AuscultifyS1 S2 S3 S4 Heart Sounds Explained: What Causes Each Sound
S1 is caused by closure of the mitral and tricuspid valves at the start of systole, and S2 by closure of the aortic and pulmonic valves at the start of diastole. S3 and S4 are extra low-pitched sounds in diastole: S3 from rapid early filling of the ventricle, S4 from atrial contraction into a stiff ventricle. Systole is the gap between S1 and S2; diastole is the longer gap from S2 to the next S1.
The cardiac cycle in one paragraph
Each beat begins when the ventricles contract. Ventricular pressure rises above atrial pressure, the mitral and tricuspid valves snap shut (S1), pressure keeps rising until it exceeds aortic and pulmonary pressure, the semilunar valves open and blood is ejected. As the ventricles relax, pressure falls below aortic and pulmonary pressure and the aortic and pulmonic valves close (S2). The ventricles keep relaxing until their pressure drops below atrial pressure, the AV valves open and blood pours in rapidly (the phase that can generate S3), filling slows, and finally the atria contract to top up the ventricles (the phase that can generate S4). Then the cycle repeats.
S1: the first heart sound
S1 is produced by the abrupt tensing of the closing mitral and tricuspid valves and their supporting apparatus. The mitral component (M1) comes first and is louder; the tricuspid component (T1) follows a few hundredths of a second later and is usually inaudible as a separate sound. S1 is loudest at the apex, higher pitched than S3 or S4, and coincides with the carotid upstroke, which is how you identify it when the rate is fast.
Loud S1: mitral stenosis with pliable leaflets (the leaflets are held wide open by the high atrial pressure and slam shut), a short PR interval, tachycardia, and high-output states such as fever, anemia, thyrotoxicosis or exercise. S1 is also loud after a long diastole in atrial fibrillation.
Soft S1: mitral regurgitation (the leaflets never coapt fully), a long PR interval in first-degree AV block (the leaflets drift closed before contraction), poor left ventricular contractility, calcified immobile mitral leaflets in advanced mitral stenosis, and anything that dampens transmission such as obesity, emphysema or pericardial effusion.
S2: the second heart sound
S2 is produced by closure of the aortic valve (A2) followed by the pulmonic valve (P2). A2 is the louder component and is heard across the precordium; P2 is normally heard only in the pulmonic area. S2 is loudest at the base, the aortic and pulmonic areas, and is higher pitched and shorter than S1.
Physiologic splitting. On inspiration, venous return to the right heart increases and pulmonic closure is delayed, so A2 and P2 separate and you hear a split S2 at the upper left sternal border. On expiration they fuse. The split is normal and is most obvious in children and young adults.
- Wide fixed split: atrial septal defect. The right heart is volume loaded in both phases of respiration, so the split does not vary.
- Wide but variable split: right bundle branch block, pulmonic stenosis, anything that delays RV emptying.
- Paradoxical (reversed) split: left bundle branch block, severe aortic stenosis, RV pacing. A2 is delayed until after P2, so the split is widest on expiration and closes on inspiration.
- Loud P2: pulmonary hypertension. If you can hear P2 clearly at the apex, suspect it.
- Soft or absent A2: severe calcific aortic stenosis, where the valve can no longer snap shut.
S3 and S4: the third and fourth heart sounds
S3 falls in early diastole, about 0.12 to 0.18 seconds after S2, when rapid ventricular filling decelerates abruptly in a compliant or volume-loaded ventricle. It is normal in children and adults under about 40 and usually indicates systolic heart failure or volume overload in older adults. Full detail in S3 heart sound.
S4 falls in late diastole, just before S1, when the atrium contracts into a stiff ventricle. It is almost always abnormal in adults and points to hypertension, LVH, aortic stenosis, hypertrophic cardiomyopathy or ischemia. It cannot occur in atrial fibrillation. Full detail in S4 heart sound, and the side-by-side comparison in S3 vs S4 heart sounds.
The four heart sounds compared
| Sound | Timing | Cause | Pitch | Best site | Chest piece |
|---|---|---|---|---|---|
| S1 | Start of systole | Mitral and tricuspid closure | Medium to high, "lub" | Apex | Diaphragm |
| S2 | Start of diastole | Aortic then pulmonic closure | High, short, "dub" | Base (aortic and pulmonic areas) | Diaphragm |
| S3 | Early diastole, after S2 | Abrupt deceleration of rapid filling | Low, dull | Apex (LV) or LLSB (RV) | Bell, light pressure |
| S4 | Late diastole, before S1 | Atrial contraction into stiff ventricle | Low, dull | Apex (LV) or LLSB (RV) | Bell, light pressure |
The site column is why the auscultation sequence matters: S2 and its splitting are judged at the base, S1 and the gallops at the apex. See cardiac auscultation areas for the five sites and bell vs diaphragm for chest-piece choice.
Which is systole and which is diastole?
Plainly: systole is between S1 and S2, and diastole is between S2 and the next S1. S1 is not "systole" and S2 is not "diastole"; each is the sound that opens its phase. At a normal rate diastole is longer than systole, so the short gap is systole and the long gap is diastole. When the rate climbs above about 100 the two gaps become similar, and you should identify S1 by palpating the carotid pulse, which rises just after S1. Every systolic murmur sits in the S1-to-S2 gap; every diastolic murmur, and both gallops, sit in the S2-to-S1 gap.
Distant or muffled heart sounds
Heart sounds are described as distant, muffled or soft when all of them are attenuated together, as opposed to a single soft S1 or S2. The cause is almost always something between the heart and your stethoscope:
- Pericardial effusion. Fluid around the heart absorbs the sound. With a large effusion the sounds may be barely audible.
- Cardiac tamponade. The same effusion plus hemodynamic compromise. Beck's triad is muffled heart sounds, hypotension and raised jugular venous pressure; pulsus paradoxus and tachycardia usually accompany it. This is an emergency, not an auscultation curiosity.
- Obesity and a thick or muscular chest wall.
- COPD and hyperinflation. Air-filled lung is a poor conductor and the heart is pushed away from the chest wall; the sounds are often best heard in the epigastrium.
- Pneumothorax and large pleural effusion, which interpose air or fluid and may shift the heart.
- Poor left ventricular contractility and shock, which reduce the force of valve closure.
When the sounds are distant, check the JVP and blood pressure before you blame body habitus, and try the epigastric and subxiphoid positions where the heart may be closer to the surface.
Hear all four sounds in Auscultify
Auscultify's library has real recordings of normal S1 and S2 at each auscultation site, split S2, S3 and S4 so you can hear the pitch and site differences described above. Six quiz modes test whether you can name the sound and the phase it falls in, missed sounds come back through spaced repetition, and the Spectrogram view (Pro) lets you see S1, S2 and any extra sound laid out on the cardiac cycle.
Train heart sounds free →FAQ
What is S1 S2 S3 S4?
S1 and S2 are the two normal heart sounds, produced by closure of the mitral and tricuspid valves (S1) and the aortic and pulmonic valves (S2). S3 and S4 are extra low-pitched diastolic sounds produced by ventricular filling: S3 by rapid early filling and S4 by atrial contraction into a stiff ventricle.
What causes S1 and S2?
S1 is caused by closure of the mitral and tricuspid valves at the start of ventricular systole. S2 is caused by closure of the aortic and pulmonic valves at the start of diastole. The sound comes from the abrupt tensing of the valve leaflets and surrounding structures, not the leaflets clapping together.
What valves close during S1?
The atrioventricular valves, the mitral and tricuspid valves, close during S1. Mitral closure slightly precedes tricuspid closure, and the mitral component is the louder of the two.
Is S1 systole and S2 diastole?
S1 marks the start of systole and S2 marks the start of diastole. Systole is the interval from S1 to S2, and diastole is the longer interval from S2 to the next S1. S3 and S4 both fall in diastole.
What causes a loud S1?
A loud S1 occurs when the mitral leaflets are wide apart at the moment of closure or the ventricle contracts forcefully: mitral stenosis with mobile leaflets, a short PR interval, tachycardia and high-output states such as fever, anemia or thyrotoxicosis.
What are the causes of distant or muffled heart sounds?
Anything that puts fluid, air or tissue between the heart and the stethoscope: pericardial effusion and cardiac tamponade, obesity, emphysema or hyperinflation, pneumothorax, a large pleural effusion, and a thick or muscular chest wall. Poor left ventricular contractility also softens the sounds.