S3 Heart Sound: Causes and Pathophysiology
Direct Answer
The S3 heart sound is caused by rapid deceleration of early diastolic blood flow into the left ventricle, resulting in sudden limitation of ventricular expansion and cardiohemic vibrations that produce an audible low-frequency sound. 1, 2
Pathophysiologic Mechanism
The S3 occurs during the rapid filling phase of early diastole when blood decelerates abruptly as it enters the ventricle. This creates a specific sequence of events:
Biomechanical Origin
The sound results from sudden intrinsic limitation of longitudinal expansion of the left ventricular wall during early diastolic filling, producing a negative jerk transmitted to the chest wall. 3
The cardiohemic system functions as a forced, damped harmonic oscillator—when transmitral flow decelerates rapidly enough, it generates oscillations of sufficient amplitude and frequency to become audible. 4
The S3 always occurs close to peak early filling velocity (E-wave) during the early flow deceleration phase on Doppler echocardiography. 5
Key Hemodynamic Determinants
The most important factors determining S3 production include:
Abnormally rapid deceleration rate of early mitral inflow (>700 cm/sec²), which is significantly higher than in patients without S3 (563 cm/sec²). 5
Elevated left ventricular filling pressures, as reflected by increased E/E' ratio on tissue Doppler imaging. 2
Decreased ventricular compliance or abnormal myocardial properties, which limit the ventricle's ability to accommodate rapid filling. 2
Clinical Causes and Contexts
Pathologic S3
An audible S3 indicates severe hemodynamic alterations and warrants comprehensive assessment for vigorous medical or surgical treatment. 6
The pathologic S3 occurs in:
Primary left ventricular systolic dysfunction (present in 46% of cases), associated with reduced ejection fraction and restrictive filling patterns. 6
Severe valvular regurgitation (mitral or aortic), where it serves as a marker of regurgitant fraction ≥40%. 6
Volume overload states with elevated pulmonary pressures (mean 55 mmHg vs. 41 mmHg in those without S3). 6
Patients with NYHA class III-IV symptoms (present in 55% vs. 18% without S3). 6
Physiologic S3
Normal young individuals and athletes can have a physiologic S3 due to enhanced early diastolic filling with rapid deceleration, despite normal ventricular function. 5
Pregnancy: Third heart sounds are present in most pregnant patients due to the 50% increase in blood volume and cardiac output, representing a normal physiologic finding. 7
The physiologic S3 shares the same mechanism as pathologic S3 (rapid flow deceleration) but occurs in the context of normal ventricular compliance and filling pressures. 5
Clinical Significance
The E/E' ratio measured by tissue Doppler imaging is the most important independent determinant of the pathologic S3, even more than invasively measured filling pressures. 2
Important Caveats
The S3 can disappear or diminish with maneuvers that reduce preload (such as head-up tilt or standing), as these decrease the E-wave deceleration rate below the threshold needed for audible oscillations. 5
The presence of S3 is not solely dependent on left ventricular systolic function—it can occur with preserved ejection fraction if diastolic dysfunction and elevated filling pressures are present. 5
In pregnancy, the S3 must be distinguished from pathologic causes by considering the overall clinical context, as it represents a normal adaptation to increased circulatory volume. 7