| Autor: |
Charalabopoulos K; Department of Physiology, Clinical Unit, Medical Faculty, University of Ioannina, Ioannina, Greece. kcharala@cc.uoi.gr, Peschos D, Zoganas L, Bablekos G, Golias C, Charalabopoulos A, Stagikas D, Karakosta A, Papathanasopoulos A, Karachalios G, Batistatou A |
| Abstrakt: |
In cirrhotic patients, in addition to hepatocytes and Kuppfer cells dysfunction circulatory anatomic shunt and ventilation/perfusion (V(A)/ Q) ratio abnormalities can induce decrease in partial pressure of oxygen in arterial blood (PaO(2)), in oxygen saturation of hemoglobin (SaO(2)) as well as various acid-base disturbances. We studied 49 cases of liver cirrhosis (LC) with ascites compared to 50 normal controls. Causes were: posthepatic 37 (75.51%), alcoholic 7 (14.24%), cardiac 2 (4.08%), and cryptogenic 3 (6.12%). Complications were: upper gastrointestinal bleeding 24 (48.97), hepatic encephalopathy 20 (40.81%), gastritis 28 (57.14%), hepatoma 5 (10.2%), renal hepatic syndrome 2 (4.01%), HbsAg (+) 24 (48.97%), and hepatic pleural effusions 7 (14.28%). Average PaO(2) and SaO(2) were 75.2 mmHg and 94.5 mmHg, respectively, compared to 94.2 mmHg and 97.1 mmHg of the control group, respectively (p value in both PaO(2) and SaO(2 )was p<0.01). Respiratory alkalosis, metabolic alkalosis, metabolic acidosis, respiratory acidosis and metabolic acidosis with respiratory alkalosis were acid-base disturbances observed. In conclusion, portopulmonary shunt, intrapulmonary arteriovenous shunt and V(A)/Q inequality can induce a decrease in PaO(2) and SaO(2) as well as various acid-base disturbances. As a result, pulmonary resistance is impaired and patients more likely succumb to infections and adult respiratory distress syndrome. |
