Normalization of ventilation/perfusion relationships after liver transplantation in patients with decompensated cirrhosis: Evidence for a hepatopulmonary syndrome

To examine the effect of liver transplantation on the respiratory and cardiovascular functions, ventilation/perfusion relationships were determined by multiple inert gas elimination technique in six patients with end‐stage liver disease 1 to 19 mo before and 2 to 6 mo after liver transplantation. Cardiac output and pulmonary vascular pressures were measured after catheterization of the pulmonary artery. All patients had normal spirometry and chest x‐ray films before transplantation. PaO 2 before transplantation was 78.8 ± 7.4 mm Hg (range = 51.8 to 102.8 mm Hg). All patients had perfusion of poorly ventilated lung regions (low ventilation/perfusion relationships) varying from 3% to 19% of cardiac output (mean = 8.5% ± 2.4% of cardiac output) and two patients had intrapulmonary shunting (3% and 20% of cardiac output). Measured and calculated PaI 2 agreed closely, indicating absence of pulmonary diffusion abnormality, as well as of extrapulmonary shunting. After transplantation, PaO 2 normalized in all patients, and both shunting and low ventilation/perfusion relationships disappeared. Cardiac output decreased from 9.1 ± 1.4 to 6.6 ± 0.5 L/min (p < 0.05), and the pulmonary vascular resistance increased from 0.69 ± 0.14 to 1.64 ± 0.43 mm Hg/L/min (p < 0.05). The systemic vascular resistance also increased (before = 8.7 ± 1.0; after = 15.3 ± 1.1 mm Hg/L/min; p < 0.001). Normalization of respiratory and cardiovascular alterations, after liver transplantation, in patients with end‐stage liver disease indicates that these changes have a direct functional relationship to the diseased liver. It is hypothesized that this is part of a “hepatopulmonary syndrome,” which in similarity to the hepatorenal syndrome disappears with improved liver function. (HEPATOLOGY 1990;12:1350–1357).