on 29-Jul-2025 (Tue)

We are building infrastructure to make humans more productive. This realization has fundamental ramifications to how we should think about and design infrastructure for data scientists— for fellow human beings, instead of for machines. For instance, if we assume that human-time is more expensive than computer-time, which is certainly true for most data scientists, it makes sense to use a highly expressive, productivity-boosting language like Python instead of a low-level language like C++, even if it makes workloads more inefficient to process.

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.

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 [1-3].

High-frequency 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.

Low-frequency 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 systole in late diastole.

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.

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 MVC 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) [15].

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.

A soft S1 is mostly related to decreased mobility or due to a semiclosed position of the leaflets prior to systole.

S1 is soft with severe MS when the mitral valve is immobile due to calcification and fibrosis, despite a significant transvalvular gradient.

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 MVC 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 [16].

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.

Splitting of S1 — 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).

The S2 consists of two components: aortic and pulmonary valve closure sounds, traditionally designated as A2 and P2, respectively [8]. Simultaneous M-mode 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.

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) [23]

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 right-sided and decreased left-sided filling due to increased pulmonary venous pooling. The inspiratory split widens mainly because of delay in P2.

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 (left-to-right shunt), which prolongs right-sided 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 3) [27,28].

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 [8,29].

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

S3 and S4 are low-frequency 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 [31]. 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 [32]. It appears to be related to a sudden limitation of the movement during ventricular filling along its long axis [33], 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 the onset of atrial systole and a-wave of the atrial pressure tracing, and with the apical impulse [34]

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, right-sided 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 unchange

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" [35]. 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 right-sided gallop sound increases during inspiration.

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) [36]. In such patients, an S3 gallop is usually associated with left atrial pressures exceeding 20 mmHg, increased LV end-diastolic pressures (>15 mmHg), and elevated serum B-type natriuretic peptide (BNP) concentrations [37-39]

An S3 gallop is almost always present in patients with hemodynamically significant chronic mitral regurgitation (MR); the absence of S3 should raise questions about the severity of 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 [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].

An S3 often occurs in high-output 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].

A phonocardiographic study of patients undergoing cardiac catheterization examined the diagnostic test characteristics of the S3 and S4 for detection of LV dysfunction [39]. These sounds were not very sensitive (40 to 50 percent) for the detection of an elevated LV end-diastolic 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 the appreciable interobserver variability in detection of an S3 on cardiac auscultation; this variability is only partially explained by the experience of the observer [45-48].

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) [49]. 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.

An S4 is heard in the vast majority of patients during the acute phase of myocardial infarction (MI) [51]. 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.

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 end-diastolic pressure (>15 mmHg) [52]. The predictive value is increased in the presence of both S3 and S4 gallops [37].

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 lower-pitched S3 and S4 will be more pronounced when listening gently with the bell, while the higher-pitched split S1 and S2 will be more pronounced when listening with the diaphragm or when applying the bell more firmly to the skin.

Auscultation to distinguish S3 and S4 from a splitting of S2 and S1 is best performed in the 45-degree 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.

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 [54]. It is occasionally heard only during inspiration and along the lower right sternal border by experienced auscultators, suggesting an early manifestation of RV constriction.

EJECTION SOUNDS —

An ejection sound is a high-frequency, "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 or click 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; it is generally best heard at the cardiac apex and may be heard at the base (at the right second intercostal space) [55]. The ejection click is often described by auscultators as a split S1. 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 [56]. 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 [57]. 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.

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 [58-61].

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.