Abstract
Perumbilical portal vein catheters and arterial and central venous catheters were inserted in 16 patients recovering from trauma or other shock-producing events, and in 5 patients who later developed shock. This permitted serial measurement of blood gases, pH, and the levels of ammonia, lactate and certain other metabolites in all three circulatory systems simultaneously. Nine of the trauma patients were never in shock, had no liver disease or injury and consequently formed a baseline group for comparison with the shock patients. In the shock patients there was a significant degree of hypoxemia in the portal venous blood and an increase in the arterialportal oxygen saturation difference. Their portal venous blood showed a lower pH and a higher pCO(2) than did the portal blood of the patients who had never been in shock. In 3 of the 4 shock patients who died, the total blood lactate showed a greater increase in portal venous than in the arterial or central venous blood. In shock there was also an increase in portal venous blood ammonia which was later accompanied by increments in arterial and central venous blood ammonia. This suggests impairment of hepatic urea synthesis, allowing escape of ammonia through the liver. These phenomena, when added to the finding previously reported of an elevated portal venous pressure in some shock patients, lend support to the hypothesis that in certain cases of shock there is increased impedance to flow of portal blood through the liver with resultant stasis in the portal-splanchnic bed and ischemichypoxic hepatocellular injury.