PharmingoGet the app
Anatomy · Thorax

Four Valves, Two Sounds, and Why You Listen in the Wrong Place

The heart has four doors, and every one of them opens and slams shut about a hundred thousand times a day — roughly forty million times a year, without maintenance, without lubrication you could name, without a single day off. What you hear through a stethoscope is not the leaflets clapping together like hands; tissue that thin makes almost no noise. The sound is the whole column of blood stopping dead against a closed door, and the walls and the chambers shuddering with it. Learn the four doors and the two shudders and you can diagnose half of cardiac disease with nothing but your ears — provided you know the single strangest fact about them: the places where you listen are not the places where the valves are.

14 min read🎯 Linked lesson: Heart valves and heart sounds· Updated 2026-07-19
THE SCENE

A boy of nine is brought to a crowded clinic for a school certificate, entirely well, complaining of nothing. The doctor warms the bell of the stethoscope in her palm, asks him to roll onto his left side, and rests it over the point where his heartbeat lifts the chest wall. In the quiet after the second sound she hears something the boy has never noticed: a sharp click, then a low rumbling that fills the pause before the next beat, like a distant train. She asks about a fever years ago, a sore throat, aching joints that moved from knee to ankle and back. His mother remembers it exactly. The strep throat healed in a week; the antibodies it raised did not stop at the throat, and for the last six years they have been quietly thickening and fusing the leaflets of one small door inside his chest. He has no symptoms yet. He will. And the whole diagnosis was made by a woman listening to a sound made by blood being forced through a doorway that no longer opens properly.

Four doors set in one plane

Before the valves, you need the frame that holds them. The four valves of the heart are not scattered about the organ; they are mounted in a single oblique plane, set into a dense collar of collagen called the fibrous skeleton of the heart. It is made of four fibrous rings — the annuli fibrosi around each valve orifice — joined by the right and left fibrous trigones and continuous with the membranous part of the interventricular septum. This skeleton does four jobs at once. It gives the valve cusps something rigid to hang from, so a ring does not simply stretch open under pressure. It provides attachment for the atrial and ventricular muscle above and below. It stops the orifices dilating as the chambers described in the heart chambers contract around them. And — the detail that matters most — it is electrically inert: fibrous tissue does not conduct, so the atria and ventricles are completely insulated from one another, and the only electrical bridge between them is the atrioventricular bundle piercing the skeleton, as traced in the conducting system of the heart. Two of these four doors are inlets, guarding the way from atrium to ventricle. Two are outlets, guarding the way out into a great artery.

The atrioventricular valves: doors on a leash

The right atrioventricular valve is the tricuspid, and it has, as promised, three cusps: anterior, posterior and septal. The left is the mitral or bicuspid valve, with two: a large anterior (aortic) cusp that hangs like a curtain between the inflow and the outflow of the left ventricle, and a longer, shallower posterior (mural) cusp. Both are made of the same thing — a fold of endocardium reinforced by a core of fibrous tissue — and both face the same problem. During ventricular systole the pressure below them rises to a level that would blow any simple flap backwards into the atrium. Something has to hold them down.

That something is a system of cords and muscles, and its timing is the clever part. From the free margin and the ventricular surface of each cusp run the chordae tendineae — fine, glistening, inelastic collagen cords, like the shrouds of a parachute. They descend to the papillary muscles, conical projections of ventricular muscle that arise from the ventricular wall. The right ventricle has three (anterior, posterior and septal); the anterior one receives the moderator band, the muscular strut that carries the right bundle branch across the cavity. The left ventricle has two, larger and stronger: the anterolateral and the posteromedial. Crucially, each papillary muscle sends chordae to BOTH cusps of its valve, so that the cusps are pulled together rather than apart. And the papillary muscles contract slightly BEFORE the rest of the ventricle — they take up the slack in the cords just as the pressure begins to rise. The cusps are therefore not pushed shut by the blood so much as held shut against it, at exactly the right tension. Too much slack and the cusp balloons backwards into the atrium (prolapse); a cord snaps or a papillary muscle dies and the cusp everts completely, and the valve leaks catastrophically.

The semilunar valves: three pockets and no cords at all

The outlet valves are built on an entirely different principle. The pulmonary valve at the mouth of the pulmonary trunk and the aortic valve at the mouth of the aorta each have three semilunar cusps — half-moon pockets of fibrous tissue covered in endothelium, with a small fibrous nodule at the midpoint of each free edge. The pulmonary cusps are described as anterior, right and left; the aortic cusps as right, left and posterior — the last also called the non-coronary cusp, for a reason you can guess. Behind each cusp the arterial wall bulges outwards into a shallow pouch: the sinus of Valsalva. There are no chordae here and no papillary muscles. Nothing holds these cusps at all.

They close by being filled from behind — and the sinuses are the reason it works. When the ventricle relaxes and the column of blood in the artery starts to fall back, it runs into the three open pockets and fills them. Each cusp balloons inwards until the three free edges meet in the middle and the nodules jam together, and the harder the blood pushes backwards the tighter the seal becomes. It is closure by back-pressure alone: passive, instantaneous and self-tightening. The sinuses of Valsalva are what stop the ballooning cusps from flattening against the arterial wall and occluding what lies behind them — and what lies behind two of the aortic sinuses is everything. The right coronary artery arises from the right sinus and the left coronary artery from the left sinus, which is exactly why the third is the non-coronary cusp. Eddies swirling in the sinuses keep the ostia open throughout systole; then, when the aortic valve shuts and pressure in the root stays high while the muscle relaxes, the coronaries fill — which is why, as the coronary arteries and cardiac veins explains, the heart is the one organ perfused in diastole. The root of the aorta is therefore not a plain tube: it is a valve housing with two doorways cut into it.

The cycle, and the two sounds it makes

Follow one beat. The ventricles are relaxed and filling; the mitral and tricuspid valves stand open and the aortic and pulmonary are shut. The ventricles begin to contract, pressure inside them shoots past the pressure in the atria, and the two atrioventricular valves slam closed. That is the FIRST heart sound, S1 — mitral and tricuspid closing together, the "lub", marking the beginning of systole. For a moment all four valves are shut and the muscle squeezes an incompressible volume: isovolumetric contraction. Then ventricular pressure exceeds arterial pressure, the semilunar valves are forced open, and blood is ejected — silently, because opening a healthy valve makes no sound. When the ventricle relaxes, pressure falls below arterial pressure, and the aortic and pulmonary valves snap shut. That is the SECOND heart sound, S2 — the "dub", marking the beginning of diastole. Neither sound is made by the cusps themselves. Both are the noise of a moving column of blood being stopped, and of the taut valve, the chamber walls and the great vessels vibrating with the arrest.

Listen closely and the second sound is often two sounds — and breathing splits it. S2 has two components: A2, the aortic valve closing, and P2, the pulmonary valve closing a fraction later. On quiet expiration they are usually fused into one sound. On INSPIRATION the negative intrathoracic pressure increases venous return to the right heart; the right ventricle takes longer to empty its larger volume, so pulmonary closure is delayed further still, while filling of the left heart is transiently reduced and aortic closure comes slightly earlier. The gap widens audibly. This is physiological splitting — it appears on inspiration and vanishes on expiration, and it is a sign of a normal heart, not a diseased one. Two further sounds may appear in diastole. S3, a low thud in early diastole, is the sound of rapid passive filling striking a compliant or over-filled ventricle: normal in children, athletes and pregnancy, but in an older adult it is the gallop of a failing, volume-loaded ventricle, the ear's version of what heart failure looks like on an echo. S4, immediately before S1, is the sound of the atrium contracting into a stiff, hypertrophied ventricle that will not accept the blood easily — and because it needs an atrial contraction to exist, S4 is impossible in atrial fibrillation, where the atria do not contract at all.

The wrong place on purpose: anatomical position versus auscultation area

All four valves lie behind the sternum in a patch you could cover with a playing card. Anatomically the four orifices are crowded together in that single oblique plane behind the body of the sternum. The pulmonary valve lies behind the medial end of the third left costal cartilage. The aortic valve is just below and medial to it, behind the left half of the sternum at the level of the third intercostal space. The mitral valve lies behind the left half of the sternum at the fourth costal cartilage, and the tricuspid behind the sternum's right half, from the fourth to the fifth costal cartilage. Put the stethoscope on any one of them and you will hear all four at once, muffled by bone. So clinicians abandoned the anatomy entirely. Sound is carried in the direction of the blood flow that produces it, so each valve is heard best DOWNSTREAM of itself, where its own jet comes closest to the chest wall.

So the four listening posts are these. AORTIC: the second right intercostal space at the sternal edge, where the ascending aorta comes closest to the front of the chest. PULMONARY: the second left intercostal space at the sternal edge, over the pulmonary trunk. TRICUSPID: the lower left sternal edge, in the fourth or fifth intercostal space, over the right ventricle. MITRAL: the apex beat, in the fifth intercostal space in the mid-clavicular line — the furthest from the valve itself and the most reliable of the four, because the apex of the left ventricle is genuinely pressed against the chest wall there. Generations have kept them with the mnemonic "All Physicians Take Money" — Aortic, Pulmonary, Tricuspid, Mitral — running clockwise from the upper right down to the apex. Notice what has happened: the aortic valve sits low and to the LEFT of the midline, and yet you listen for it high and to the RIGHT. The listening post is not a lie about the anatomy; it is a map of where the sound goes, and the surface landmarks used to find it are the same rib-counting landmarks set out in thoracic surface anatomy and procedures.

THE ANALOGY

Think of a house with four doors and a neighbour trying to work out which one is faulty — but she cannot enter the house, and all four doors are on the same wall, side by side behind a thick stone facade. Standing at the facade she hears only a jumble. So she stops listening at the doors and starts listening in the corridors they open into. A door that sticks and has to be forced makes a harsh scraping noise that carries up its corridor; a door that no longer latches lets a draught whistle backwards down the corridor behind it. Each fault has a signature sound, and each sound travels in the direction the air is moving. This is exactly the auscultation map: the aortic corridor runs up and to the right, the pulmonary up and to the left, the mitral corridor runs down and out to the apex and on into the armpit. You are never listening to a valve. You are standing downstream of it, listening to what it did to the flow.

Murmurs: only two things can go wrong

A door either will not open, or will not shut. Everything else is detail. A murmur is the sound of turbulent flow, and turbulence in a valve means one of exactly two mechanical failures. STENOSIS is a narrowed orifice: the leaflets are thickened, stiffened, calcified or fused at their commissures, so forward flow has to be forced through a hole that is too small, and the pressure load falls on the chamber behind. REGURGITATION, also called incompetence, is a leaking closure: the leaflets do not meet, so blood runs backwards through a door that should be shut, and a volume load falls on the chamber that has to handle the same blood twice. Now add timing, and you can name the lesion before you have touched a scanner. In SYSTOLE the outlet valves should be open and the inlet valves shut — so a systolic murmur means either an obstructed outlet (aortic stenosis, pulmonary stenosis) or a leaking inlet (mitral regurgitation, tricuspid regurgitation). In DIASTOLE the inlet valves should be open and the outlet valves shut — so a diastolic murmur means either an obstructed inlet (mitral stenosis, tricuspid stenosis) or a leaking outlet (aortic regurgitation, pulmonary regurgitation).

The four common lesions each have a portrait. Aortic stenosis: a harsh crescendo–decrescendo ejection murmur at the upper right sternal edge, radiating up into the carotid arteries, with a slow-rising pulse. Mitral regurgitation: a blowing pansystolic murmur at the apex, radiating into the axilla, following the jet backwards into the left atrium. Aortic regurgitation: a soft early-diastolic decrescendo murmur down the left sternal edge, easily missed, with a collapsing pulse. Mitral stenosis: an opening snap after S2 and then a low mid-diastolic rumble at the apex, heard with the bell and almost nowhere else. This is also the moment to understand a ritual every patient has experienced — being asked to roll onto the left side, or to sit forward, breathe out and hold. Rolling left swings the apex of the heart against the chest wall and brings the mitral valve into contact with it, so a mitral rumble that was inaudible becomes obvious. Sitting forward in held expiration empties the lungs and pulls the aortic root towards the sternum, unmasking a soft aortic regurgitant murmur. They are not superstitions. They are anatomy, performed.

💡 CLINICAL PEARL

The two papillary muscles of the mitral valve do not have equal insurance. The anterolateral papillary muscle receives a dual blood supply — from the left anterior descending and the circumflex arteries — while the posteromedial one is usually fed by a single vessel, the posterior descending artery, which in most hearts comes from the right coronary. One muscle has two independent supplies; the other has one. So when an inferior myocardial infarction closes the right coronary, it is almost always the posteromedial papillary muscle that dies, and two to seven days later, as the necrotic muscle softens, it can rupture. The patient who was recovering suddenly develops a loud new pansystolic murmur and flash pulmonary oedema, because the mitral valve has lost half its tethering and is now wide open in systole. It is one of the sharpest examples in the body of an anatomical fact — a single artery instead of two — deciding which patient survives their heart attack and which one crashes on day four.

Four failing valves, four different lives

The rheumatic valve: a woman of thirty-five, a childhood sore throat in a crowded city, presents with breathlessness in pregnancy and an irregular pulse. Rheumatic fever fused the commissures of her mitral valve into a narrow fish-mouth orifice; blood dams back into the left atrium, which dilates until it fibrillates. Mitral stenosis remains the commonest rheumatic valve lesion in the world, and controlling the rate of the atrial fibrillation it breeds becomes a lifelong task. The worn valve: a man of seventy-eight who blacks out briefly while climbing stairs and gets chest pain walking uphill — decades of calcium laid down in a normal tricuspid aortic valve, or a lifetime of turbulence through a congenitally bicuspid one, have narrowed his outflow; the hypertrophied ventricle cannot be perfused fast enough, so he has angina with clean coronaries, and the fixed outflow cannot raise cardiac output on exertion, so he faints. The floppy valve: a slim young woman with atypical chest pain and palpitations, in whom the doctor hears a mid-systolic click followed by a late systolic murmur — mitral valve prolapse, the commonest valve abnormality in the developed world and usually entirely benign. The infected valve: a febrile patient with a new murmur, splinter haemorrhages and positive blood cultures, in whom vegetations of platelets, fibrin and bacteria have colonized a cusp — infective endocarditis, which in people who inject drugs strikes the TRICUSPID valve first, because that is the first valve the venous blood reaches. Two treatments end these stories: surgical replacement with a mechanical valve (durable, but requiring lifelong anticoagulation) or a bioprosthesis, and — for the frail elderly with aortic stenosis — TAVI, a new valve threaded up the femoral artery and deployed inside the diseased one without opening the chest at all.

Key points
  • All four valves are mounted in one oblique plane in the fibrous skeleton — four annuli fibrosi joined by the right and left fibrous trigones — which anchors the cusps, prevents the orifices dilating and electrically insulates atria from ventricles.
  • Tricuspid = right AV valve, three cusps (anterior, posterior, septal). Mitral / bicuspid = left AV valve, two cusps (anterior/aortic and posterior/mural).
  • Chordae tendineae run from the cusp margins to papillary muscles — three on the right (the anterior receiving the moderator band), two on the left (anterolateral, posteromedial); each muscle tethers BOTH cusps.
  • The papillary muscles contract just BEFORE ventricular systole, taking up the slack so the cusps are held shut rather than everting into the atrium (prolapse).
  • Semilunar valves (pulmonary and aortic) have three cusps each, NO chordae and NO papillary muscles; they close passively when back-pressure fills the sinuses of Valsalva behind them.
  • The aortic cusps are right, left and posterior — the posterior being the NON-CORONARY cusp, because the right and left coronary arteries arise from the right and left sinuses; the coronaries fill in diastole.
Key points
  • S1 ("lub") = mitral + tricuspid closing at the start of systole. S2 ("dub") = aortic + pulmonary closing at the start of diastole. Opening a normal valve is silent.
  • S2 splits physiologically on INSPIRATION: increased venous return delays right ventricular emptying and therefore pulmonary (P2) closure, widening the gap after aortic (A2).
  • S3 = rapid passive filling in early diastole (normal in the young, a gallop in heart failure). S4 = atrial contraction into a stiff ventricle — impossible in atrial fibrillation.
  • Anatomically all four valves lie behind the sternum between the third and fifth costal cartilages; the auscultation areas lie DOWNSTREAM because sound travels with the blood.
  • Listen: Aortic 2nd right ICS, Pulmonary 2nd left ICS, Tricuspid lower left sternal edge (4th/5th), Mitral at the apex, 5th ICS mid-clavicular line — "All Physicians Take Money".
  • Systolic murmurs = obstructed outlet (aortic/pulmonary stenosis) or leaking inlet (mitral/tricuspid regurgitation). Diastolic murmurs = obstructed inlet (mitral stenosis) or leaking outlet (aortic regurgitation).
⚠️ Common mistakes
  • Believing the heart sounds are made by the leaflets slapping together. The cusps are thin membranes and make almost no noise; the sound is the sudden arrest of a moving column of blood and the vibration of the taut valve, chamber walls and great vessels.
  • Assuming the auscultation area marks the valve's position. It does not: the aortic valve lies behind the LEFT half of the sternum at the 3rd intercostal space, yet is heard at the 2nd RIGHT intercostal space, because sound is carried downstream with the flow.
  • Treating any split second sound as abnormal. Splitting that appears on inspiration and disappears on expiration is physiological; it is fixed, wide or reversed splitting that signals disease.
🎓 Questions students ask
Why do the atrioventricular valves need chordae and papillary muscles when the aortic and pulmonary valves manage without them?
Because of the pressure difference on the two sides of each door. The semilunar valves close against arterial pressure, which is high but is opposed by a ventricle that has already relaxed towards zero — and their cusps are small, deep pockets that seal more tightly the harder they are pushed. The atrioventricular valves face a far more violent gradient: behind them a ventricle generating up to 120 mmHg or more, and in front of them an atrium at only a few mmHg. A large, floppy curtain of a cusp exposed to that would simply invert into the atrium. The chordae and papillary muscles are a tethering system that converts a flap into a parachute — free to swing open but physically unable to travel past the closed position. Take the tether away, by rupture or infarction, and the cusp everts instantly.
Why does aortic stenosis cause angina even when the coronary arteries are completely normal?
Two forces meet and both point the same way. To force blood through a narrowed orifice the left ventricle must generate far higher pressure, and it responds by hypertrophying — so there is now much more muscle demanding oxygen. At the same time, the high pressure in the thick-walled cavity compresses the vessels running through it, and because the ventricle is ejecting for longer against the obstruction, the diastolic window in which the coronaries actually fill is shortened. Demand rises, supply falls, and the patient gets classic exertional chest pain on entirely clean arteries. The same reasoning explains the exertional syncope: the fixed obstruction means cardiac output cannot rise to meet exercising muscle, so when peripheral vessels dilate the blood pressure falls and the patient blacks out. Angina, syncope and breathlessness are the triad, and the pain will not behave like the pain of an acute coronary syndrome because the mechanism behind it is mechanical, not thrombotic.
Is a murmur always a sign of disease?
No. A murmur only means turbulent flow, and flow can be turbulent for reasons that have nothing to do with a damaged valve. Anything that increases the velocity or the volume of blood crossing a normal orifice can produce an innocent or flow murmur: fever, anaemia, thyrotoxicosis, pregnancy, exercise, and childhood — where a soft systolic murmur is extremely common and usually means nothing at all. The features that reassure are consistent: soft, early or mid-systolic, short, confined to the left sternal edge or pulmonary area, no radiation, no thrill, normal heart sounds and a symptom-free patient. The features that worry are the opposite: any diastolic murmur at all, a pansystolic murmur, a loud one with a palpable thrill, radiation to the carotids or axilla, an added click or snap, or a patient with breathlessness, chest pain or blackouts. Timing and company matter far more than loudness.
Test yourself

A 78-year-old man reports blacking out while climbing stairs. You hear a harsh crescendo–decrescendo murmur that begins after the first heart sound, is loudest in the second right intercostal space at the sternal edge, and radiates to both carotid arteries. Where does the responsible valve actually lie, and why is it heard where it is?

🫁 In one breath
  • Four valves sit in one oblique plane in the fibrous skeleton of the heart: the tricuspid (anterior, posterior, septal cusps) and mitral (anterior, posterior cusps) as inlets, the pulmonary and aortic (three semilunar cusps each) as outlets.
  • The AV valves are held shut by chordae tendineae running to papillary muscles that contract just before systole; the semilunar valves have no chordae and close passively as back-pressure fills the sinuses of Valsalva, from two of which the coronary arteries arise.
  • S1 is mitral and tricuspid closure at the start of systole and S2 is aortic and pulmonary closure at the start of diastole, with physiological splitting of S2 on inspiration; S3 signals rapid filling of a compliant or failing ventricle and S4 an atrial kick into a stiff one.
  • Sound travels downstream, so you listen aortic at the 2nd right space, pulmonary at the 2nd left, tricuspid at the lower left sternal edge and mitral at the apex — nowhere near the valves themselves — and the murmur you hear is either stenosis (obstructed forward flow) or regurgitation (backward leak), named by its timing in the cycle.
📚 Sources
  • Drake RL, Vogl AW, Mitchell AWM. Gray's Anatomy for Students — Thorax: the heart, valves and surface projections.
  • Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy — The heart: valves, fibrous skeleton and auscultation areas.
  • Netter FH. Atlas of Human Anatomy — Heart: valves in situ, the fibrous skeleton and the aortic sinuses.
  • Last RJ. Last's Anatomy: Regional and Applied — The heart and pericardium.
  • Snell RS. Clinical Anatomy by Regions — The thorax: valvular disease, murmurs and auscultation.
  • TeachMeAnatomy — The Heart Valves; Heart Sounds and Auscultation.

More in Thorax →

Learn pharmacology and anatomy the fun way

Short lessons, interactive quizzes, a real 3D anatomy model, and a streak you'll actually keep.

Download on the App StoreGet it on Google Play