on 30-May-2025 (Fri)

S1 is heard well across the entire precordium, both with the bell and diaphragm of the stethoscope. It is usually loudest at or near the apex and contains more low- frequency energy than does S2, which explains why, when mimicking the sound, the term lub is used for S1 and the sharper term dup for S2

Although its two recordable components coincide with closure of the mitral and tricuspid valves, the force of valve closure itself is insufficient to generate sound.4 Instead, their closure probably causes moving columns of blood to abruptly decelerate, which sets up vibrations in the chordae tendineae, ventricles, and blood as a unit (i.e., cardiohemic system).5

The most important abnormalities of S1 relate to its intensity; the sound can be abnormally loud, abnormally faint, or vary in intensity abnormally from beat to beat.

The primary variables governing intensity of S1 are strength of ventricular contraction and the position of the atrioventricular leaflets at the onset of ven- tricular systole

The stronger the ventricular contraction, the louder the S1. Strong contractions, which have a high dP/dT (i.e., large increase in pressure with respect to time), intensify S1 because the valves close with more force and generate more vibrations in the cardiohemic system.6-8

If the mitral valve is wide open at the onset of ventricular systole, it will take longer to close completely than if it had been barely open. Even this small delay in closure intensifies S1 because closure occurs on a later and steeper portion of the left ven- tricular (LV) pressure curve (i.e., dP/dT is greater).9

Studies show that, with PR intervals less than 0.20 seconds, the intensity of S1 varies inversely with the PR interval (the shorter the PR interval the louder the sound). With PR intervals greater than 0.20 seconds, S1 is faint or absent.8-10

The PR interval is the main variable determining the position of the valves at the beginning of ventricular systole. If the PR interval is short, ventricular sys- tole immediately follows atrial systole (i.e., the R wave immediately follows the P wave). Because atrial systole kicks the valve open, a short PR guarantees that the valve will be wide open at the onset of ventricular systole. In contrast, a long PR interval allows time for the cusps of the atrioventricular valves to float back together before ventricular systole occurs

S1 may be abnormally loud because of unusually vigorous ventricular contractions or because of delayed closure of the mitral valve

Vigorous contractions, such as those occurring from fever and sympathetic stimulation (e.g., beta-adrenergic inhalers, thyrotoxicosis), increase dP/dT and intensify S1.6

PROLAPSED MITRAL VALVE In patients with the murmur of mitral regurgitation, a loud S1 is a clue to the diagnosis of early prolapse of the mitral valve (many patients with mitral regurgitation have a normal or soft S1).11,12 S1 is loud in these patients because the prolapsing leaflets stop moving and tense later than normal, when dP/dT in the ventricle is greater.11

Ninety percent of patients with pure uncomplicated mitral stenosis have a loud S1.13 Because the murmur of mitral stenosis is often difficult to hear, a traditional teaching is that clinicians should suspect mitral stenosis in any patient with a loud, unex- plained S1 and listen carefully for the murmur with the patient lying on the left side.

Mitral stenosis delays closure of the mitral valve because the pressure gradient between the left atrium and left ventricle keeps the leaflets open until the moment of ventricular systole. After successful valvuloplasty, the loud S1 becomes softer.13

LEFT ATRIAL MYXOMA Many patients with left atrial myxoma (seven of nine in one series) also have a loud S1 because the tumor falling into the mitral orifice during diastole delays closure of the valve.14

S1 is unusually faint if ventricular contractions are weak or if the mitral valve is already closed when ventricular systole occurs

ACUTE AORTIC REGURGITATION In patients with the murmur of aortic regurgitation, the faint or absent S1 is an impor- tant clue that the regurgitation is acute (e.g., endocarditis) and not chronic.

Patients with acute aortic regurgitation have much higher LV end-diastolic pressures than those with chronic regurgitation, because the acutely failing valve has not allowed time for the ventricle to enlarge, as it does to compensate for chronic regurgitation. The high pressures in the ventricle eventually exceed diastolic left atrial pressures, closing the mitral valve before ventricular systole and thus making S1 faint or absent.16

Any delay in the closure of the tricuspid valve, the second component of S1, accen- tuates splitting of S1. This finding therefore occurs in patients with right bundle branch block (RBBB) or in LV ectopic or paced beats, all of which delay the onset of right ventricular (RV) systole and also cause wide physiologic splitting of S2 (see later).5,27

In patients with complete heart block, S1 intensity is predictable, varying inversely with the PR interval for intervals less than 0.2 second, becoming inaudible for intervals 0.2 to 0.5 second, and becoming louder again with intervals more than 0.5 second (because the mitral valve reopens).10

The first component (M1) of S1 is attributed to mitral valve closure (MVC) and the second (T1) to closure of the tricuspid valve [8-11]. 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 [12,13]. A second hypothesis suggests that the principal high-frequency 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 the contractile state and ejection [14].

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 following factors influence the intensity of S1:

● Mitral valve position at the onset of systole (wide versus partially open).

● Cardiac cycle length.

● 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 affects the timing of atrial contraction, and hence the position of the mitral leaflets at the onset of LV contraction.

● Force of ventricular systolic contraction.

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 end-diastole (mitral or tricuspid valve obstruction as in less than severe ["progressive"] mitral stenosis (table 2 and movie 1), or tricuspid stenosis, or atrial myxoma).

• Increased transvalvular flow (left-to-right shunt in patent ductus arteriosus, ventricular septal defect, and high output state).

• Short diastole.

• Short PR intervals (eg, with preexcitation).

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 MVC. In contrast, MR due to perforation of the valve leaflets from bacterial endocarditis may not be associated with a reduced intensity of S1

S1 is soft in some patients with left bundle branch block without any other obvious abnormality; the mechanism is unclear. Decreased MVC 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 calcification to the mitral valve and in the presence of a normal PR interval [15]. Semiclosure of the mitral valve due to a forceful 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 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 MVC 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.

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.

Wide splitting of S1 is a feature of Ebstein anomaly which is associated with right bundle branch block [17]. 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 [18].