Hepatic blood flow and splanchnic oxygen consumption in patients with liver failure. Effect of high-volume plasmapheresis

Liver failure represents a major therapeutic challenge, and yet basic patho physiological questions about hepatic perfusion and oxygenation in this con dition have been poorly investigated, In this study, hepatic blood flow (HB F) and splanchnic oxygen delivery (DO2,sp) and oxygen consumption (VO2,sp) were assessed in patients with liver failure defined as hepatic encephalopa thy grade II or more. Measurements were repeated after high-volume plasmaph eresis (HVP) with exchange of 8 to 10 L of plasma, HBF was estimated by use of constant infusion of D-sorbitol and calculated according to Fick's prin ciple from peripheral artery and hepatic vein concentrations. In 14 patient s with acute liver failure (ALF), HBF (1.78 +/- 0.78 L/min) and VO2,sp (3.9 +/- 0.9 mmol/min) were higher than in 11 patients without liver disease (1 .07 +/- 0.19 L/min, P <.01) and (2.3 +/- 0.7 mmol/min, P <.001). In 9 patie nts with acute on chronic liver disease (AOCLD), HBF (1.96 +/- 1.19 L/min) and VO2,sp (3.9 +/- 2.3 mmol/min) were higher than in 18 patients with stab le cirrhosis (1.00 +/- 0.36 L/min, P <.005; and 2.0 +/- 0.6 mmol/min, P <.0 05). During HVP, HBF increased from 1.67 +/- 0.72 to 2.07 +/- 1.11 L/min (n =11) in ALF, and from 1.89 +/- 1.32 to 2.34 +/- 1.54 L/min (n=7) in AOCLD, P <.05 in both cases, In patients with ALF, cardiac output (thermodilution) was unchanged (6.7 +/- 2.5 vs. 6.6 +/- 2.2 L/min, NS) during HVP. Blood fl ow was redirected to the liver as the systemic vascular resistance index in creased (1,587 +/- 650 vs. 2,020 +/- 806 Dyne . s . cm(-5) . m(2), P <.01) whereas splanchnic vascular resistance was unchanged, In AOCLD, neither sys temic nor splanchnic vascular resistance was affected by HVP, but as cardia c output increased from 9.1 +/- 2.8 to 10.1 +/- 2.9 L/min (P <.01) more blo od was directed to the splanchnic region, In all liver failure patients tre ated with HVP (n=18), DO2,sp increased by 15% (P <.05) whereas VO2,sp was u nchanged. Endothelin-1 (ET-1) and ET-3 were determined before and after HVP , Changes of ET-1 were positively correlated with changes in HBF (P <.005) and VO2,sp (P <.05), indicating a role for ET-1 in splanchnic circulation a nd oxygenation, ET-3 was negatively correlated with systemic vascular resis tance index before HVP (P <.05) but changes during HVP did not correlate. O ur data suggest that liver failure is associated with increased HBF and VO2 ,sp. HVP further increased HBF and DO2,sp but VO2,sp was unchanged, indicat ing that splanchnic hypoxia was not present.