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代谢性碱中毒对肺气体交换的影响。

Effects of metabolic alkalosis on pulmonary gas exchange.

作者信息

Brimioulle S, Kahn R J

机构信息

Department of Intensive Care, Erasme University Hospital, Brussels, Belgium.

出版信息

Am Rev Respir Dis. 1990 May;141(5 Pt 1):1185-9. doi: 10.1164/ajrccm/141.5_Pt_1.1185.

DOI:10.1164/ajrccm/141.5_Pt_1.1185
PMID:2339841
Abstract

In order to investigate whether the changes in PaO2 reported during acid-base disturbances are due to modifications of ventilation/perfusion relationships or only to extrapulmonary factors, we studied the hemodynamics and blood gases of eight critically ill patients maintained in constant mechanical ventilation, before and after selective correction of metabolic alkalosis by infusion of 1 N hydrochloric acid (HCl). HCl infusion decreased arterial pH from 7.55 to 7.40 (p less than 0.001) and increased PaO2 from 76 to 98 mm Hg (p less than 0.05) at the end of the study. Cardiac output and oxygen consumption did not change. In patients with initial venous admixture (QS/QT) less than 20% (n = 4), QS/QT did not change, and hemoglobin saturation decreased, whereas PaO2 increased from 87 to 96 mm Hg (p less than 0.10), indicating a shift in the oxyhemoglobin dissociation curve caused by the Bohr effect. In patients with QS/QT greater than 20% (n = 4), QS/QT decreased from 27 to 22% (p less than 0.05), hemoglobin saturation increased from 93 to 96% (p less than 0.05), and PaO2 increased from 65 to 100 mm Hg (p less than 0.05), which reflects an improvement in ventilation/perfusion relationships, probably because of enhanced hypoxic pulmonary vasoconstriction. These data indicate that metabolic alkalosis deteriorates pulmonary ventilation/perfusion relationships in patients with marked respiratory failure (QS/QT greater than 20%), and that reversing this effect with HCl infusion can improve PaO2 significantly.

摘要

为了研究酸碱紊乱期间所报告的动脉血氧分压(PaO₂)变化是由于通气/灌注关系的改变还是仅由肺外因素引起,我们对8例接受持续机械通气的重症患者进行了研究,在通过输注1N盐酸(HCl)选择性纠正代谢性碱中毒之前和之后,观察其血流动力学和血气情况。在研究结束时,输注HCl使动脉pH从7.55降至7.40(p<0.001),PaO₂从76mmHg升至98mmHg(p<0.05)。心输出量和氧耗量未发生变化。初始静脉血掺杂(QS/QT)小于20%的患者(n = 4),QS/QT未改变,血红蛋白饱和度降低,而PaO₂从87mmHg升至96mmHg(p<0.10),这表明由波尔效应引起氧合血红蛋白解离曲线的移位。QS/QT大于20%的患者(n = 4),QS/QT从27%降至22%(p<0.05),血红蛋白饱和度从93%升至96%(p<0.05),且PaO₂从65mmHg升至100mmHg(p<0.05),这反映了通气/灌注关系的改善,可能是由于缺氧性肺血管收缩增强所致。这些数据表明,代谢性碱中毒会使严重呼吸衰竭(QS/QT大于20%)患者的肺通气/灌注关系恶化,而通过输注HCl逆转这种效应可显著提高PaO₂。

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