The incidence of mitral valve stenosis is associated with scarring of the valve due to rheumatic fever. Fibrosis restricts the mobility of the valve leaflets and commissures that eventually leads to valve funneling or retraction. The normal mitral valve diameter is 4-6 cm2. Hemodynamic changes occur when the valve aperture is diminished to 1.5-2.5 cm2, and pulmonary congestion occurs with further reduction of valve size to 1.1-1.5 cm2. The pulmonary wedge pressure with patients experiencing dyspnea is greater than 15-20 mmHg.
Mitral valve stenosis represents an inflow tract obstruction to the left ventricle that inhibits filling of the ventricle thereby restricting excessive volume to the left atrium. Clinically, this provides diminished cardiac output in conjunction with left atrial volume overload, leading to pulmonary congestion.
Directly related to higher left atrial pressure, is backward failure that ultimately leads to pulmonary hypertension, right ventricular failure, and atrial fibrillation. A high pulmonary capillary wedge pressure should be anticipated as a reflection of the increased pressure gradient required to provide flow from the atrium past the stenotic valve. In these cases the wedge pressure is not considered to be an accurate assay of left ventricular end-diastolic pressure. In cases where the wedge pressure is low, it may represent an accurate marker for reduced ventricular filling.
Transvalvular blood flow is diastolic dependent with mitral stenosis, therefore tachycardia should be avoided as it will result in decreased left ventricular filling, increased pulmonary congestion, and decreased cardiac output. Bradycardia may also result in reduced cardiac output.
Therapeutic concerns significant for mitral stenosis, indicate slow controlled changes in terms of volume management. This approach is based on the existence of an essentially fixed cardiac output, and restricted ranges of tolerable right sided pressures.
Diuretic therapy may reduce the pressure gradient, and in conjunction with induction agents and positive pressure ventilation, may result in decreased ventricular filling and cardiac output.
Systemic vasodilation has not been found to improve cardiac output while inotropes are rarely helpful unless contractility is below baseline. Digoxin is a capable choice for controlling atrial fibrillation associated with mitral stenosis.
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