The hemodynamic status of preascitic cirrhosis: An evaluation under steady‐state conditions and after postural change

Abstract

To assess the hemodynamic status of patients with compensated cirrhosis, mean arterial pressure, cardiac index and peripheral vascular resistance and markers of central (plasma concentrations of atrial natriuretic factor) and arterial volemia (plasma norepinephrine concentration, plasma renin activity) were studied in 10 patients and 10 healthy control subjects under steady‐state conditions (after 2 hr of standing) and after assumption of the supine position (30, 60, and 120 min). After standing, neither hemodynamics nor markers of effective volemia differed significantly between controls and patients. By evaluating the areas under the curve during the 2 hr of supine posture, the increase in cardiac output and plasma natriuretic factor and the decrease in peripheral vascular resistance were greater in patients (2.59 ± 0.43 [S.E.M.] L/min/hr; 32.8 ± 7.2 pg/ml/hr − 1,103 ± 248.4 dyn · sec/cm5/hr, respectively) than in controls (0.53 ± 0.24 L/min/hr, p = 0.005; 17.4 ± 4.7 pg/ml/hr, p = 0.005; − 265.5 ± 206.2 dyn · sec/cm5/hr, p = 0.02). The declines in heart rate, plasma norepinephrine concentration and plasma renin activity did not differ significantly. Mean arterial pressure did not significantly change. Our results suggest that during periods of upright posture, cirrhotic patients in the preascitic stage, who are known to have expanded blood volume, compensate for dilatation of the splanchnic vascular bed through total hypervolemia. The latter becomes excessive during recumbency, leading to supernormal increases in venous return, central volemia and cardiac index. The decline in peripheral vascular resistance appears to be a compensatory mechanism to maintain steady arterial blood pressure. Thus increased cardiac index and reduced peripheral vascular resistance in recumbent compensated cirrhotic patients may represent a physiological adaptation rather than a primitive vascular abnormality. (HEPATOLOGY 1992;16:341–346.) Copyright © 1992 American Association for the Study of Liver Diseases