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Mitral stenosis is a valvular heart disease characterized by the narrowing of the orifice of the mitral valve of the heart.
In normal cardiac physiology, the mitral valve opens during left ventricular diastole, to allow blood to flow from the left atrium to the left ventricle. Blood flows in the proper direction because during this phase of the cardiac cycle the pressure in the left ventricle is lower than the pressure in the left atrium, and the blood flows down the pressure gradient. In the case of mitral stenosis, the valve does not open completely, and to transport the same amount of blood the left atrium needs a higher pressure than normal to overcome the increased gradient.
Most cases of mitral stenosis are due to disease in the heart secondary to rheumatic fever and the consequent rheumatic heart disease. Less common causes of mitral stenosis are calcification of the mitral valve leaflets, and as a form of congenital heart disease. However, there are primary causes of mitral stenosis that emanate from a cleft mitral valve. Other causes include Bacterial endocarditis where the vegetations may favor increase risk of stenosis.
The normal area of the mitral valve orifice is about 4 to 6 cm2. Under normal conditions, a normal mitral valve will not impede the flow of blood from the left atrium to the left ventricle during (ventricular) diastole, and the pressures in the left atrium and the left ventricle during diastole will be equal. The result is that the left ventricle gets filled with blood during early diastole, with only a small portion of extra blood contributed by contraction of the left atrium (the “atrial kick”) during late ventricular diastole.
When the mitral valve area goes below 2 cm2, the valve causes an impediment to the flow of blood into the left ventricle, creating a pressure gradient across the mitral valve. This gradient may be increased by increases in the heart rate or cardiac output. As the gradient across the mitral valve increases, the amount of time necessary to fill the left ventricle with blood increases. Eventually, the left ventricle requires the atrial kick to fill with blood. As the heart rate increases, the amount of time that the ventricle is in diastole and can fill up with blood (called the diastolic filling period) decreases. When the heart rate goes above a certain point, the diastolic filling period is insufficient to fill the ventricle with blood and pressure builds up in the left atrium, leading to pulmonary congestion.
When the mitral valve area goes less than 1 cm2, there will be an increase in the left atrial pressures (required to push blood through the stenotic valve). Since the normal left ventricular diastolic pressures is about 5 mmHg, a pressure gradient across the mitral valve of 20 mmHg due to severe mitral stenosis will cause a left atrial pressure of about 25 mmHg. This left atrial pressure is transmitted to the pulmonary vasculature and causes pulmonary hypertension. Pulmonary capillary pressures in this level cause an imbalance between the hydrostatic pressure and the oncotic pressure, leading to extravasation of fluid from the vascular tree and pooling of fluid in the lungs (congestive heart failure causing pulmonary edema).
Increases in the heart rate will allow less time for the left ventricle to fill, also causing an increase in left atrial pressure and pulmonary congestion.
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