Tissue hypoxia during fulminant hepatic failure

  title={Tissue hypoxia during fulminant hepatic failure},
  author={David J Bihari and Alexander E. S. Gimson and Michael J Waterson and R. Williams},
  journal={Critical Care Medicine},
To assess the adequacy of tissue oxygenation in fulminant hepatic failure, we measured arterial oxygen delivery, the affinity of hemoglobin for oxygen, mixed venous oxygen tension, and lactate concentration in 32 patients suffering grade IV encephalopathy.In the patients who died, median systemic vascular resistance and oxygen extraction ratio were significantly (p < .005) lower than in those who survived (1268 vs. 1866 dyne. sec/cm5 m2 and 20% vs. 25%, respectively) despite a significantly (p… 
Cerebral blood flow and metabolism in fulminant liver failure
The depressed cerebral metabolic rate for oxygen in patients with fulminant liver failure is inappropriate to metabolic requirements, as demonstrated by both cerebral lactate production and the increase in cerebral oxygen consumption after improvement in cerebral blood flow.
Hemodynamic parameters in a surgical devascularization model of fulminant hepatic failure in the minipig.
The parameters are believed to be quite adequate, as they were able to maintain satisfactory hemodynamic stability in all experimental animals with induced acute hepatic failure.
Fibronectin replacement in patients with fulminant hepatic failure
No significant changes were observed in cardiopulmonary function or oxygen utilization and it is possible this is because clearance of opsonized particles is limited by damage to Kupffer cells.
Hyperlactatemia in patients with non-acetaminophen-related acute liver failure.
Hyperlactatemia is not a prognosis factor due to byproduct of the overall acceleration in glycolysis, and the presence of infection was an independent predictor of survival.
Improvement by acetylcysteine of hemodynamics and oxygen transport in fulminant hepatic failure.
The increase in oxygen delivery and consumption in response to acetylcysteine may account for its beneficial effect on survival in patients with fulminant hepatic failure induced by acetaminophen.
The effect of N‐acetylcysteine on oxygen transport and uptake in patients with fulminant hepatic failure
It is concluded that N‐acetylcysteine infusion does not result in clinically relevant improvements in global Vo2, or in clinical markers of tissue hypoxia in patients with severe fulminant hepatic failure.
Relationship between oxygen transport and oxygen uptake in patients with cirrhosis: Effects of vasoactive drugs
O2 uptake may be abnormally dependent on O2 transport in patients with cirrhosis, and the effects of three vasoactive drugs that change O2 Transport are studied.