NOREPINEPHRINE INDUCED PULMONARY CONGESTION IN PATIENTS WITH AORTIC VALVE REGURGITATION*

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Abstract
A comparison was made of the pluripotential effects of norepinephrine (0.2 [mu]g/kg/min. for 15 min.) in the normal human (7) and in compensated aortic regurgitation (8) to assess the role of blood redistribution upon cardiopulmonary hemodynamics. Indicator dilution curves were obtained to evaluate the cardiac output, regurgitant flow and central volume. Intravascular pressures from the brachial artery, pulmonary artery were recorded, with the pulmonary "capillary" as an index of left ventricular filling pressure. A disparity of response between the 2 groups was most manifest in the pulmonary "capillary" and artery pressure alterations, a nearly 4-fold rise to pulmonary congestion levels in the aortic regurgitation group contrasted with a 5 mm Hg mean rise occurring in the normal. Whereas this small increment of left ventricular filling pressure was associated with a sizable stroke work increase in the normal, no significant change in contractility was found in the aortic regurgitant group, despite markedly elevated filling pressures. Displacement of blood from the peripheral venous system appeared to be the major mechanism involved since venous occlusion tourniquets restored to normal the norepinephrine cardiovascular response in aortic regurgitation.