Systemic oxygen delivery and consumption during acute lung injury in dogs

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 (F_lO₂ = 1.0) and a second group (n = 7) was maintained with PEEP (F_lO₂ = 1.0) after receiving oleic acid. A third group (n = 8) received no oleic acid (F_lO₂ = 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.