When oxygen delivery (QO2 = Qt × CaO2) is reduced in healthy animals, oxygen uptake by tissues (VO2) is maintained by an increase in the O2 extraction ratio ((CaO2 - CvO2)/CaO2) until a critical level of delivery QO2C is reached, below which VO2 becomes dependent on QO2. In patients with adult respiratory distress syndrome (ARDS), VO2 becomes dependent on O2 delivery even at high levels of QO2 implying a systemic O2 extraction defect. To determine whether lung injury, or its management with positive end-expiratory pressure (PEEP) and high inspired oxygen fractions (F1O2), might disrupt O2 extraction by peripheral tissues, we compared the critical O2 delivery and extraction ratio in 30 anesthetized and paralyzed dogs in four groups. One group (n = 7) received oleic acid to produce an acute lung injury (FlO2 = 1.0) and a second group (n = 7) was maintained with PEEP (FlO2 = 1.0) after receiving oleic acid. A third group (n = 8) received no oleic acid (FlO2 = 1.0), and a fourth group received no oleic acid and was ventilated with room air. The critical O2 delivery was determined in each animal as QO2 was lowered in a stepwise manner by controlled blood removal. Neither the critical QO2 nor critical O2 extraction ratios were different (P > .05) among oleic acid, PEEP-treated, or hyperoxic control animals. Similarly, the critical QO2 determined from the point at which arterial lactate began to increase showed no difference among groups. Thus, neither acute lung injury produced with oleic acid nor its treatment with PEEP was associated with a peripheral O2 extraction defect. However, a linear regression across all groups demonstrated a positive correlation between the arterial PO2 and corresponding critical O2 delivery (r = < P < .05). These results suggest that high arterial O2 tensions may contribute to an impairment of peripheral O2 extraction.
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine