Cardiac function was evaluated in 17 patients with cardiac valvular insufficiency scheduled for valve replacement 1) immediately prior to the induction of anesthesia, 2) during stable anesthetic and surgical conditions after the chest was opened, and 3) during a constant sodium nitroprusside infusion about 15 min later but prior to cannulation for cardiopulmonary bypass. Preoperative awake hemodynamic measurements indicated that these patients were in a state of compensatory cardiac failure with a low cardiac index of 2.20 ± 0.15 1/min/m2 and a high systemic vascular resistance of 1,560 ± 150 dynes.sec.cm-5. Pulmonary capillary wedge pressure was 13 ± 3 torr, central venous pressure 4 ± 1 torr, and stroke volume index was 29.6 ± 2.1 ml/beat/m2. During steady-state anesthesia with the operation in progress, there were significant increases in systemic vascular resistance to 2,370 ± 160 dynes.sec.cm-5 and pulmonary capillary wedge pressure to 24 ± 2 torr, and significant decreases in cardiac index to 1.63 ± 0.08 1/min/m2 and stroke volume index to 19.4 ± 1.3 ml/beat/m2, demonstrating cardiac decompensation.
At this time, an infusion of sodium nitroprusside, 20–96 μg/min, produced significant decreases in systemic vascular resistance to 1,490 ± 130 dynes.sec.cm-5 and pulmonary capillary wedge pressure to 16 ± 2 torr. Cardiac index increased to 2.21 ± 0.15 1/min/m2 and stroke volume index to 24.4 ± 1.9 ml/beat/m2. These results indicate that patients in compensated cardiac failure secondary to valvular insufficiency respond to anesthesia and operation with a marked deterioration in cardiac function primarily due to a further increase of the already high systemic vascular resistance. Sodium nitroprusside, by decreasing vascular tone and thus ventricular afterload, reverses some of the cardiovascular depression and failure in these patients, thereby mitigating the deleterious effects of anesthesia and operation.