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允许性高碳酸血症会损害急性呼吸窘迫综合征患者的肺气体交换。

Permissive hypercapnia impairs pulmonary gas exchange in the acute respiratory distress syndrome.

作者信息

Feihl F, Eckert P, Brimioulle S, Jacobs O, Schaller M D, Mélot C, Naeije R

机构信息

Department of Internal Medicine, Lausanne University Hospital, Lausanne, Switzerland.

出版信息

Am J Respir Crit Care Med. 2000 Jul;162(1):209-15. doi: 10.1164/ajrccm.162.1.9907119.

DOI:10.1164/ajrccm.162.1.9907119
PMID:10903243
Abstract

Current recommendations for mechanical ventilation in the acute respiratory distress syndrome (ARDS) include the use of small tidal volumes (VT), even at the cost of respiratory acidosis. We evaluated the effects of this permissive hypercapnia on pulmonary gas exchange with the multiple inert gas elimination technique (MIGET) in eight patients with ARDS. After making baseline measurements, we induced permissive hypercapnia by reducing VT from 10 +/- 2 ml/kg to 6 +/- 1 ml/kg (mean +/- SEM) at constant positive end-expiratory pressure. After restoration of initial VT, we infused dobutamine to increase cardiac output (Q) by the same amount as with hypercapnia. Permissive hypercapnia increased Q by an average of 1.4 L. min(-)(1). m(2), decreased arterial oxygen tension from 109 +/- 10 mm Hg to 92 +/- 11 mm Hg (p < 0.05), markedly increased true shunt (Q S/Q T), from 32 +/- 6% to 48 +/- 5% (p < 0.0001), and had no effect on the dispersion of VA/Q.VA/Q. On reinstatement of baseline V T with maintenance of a high Q, Q S/Q T remained increased, to 38 +/- 6% (p < 0.05), and Pa(O(2 ))remained decreased, to 93 +/- 4 mm Hg (p < 0. 05). These results agreed with effects of changes in VT and Q predicted by the mathematical lung model of the MIGET. We conclude that permissive hypercapnia increases pulmonary shunt, and that deterioration in gas exchange is explained by the combined effects of increased Q and decreased alveolar ventilation.

摘要

目前针对急性呼吸窘迫综合征(ARDS)机械通气的建议包括使用小潮气量(VT),即便以呼吸性酸中毒为代价。我们采用多惰性气体排除技术(MIGET)评估了八例ARDS患者中这种允许性高碳酸血症对肺气体交换的影响。在进行基线测量后,我们通过在呼气末正压恒定的情况下将VT从10±2 ml/kg降至6±1 ml/kg(平均值±标准误)来诱导允许性高碳酸血症。恢复初始VT后,我们输注多巴酚丁胺以使心输出量(Q)增加至与高碳酸血症时相同的量。允许性高碳酸血症使Q平均增加1.4 L·min⁻¹·m⁻²,动脉血氧分压从109±10 mmHg降至92±11 mmHg(p<0.05),真性分流(QS/QT)显著增加,从32±6%增至48±5%(p<0.0001),且对VA/Q的离散度无影响。在维持高Q的情况下恢复基线VT时,QS/QT仍升高至38±6%(p<0.05),动脉血氧分压(PaO₂)仍降低至93±4 mmHg(p<0.05)。这些结果与MIGET数学肺模型预测的VT和Q变化的影响一致。我们得出结论,允许性高碳酸血症会增加肺内分流,气体交换恶化可由Q增加和肺泡通气减少的联合作用来解释。

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