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不同猪肺损伤模型中的通气-灌注分布

Ventilation-perfusion distributions in different porcine lung injury models.

作者信息

Neumann P, Hedenstierna G

机构信息

Department of Clinical Physiology, University of Uppsala, Sweden.

出版信息

Acta Anaesthesiol Scand. 2001 Jan;45(1):78-86. doi: 10.1034/j.1399-6576.2001.450113.x.

Abstract

BACKGROUND

Acute lung injury is characterized by hypoxemia which may be caused by hypoventilation, ventilation-perfusion (V(A)/Q) mismatch, intrapulmonary shunting and oxygen diffusion impairment. The multiple inert gas elimination technique (MIGET) allows analysis of these four causes of hypoxemia and is therefore the most comprehensive approach to investigate blood gas abnormalities. Using MIGET, we studied whether specific patterns of gas exchange abnormalities occur in different lung injury models and whether gas exchange abnormalities can be related to pathogenic aspects of lung injury.

METHODS

Lung injury was induced with oleic acid injection, endotoxin infusion or repeated lung lavage in groups of 6 mechanically ventilated pigs.

RESULTS

PaO2 decreased and PaCO2 increased significantly in all three lung injury models, but gas exchange was more impaired in the oleic acid and lavage, as compared to the endotoxin group. Shunt was the major cause of hypoxemia in our lung injury models, whereas V(A)/Q mismatch contributed to venous admixture only after oleic acid injection and lung lavage. Oxygen diffusion limitation was not observed. Although alveolar ventilation was maintained after induction of lung injury, hypercapnia developed due to an increase of the ventilatory mean towards higher V(A)/Q ratios, increased shunt and increased carbon dioxide production.

CONCLUSIONS

Shunt and ventilation-perfusion mismatch fully explain the gas exchange disturbances observed in our lung injury models. Although V(A)/Q distributions can be related to pathogenic aspects of the three study groups, we did not observe specific V(A)/Q patterns which allow diagnosis of the type of lung injury from a recovered V(A)/Q distribution.

摘要

背景

急性肺损伤的特征为低氧血症,其可能由通气不足、通气/灌注(V(A)/Q)不匹配、肺内分流及氧弥散障碍所致。多惰性气体清除技术(MIGET)可分析低氧血症的这四种病因,因此是研究血气异常最全面的方法。我们使用MIGET研究了不同肺损伤模型中是否会出现特定的气体交换异常模式,以及气体交换异常是否与肺损伤的致病因素有关。

方法

对6组机械通气猪分别注射油酸、输注内毒素或反复进行肺灌洗以诱导肺损伤。

结果

在所有三种肺损伤模型中,动脉血氧分压(PaO2)均显著降低,动脉血二氧化碳分压(PaCO2)均显著升高,但与内毒素组相比,油酸组和肺灌洗组的气体交换受损更严重。分流是我们肺损伤模型中低氧血症的主要原因,而V(A)/Q不匹配仅在注射油酸和肺灌洗后导致静脉血掺杂。未观察到氧弥散受限。虽然肺损伤诱导后维持了肺泡通气,但由于通气均值向更高的V(A)/Q比值增加、分流增加和二氧化碳产生增加,出现了高碳酸血症。

结论

分流和通气/灌注不匹配充分解释了我们肺损伤模型中观察到的气体交换紊乱。虽然V(A)/Q分布可能与三个研究组的致病因素有关,但我们未观察到能从恢复的V(A)/Q分布诊断肺损伤类型的特定V(A)/Q模式。

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