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.
ASJC Scopus subject areas
- Physiology (medical)