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慢性高碳酸血症呼吸衰竭的病理生理学。

Pathophysiology of Chronic Hypercapnic Respiratory Failure.

机构信息

Charles Sturt University, 346 Leeds Parade, Orange, NSW 2800, Australia; Department of Medicine, Orange Health Service, Orange, NSW 2800, Australia; University of Sydney, Camperdown, NSW 2006, Australia.

Department of Respiratory & Sleep Medicine, Royal Prince Alfred Hospital, Camperdown, NSW 2050, Australia.

出版信息

Sleep Med Clin. 2024 Sep;19(3):379-389. doi: 10.1016/j.jsmc.2024.04.001. Epub 2024 May 28.

Abstract

Chronic hypercapnic respiratory failure occurs in several conditions associated with hypoventilation. The mechanisms underlying the development of chronic hypercapnia include a combination of processes that increase metabolic CO production, reduce minute ventilation (V'e), or increase dead space fraction (Vd/Vt). Fundamental to the pathophysiology is a mismatch between increased load and a reduction in the capacity of the respiratory pump to compensate. Though neural respiratory drive may be decreased in a subset of central hypoventilation disorders, it is more commonly increased in attempting to maintain the load-capacity homeostatic balance.

摘要

慢性高碳酸血症性呼吸衰竭发生于多种与通气不足相关的疾病中。慢性高碳酸血症发生的机制包括一系列增加代谢性 CO2 生成、减少分钟通气量(V'e)或增加死腔量(Vd/Vt)的过程。病理生理学的基础是增加的负荷与呼吸泵代偿能力降低之间的不匹配。虽然在部分中枢性通气不足疾病中神经呼吸驱动可能降低,但为了维持负荷-容量的内稳态平衡,它通常会增加。

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