What Causes the S3 Heart Sound
The S3 heart sound is caused by rapid deceleration of blood flow during early ventricular diastolic filling, which creates cardiohemic vibrations when blood encounters a stiff or volume-overloaded ventricle. 1, 2
Pathophysiologic Mechanism
The S3 occurs during the rapid filling phase of ventricular diastole and is fundamentally related to the kinematics of blood flow deceleration 1, 2:
The sound is generated when transmitral blood flow decelerates rapidly (typically >700 cm/sec²) during early diastole, causing the cardiohemic system to oscillate like a forced, damped harmonic oscillator 2, 3
Myocardial viscoelasticity is the primary mechanical property responsible for converting the kinetic energy of rapid deceleration into audible vibrations 4
The S3 always occurs close to peak early filling velocity (E-wave) during early flow deceleration on Doppler echocardiography 2, 3
Clinical Conditions Associated with S3
Pathologic S3 (Volume Overload States)
S3 is associated with elevated left ventricular filling pressures and volume overload 1:
Heart failure with systolic dysfunction is the most common cause, with S3 present in 46% of patients with primary left ventricular dysfunction 5
Severe valvular regurgitation (mitral or aortic) creates volume overload conditions that produce S3, with the sound serving as a marker of regurgitant fraction ≥40% 5
Restrictive filling patterns with rapid early diastolic inflow and elevated pulmonary pressures (mean 55 mmHg vs 41 mmHg in those without S3) 5
Physiologic S3 (High Flow States)
Young healthy individuals with hyperdynamic circulation can have S3 due to rapid early filling velocity without underlying cardiac disease 6, 3
Athletes commonly demonstrate S3 related to enhanced early diastolic filling with rapid deceleration rates (726 cm/sec²) that disappear with reduced preload (head-up tilt) 3
Key Hemodynamic Determinants
The presence and intensity of S3 depends on several interrelated factors 5, 4:
Greater filling volume entering the ventricle during early diastole increases the likelihood of S3 5
Increased ventricular compliance (dilated chambers) amplifies sound generation, with marked dilatation strongly associated with audible S3 (OR = 20 in mitral regurgitation) 5, 4
Reduced ejection fraction (<50%) in conditions like aortic regurgitation increases S3 probability (OR = 19) 5
Elevated left atrial pressure drives more rapid early filling and deceleration 1, 5
Clinical Significance
S3 is a reliable indicator of cardiac decompensation and substantially increases perioperative risk 6, 1:
Patients with S3 are more likely to have NYHA class III-IV symptoms (55% vs 18% without S3) 5
S3 combined with history of heart failure, pulmonary edema, bilateral rales, or pulmonary vascular redistribution is an independent predictor of perioperative complications 6, 1
The sound indicates severe hemodynamic alterations requiring comprehensive assessment and consideration of aggressive medical or surgical treatment 5
Important Caveats
Interobserver agreement for detecting S3 by auscultation is only moderate at best (kappa = 0.40-0.50), with some observer pairs showing only slight agreement (kappa = 0.10-0.30) 7. This limitation means:
Echocardiography should be performed to assess ventricular function when S3 is suspected, rather than relying solely on auscultation 1
The clinical context (symptoms, other physical findings, BNP levels) is essential for interpretation 1, 8
Not all hearts with rapid deceleration produce audible S3 - the oscillations must have sufficient amplitude and frequency (typically requiring deceleration >700 cm/sec²) to be heard 2, 3