Effects of a dobutamine-induced increase in splanchnic blood flow on hepatic metabolic activity in patients with septic shock

Background: Septic shock leads to increased splanchnic blood flow (Qspl) and oxygen consumption (VO(2)spl). The increased Qspl, however, may not match the splanchnic oxygen demand, resulting in hepatic dysfunction. This concept of ongoing tissue hypoxia that can be relieved by increasing splanchnic oxygen delivery (DO(2)spl), however, was challenged because most of the elevated VO(2)spl was attributed to increased hepatic glucose production (HGP) resulting from increased substrate delivery. Therefore the authors tested the hypothesis that a dobutamine-induced increase in Qspl and DO(2)spl leads to increased VO(2)spl associated with accelerated HGP in patients with septic shock. Methods: Twelve patients with hyperdynamic septic shock in whom blood pressure had been stabilized (mean arterial pressure greater than or equal to 70 mmHg) with volume resuscitation and norepinephrine received dobutamine to obtain a 20% increase in cardiac index (CI). Qspl, DO(2)spl, and VO(2)spl were assessed using the steady-state indocyanine green clearance technique with correction for hepatic dye extraction, and HGP was determined from the plasma appearance rate of stable, non-radioactive-labeled glucose using a primed-constant infusion approach. Results: Although the increase in CI resulted in a similar increase in Qspl (from 0.91 +/- 0.21 to 1.21 +/- 0.34 1 . min(-1) . m(2); P < 0.001) producing a parallel increase of DO(2)spl (from 141 +/- 33 to 182 +/- 44 ml . min(-1) . m(2); P < 0.001), there was no effect on VO(2)spl (73 +/- 16 and 82 +/- 21 ml . ml . min(-1) . m(2), respectively). Hepatic glucose production decreased from 5.1 +/- 1.6 to 3.6 +/- 0.9 mg . kg(-1) . min(-1) (P < 0.001). Conclusions: In the patients with septic shock in whom blood pressure had been stabilized with volume resuscitation and norepinephrine, no delivery-dependency of VO(2)spl could be detected. Oxygen consumption was not related to the accelerated HGP either, and thus the concept that HGP dominates VO(2)spl must be questioned in well-resuscitated patients with septic shock.