What is the mechanism by which heart sounds are produced in a healthy adult?

Mechanism of Heart Sound Production

Heart sounds are produced by the sudden deceleration or acceleration of blood columns following valve closure or opening, which causes vibrations of the cardiac structures and valves that propagate through the cardiohemic system as audible sounds. 1, 2, 3

First Heart Sound (S1)

S1 is generated primarily by closure of the atrioventricular valves (mitral and tricuspid), with the audible components occurring precisely when these valves complete their closure. 1

Timing and Components

• The mitral component (M1) occurs approximately 0.06 seconds after the Q wave on ECG, coinciding with complete mitral valve closure 1
• The tricuspid component (T1) follows at approximately 0.09 seconds after the Q wave, reflecting tricuspid valve closure 1
• The sound results from sudden deceleration of blood when the valves close, causing the valve leaflets to act as elastic membranes that vibrate and generate compression waves in the blood 3

Mechanism Details

• Ventricular myocardial contraction during isovolumetric contraction generates vibrations in the muscular wall that contribute to S1 4
• A transient myocardial quiver occurs across the interventricular septum approximately 4 milliseconds after S1 onset 2
• The amplitude and frequency of S1 correlate with the slope of the left ventricular pressure-time curve during isovolumetric contraction 4

Second Heart Sound (S2)

S2 is produced by closure of the semilunar valves (aortic and pulmonic), with the sound beginning after complete valve coaptation when the closed leaflets vibrate as elastic membranes. 2, 3

Timing and Components

• The aortic component (A2) occurs first, followed by the pulmonic component (P2) 2
• S2 onset is synchronous with coaptation of the aortic valve cusps and a sharp vibration on the aortic wall 2
• The closed valve oscillates for 30-45 milliseconds after cusp coaptation 2

Mechanism Details

• The semilunar valves act as elastic membranes when closed, and their stretch and recoil generate compression and expansion of blood, producing transient pressure changes that manifest as sound 3
• The magnitude of initial valve stretch relates to the differential pressure between the arterial and ventricular chambers, explaining why S2 amplitude varies with diastolic pressure 3
• Sound amplitude is higher in the ventricles than in the arterial cavities, with opposite directional inscription of sound components between ventricular and arterial chambers 3

Additional Heart Sounds

Ejection Sounds

• Ejection sounds occur when semilunar valves achieve fully opened position, coinciding exactly with valve opening in most cases 1
• Aortic ejection sounds occur approximately 0.13 seconds after the Q wave 1
• Pulmonic ejection sounds occur approximately 0.10 seconds after the Q wave in valvular stenosis, or 0.18 seconds in non-stenotic right-sided abnormalities 1

Third Heart Sound (S3)

• S3 is a normal finding in most pregnant women due to increased blood volume and cardiac output 5
• It represents rapid ventricular filling in early diastole 5

Clinical Implications

The frequency and energy content of heart sounds depend on valve structure, pressure gradients across valves, and the mechanical properties of cardiac tissues. 6

• Mechanical heart valves produce higher frequency components and greater energy compared to native valves 6
• Calcific changes in valves can reduce or eliminate associated sounds by decreasing valve elasticity 3
• The lungs, thorax structure, and recording location affect the transmission and characteristics of heart sounds 6