Pathological supply dependence of O₂ uptake during bacteremia in dogs

When systemic deliver of O₂ [Q̇O₂ = cardiac output x arterial O₂ content [(Ca(O₂)] is reduced, the systemic O₂ extraction ratio [(Ca(O₂) - concentration of O₂ in venous blood/Ca(O₂] increases until a critical limit is reached below which O₂ uptake (V̇O₂) becomes limited by delivery. Many patients with adult respiratory distress syndrome exhibit supply dependence of V̇O₂ even at high levels of Q̇O₂, which suggests that a peripheral O₂ extraction defect may be present. Since many of these patients also suffer from serious bacterial infection, we tested the hypothesis that bacteremia might produce a similar defect in the ability of tissues to maintain V̇O₂ independent of Q̇O₂, as Q̇O₂ reduced. The critical O₂ delivery (Q̇O(₂crit)) and critical extraction ratio (ER(crit)) were compared in a control group of dogs and a group receiving a continuous infusion of Pseudomonas aeruginosa (5 x 10⁷ organisms/min). Dogs were anesthetized, paralyzed, and ventilated with room air. Systemic Q̇O₂ was reduced in stages by hemorrhage as hematocrit was maintained. At each stage, systemic V̇O₂ and Q̇O₂ were measured, and the critical point was determined from a plot of V̇O₂ vs. Q̇O₂. The mean Q̇O(₂crit) and ER(crit) of the bacteremic group (11.4 ± 2.2 ml·min^-1·kg^-1 and 0.51 ± 0.09) were significantly different from control (7.4 ± 1.2 and 0.71 ± 0.10) (P < 0.05). These results suggest that bacterial infection can reduce the ability of peripheral tissues to extract O₂ from a limited supply, causing V̇O₂ to become limited by O₂ delivery at a stage when a smaller fraction of the delivered O₂ has been extracted. This effect may be due to a change in microvascular regulation of blood flow, which interferes with an optimal distribution of Q̇O₂ in accordance with tissue O₂ needs.