We tested whether oxygen consumption (V̇o2) was dependent on oxygen delivery (Q̇o2) in 10 patients with septic shock when Q̇o2 was changed by the use of the inotropic agent, dobutamine. The mean acute physiology and chronic health evaluation (APACHE) II score of the patients was 27.3 ± 8.1 with a mean blood pressure on entry of 66.8 ± 12.4 mm Hg, and all had been volume resuscitated to a pulmonary artery occlusion pressure of greater than 10 mm Hg. We measured V̇o2 by analysis of respiratory gases NOW) while calculating V̇o2 by the Fick equation NOV) at three different OZ deliveries. When the dobutamine infusion rate was increased from 2.5 ± 4.0 to 12.3 ± 6.0 μg/kg/min, thermodilution cardiac output increased from 7.7 ± 2.6 to 10.1 ± 2.7 L/min (P < .01). Accordingly, dobutamine increased Q̇o2 from 13.5 ± 3.8 to 18.2 ± 4.3 mL/min per kg (increase of 36.4% ± 19.7%; P < .01), but V̇o2G did not increase (3.2 ± 0.5 to 3.2 ± 0.6 mL/ min per kg). During these same interventions, the V̇o2F tended to increase (2.9 ± 0.7 to 3.4 ± 0.8 mL/min per kg, P < .06), presumably a spurious correlation because of measurement errors shared by the calculation of V̇o2F and Q̇o2. Neither lactic acidosis nor acute respiratory distress syndrome (ARDS) conferred supply dependence of V̇o2G, but the presence of ARDS was predictive of death in this cohort. It is concluded that V̇o2 is independent of Q̇o2 in patients with septic shock and lactic acidosis. These data confirm that maximizing Q̇o2 beyond values achieved by initial fluid and vasoactive drug resuscitation of septic shock does not improve tissue oxygenation as determined by respiratory gas measurement of V̇o2.
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine