Heart Valves

What the four valves actually do

Blood moves through the heart in one direction only, and the heart valves are what enforce that rule. Picture two pumps side by side. The right heart receives deoxygenated blood from the body and pushes it to the lungs; the left heart receives oxygenated blood from the lungs and pushes it to the body. Each pump has an inlet valve and an outlet valve, giving four valves in total, all seated on a tough ring of connective tissue called the fibrous skeleton or valve plane.

On the right side, blood enters the right ventricle through the tricuspid valve and leaves through the pulmonary valve. On the left side, blood enters the left ventricle through the mitral valve (also called the bicuspid valve) and leaves through the aortic valve. The tricuspid and mitral valves are grouped together as the atrioventricular (AV) valves because they sit between an atrium and a ventricle. The pulmonary and aortic valves are the semilunar valves, named for their three half-moon-shaped cusps.

The crucial point is that valves are passive. They have no muscle of their own and receive no nerve signal telling them when to open. They respond only to the pressure gradient across their leaflets. When the pressure behind a valve rises above the pressure ahead of it, the leaflets are pushed apart and blood flows through. The instant that gradient reverses — even by a few millimeters of mercury — the leaflets billow back, meet in the middle, and seal. Get four valves opening and closing in the right order, and you have a one-way circulatory pump that runs without conscious thought for a century.

Valve timing across the cardiac cycle

The whole sequence is choreographed by pressure, and following one heartbeat makes it concrete. Start in diastole, when the ventricles are relaxed and filling. Pressure in the atria is slightly higher than in the relaxed ventricles, so the tricuspid and mitral valves are open and blood drains passively from atria to ventricles. The aortic and pulmonary valves are shut, held closed by the much higher pressure sitting in the aorta (about 80 mmHg) and pulmonary artery.

Late in diastole the atria give a small contraction — the "atrial kick" — topping off the ventricles with the last 15 to 25 percent of their filling volume. Then the ventricles contract. As ventricular pressure shoots up, it almost instantly exceeds atrial pressure, and the AV valves snap shut. That closure is the first heart sound, S1, the "lub." For a brief moment all four valves are closed and the ventricle squeezes an incompressible volume of blood — isovolumetric contraction. Pressure climbs steeply until left-ventricular pressure crosses aortic pressure (and right-ventricular pressure crosses pulmonary pressure). At that crossover the semilunar valves are forced open and blood is ejected.

Ejection slows as the ventricle empties, and the moment ventricular pressure drops back below arterial pressure, blood begins to fall back toward the heart. It is caught in the small pockets — the sinuses of Valsalva — behind each semilunar cusp, and these eddies float the leaflets shut before any meaningful backflow occurs. That closure is the second heart sound, S2, the "dub." The ventricle then relaxes against closed valves — isovolumetric relaxation — until its pressure falls below atrial pressure, the AV valves reopen, and filling begins again. At a resting heart rate of 75 beats per minute the entire cycle takes about 0.8 seconds, of which roughly two thirds is diastole.

The mitral and tricuspid apparatus

The AV valves face a mechanical problem the semilunar valves do not. During ventricular contraction the pressure trying to blow them backward into the atrium is enormous — peak left-ventricular pressure reaches about 120 mmHg, while the left atrium sits near 8 to 12 mmHg. A simple flap would invert like an umbrella in a storm. The solution is a tethering system. Thin tendon-like cords called the chordae tendineae run from the free edges of the leaflets down to papillary muscles projecting from the ventricular wall.

The timing is elegant: the papillary muscles contract a fraction of a second before the main mass of the ventricle, so by the moment full pressure hits, the chordae are already taut and the leaflets are held precisely at their closing position — like the strings of a parachute keeping the canopy from collapsing. If a papillary muscle ruptures, as can happen during a heart attack that damages the underlying ventricular muscle, the mitral valve suddenly flails and acute, life-threatening regurgitation follows. The mitral valve has two leaflets and the tricuspid has three; both rely on the same annulus–leaflet–chordae–papillary-muscle quartet, which is why surgeons speak of repairing the mitral apparatus rather than just the valve.

The numbers clinicians care about

Valve disease is graded by measurable thresholds, mostly obtained by echocardiography. A normal aortic valve opens to an area of 3.0 to 4.0 cm². As it narrows, blood must accelerate to get through, and the pressure gradient across the valve rises. Severe aortic stenosis is defined by a valve area below 1.0 cm², a mean gradient above 40 mmHg, or a peak jet velocity above 4 m/s. Once a patient with severe aortic stenosis develops the classic symptoms — angina, syncope, or heart failure — untreated survival averages only a few years, which is why valve replacement is recommended once symptoms appear.

Regurgitation is graded by how much blood leaks backward. In severe mitral regurgitation, the regurgitant fraction exceeds 50 percent, meaning more than half of what the ventricle ejects sloshes back into the atrium instead of moving forward. The left ventricle compensates by dilating to maintain forward output, but chronic volume overload eventually exhausts it. A regurgitant orifice area above 0.4 cm² and a regurgitant volume above 60 mL per beat are the echocardiographic flags for severe disease.

Stenosis vs regurgitation

The two ways a valve can fail load the heart very differently. A narrowed valve creates a pressure problem; a leaky valve creates a volume problem. The contrast is worth laying out directly.

Feature	Stenosis (narrowed valve)	Regurgitation (leaky valve)
Core defect	Valve cannot open fully	Valve cannot close fully
Hemodynamic burden	Pressure overload	Volume overload
Ventricular response	Concentric hypertrophy (thick walls)	Eccentric hypertrophy / dilation
Pressure gradient	High across the valve (e.g. >40 mmHg in severe AS)	Backward leak, low forward gradient
Murmur timing	Often systolic ejection (AS, PS) or diastolic (MS)	Often holosystolic (MR, TR) or early diastolic (AR)
Classic example	Calcific aortic stenosis	Degenerative mitral regurgitation
Typical fix	Replace the valve (surgical or TAVR)	Repair when possible, especially mitral

Both lesions can coexist on the same valve. Rheumatic heart disease, still common worldwide, classically thickens and fuses the mitral leaflets so the valve neither opens nor closes properly — mixed mitral stenosis and regurgitation.

When valves go wrong

• Calcific aortic stenosis. The most common valve disease in the developed world. Decades of mechanical stress lay down calcium on the aortic cusps until they stiffen and barely open. It is essentially the valvular cousin of atherosclerosis, driven by age, hypertension, and lipid deposition.
• Bicuspid aortic valve. A congenital two-cusp valve in 1–2 percent of people. The abnormal flow accelerates wear, so these patients develop stenosis decades early and also carry a higher risk of aortic aneurysm.
• Mitral valve prolapse. A floppy, billowing leaflet found in 2–3 percent of adults. Usually benign, but it is the leading cause of degenerative mitral regurgitation when a leaflet or chord eventually gives way.
• Rheumatic heart disease. An autoimmune sequel to untreated streptococcal throat infection that scars the mitral and aortic valves. Rare now in wealthy countries but a major cause of valve disease and death globally.
• Infective endocarditis. Bacteria seed a valve and grow vegetations that destroy the leaflets and shower emboli. It can convert a competent valve into a severely regurgitant one within days, and it links valve disease to sepsis.
• Functional regurgitation. A normal valve made incompetent because the ventricle has dilated around it — common in heart failure, where the stretched annulus stops the leaflets from meeting.

Fixing a broken valve

For decades the only option was open-heart surgery: replacing the diseased valve with a mechanical prosthesis (durable for life but requiring lifelong anticoagulation with warfarin) or a bioprosthetic valve made from bovine or porcine tissue (no long-term blood thinner, but wears out in 10–20 years). The choice trades durability against the bleeding risk of anticoagulation, which is why younger patients often receive mechanical valves and older patients tissue valves.

The biggest change in modern cardiology is the catheter. Transcatheter aortic valve replacement (TAVR) threads a collapsed bioprosthetic valve up through the femoral artery and deploys it inside the diseased aortic valve, crushing the old leaflets aside — no chest incision, no heart-lung machine. Once reserved for patients too frail for surgery, it is now offered across the risk spectrum. On the mitral side, edge-to-edge clip devices grab the leaking leaflets and pin them partly together to reduce regurgitation. The guiding principle, especially for the mitral valve, is to repair native tissue when feasible — preserving the chordae and annulus protects long-term ventricular function better than ripping the whole apparatus out.

This article is for education and is not medical advice. If you have symptoms such as chest pain, breathlessness, or fainting, or have been told you have a heart murmur, seek evaluation from a qualified clinician.