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Journal Article
Research Support, U.S. Gov't, P.H.S.
Comparison of intraoperative nitroprusside unloading in mitral and aortic regurgitation.
To compare the hemodynamic effect of vasodilator therapy on different regurgitant lesions, we infused sodium nitroprusside intraooperatively in 12 patients with mitral regurgitation and 15 with aortic regurgitation. During the critical period preceding establishment of cardiopulmonary bypass, both groups had developed intense vasoconstriction and cardiac decompensation. All demonstrated improved cardiac function with vasodilator therapy; however, the degree of improvement with nitroprusside differed in the two groups. Stroke volume increased 10 ml. per beat per meter squared in those patients with aortic regurgitation and only 6 ml. per beat per meter squared in those with mitral regurgitation (p less than 0.05). The percent increase in stoke volume induced by nitroprusside was inversely correlated to the preoperative left ventricular ejection fraction (r = 0.44, p less than 0.02). Patients with aortic regurgitation had lower preoperative left ventricular ejection fractions than those with mitral regurgitation (0.53 versus 0.63, p less than 0.02). Therefore, we conclude that patients with aortic regurgitation derived greater intraoperative hemodynamic benefit from unloading with nitroprusside, because they came to surgery with greater impairment of left ventricular contractility. Although nitroprusside improved cardiac function in both groups, only the patients with aortic regurgitation achieved normal pulmonary artery pressure (17 torr) and pulmonary vascular resistance (2.1 units) as a result of unloading. Those with mitral regurgitation continued to have pulmonary hypertension (28 torr) and increased pulmonary vascular resistance (3.9 units) despite vasodilator therapy. Thus the data suggest that patients with mitral regurgitation derived less hemodynamic benefit from intraoperative nitroprusside therapy because they were also limited by right ventricular dysfunction and a less responsive pulmonary vasculature.
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