The normal area of the mitral valve orifice is about 4 to 6 cm².
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.
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 ventricular diastole will be equal.
 The result is that the left ventricle gets filled with blood during early ventricular 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).

The constant pressure overload of the left atrium will cause the left atrium to increase in size.
 As the left atrium increases in size, it becomes more prone to develop atrial fibrillation (AF).
 When atrial fibrillation develops, the atrial kick is lost (since it is due to the normal atrial contraction).

In individuals with severe mitral stenosis, the left ventricular filling is dependent on the atrial kick.
 The loss of the atrial kick due to atrial fibrillation ( i.e. blood cannot flow into the left ventricle thus accumulating in the left atrium )  can cause a precipitous decrease in cardiac output and sudden congestive heart failure.

Patients with mitral stenosis prompts a series of hemodynamic changes that frequently cause deterioration of the patient's clinical status.
A reduction in cardiac output, associated with acceleration of heart rate and shortening of the diastolic time, frequently leads to congestive heart failure.
In addition, when AF sets in, systemic embolization becomes a real danger.

Mitral stenosis typically progresses slowly (over decades) from the initial signs of mitral stenosis to NYHA functional class II symptoms to the development of atrial fibrillation to the development of NYHA functional class III or IV symptoms.
 Once an individual develops NYHA class III or IV symptoms, the progression of the disease accelerates and the patient's condition deteriorates.
The normal area of the mitral valve orifice is about 4 to 6 cm². 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. 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 ventricular diastole will be equal.  The result is that the left ventricle gets filled with blood during early ventricular 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).
The constant pressure overload of the left atrium will cause the left atrium to increase in size.  As the left atrium increases in size, it becomes more prone to develop atrial fibrillation (AF).  When atrial fibrillation develops, the atrial kick is lost (since it is due to the normal atrial contraction).
In individuals with severe mitral stenosis, the left ventricular filling is dependent on the atrial kick.  The loss of the atrial kick due to atrial fibrillation ( i.e. blood cannot flow into the left ventricle thus accumulating in the left atrium )  can cause a precipitous decrease in cardiac output and sudden congestive heart failure.
Patients with mitral stenosis prompts a series of hemodynamic changes that frequently cause deterioration of the patient's clinical status. A reduction in cardiac output, associated with acceleration of heart rate and shortening of the diastolic time, frequently leads to congestive heart failure. In addition, when AF sets in, systemic embolization becomes a real danger.
Mitral stenosis typically progresses slowly (over decades) from the initial signs of mitral stenosis to NYHA functional class II symptoms to the development of atrial fibrillation to the development of NYHA functional class III or IV symptoms.  Once an individual develops NYHA class III or IV symptoms, the progression of the disease accelerates and the patient's condition deteriorates.
Mitral valve stenosis