Left ventricular function was assessed in 10 patients with alcoholic cirrhosis and ascites without clinical evidence of heart disease. In the resting state pulmonary wedge pressure (PWP) was normal (average 9.7 mm Hg), cardiac output (CO) was elevated (average 9.7 L/min) and systemic vascular resistance (SVR) was low (average 825 dynes sec cm-5). During infusion of angiotensin in a dose sufficient to raise diastolic arterial pressure 20 mm Hg, SVR increased to 1140 dynes sec cm-5 (P < 0.01) and PWP rose to 19.2 mm Hg (P < 0.001) with no change in CO. Resting hemodynamics were essentially unchanged in 7 patients restudied 45-60 min after intravenous administration of 0.5 mg ouabain. Repeat infusion of angiotensin after ouabain again resulted in a rise in PWP to an average of 17.0 mm Hg (P < 0.001) with no significant change in CO. In 7 additional cirrhotic patients with ascites, systolic time intervals were unchanged by 0.5 mg ouabain whereas in 4 normal volunteers the same dose resulted in significant shortening of total electromechanical systole, pre ejection period and left ventricular ejection time. These data indicate that depression of the left ventricular response to an increase in afterload is a uniform finding in alcoholic patients with cirrhosis and ascites. The absence of clinical symptoms of heart disease, therefore, could be attributed to the low systemic vascular resistance characteristic of cirrhosis. Since acute administration of ouabain neither improved left ventricular function nor altered systolic time intervals, digitalis may have a limited place in the therapy of this form of cardiac impairment.