Objective: To demonstrate that oxygen consumption (VO2) can be dependent on oxygen delivery (DO2) during hemodynamic instability and independent of DO2 following stabilization.
Design: We retrospectively reviewed hemodynamic and blood gas data collected from ten patients in whom DO2 was acutely altered during an episode of septic shock (phase A) and after recovery from this episode (phase B).
Setting: General intensive care unit of a university hospital.
Interventions: DO2 was altered by fluid challenge, administration of vasoactive agents, or application of positive end-expiratory pressure.
Results: In phase A, changes in VO2 (121 ± 32 vs 165 ± 36 ml/min · m2; p<0.001) paralleled changes in DO2 (415 ± 153 vs 607 ± 217 ml/min · m2; p<0.001), but oxygen extraction (O2ER) remained stable (31.9 ± 11.2 vs. 30.2 ± 8.9 %; NS). In phase B, changes in DO2 (412 ± 118 vs 526 ± 152 ml/min · m2; p<0.001) were associated with opposite changes in O2ER (36.1 ± 4.2 vs 28.9 ± 4.9t%; p<0.001), and VO2 was unchanged (147 ± 35 vs 149 ± 33 ml/min · m2; NS). The mean VO2/DO2 slope was greater in phase A than in phase B (0.26 ± 0.09 vs. 0.08 ± 0.08; p<0.004). Blood lactate levels were higher in phase A than in phase B (3.3 ± 1.8 vs 1.6 ±0.6 mEq/l; p<0.05).
Conclusions: Oxygen supply independency and dependency can be found at different times in the same critically ill patient. Our findings are consistent with the concept that VO2/DO2 dependency is a marker of septic shock. Interventions to increase DO2 are probably justified when this phenomenon is present.
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