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高氧导致的氧消耗可逆性降低。

Reversible decrease of oxygen consumption by hyperoxia.

作者信息

Reinhart K, Bloos F, König F, Bredle D, Hannemann L

机构信息

Department of Anesthesiology and Intensive Care Medicine, Free University of Berlin, Germany.

出版信息

Chest. 1991 Mar;99(3):690-4. doi: 10.1378/chest.99.3.690.

Abstract

The hemodynamic and metabolic effects of 90 minutes normobaric hyperoxia were studied in 20 critically ill patients (11 septic, 9 nonseptic) requiring mechanical ventilation with inspired O2 fraction (FIO2) less than 0.40. Thirty minutes after increasing the FIO2 to 1.0, arterial PO2 had increased from about 100 to about 400 mm Hg, and whole body oxygen uptake (VO2) was decreased 10 percent (p less than 0.05) due to an 18 percent decrease in O2 extraction ratio. During the subsequent 60 minutes of hyperoxia, there was no further significant change in VO2. Cardiac index did not change in hyperoxia, but it increased 10 percent (p less than 0.05) in recovery as systemic vascular resistance decreased. VO2 returned to baseline after 30 minutes recovery at original FIO2 due to increased O2 extraction as well as the increased cardiac output. The decrease in VO2 without a decrease in O2 delivery may reflect maldistribution of blood flow and functional O2 shunting to protect tissue from unphysiologically high PO2. While brief oxygenation is advisable before periods of hypoventilation, the present data suggest that hyperoxic ventilation in these patients with already adequate O2 delivery was counterproductive.

摘要

对20例需要机械通气且吸入氧分数(FIO2)低于0.40的危重症患者(11例脓毒症患者,9例非脓毒症患者)研究了90分钟常压高氧的血流动力学和代谢效应。将FIO2提高到1.0后30分钟,动脉血氧分压从约100 mmHg升至约400 mmHg,全身氧摄取量(VO2)下降了10%(p<0.05),这是由于氧摄取率下降了18%。在随后的60分钟高氧期间,VO2没有进一步显著变化。高氧期间心脏指数未改变,但恢复过程中随着全身血管阻力下降心脏指数增加了10%(p<0.05)。由于氧摄取增加以及心输出量增加,在以原始FIO2恢复30分钟后VO2恢复至基线水平。VO2下降而氧输送未下降可能反映了血流分布不均和功能性氧分流,以保护组织免受非生理性高氧分压的影响。虽然在通气不足期间进行短暂氧合是可取的,但目前的数据表明,在这些氧输送已充足的患者中进行高氧通气会适得其反。

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