# Heart valve

(Redirected from Heart valves)
Heart valves
Valve positions in heart
System Cardiovascular

A heart valve normally allows blood to flow in only one direction through the heart. The four valves commonly represented in a mammalian heart determine the pathway of blood flow through the heart. A heart valve opens or closes incumbent upon differential blood pressure on each side.[1][2][3]

The four main valves in the heart are:

• The two atrioventricular (AV) valves, the mitral valve (bicuspid valve), and the tricuspid valve, which are between the upper atria and the lower ventricles.
• The two semilunar (SL) valves, the aortic valve and the pulmonary valve, which are in the arteries leaving the heart.

The mitral valve and the aortic valve are in the left heart and the tricuspid valve and the pulmonary valve are in the right heart.

There are also the coronary sinus and the inferior vena cava valves.

## Structure

Blood flow through the valves

Heart valves separate the atria from the ventricles, or the ventricles from a blood vessel. Heart valves are situated around the fibrous rings of the cardiac skeleton. The valves incorporate leaflets or cusps which are pushed open to allow blood flow and which then close together to seal and prevent backflow. Each valve has three cusps, except for the mitral valve, which only has two. There are nodules at the tips of the cusps which make the seal tighter.

The pulmonary valve has left, right, and anterior cusps.[4] The aortic valve has left, right, and posterior cusps.[5] The tricuspid valve has anterior, posterior, and septal cusps and the mitral valve has only two cusps, anterior and posterior.

### Atrioventricular valves

Main articles: Mitral valve and Tricuspid valve
3D - loop of a heart viewed from the top, with the apical part of the ventricles removed and the mitral valve clearly visible. Due to missing data the leaflets of the tricuspid and aortic valves are not clearly visible, but the openings are; the pulmonary valve is not visible. On the left are two standard 2D views (taken from the 3D dataset) showing tricuspid and mitral valves (above) and aortal valve (below).

These are the mitral and tricuspid valves situated between the atria and the ventricles that prevent backflow from the ventricles into the atria during systole. They are anchored to the walls of the ventricles by chordae tendineae, which prevent the valves from inverting.

The chordae tendineae are attached to papillary muscles that cause tension to better hold the valve. Together, the papillary muscles and the chordae tendineae are known as the subvalvular apparatus. The function of the subvalvular apparatus is to keep the valves from prolapsing into the atria when they close. The subvalvular apparatus has no effect on the opening and closure of the valves, however, which is caused entirely by the pressure gradient across the valve. The peculiar insertion of chords on the leaflet free margin however provides systolic stress sharing between chords according to their different thickness.[6]

The closure of the AV valves is heard as lub, the first heart sound (S1). The closure of the SL valves is heard as dub, the second heart sound (S2).

The mitral valve is also called the bicuspid valve because it contains two leaflets or cusps. The mitral valve gets its name from the resemblance to a bishop's mitre (a type of hat). It is on the left side of the heart and allows the blood to flow from the left atrium into the left ventricle.

During diastole, a normally-functioning mitral valve opens as a result of increased pressure from the left atrium as it fills with blood (preloading). As atrial pressure increases above that of the left ventricle, the mitral valve opens. Opening facilitates the passive flow of blood into the left ventricle. Diastole ends with atrial contraction, which ejects the final 20% of blood that is transferred from the left atrium to the left ventricle. This amount of blood is known as end diastolic volume (EDV), and the mitral valve closes at the end of atrial contraction to prevent a reversal of blood flow.

The tricuspid valve has three leaflets or cusps and is on the right side of the heart, between the right atrium and the right ventricle which stops the backflow of blood between the two.

### Semilunar valves

Main articles: Aortic valve and Pulmonary valve

The semilunar valves, the aortic and the pulmonary valves, are located at the base of the aorta and the pulmonary trunk or artery, and the aorta. These two arteries receive blood from the ventricles and their semilunar valves permit blood to be forced into the arteries, and prevent backflow from the arteries into the ventricles. These valves do not have chordae tendineae, and are more similar to the valves in veins than they are to the atrioventricular valves. Closure of the semilunar valves causes the second heart sound.

The aortic valve lies between the left ventricle and the aorta, and has three cusps. During ventricular systole, pressure rises in the left ventricle and when it is greater than the pressure in the aorta, the aortic valve opens, allowing blood to exit the left ventricle into the aorta. When ventricular systole ends, pressure in the left ventricle rapidly drops and the pressure in the aorta forces aortic valve to close. The closure of the aortic valve contributes the A2 component of the second heart sound (S2).

The pulmonary valve (sometimes referred to as the pulmonic valve) lies between the right ventricle and the pulmonary artery, and has three cusps. Similar to the aortic valve, the pulmonary valve opens in ventricular systole, when the pressure in the right ventricle rises above the pressure in the pulmonary artery. At the end of ventricular systole, when the pressure in the right ventricle falls rapidly, the pressure in the pulmonary artery will close the pulmonary valve.

The closure of the pulmonary valve contributes the P2 component of the second heart sound (S2). The right heart is a low-pressure system, so the P2 component of the second heart sound is usually softer than the A2 component of the second heart sound. However, it is physiologically normal in some young people to hear both components separated during inhalation.

## Physiology

In general, motion of the heart valves is determined using the Navier-Stokes equation; using boundary conditions of the blood pressures, pericardial fluid, and external loading as the constraints. Motion of the heart valves is used as a boundary condition in the Navier-Stokes equation in determining the fluid dynamics of blood ejection from the left and right ventricles into the aorta and the lung.

Wiggers diagram, showing various events during a cardiac cycle, with closures and openings of the aortic and mitral marked in the pressure curves.
This is further explanation of the echocardiogram above. MV: Mitral valve, TV: Tricuspid valve, AV: Aortic valve, Septum: Interventricular septum. Continuous lines demarcate septum and free wall seen in echocardiogram, dotted line is a suggestion of where the free wall of the right ventricle should be. The red line represents where the upper left loop in the echocardiogram transects the 3D-loop, the blue line represents the lower loop.

### Relationship between pressure and flow in open valves

The pressure drop, ${\Delta}p$, across an open heart valve relates to the flow rate, Q, through the valve:

$a{{\partial}Q\over{\partial}t} + bQ^2 = {\Delta}p$

If:

-Inflow energy conserved

-Stagnant region behind leaflets

-Outflow momentum conserved

-Flat velocity profile

### Valves with a single degree of freedom

Usually the aortic and mitral valves are incorporated in valve studies within a single degree of freedom. These relationships are based on the idea of the valve being a structure with a single degree of freedom. These relationships are based upon the Euler equations.

Equations for the aortic valve in this case:

${\rho}\left({{\partial}u\over{\partial}t} + {u{\partial}u\over{\partial}x}\right) + {{\partial}p\over{\partial}x} = 0$

${{\partial}A\over{\partial}t} + {{\partial}\over{\partial}x}(Au) = 0$

$A(x,t) = A_0 \left(1-[1-{\Lambda}(t)]{x\over{L}}\right)^2$

$\int_{0}^{L} p(x,t) {{\partial}A\over{\partial}x}\, dx = [A_0 - A(L,t)]p(L,t)$

where:

u=axial velocity

p=pressure

A=cross sectional area of valve

L=axial length of valve

${\Lambda}$(t)=single degree of freedom; when ${\Lambda}^2 (t) = {A(L,t)\over{A_0}}$

Atrioventricular valve

## Clinical significance

An artificial heart valve may be used to surgically replace a patient's damaged valve.

One of the two forms of valvular heart disease can result from regurgitation or insufficiency, which occurs when a valve becomes insufficient and malfunctions, allowing some blood to flow in the wrong direction (regurgitate). This insufficiency can affect any of the valves as in aortic insufficiency, mitral insufficiency, pulmonary insufficiency and tricuspid insufficiency.

The other form of valvular heart disease is stenosis, a narrowing of the valve. This is a result of the valve becoming thickened and any of the heart valves can be affected, as in mitral valve stenosis, tricuspid valve stenosis, pulmonary valve stenosis and aortic valve stenosis. Stenosis of the mitral valve is a common complication of rheumatic fever.

A major valvular heart disease is mitral valve prolapse, which is the myxomatous degeneration (a weakening of connective tissue) of the valve. This sees the displacement of a thickened mitral valve cusp into the left atrium during systole.

Inflammation of the valves can be caused by infective endocarditis , usually a bacterial infection but can sometimes be caused by other organisms. Bacteria can more readily attach to damaged valves.[7] Another type of endocarditis which doesn't provoke an inflammatory response, is nonbacterial thrombotic endocarditis. This is commonly found on previously undamaged valves.[7]

A form of cardiac fibrosis involves the abnormal thickening of the valves due to a proliferation of fibroblasts. These cells secrete collagen and when over-activated cause tissue build up on the valves, primarily on the tricuspid valve, but also on the pulmonary valve. The thickening and loss of flexibility may eventually lead to valvular dysfunction and right-sided heart failure.

The most common form of valvular anomaly is a congenital heart defect (CHD), called a bicuspid aortic valve. This results from the fusing of two of the cusps during embryonic development forming a bicuspid valve instead of a tricuspid valve. This condition is often undiagnosed until calcific aortic stenosis has developed, and this usually happens around ten years earlier than would otherwise develop.[8][9]

Less common CHD's are tricuspid and pulmonary atresia, and Ebstein's anomaly. Tricuspid atresia is the complete absence of the tricuspid valve which can lead to an underdeveloped or absent right ventricle. Pulmonary atresia is the complete closure of the pulmonary valve. Ebstein's anomaly is the displacement of the septal leaflet of the tricuspid valve causing a larger atrium and a smaller ventricle than normal.

Damaged and defective heart valves can be repaired, or replaced with artificial heart valves.

## References

1. ^ "Heart Valves". Heart and Stroke Encyclopedia. American Heart Association, Inc. Retrieved 2010-08-05.
2. ^ Klabunde, RE (2009-07-02). "Pressure Gradients". Cardiovascular Physiology Concepts. Richard E. Klabunde. Retrieved 2010-08-06.
3. ^ Klabunde, RE (2007-04-05). "Cardiac Valve Disease". Cardiovascular Physiology Concepts. Richard E. Klabunde. Retrieved 2010-08-06.
4. ^ Anatomy photo:20:21-0102 at the SUNY Downstate Medical Center - "Heart: The Pulmonic Valve"
5. ^ Anatomy photo:20:29-0104 at the SUNY Downstate Medical Center - "Heart: The Aortic Valve and Aortic Sinuses"
6. ^ S Nazari et al.: Patterns Of Systolic Stress Distribution On Mitral Valve Anterior Leaflet Chordal Apparatus. A Structural Mechanical Theoretical Analysis. J Cardiovasc Surg (Turin) 2000 Apr;41(2):193-202 (video)
7. ^ a b Mitchell RS, Kumar V, Robbins SL, Abbas AK, Fausto N (2007). Robbins Basic Pathology (8th ed.). Saunders/Elsevier. pp. 406–8. ISBN 1-4160-2973-7.
8. ^ Bertazzo, S. et al. Nano-analytical electron microscopy reveals fundamental insights into human cardiovascular tissue calcification. Nature Materials 12, 576-583 (2013).
9. ^ Miller, J. D. Cardiovascular calcification: Orbicular origins. Nature Materials 12, 476-478 (2013).