Search

Hepatic and systemic hemodynamics were measured in 19 cirrhotic patients with variceal bleeding enrolled in a controlled trial of propranolol for the prevention of rebleeding. The patients were studied on three separate occasions. The first study was performed before randomization within 24 h of the bleeding episode, once hemodynamic stabilization had been achieved. The second study was performed after 10 days of treatment, and the third after 6 mo without rebleeding. Propranolol dosage was titrated according to blood levels. Wedged and free hepatic venous pressures and the hepatic venous pressure gradient were recorded. Hepatic blood flow and cardiac output were also measured. Before treatment, the groups of patients treated with propranolol (n = 11) or placebo (n = 8) were comparable according to clinical, biochemical, and hemodynamic parameters. After 10 days, hepatic venous pressure gradient decreased similarly in the two groups (-20% in the propranolol group, -25% in the placebo group). Cardiac output fell only in the propranolol group (-40%). Hepatic blood flow remained unchanged in either group. After 6 mo, hepatic venous pressure gradient remained lower than the values from the first (within 24 h of bleeding) study in both the propranolol group (n = 5) and the placebo group (n = 6). Our results suggest that portal pressure increases shortly after hemorrhage with a return to baseline values 10 days later, and that propranolol does not further magnify these changes. Spontaneous changes in hepatic hemodynamics after variceal hemorrhage must be taken into account when evaluating the effect of pharmacologic agents on portal pressure.

The simultaneous measurement of wedged hepatic vein pressure (WHVP) and portal vein pressure (PVP) was performed in 156 cirrhotic patients. In the 110 alcoholic cirrhotic patients (97 micronodular and 13 macronodular cirrhosis), WHVP and PVP were closely related (25.8 +/- 6.3 vs. 25.9 +/- 6.3 mm Hg; p = not statistically significant). The difference between the two parameters was greater than 4 mm Hg in only six patients. In the 46 patients with nonalcoholic cirrhosis (41 macronodular and 1 micronodular cirrhosis; 4 primary biliary cirrhosis), PVP was significantly higher than was WHVP (25.8 +/- 6.2 vs. 21.7 +/- 6.8 mm Hg; p less than 0.001); in 20 patients, PVP exceeded WHVP by more than 4 mm Hg, and the mean difference was 7.5 mm Hg. There was no correlation between the porto-hepatic gradient and total hepatic blood flow measured by the indocyanine green single injection method or the portal fraction of total hepatic blood flow measured by indicator dilution curves. It is concluded that: (i) measurement of WHVP in alcoholic cirrhosis provides a reliable estimate of the severity of the portal hypertension, and (ii) hemodynamic evaluation of nonalcoholic cirrhosis should include PVP measurement in order to avoid underestimation of the porto-hepatic gradient.