The patient first felt winded one night after doing the dishes. She was breathing so hard by morning that she was barely able to get out of bed. And a cough had started. “The flu” went through her mind. She stayed home from work to rest, but all day she just couldn't catch her breath. The cough got worse and was making her chest hurt, and she felt her heart racing. She was exhausted by evening, but knew she wasn't going to be able to sleep. The temperature was below 0°F outside, but she bundled up and drove herself the three miles to the emergency department.
Barely able to speak by the time she stepped up to the triage desk, she was only able to get out “You need to slow my heart down.” The nurse knew that look. The patient sat down hard in the wheelchair rescuing her from the burden of standing. “Medical Resus” was paged overhead, and the nurse rushed the patient back.
This ECG demonstrated atrial fibrillation with rapid ventricular response with ST-segment depression in the lateral leads concerning for myocardial ischemia. Ultrasound revealed a remarkable hypertrophied and calcified mass on the ventricular side of the mitral valve with severely impaired opening of the mitral valve during diastole. The anterior leaflet billowed while remaining fixed at the commissure, visually described as a “hockey stick.” The patient's presentation and ultrasound were diagnostic of severe mitral stenosis.
A stenotic mitral valve significantly changes cardiac hemodynamics once the valve area falls to less than 2 cm2 (normal 4-6 cm2). High velocities and a large transmitral pressure gradient are needed because the entire cardiac output must pass through the stenosis. These higher gradients are generated by increased left atrial pressure in systole and diastole, and are transmitted upstream to the pulmonary vasculature and right side of the heart causing pulmonary edema, pulmonary hypertension, and elevated central venous pressures. Despite these higher pressures, the left ventricular end diastolic pressure remains low from the reduced preload, and cardiac output is therefore depressed. The systemic vasculature compensates with higher resistance.
The transmitral gradients are highly heart rate-dependent, and patients who develop rapid atrial fibrillation can quickly deteriorate. There is reduced filling time that demands much higher filling pressures, which in turn causes significant pulmonary edema and occasional hemoptysis from pulmonary venous rupture. Treatment of mitral stenosis is directed at controlling the heart rate and maintaining sinus rhythm (e.g., digoxin, diltiazem, beta-blockade). Left ventricle contractility is generally preserved in mitral stenosis. Beta-blockade does result in decreased right ventricular contractility, which in pulmonary hypertension can further compromise the cardiac output and systemic blood pressure. The loss in right ventricle contractility, however, is more than offset by the beneficial effects of reducing the heart rate. Loop diuretics should be used for diuresis and their venodilation effects (mediated by angiotensin II and prostaglandins) to reduce pulmonary vascular congestion. Left atrial dilation and stasis substantially increase the risk of thromboembolism, especially for atrial fibrillation, and therefore anticoagulation is critical. Surgical intervention is ultimately required, and involves carefully choosing balloon mitral valvuloplasty, mitral valve commissurotomy, or mitral valve replacement.
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