Effects of nitroprusside on venous return and central blood volume in the absence and presence of acute heart failure.

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The effects of nitroprusside (380–760 ug/min) on the systemic venous return, the central blood volume and the equilibrium point between the venous return and cardiac output curves were studied in eight dogs using a right-heart bypass preparation at constant total blood volume. Experiments were performed before and after the production of acute left ventricular failure. During control, nitroprusside infusion shifted the venous return curve, with a reduction in its plateau (3.1 to 2.4 l/min;p < 0.005), the central blood volume fell (−2.4 ± 0.4 ml/kg; p < 0.05) and the cardiac output at equilibrium was reduced (3.1 to 2.4 1/min; p < 0.005). Cardiac failure (produced by acute coronary artery ligation) increased the central blood volume (+6.3 ± 0.6 ml/kg; p < 0.01), leading to a decrease in both the systemic blood volume and the plateau of the venous return curve (3.2 to 2.6 1/min; p < 0.003). The cardiac output at equilibrium was also reduced (3.2 to 1.9 1/min; p < 0.001). In this setting, nitroprusside infusion decreased the central blood volume (−7.4 ml/kg; p < 0.01), but the venous return curve was not altered. The cardiac output curve was markedly shifted upward due to reduced afterload on the failing left ventricle; however, in the absence of a downward shift of the venous return curve, the cardiac output at equilibrium increased from 1.9 to 2.6 1/min (p < 0.05). We conclude that the differing effects of nitroprusside in acute cardiac failure are due primarily to an increased shift of blood from the central circulation in the failure state compared with the normal circulation. This shift counteracts the systemic venodilatation produced by nitroprusside and allows the markedly improved left ventricular function consequent to reduced afterload to be expressed as increased venous return and cardiac output.