The First Heart SoundLUB

Dr. Varun V

“The rubbery mass of the heart muscle which from a physical stand point seems like an ideal sound deadening substance, apparently gives of no audible vibrations. Its contraction or filling or even its forceful impact against the chest wall contributes nothing to the heart sound. The fact that audible vibrations can be obtained from thin strips of muscle isolated from the ventricle is of no significance, for it is easy to produce sounds with a thin rubber band but almost impossible with a rubber ball as thick walled as the heart.”

William Dock, M.D 1938

The first heart sound signals the onset of left ventricular contraction and consists of two major audible components (M1 and T1) and two inaudible components.

The first inaudible low frequency vibrations coincide with the beginning of the LV contraction and are muscular in origin.

It is followed by high frequency audible M1 and T1 components, which are produced due to the closure of mitral and tricuspid valves (William Dock)

The last inaudible low frequency vibrations coincide with opening of the semilunar valves with ejection of blood into the aorta and the pulmonary trunk.

However, electrical initiation of LV systole begins 50 to 60 msec before S1 is heard.

LV pressure rises above LA pressure well before forward flow across the mitral valve ceases & valve leaflets have reached their maximally closed position.

Mechanism of first major audible vibration of S1

Luisada Theory

Onset of isovolumetric contraction results in prominent tensing of LV walls, septum and mitral valve apparatus, which produces a sound transient.

He was against the term M1.

Criage and Leatham

First major component of S1 (M1) is coincident with the maximal closing excursion of mitral cusps.

M1 reflects the sudden tensing of the closed mitral leaflets which sets the surrounding cardiac structures and blood into vibration.

Most, but not all, echophonocardiographic studies indicate that Mitral valve closure (M1) coincides with first major recordable sound of S1.

Mechanism of second major audible vibration of S1

Luisada and Shaver Theory

The second major audible vibration of S1 is an ejection component coincident with opening of the Aortic valve.

Craige and Leatham

They have obtained echophonocardiograms confirming coincidence of tricuspid valve closure (T1) with the second component of S1

Most investigators concur that the last recordable component of S1 coincides with onset of ejection into the Aorta.

Factors Affecting Intensity of S1

PR interval

Short PR interval results in late Mitral valve closure and a loud S1.

When PR is short, LV isovolumetric systolic pressure is high at the time of LV-LA pressure crossover, causing more rapid mitral valve closing motion and loud S1.

Maximal intensity of S1 occurs at a PR interval range of 80 to 140 msec.

PR interval >200 msec results in soft S1 as the Mitral valve has already closed prior to development of LV pressure.

LV Contractility

The more vigorous the LV contraction, the louder the S1.

Depressed LV contractilty and a decreased rate of LV pressure development will result in a decreased intensity of S1.

Hyper-adrenergic states like excitement, fever or exercise commonly increases S1 amplitude.

In general, position of mitral valve leaflets at end-diastole and their closing velocity are more important than the state of LV contractility.

Mitral Leaflets and Left Ventricle

Mobile but abnormally stiff mitral valve leaflets such as those found in Mitral Stenosis, produce a loud S1, unless they are severely distorted, calcified or fibrotic.

How to listen to S1?

Timing

S1 should be timed simultaneously with palpation of the carotid pulse or apical impulse.

S1 immediately precedes the palpable carotid arterial upstroke.

It will appear to initiate the outward LV thrust of apex beat.

Characteristics

S1 is of medium to high frequency.

Usually lower pitched than S2.

S1 splitting is better detected medial to the apex or at the left lower sternal border.

T1 is usually softer at the apex and louder at the lower left sternal border.

S1 is usually not prominent at the base.

Splitting of S1 is best detected in expiration.

T1 more prominent with inspiration.

When apparent splitting of S1 is heard at the base, one should suspect presence of an ejection sound or early mid-systolic click.

Ejection Click vs. Split S1

Ejection click is usually more intense than T1.

Ejection click is better hear at the base.

Aortic click is best heard at the apex.

Pulmonic ejection click will vary with respiration if caused by pulmonic stenosis.

S1 vs. S4

S4 is usually audible at the apex mostly in left lateral position.

S4 is not heard in left lower sternal border where splitting is best detected.

S4 may vary in intensity with respiration.

Abnormalities of S1

Increased intensity of S1

Short PR interval such as in WPW and Lown-Ganong-Levine syndrome.

It may equal or exceed the intensity of S2 at the base.

Loud S1 is often associated with a hypertrophied, non-compliant left ventricle, because of elevated LVEDP that causes a late and abrupt acceleration of mitral valve closure.

Mitral valve prolapse with early or holosystolic prolapse, S1 may be very loud.

Mechanism of loud S1 is in Mitral Stenosis.

Persistently elevated LA pressure in late diastole allows ventricular pressure to rise considerably higher than normal during isovolumetric systole.

A wide closing excursion of mitral valve leaflets, which are held open deep within the left ventricle during late diastole, resulting in delayed M1 and may follow T1.

The stiff, noncompliant leaflet and chordal tissue probably resonate with an increased sound amplitude.

Left Atrial Myxoma S1 may be loud and delayed due to obstructing tumor which results

in elevated LA pressure as it keeps the mitral valve cusps apart in late diastole.

Decreased intensity of S1

Long PR interval

Audible reduction in S1 amplitude occurs at PR intervals > 0.16sec.

S1 is markedly attenuated with a PR > 0.20sec.

Impaired LV function with depressed rate of rise of isovolumetric pressure. Thus S1 is soft in AR, MR and CCF.

Cardiomyopathy, Myocarditis, Myxedema, Ventricular aneurysm – reduced myocardial contractility hence soft S1.

In acute AR a markedly elevated LVEDP results in premature closure of Mitral Valve, thus reducing the intensity of S1

S1 intensity is usually decreased in LBBB, in part because of reduced LV contractility and in part because of the delay in onset of LV contraction.

M1 may follow T1 in patients with LBBB

Abnormal Splitting of S1

Wide splitting of S1 can result from an electrical delay in ventricular activation which results in asynchrony of contraction.

RBBB, PVC with RBBB configuration and LV pacing have been associated with prominent splitting of S1.

In acute MI LV pre-ejection time may be prolonged which may result in splitting of S1.

Prominent splitting of S1 is common in Ebstein’s anomaly – the delayed closing of septal leaflet of the tricuspid valve produces a loud and early systolic closing sound.

Tricuspid valve closure sound is exaggerated in patients with ASD.

Variable S1

Whenever the relationship between the position of mitral valve leaflets and LV pressure rise is inconstant, the intensity as well as spitting interval of S1 will vary.

Thus 2nd or 3rd degree heart block and AV dissociation will result in S1 of variable intensity.

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