Arteriovenous shunting, hemodynamic changes, and renal sodium retention in liver cirrhosis

Arterial vasodilation has been postulated to initiate sodium retention in cirrhosis. This work was designed to analyze whether arteriovenous shunting underlies vasodilation and influences renal function in cirrhosis.

The femoral arteriovenous difference in oxygen content (Ca-VO2) was measured in 10 healthy subjects (control group) and 31 cirrhotic patients: 9 without ascites (group 1), 10 with ascites and a urinary sodium excretion rate (UNaV) of > 10 mEq/24 h (group 2), and 12 with ascites and UNaV of < or = 10 mEq/24 h (group 3). In 8 subjects from each group, femoral blood flow and the cardiac output were determined by duplex-Doppler ultrasonography. In 9 cases arteriovenous shunting in the femoral territory was estimated using 30 +/- 5-microns radiolabeled microspheres.

Ca-VO2 was lower in group 3 than in controls or group 1. Ca-VO2 correlated inversely with femoral blood flow, plasma renin activity, plasma aldosterone concentration, and degree of shunting measured by microspheres. Ca-VO2 correlated directly with systemic vascular resistance and prothrombin index.

In decompensated cirrhotic patients, there is an increased arteriovenous shunt for oxygen in the lower extremities that is associated with increased arterial blood flow, decreased systemic vascular resistance, and worsening of liver function. This shunt is due partly to opening of arteriovenous precapillary connections.