Alicia hears lub-dub and imagines two doors slamming shut. Tricia says the first sound is the mitral valve and the second is the aortic valve. Kai Kai notices that each sound comes from a whole mechanical transition involving several valves, blood columns, chamber walls and surrounding tissue. The familiar mnemonic is useful, but the real acoustics are richer.
Heart sounds work by converting rapid mechanical events in the beating heart into vibrations that travel through blood, tissue and the chest wall to the listener. S1 is associated mainly with closure of the mitral and tricuspid valves at the start of ventricular systole. S2 is associated mainly with closure of the aortic and pulmonary valves at the end of ejection. The audible sound is not simply the leaflet edges colliding; it reflects coupled vibration of valves, blood and cardiac structures.
This article supports How the Heart Works. How Heart Valves Work owns the valve mechanics. How the Cardiac Cycle Works owns the beat sequence. Here the reader job is acoustics: how a mechanical transition becomes a sound and what that sound can and cannot tell us.
The discussion is educational physiology, not a guide to diagnosing murmurs, valve disease or heart conditions from self-auscultation.
1. A heart sound is a vibration, not a valve name
When a valve closes, blood decelerates abruptly and the surrounding structures experience changing forces. Valve leaflets, chordae, ventricular walls, arterial roots and blood columns can all participate in the resulting vibration.
The NCBI review Physiology, Heart Sounds describes S1 and S2 as acoustic consequences of structural and haemodynamic events associated with valve closure. This language is more accurate than saying the valve itself makes a single isolated click.
Sound therefore tells us that a rapid mechanical transition occurred. It does not directly measure how much blood crossed the valve.
2. S1 marks the beginning of ventricular systole
S1 occurs as ventricular pressure rises above atrial pressure and the atrioventricular valves close. The mitral component, M1, usually precedes and dominates the tricuspid component, T1.
Closure happens early in isovolumetric contraction, before the aortic and pulmonary valves have opened. The ventricle is already producing force even though ejection has not yet begun.
This timing makes S1 a useful acoustic marker for the start of mechanical systole, but it should not be confused with the exact onset of electrical ventricular depolarisation on the ECG.
3. Mitral and tricuspid closure are not perfectly simultaneous
The left and right ventricles do not develop pressure in perfectly identical timing. Their atrioventricular valves therefore need not close at exactly the same instant.
In ordinary conditions the M1 and T1 components are close enough in time that the ear usually perceives one first heart sound.
The single audible S1 is therefore already a compressed sensory representation of two related mechanical events.
4. S1 loudness depends on more than valve anatomy
Sound amplitude depends on the speed and force of the transition, valve position before closure, contractile state, pressure development and how the vibration is transmitted through tissue.
A valve starting more widely open can undergo a larger movement before closure than one already near the closed position. The timing between atrial and ventricular activation can therefore influence S1 intensity.
A louder sound is not a direct measure of a healthier or stronger heart. Acoustic amplitude mixes source mechanics with transmission and recording conditions.
5. S2 marks the end of ventricular ejection
S2 occurs when the pressure-flow conditions at the semilunar valves reverse and the aortic and pulmonary valves close. The aortic component is called A2 and the pulmonary component P2.
These events occur near the transition from ventricular systole to diastole. The ventricles have finished useful forward ejection and are entering isovolumetric relaxation.
The classic description in The Second Heart Sound treats S2 as a short burst of vibrations generated by haemodynamic events around semilunar valve closure.
6. A2 usually precedes P2
In ordinary physiology the aortic valve usually closes slightly before the pulmonary valve. The interval between A2 and P2 can become audible under appropriate conditions.
This is physiological splitting of S2. It reflects small timing differences between left- and right-sided ejection rather than a second separate heartbeat.
The fact that one sound contains two components illustrates again why the ear hears a compressed version of multiple mechanical events.
7. Inspiration can widen normal S2 splitting
During spontaneous inspiration, intrathoracic pressure falls and venous return to the right heart can increase. The right ventricle may then eject for slightly longer, delaying pulmonary valve closure.
At the same time, left-sided filling and ejection timing can change in the opposite direction because the pulmonary circulation temporarily stores more blood.
The result can be a wider A2–P2 interval during inspiration and a narrower interval during expiration. Breathing therefore modulates a heart sound through circulation mechanics, not because the lungs directly pull a valve open or closed.
8. Splitting is fundamentally a timing measurement
To understand splitting, ask which mechanical event occurred first and how much later the second event occurred.
The ear detects two bursts when their separation exceeds the listener’s temporal-resolution threshold and the components are sufficiently strong.
A split sound therefore combines physiology with sensory resolution. Two closure events can remain distinct in the heart even when the listener perceives them as one sound.
9. Frequency determines pitch
Rapid vibrations create higher-frequency acoustic components; slower oscillations create lower-frequency components. Human auscultation is sensitive only across a limited frequency range, and the chest wall filters the signal further.
S1 is generally lower pitched and somewhat longer than S2. S2 contains sharper higher-frequency components.
The words low and high pitched refer to frequency, not loudness. A quiet sound can be high pitched, and a loud sound can be low pitched.
10. Loudness depends on amplitude and transmission
Acoustic amplitude at the chest surface depends on both the source vibration and the pathway between source and stethoscope.
Blood, myocardium, lungs, ribs, fat and skin all affect transmission. Position, breathing and stethoscope pressure can therefore change what reaches the ear.
A quieter chest-wall sound does not necessarily mean the intracardiac event itself became proportionally weaker.
11. The stethoscope is a mechanical-acoustic filter
The chest piece couples vibration from the body into an air column and ultimately to the listener’s ears. The diaphragm and bell emphasise different frequency ranges depending on design and applied pressure.
High-frequency sounds are generally more evident with the diaphragm, while low-frequency sounds can be appreciated with a lightly applied bell on traditional acoustic stethoscopes.
The device therefore does not merely amplify everything equally. It shapes which parts of the acoustic spectrum are easiest to hear.
12. Auscultation locations are listening windows, not exact valve positions
The classic aortic, pulmonary, tricuspid and mitral auscultation areas are chest locations where particular sound components often transmit well.
They are not drawn directly over the anatomical valve leaflets. Sound propagates through blood and tissue along favourable pathways.
This distinction explains why the best listening point can lie some distance from the structure that generated much of the vibration.
13. Timing with the pulse helps identify systole
The carotid pulse rises shortly after the onset of ventricular systole and can help a listener identify which acoustic event is S1 when the rhythm is unfamiliar.
A more distant pulse, such as at the wrist, arrives later because the arterial pressure wave takes time to propagate. The NCBI Clinical Methods overview notes why the carotid is preferable for timing.
This is another example of aligning two different signals—sound and pulse—to infer a common mechanical sequence.
14. ECG timing separates electrical and acoustic events
The QRS complex begins ventricular electrical depolarisation before S1 occurs. Excitation–contraction coupling and pressure development intervene between the two.
The T wave overlaps the later part of ventricular mechanical systole, while S2 occurs near the end of ejection as semilunar valves close.
Recording ECG and phonocardiography together therefore lets us align the electrical and acoustic clocks rather than assuming they are simultaneous.
15. Phonocardiography turns sound into a waveform
A phonocardiogram records acoustic vibration over time. Instead of relying only on the ear, the signal can be displayed as amplitude versus time and analysed by frequency.
Digital systems can synchronise the acoustic trace with ECG or pressure measurements, allowing component timing to be quantified.
The waveform is still dependent on sensor placement, filtering and noise. A digital trace does not remove the measurement chain; it makes that chain more explicit.
16. S3 and S4 are low-frequency filling sounds
Additional low-frequency heart sounds can occur during diastole. S3 occurs in early diastole during rapid ventricular filling, while S4 occurs later in diastole in association with atrial contraction against the ventricle.
Their presence and significance depend strongly on age, physiology and clinical context. This article does not use them as diagnostic labels.
Mechanistically, their timing reminds us that rapid filling and chamber-wall vibration can generate acoustic events even when no valve is closing.
17. A murmur is sustained vibration produced by moving blood and structures
Murmurs last longer than the brief S1 and S2 events because the underlying flow disturbance persists over a larger fraction of systole or diastole.
The acoustic energy can arise from high-velocity jets, vortices, vibrating walls and flow through changing geometries.
The simplified phrase turbulent blood flow is useful but incomplete. Flow can generate sound through several interacting mechanisms, and the relationship between Reynolds number, geometry and audible vibration is not one universal threshold.
18. Sound timing is often more informative than loudness alone
Knowing whether a sound occurs in early systole, late systole, early diastole or late diastole places it inside the cardiac cycle.
Loudness varies with the source and transmission path, whereas timing links the sound to valve state, filling or ejection.
This is why an experienced listener first locates systole and diastole before trying to interpret finer acoustic qualities.
19. Breathing changes both mechanics and acoustics
Respiration changes venous return, intrathoracic pressure, lung volume and the distance and acoustic path between the heart and chest wall.
A change in what the listener hears can therefore combine a true change in intracardiac timing with a change in transmission.
The same observation can have both physiological and acoustic causes. Good reasoning keeps those pathways separate.
20. Body position changes the acoustic window
Changing posture can move the heart relative to the chest wall and alter venous return. Some sounds become easier to hear when the relevant cardiac structure lies closer to the stethoscope.
The left lateral position, for example, brings the apex region closer to the chest wall in many people.
This shows why auscultation is not simply placing a sensor at one permanent coordinate. Geometry of the whole thorax matters.
21. Worked problem: same valve event, different sound amplitude
Imagine two model recordings generated by identical intracardiac vibrations. In Model A, the sensor sits over a favourable transmission path. In Model B, more air-filled lung lies between source and sensor.
B can record a lower amplitude even though the source event is unchanged. The difference belongs to transmission, not necessarily to the valve or myocardium.
This is the acoustic equivalent of a distant speaker sounding quieter without the speaker itself changing power.
22. Worked problem: one sound or two?
Suppose A2 occurs at 400 ms and P2 at 430 ms after an arbitrary cycle marker. A second recording has the same components at 400 and 405 ms.
The first interval is 30 ms; the second is 5 ms. Depending on frequency, amplitude and listener resolution, the first is more likely to be perceived as two components while the second may merge into one audible event.
The mechanical components exist in both cases. Perception adds another layer to the measurement.
23. Worked problem: sound does not equal flow
Two model hearts produce identical S1 amplitude. Heart A ejects 70 mL and Heart B ejects 50 mL per beat.
There is no contradiction because S1 is not a stroke-volume meter. It reflects a rapid mechanical transition at atrioventricular valve closure.
To compare flow, another measurement such as chamber-volume change or Doppler-derived flow is required.
24. Worked problem: electrical regularity does not guarantee identical acoustics
Suppose successive ECG cycles have identical RR intervals but filling varies with respiration. The valve positions and pressure trajectories at closure can differ slightly from beat to beat.
The resulting sound intensity or S2 splitting can therefore vary even while electrical rate remains regular.
Electrical timing constrains mechanical timing but does not specify every acoustic detail.
25. The heart-sound mechanism in one causal chain
Electrical activation changes myocardial force. Chamber pressure rises. Pressure relationships close the atrioventricular valves and rapidly decelerate blood, generating vibrations that form S1. Ventricular pressure then opens the semilunar valves and blood is ejected. As ejection decelerates and arterial pressure again exceeds ventricular pressure, the semilunar valves close and surrounding structures vibrate, forming S2. Respiration changes right- and left-sided timing and can alter the separation of A2 and P2. These vibrations propagate through blood, myocardium, lungs and chest wall before reaching the stethoscope or sensor.
Alicia keeps lub-dub as a useful mnemonic but no longer imagines two isolated doors. Tricia separates M1 from T1 and A2 from P2. Kai Kai places the sounds on the ECG and pressure timelines. The acoustics now belong to the mechanism.
The deeper lesson is that a sound is evidence of motion and force, not a transparent label for one structure. Listening becomes scientific when the vibration is placed back into the pressure, valve and timing sequence that produced it.
Evidence trail and connected reading
For a concise physiology overview, see NCBI Bookshelf: Physiology, Heart Sounds. For classic S2 timing and splitting, see The Second Heart Sound. For timing heart sounds against the pulse, see Clinical Methods: An Overview of the Cardiovascular System.
Return to the parent: How the Heart Works. Continue to How Heart Valves Work, How the Cardiac Cycle Works and How the ECG Works.