EFFECTS OF PROPRANOLOL ON ARTERIAL OXYGENATION AND OXYGEN-TRANSPORT TO TISSUES IN PATIENTS WITH CIRRHOSIS

Patients with cirrhosis may show ventilation-perfusion (V̇/Q̇) inequality in the absence of any intrinsic heart of lung disease. However, the high cardiac output of cirrhosis generally prevents or minimizes the appearance of a severe degree of arterial hypoxemia. Propranolol has been used to reduce cardiac output and portal pressure in these patients. We wondered whether it might alter arterial oxygenation and reduce O2 transport to tissues. We studied eight patients (three women) 54 ± 3 (SEM) yr of age before and after intravenous propranolol (0.1 mg/kg followed by 2 mg/h). Cardiac output (Q̇T) fell from 7.8 ± 0.7 to 6.0 ± 0.7 L/min (p < 0.05), and portal pressure was reduced (22 ± 2 to 19 ± 2 mm Hg, p < 0.01). Arterial PO2 did not change (88 ± 4 to 89 ± 5 mm Hg) because the fall in mixed venous PO2 (43 ± 1 to 40 ± 1 mm Hg, p < 0.01) that followed the lower Q̇T was counterbalanced by a lower intrapulmonary shunt (multiple inert gas technique) (4 ± 2 to 2 ± 1%, p < 0.05) an a shift of the V̇A/Q̇ distributions toward a higher V̇A/Q̇ ratio. Paralleling the fall in Q̇T, oxygen transport to tissue (Q̇O2) was reduced (19 ± 2 to 14± 1 ml/min/kg, p < 0.01). However, O2 uptake (V̇O2) remained constant (3.4 ± 0.2 to 3.6 ± 0.2 ml/min/kg) because O2 extraction by the tissues increased appropriately (22 ± 2 to 28 ± 1%, p < 0.01). This implies an independence of V̇O2 and Q̇O2 in this range and suggests that these patients had a normal capacity to regulate O2 extraction in the face of a reduced O2 delivery.