Mitral Stenosis
In mitral stenosis, valve leaflets become diffusely thickened by fibrosis and calcification. The mitral commissures fuse, the chordae tendineae fuse and shorten, the valvular cusps become rigid, and the apex of the valve becomes narrowed, obstructing blood flow from the left atrium to the left ventricle.
As a result of these changes, left atrial volume and pressure rise, and the atrial chamber dilates. The increased resistance to blood flow causes pulmonary hypertension, right ventricular hypertrophy and, eventually, right-sided heart failure. What’s more, inadequate filling of the left ventricle reduces cardiac output.
Two-thirds of all patients with mitral stenosis are female.
Causes
Mitral stenosis most commonly results from rheumatic fever; however, it may also be associated with congenital anomalies.
Complications
Pulmonary hypertension caused by mitral stenosis can rupture pulmonary-bronchial venous connections, which results in hemorrhage. Pulmonary hypertension
also increases transudation of fluid from pulmonary capillaries, which can cause fibrosis in the alveoli and pulmonary capillaries. This action reduces vital capacity, total lung capacity, maximal breathing capacity, and oxygen uptake per unit of ventilation.
also increases transudation of fluid from pulmonary capillaries, which can cause fibrosis in the alveoli and pulmonary capillaries. This action reduces vital capacity, total lung capacity, maximal breathing capacity, and oxygen uptake per unit of ventilation.
Physical findings in mitral stenosis
With mitral stenosis, inspection may reveal peripheral and facial cyanosis, particularly in severe cases. The patient’s face may appear pinched and blue, and she may have a malar rash. You may note jugular vein distention and ascites in the patient with severe pulmonary hypertension or associated tricuspid stenosis.
Palpation may reveal peripheral edema, hepatomegaly, and a diastolic thrill at the cardiac apex.
Auscultation may detect a loud S1 or opening snap and a diastolic murmur at the apex, along the left sternal border, or at the base of the heart. In a patient with pulmonary hypertension, the S2 may be accentuated and the two components of the S2 closely split. You may hear a pulmonary systolic ejection click in a patient with severe pulmonary hypertension. Crackles also may be audible.
Thrombi may form in the left atrium and—if they embolize—travel to the brain, kidneys, spleen, and extremities, possibly causing infarction. Embolization occurs most commonly in patients with arrhythmias.
