Effect of Velocity of Contraction on S1 Intensity
The intensity of the first heart sound (S1) increases with faster velocity of ventricular contraction, as S1 amplitude correlates directly with the rate of left ventricular pressure rise (dP/dt) during isovolumetric contraction. 1
Physiologic Mechanism
The relationship between contraction velocity and S1 intensity is fundamentally linked to hemodynamic forces:
S1 amplitude demonstrates a linear relationship with the slope of the left ventricular pressure-time curve (dP/dt), meaning faster rates of pressure development during isovolumetric contraction generate louder heart sounds 1
The sound generation occurs through vibrations of the cardiohemic system caused by sudden deceleration of blood columns when the atrioventricular valves complete closure, with the high-frequency components (M1 and T1) precisely coinciding with completion of mitral and tricuspid valve closure 2
Increased contractility and faster contraction velocities result in more rapid valve closure and greater closing energy, which translates to increased S1 intensity 3
Clinical Applications
Conditions with Increased Contraction Velocity
During normal pregnancy, S1 becomes louder than normal with prominent splitting due to the 50% increase in circulating blood volume and enhanced cardiac output, which increases the velocity of ventricular contraction 4, 5
In early systolic mitral valve prolapse, the S1 amplitude ratio (S1/A2) is markedly elevated (6.2 ± 3.1 vs 1.4 ± 0.7 in controls) because initial leaflet coaptation occurs with high closing velocity 6
Conditions with Decreased Contraction Velocity
In left bundle branch block, S1 intensity is reduced because delayed onset of left ventricular contraction and increased isometric contraction time result in slower pressure rise and decreased valve closing velocity 7
In flail mitral leaflet without normal coaptation, the S1 amplitude ratio drops dramatically (0.3 ± 0.5) due to loss of normal closing dynamics 6
Important Clinical Caveat
Initial conditions like valve closure velocity, while intuitively important, are actually less significant than the rate of ventricular pressure development itself in determining S1 intensity 1. This explains why S1 intensity primarily reflects myocardial contractile function rather than simply the speed at which valves close.
The hemodynamic theory—where S1 is generated by vibrations of the ventricular wall during rapid pressure rise—better explains S1 characteristics than the valvular theory alone, though both mechanisms contribute 1.