Pulmonary Hemodynamics and Gas Exchange during Exercise in Liver Cirrhosis

We have recently shown that ventilation-perfusion ( a/) mismatching at rest in cirrhosis is due to an abnormal pulmonary vascular tone. It has been suggested that in patients with cirrhosis, O2 transfer might become diffusion-limited during exercise. This study examined pulmonary hemodynamics and mechanisms modulating gas exchange during exericise (60 to 70% O2max) in six patients (41 ± 5 yr, ± SEM) with cirrhosis but with normal lung function tests. At rest, t was high (8.4 ± 0.5 L/min), pulmonary vascular resistance (PVR) was low (0.61 ± 0.17 mm Hg/L/min), and there was mild to moderate a/ mismatching (Logsd Q, 0.79 ± 0.09; normal range, 0.3 to 0.6). However, hyperventilation (PaCO2, 29 ± 2 mm Hg) and high t (thus, high P O2, 41 ± 2 mm Hg) contributed to the maintenance of PaO2 within normal values (99 ± 7 mm Hg). Exercise O2 (1,278 ± 122 ml/min) was normal relative to work load, but, contrary to that in normal subjects, t was higher and PVR did not fall. During exercise, PaO2 showed a trend to decrease (to 90 ± 5 mm Hg) and PaCO2 to rise (to 35 ± 2 mm Hg), but the differences failed to reach statistical significance (p = 0.07 each). Pa O2 fell significantly with exercise (41 ± 2 to 33 ± 0.3 mm Hg, p < 0.05), but neither AaPaO2 (15 ± 7 to 21 ± 6 mm Hg) nor a/ inequality (Logsd, 0.82 ± 0.11) changed. No systematic difference was noticed between predicted and measured PaO2 values, suggesting no O2 diffusion impairment during exercise. We conclude that exercise in patients with liver cirrhosis (1) perpetuates the hyperdynamic cardiovascular state observed at rest, (2) cannot modify PVR because the pulmonary circulation is already maximally dilated at rest, and (3) does not change the efficiency of the lung as a gas exchanger. Specifically, no limitation for the O2 transfer ensues. We suggest that changes in PaO2 with exercise are fully explained by the interplay of the extrapulmonary factors, namely, t, e, and O2.