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慢性阻塞性肺疾病患者氧疗时高碳酸血症的原因。

Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease.

作者信息

Hanson C W, Marshall B E, Frasch H F, Marshall C

机构信息

Department of Anesthesia, Hospital of the University of Pennsylvania, Philadelphia 19104, USA.

出版信息

Crit Care Med. 1996 Jan;24(1):23-8. doi: 10.1097/00003246-199601000-00007.

Abstract

OBJECTIVES

To compare data derived from a computer model of the pulmonary circulation with data from a case series of patients with chronic obstructive pulmonary disease (COPD). To evaluate the specific factors contributing to CO2 retention due to oxygen therapy in patients with acute exacerbations of COPD.

DESIGN

Data from a computer model of the pulmonary circulation were compared with a previous case series.

PATIENTS

Patient data were derived from previous case series.

INTERVENTIONS

Simulated application of oxygen therapy.

MEASUREMENTS AND MAIN RESULTS

The computer model of the pulmonary circulation generates data comparable with those data from a series of patients with COPD treated with supplemental oxygen and permits identification of the causes for hypercarbia. Therapy with supplemental oxygen alters hypoxic pulmonary vasoconstriction and modulates the Haldane effect, resulting in changes in physiologic deadspace.

CONCLUSION

Changes in physiologic deadspace are sufficient to account for the hypercarbia developed by patients with acute exacerbations of COPD when treated with supplemental oxygen.

摘要

目的

比较来自肺循环计算机模型的数据与慢性阻塞性肺疾病(COPD)患者病例系列的数据。评估导致COPD急性加重患者因氧疗而出现二氧化碳潴留的具体因素。

设计

将肺循环计算机模型的数据与先前的病例系列进行比较。

患者

患者数据来自先前的病例系列。

干预措施

模拟氧疗应用。

测量与主要结果

肺循环计算机模型生成的数据与一系列接受补充氧气治疗的COPD患者的数据具有可比性,并能够确定高碳酸血症的原因。补充氧气治疗会改变低氧性肺血管收缩并调节哈氏效应,从而导致生理死腔发生变化。

结论

生理死腔的变化足以解释COPD急性加重患者接受补充氧气治疗时出现的高碳酸血症。

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