Defense mechanisms to increasing back pressure for hepatic oxygen transport and venous return in porcine fecal peritonitis.

High central venous pressure (CVP) acutely decreases venous return. How this affects hepatic oxygen transport in sepsis remains unclear. The aim of this study was to evaluate the effects of repeated increases of CVP via standard nursing procedures (NPs) on hepato-splanchnic and renal oxygen transport in a prolonged porcine sepsis model. Twenty anesthetized and mechanically ventilated pigs with regional hemodynamics monitored were randomized to fecal peritonitis or controls (n=10 / group). Resuscitation was started after 8-hour of observation and continued for 3 days. NPs were performed at baseline and 8h, 32h, 56h and 72h after resuscitation started. NPs increased CVP by 4-7 mmHg in both groups. In controls, this was associated with less decrease in hepatic arterial (Qha, 62±70 ml/min) than portal venous flow (Qpv, 364±151 ml/min). Portal venous oxygen content, and hepatic O2 delivery (DO2) and consumption (VO2) decreased by 11±6 ml/dl, 0.9±0.3 and 0.4±0.3 ml/min/kg respectively. In septic animals, hepatic DO2 decreased more in response to increasing CVP (1.5±0.9 ml/min/kg), which was attributable to a larger fall both in Qha (88±66 ml/min) and in portal O2 content (14±10 ml/dl, all p<0.05).This resulted in numerically lower hepatic VO2 since O2 extraction did not increase significantly. In control conditions, a smaller decrease of Qha compared to Qpv helped to limit the reduction in hepatic VO2 in response to acute CVP increase. In sepsis, the contribution of Qha to maintain hepatic DO2 was reduced which jeopardized hepatic VO2 further. Renal arterial flow was similarly affected by CVP increase as Qha.