Hypoxic pulmonary vasoconstriction in liver cirrhosis.

Impairment of hypoxic pulmonary vasoconstriction (HPV) is frequently cited as an explanation for the hypoxemia of liver cirrhosis. We investigated the pulmonary and systemic hemodynamic responses to acute inspiratory hypoxia, 12.5 percent oxygen in nitrogen during 10 minutes, in 24 patients with mildly to moderately decompensated liver cirrhosis and arterial hypoxemia. A mean increase of 50 percent in pulmonary vascular resistance (PVR) was observed, which is comparable to reported responses of normal subjects to a similar degree of hypoxia. Seven of the 24 patients showed an increase in PVR of less than 20 percent. Compared with the other patients, no difference could be found between both groups in baseline blood gas and hemodynamic determinations, physical examination, liver function tests, and laboratory tests that may be disturbed by circulating endotoxin. Five of the 24 patients had a hyperkinetic circulatory state, but only one of them failed to increase PVR in response to hypoxia. Considering the whole group of 24 patients, there was no correlation between PaO2, PVR, and PVR response to hypoxia. Impairment of HPV is probably not the right explanation for most cirrhotic patients with arterial hypoxemia.