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.

Portal hypertension and cirrhosis can result in complex changes in the pulmonary vascular bed, the most important among them being the hepatopulmonary syndrome and portopulmonary hypertension. When pulmonary hypertension accompanies cirrhosis and portal hypertension, it is seldom diagnosed. Its prevalence is estimated to range from 1% to 2% in patients with portal hypertension or cirrhosis, regardless of gender, and the condition is predominantly seen in patients in their 40s. Etiologic factors have not been sufficiently well defined to explain the increase in pulmonary artery pressure and pulmonary vascular resistance. Most patients are asymptomatic until developing dyspnea on exertion, which generally occurs when the mean pulmonary artery pressure exceeds 40 mmHg. Concomitant hepatic disease with progressive hypoxemia or right ventricular failure increase mortality rates. Further studies are needed in order to determine the benefits of using oral, inhaled or intravenous vasodilators, as well as to evaluate the outcomes of liver transplant, which may be the sole definitive therapeutic option.

Keywords: Key words: Oxygen free radicals. Antioxidant substances. Oxidative stress. Lung diseases.