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 (Qsp l) and oxygen consumption (VO(2)spl). The increased Qspl, however, may not match the splanchnic oxygen demand, resulting in hepatic dysfunct ion. This concept of ongoing tissue hypoxia that can be relieved by in creasing splanchnic oxygen delivery (DO(2)spl), however, was challenge d because most of the elevated VO(2)spl was attributed to increased he patic glucose production (HGP) resulting from increased substrate deli very. Therefore the authors tested the hypothesis that a dobutamine-in duced increase in Qspl and DO(2)spl leads to increased VO(2)spl associ ated with accelerated HGP in patients with septic shock. Methods: Twel ve patients with hyperdynamic septic shock in whom blood pressure had been stabilized (mean arterial pressure greater than or equal to 70 mm Hg) with volume resuscitation and norepinephrine received dobutamine t o 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 det ermined from the plasma appearance rate of stable, non-radioactive-lab eled glucose using a primed-constant infusion approach. Results: Altho ugh 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 . mi n(-1) . m(2); P < 0.001), there was no effect on VO(2)spl (73 +/- 16 a nd 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 wh om blood pressure had been stabilized with volume resuscitation and no repinephrine, no delivery-dependency of VO(2)spl could be detected. Ox ygen consumption was not related to the accelerated HGP either, and th us the concept that HGP dominates VO(2)spl must be questioned in well- resuscitated patients with septic shock.