Presence of arterial hypoxemia in hepatic cirrhosis is a well-documented fact. Physiopathogenic mechanisms have been widely studied. It is assumed that there are alterations in pulmonary vessels which determine small and numerous arteriovenous shunts. Presence of anatomic intrapulmonary shunts, although well-documented, is small and could hardly explain such low levels of arterial oxigenation in cirrhotic patients. It is a premise that alterations occur in the pulmonary dynamics and that the diffusion of gases may be altered. Purpose: To evaluate the pulmonary function and arterial oxygenation levels in 55 patients with hepatic cirrhosis, with no other pulmonary, cardiac or hematologic diseases. They were submitted to evaluation of the pulmonary function through measurement of the forced vital capacity, forced expiratory volume in one second, and residual volume as well as diffusion capacity for carbon monoxide. Finally, arterial oxygenation was evaluated through arterial gasometry during air breathing and with 100% oxygen. Analysis of results allowed the authors to observe the presence of normal pulmonary flows and volumes (average of: FVC = 104.6%; FEV1 = 102.4%; residual volume = 117.4%); and diffusion capacity was diminished (average = 70.8%) in relation to predicted values. Arterial blood gases showed a mean PaO2 of 81.20 mmHg during air breathing and 515.4 mmHg when 100% oxygen was breathed. No correlations among PaO2 (with air breathing and with oxygen) and diffusion capacity were observed. In this study, flows and pulmonary volumes were normal in relation to the predicted values; however, diffusion of carbon monoxide was diminished. This diminished diffusion corroborates the existing idea of the so-called diffusion-perfusion imbalance as one of the mechanisms involved in the physiopathology of the hepatic pulmonary syndrome, even with no evidence of intrapulmonary morphological arteriovenous shunt.

Keywords: Hepatopulmonary syndrome. Pulmonary function. Hepatic cirrhosis.