A 77-year-old woman with severe mitral stenosis was scheduled for mitral valve repair or replacement and tricuspid valve annuloplasty. On admission to the hospital, she had severe pulmonary edema and atrial fibrillation, with a rapid ventricular response. She weighed 55 kg. Cardiac catheterization revealed mitral stenosis, pulmonary hypertension, and tricuspid regurgitation.
What are the etiology and pathophysiology of mitral stenosis?
Mitral stenosis is frequently rheumatic in origin. In many patients, there is a latency period of 30–40 years between the episode of rheumatic fever and the onset of clinical symptoms. Dyspnea is the most common symptom. The initial presentation is often due to an episode of atrial fibrillation resulting from atrial dilation or an exacerbation of symptoms from an unrelated condition, such as pregnancy, thyrotoxicosis, anemia, fever, or sepsis. Other common symptoms include fatigue, palpitations, chest pain, thromboembolic events, and hemoptysis (from pulmonary vascular congestion).
The normal adult mitral valve orifice is 4–6 cm 2 . As the orifice narrows to <2 cm 2 , the pressure gradient between the left atrium and left ventricle increases to maintain adequate flow and filling of the left ventricle. The high left atrial pressure causes pulmonary venous congestion, which eventually leads to pulmonary edema, particularly in the presence of tachycardia ( Figure 5-1 ). Tachycardia shortens diastole and diminishes the time available for flow across the mitral valve; this impairs left atrial emptying and left ventricular filling. Cardiac output decreases, pulmonary congestion increases, and decompensation ensues. A mitral valve area <1 cm 2 is considered critical. However, the decision to perform valve surgery is usually based on the severity of symptoms (i.e., New York Heart Association [NYHA] classification). The 10-year survival rate for patients with symptoms of dyspnea on exertion is approximately 80% without surgery. The 10-year survival rate for patients with disabling NYHA class III (dyspnea with minimal activity) and class IV (dyspnea at rest) symptoms is approximately 15% without surgery.
It previously had been thought that the left ventricle is “protected” from pressure or volume overload. Although some degree of left ventricular “protection” may be present for most cases of mild mitral stenosis, as the disease progresses, it is likely to cause varying degrees of left ventricular failure. Additionally, left ventricular contractility may be impaired by rheumatic involvement of papillary muscles and mitral anulus. Left ventricular posterobasal regional wall motion abnormalities may result. However, it is possible that left ventricular function might also be impaired by a leftward shift of the interventricular septum owing to right ventricular pressure overload. Pulmonary hypertension and right ventricular failure are often observed in mitral stenosis.
How are preload, afterload, heart rate, and contractility managed in patients with mitral stenosis?
The goals for preload, afterload, heart rate, and contractility are the major guiding principles of intraoperative management for patients with mitral stenosis. High left atrial pressures are required to maintain filling of the left ventricle (preload) through the stenotic mitral valve. Hypovolemia and venodilating drugs should be avoided. Afterload (systemic vascular resistance) should be kept high to maintain perfusion pressure in the face of a relatively low and fixed cardiac output. Heart rate should be kept slow to maximize diastolic filling of the left ventricle. Contractility should be maintained to preserve stroke volume. The hemodynamic goals in mitral stenosis are summarized in Table 5-1 .
|Heart rate||Slow||β-adrenergic blockers||Dopamine|
|Afterload||High||Phenylephrine||Angiotensin-converting enzyme inhibitors (except for right ventricular failure)|
|Contractility||Normal to increased||Norepinephrine||High-dose volatile anesthetics|
|High-dose β-adrenergic blockers|