Heart Sounds & Pathophysiology: Why Each Sound Happens

Connecting what you hear to what's happening hemodynamically · Updated 2026

You can memorize that aortic stenosis is a crescendo-decrescendo systolic murmur. But if you understand why — because flow velocity across the narrowed valve peaks in mid-systole — the sound stops being a fact to recall and becomes a pattern you can reason through. Here's the pathophysiology behind the sounds you need to know.

Normal heart sounds

S1 — mitral and tricuspid valve closure

S1 marks the beginning of systole. It's produced by the sudden tensing and closure of the mitral and tricuspid valves as ventricular pressure exceeds atrial pressure. Mitral closure (M1) comes slightly before tricuspid closure (T1), but the split is usually inaudible.

Loud S1: short PR interval, mitral stenosis (mobile leaflets), high-output states. Soft S1: long PR interval, mitral regurgitation, reduced contractility, calcified mitral valve.

S2 — aortic and pulmonic valve closure

S2 marks the beginning of diastole. Aortic closure (A2) precedes pulmonic closure (P2). On inspiration, increased venous return to the right heart delays pulmonic valve closure, producing a physiologic split heard best at the pulmonic area.

Fixed split: ASD (right heart volume overload equalizes timing). Paradoxical split: LBBB, severe aortic stenosis (delayed A2 falls after P2). Wide split: pulmonic stenosis, RBBB.

Extra heart sounds

S3 — rapid ventricular filling

A low-pitched sound in early diastole, just after S2. It occurs when blood rushing into the ventricle meets a suddenly decelerating column of blood. In young patients with compliant ventricles, this is normal. In adults over 40, it suggests volume overload — heart failure, mitral regurgitation, high-output states.

Mnemonic: "Ken-TUCK-y" = S1-S2-S3.

S4 — atrial kick into a stiff ventricle

A low-pitched sound in late diastole, just before S1. It's produced by atrial contraction forcing blood into a non-compliant ventricle — diastolic dysfunction. Causes: LVH (from hypertension or aortic stenosis), hypertrophic cardiomyopathy, acute MI.

Mnemonic: "TEN-nes-see" = S4-S1-S2. Note: S4 is absent in atrial fibrillation (no organized atrial contraction).

Systolic murmurs

Aortic stenosis

Sound: crescendo-decrescendo (diamond-shaped) systolic murmur at RUSB, radiating to the carotids.

Why: the narrowed aortic valve creates a pressure gradient. Flow velocity accelerates as the ventricle contracts, peaks at mid-systole (maximum pressure difference), then decelerates as the ventricle relaxes — producing the characteristic diamond shape. As stenosis worsens, the peak shifts later in systole and S2 becomes soft (calcified valve can't snap shut).

Mitral regurgitation

Sound: high-pitched blowing pansystolic (holosystolic) murmur at the apex, radiating to the axilla.

Why: the incompetent mitral valve allows blood to flow backward from LV to LA throughout the entire duration of systole — the pressure gradient is present from S1 to S2 continuously, so the murmur occupies all of systole. Unlike AS, there's no crescendo-decrescendo because the gradient doesn't peak and fall.

Mitral valve prolapse

Sound: mid-systolic click followed by a late systolic murmur.

Why: the mitral leaflet billows back into the atrium mid-systole (click). If the prolapse is severe enough, the leaflets separate and regurgitation begins (late systolic murmur). Standing (reduced preload) makes the click earlier and the murmur longer; squatting (increased preload) delays the click.

HOCM (hypertrophic obstructive cardiomyopathy)

Sound: harsh crescendo-decrescendo systolic murmur at LLSB.

Why: the thickened septum obstructs the LVOT during systole. Anything that decreases LV volume (standing, Valsalva, dehydration) worsens obstruction and makes the murmur louder — the opposite of most other murmurs. This is the key bedside differentiator.

Diastolic murmurs

Aortic regurgitation

Sound: high-pitched decrescendo diastolic murmur, best heard sitting forward at end-expiration with the diaphragm.

Why: blood leaks back through the incompetent aortic valve as soon as the ventricle relaxes (early diastole). The regurgitant flow is fastest at the start and slows as pressures equalize — hence the decrescendo pattern.

Mitral stenosis

Sound: low-pitched rumbling diastolic murmur at the apex, heard with the bell in left lateral decubitus. Often preceded by an opening snap.

Why: the stenotic mitral valve resists blood flow from LA to LV during diastole. The opening snap occurs when the stiff valve is forced open by rising atrial pressure. The rumble is the turbulent flow through the narrowed orifice. Pre-systolic accentuation occurs because atrial contraction (in sinus rhythm) pushes more blood through the stenotic valve just before S1.

Continuous murmurs

Patent ductus arteriosus (PDA)

Sound: continuous "machinery" murmur at the left infraclavicular area.

Why: aortic pressure exceeds pulmonary artery pressure in both systole and diastole, so blood shunts left-to-right continuously. The murmur peaks at S2 (maximum gradient) and is loudest in systole but doesn't stop — distinguishing it from separate systolic and diastolic murmurs.

Pericardial friction rub

Sound: scratchy, grating, superficial sound with up to three components (atrial systole, ventricular systole, early diastolic filling).

Why: inflamed pericardial surfaces rub against each other with each cardiac motion. Best heard with the diaphragm, patient sitting forward. It's typically positional — changes or disappears with body position — which distinguishes it from murmurs.