertrophy). (See 'Clinical significance of S4' above.) ● Other early diastolic high­frequency sounds include an opening snap of the mitral or tricuspid valve (appreciated in mitral or tricuspid stenosis) or a tumor plop associated with an atrial myxoma. (See 'Early diastolic high­frequency sounds' above.) ● A pericardial rub is characteristically a scratching or grating sound that may have one, two, or three components. (See 'Pericardial friction rub and other adventitious sounds' above.) ACKNOWLEDGMENT UpToDate wishes to acknowledge the past work of the late Kanu Chatterjee, MD, as an author for this topic. Use of UpToDate is subject to the Subscription and License Agreement. Topic 1079 Version 14.0 GRAPHICS Causes of first heart sound (S1) abnormalities Abnormality Causes Increased intensity Atrioventricular valve obstruction Mitral Mitral stenosis and left atrial myxoma Tricuspid Tricuspid stenosis and right atrial myxoma Increased transvalvular flow Mitral Patent ductus arteriosus; ventricular septal defect; atrial septal defect Tricuspid Forceful ventricular systole Hyperkinetic heart syndrome; tachycardia (eg, exercise); mitral valve prolapse Short PR interval Pre­excitation syndrome; Lown­Ganong­Levine syndrome Decreased intensity Immobility of mitral valve Calcific mitral stenosis Lack of apposition of the mitral leaflets Rheumatic mitral regurgitation Presystolic semiclosure of the atrioventricular valves Long PR interval; acute aortic regurgitation; significant aortic stenosis; dilated cardiomyopathy Conduction anomaly Left bundle branch block Wide splitting of S1 Conduction abnormalities Complete right bundle branch block; left ventricular pacing; pre­excitation syndrome (left ventricular connection); Ebstein's anomaly Mechanical Tricuspid stenosis; atrial septal defect; Ebstein anomaly Reversed splitting of S1 Arrhythmia Premature beats (right ventricular origin) Mechanical Severe mitral stenosis and left atrial myxoma Graphic 65274 Version 2.0 Cause of loud S1 with mitral stenosis This schematic representation shows the transition between left atrial (LA) and left ventricular (LV) pressures at end­ diastole in the normal heart (A) and in a patient with mitral stenosis (B). In B, a significant pressure gradient remains at end­diastole. Note that at low LA pressures, the rate of LV pressure development (dP/dt) is much slower than when crossover occurs at higher LA pressures. Hence, the rate of mitral valve closure is increased in mitral stenosis, the principal cause of a loud S1. S1: first heart sound. Courtesy of Theo Meyer, MD. Graphic 119876 Version 1.0 Abnormalities of the second heart sound (S2) and their mechanisms Wide splitting of S2 with maintained inspiratory delay of P2 Delayed activation and completion of right ventricular ejection Complete right bundle branch block Artificial left ventricular pacing Pre­excitation of the left ventricle (Wolff­Parkinson­White syndrome) Premature beats and idioventricular rhythm originating from the left ventricle Prolonged right ventricular ejection time Pulmonary hypertension with right heart failure Right ventricular outflow obstruction (eg, pulmonic stenosis, acute massive pulmonary embolus) Increased pulmonary hangout time Idiopathic dilatation of the pulmonary artery Mild pulmonic stenosis Postoperative atrial septal defect Decreased left ventricular ejection time (early A2) Mitral regurgitation Ventricular septal defect with low pulmonary vascular resistance Constrictive pericarditis Fixed splitting of S2 Unchanged right ventricular stroke volume during respiration; severe right ventricular failure due to any cause Interatrial communication; atrial septal defect; common atrium Reversed splitting of S2 Delayed left ventricular activation and completion of ejection Left bundle branch block Artificial right ventricular pacing Pre­excitation of the right ventricle (Wolff­Parkinson­White syndrome) Premature beats of right ventricular origin Prolonged left ventricular ejection time Increased resistance to left ventricular ejection (aortic stenosis, obstructive hypertrophic cardiomyopathy, hypertension) Isolated increase in left ventricular forward stroke volume (aortic regurgitation, patent ductus arteriosus) Myocardial dysfunction (mild to moderate left ventricular failure, myocardial ischemia or infarction) Increased aortic hangout time (not the sole cause) Aortic regurgitation Patent ductus arteriosus Aortic stenosis Single S2 Apparent: obesity, emphysema, pericardial effusion Absent A2: severe aortic stenosis, severe aortic regurgitation Absent P2: absent pulmonary valve, pulmonary atresia, tetralogy of Fallot, truncus arteriosus Fusion of A2 and P2: Eisenmenger ventricular septal defect, common ventricle Graphic 77038 Version 3.0 Splitting of the second heart sound Wide splitting of second heart sound (S2) may be due to delayed closure of pulmonic valve as in right bundle branch block, pulmonic stenosis, and atrial septal defect, or to early closure of aortic valve as in mitral regurgitation and ventricular septal defect. In atrial septal defect, splitting is both wide and fixed. S1: first heart sound; A2: aortic valve closure sound; P2: pulmonic valve closure sound; T1: tricuspid valve closure sound; M1: mitral valve closure sound. Reprinted with permission from: Shaver JA, Leonard JJ, Leon DF. Auscultation of the Heart. Examination of the Heart, Part 4. American Heart Association, Dallas 1990. Copyright ©1990, American Heart Association, Inc. Graphic 55198 Version 11.0 Causes of a high frequency sound in early diastole Mitral opening snap Organic mitral stenosis Rarely, pure mitral regurgitation Tricuspid opening snap Organic tricuspid stenosis Functional tricuspid stenosis (rare) Atrial septal defect "Tumor plop" Left atrial myxoma Right atrial myxoma Opening clicks of mitral stenosis Mitral valve prolapse Graphic 73281 Version 1.0 Normal auscultatory findings of prosthetic valves according to type and location Auscultatory Findings Valve prosthesis Mitral Ball valves (eg, Starr­Edwards) Tilting disc valves (eg, Medtronic­Hall) Bioprosthetic valves Bileaflet valves (eg, St. Jude) Aortic A2­MO interval 0.07 to 0.11 seconds S1­AO interval 0.07 seconds MO louder than MC AO louder than AC Soft systolic murmur Soft, harsh systolic ejection murmur No diastolic murmur "Seating puff" ­ diastolic rumble A2­MO interval 0.05 to 0.09 second S1­AO interval 0.04 seconds MO is soft or may not be audible AC louder than AO Soft systolic murmur Soft systolic ejection murmur Soft and short diastolic rumble "Seating puff" ­ diastolic rumble A2­MO interval 0.1 seconds S1­AO interval 0.03 to 0.08 seconds MC louder than MO AC louder than AO MO is audible in approximately 50% AO may be absent Soft apical systolic murmur Soft systolic ejection murmur Soft diastolic ramble No diastolic rumble Loud AO and AC Soft systolic ejection murmur A2: aortic valve closure sound; MO: mitral prosthesis opening sound; MC: mitral prosthesis closing sound; S1: first heart sound; AO: aortic prosthesis opening sound; AC: aortic prosthesis closing sound. Data from Smith ND, Ralzada V, Abrams J: Auscultation of the normally functioning prosthetic valve. Ann Intern Med 95:594, 1981. Graphic 61951 Version 5.0
