Limited physical activity is generally recommended in women with mitral stenosis. If symptoms of pulmonary congesJ tion develop, activity is further reduced, dietary sodium is restricted, and diuretics are given (Siva, 2005). Also, �-blocker drug therapy slows the ventricular response to activity. If new onset atrial ibrillation develops, intravenous verapamil, 5 to 10 mg, is given, or electrocardioversion is performed. For chronic :) 15 ibrillation, digoxin, a �-blocker, or a calcium-channel blocker ; E can slow ventricular response. Therapeutic anticoagulation is = E 10 indicated with persistent ibrillation, left atrial thrombus, and/ ) A B C or a history of embolism (Nanna, 2014). ..m 5 0 Surgical intervention is considered for women with sympc tomatic severe mitral stenosis and in those with lesser degrees E0 of mitral stenosis-mitral-valve area 1.5 to 2.0 cm2-compli.
hypertension. Balloon valvuloplasty is preferred if the valve is pliable (Bui, 2014). In one review of 71 pregnant women with surements (red graph line) in eight women with mitral valve stenosis. Shaded yellow and blue boxes are mean (± 1 SO) pres neous valvuloplasty, 98 percent were either NYHA class I or sures in nonlaboring normal women at term. A. First-stage labor.
II at delivery (Esteves, 2006). At a mean of 44 months, the
B. Second-stage labor 15 to 30 minutes before delivery. C. Postpartotal event-free maternalsurvival rate was 54 percent. However, tum 5 to 15 minutes. D. Postpartum 4 to 6 hours. E. Postpartum 18 eight women required another surgical intervention. All of the to 24 hours. (Data from Clark, 1985, 1989.) from a now-empty, contracted uterus and from the lower extremities and pelvis (Clark, 1985).
Most prefer vaginal delivery in women with mitral stenosis.
Elective induction is reasonable so that labor and delivery are attended by a scheduled, experienced team. With severe steno sis and chronic heart failure, insertion of a pulmonary artery catheter may help guide management.
A trivial degree of mitral insuiciency is found in most normal patients. But if mitral valve lealets align improperly during systole, abnormal degrees of mitral regurgitation can develop. his is eventually followed by left ventricular dilation and eccentric hypertrophy (see Table 49-6). Acute mitral insuiciency is caused by chordae tendineae rupture, papillary muscle infarction, or leaflet perforation from infective endocarditis. Chronic mitral regurgitation, in contrast, may derive from rheumatic fever, connective tissue diseases, mitral valve prolapse, or left ventricular dilation of any etiology-for example, dilated cardiomyopathy. Less common causes include a calcified mitral annulus, possibly some appetite suppressants, and in older women, ischemic heart disease. Mitral valve vegetations-Libman-Sacks endocarditis-are relatively common in women with antiphospholipid antibodies (Shrof, 2012). These sometimes coexist with systemic lupus erythematosus.
In nonpregnant patients, symptoms from mitral valve insufficiency are rare, and valve replacement is seldom indicated unless infective endocarditis develops. During pregnancy, mitral regurgitation is similarly well tolerated, probably because the lowered systemic vascular resistance yields less regurgitation. Heart failure rarely develops during pregnancy, and occasionally tachyarrhythmias or severely depressed systolic function require treatment.