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阻塞性睡眠呼吸暂停的病理生理学

Pathophysiology of obstructive sleep apnoea.

作者信息

Deegan P C, McNicholas W T

机构信息

Dept of Respiratory Medicine, University College, Dublin, Ireland.

出版信息

Eur Respir J. 1995 Jul;8(7):1161-78. doi: 10.1183/09031936.95.08071161.

DOI:10.1183/09031936.95.08071161
PMID:7589402
Abstract

The pathophysiology of obstructive sleep apnoea (OSA) is complex and incompletely understood. A narrowed upper airway is very common among OSA patients, and is usually in adults due to nonspecific factors such as fat deposition in the neck, or abnormal bony morphology of the upper airway. Functional impairment of the upper airway dilating muscles is particularly important in the development of OSA, and patients have a reduction both in tonic and phasic contraction of these muscles during sleep when compared to normals. A variety of defective respiratory control mechanisms are found in OSA, including impaired chemical drive, defective inspiratory load responses, and abnormal upper airway protective reflexes. These defects may play an important role in the abnormal upper airway muscle responses found among patients with OSA. Local upper airway reflexes mediated by surface receptors sensitive to intrapharyngeal pressure changes appear to be important in this respect. Arousal plays an important role in the termination of each apnoea, but may also contribute to the development of further apnoea, because of reduction in respiratory drive related to the hypocapnia which results from postapnoeic hyperventilation. A cyclical pattern of repetitive obstructive apnoeas may result. A better understanding of the integrated pathophysiology of OSA should help in the development of new therapeutic techniques.

摘要

阻塞性睡眠呼吸暂停(OSA)的病理生理学很复杂,尚未完全明确。上气道狭窄在OSA患者中非常常见,在成人中通常是由非特异性因素引起的,如颈部脂肪堆积或上气道骨骼形态异常。上气道扩张肌的功能障碍在OSA的发病过程中尤为重要,与正常人相比,患者在睡眠期间这些肌肉的紧张性和相位性收缩均有所减少。在OSA中发现了多种有缺陷的呼吸控制机制,包括化学驱动受损、吸气负荷反应缺陷和上气道保护反射异常。这些缺陷可能在OSA患者中发现的上气道肌肉异常反应中起重要作用。由对咽内压力变化敏感的表面受体介导的局部上气道反射在这方面似乎很重要。觉醒在每次呼吸暂停的终止中起重要作用,但也可能导致进一步的呼吸暂停,因为呼吸暂停后过度通气导致的低碳酸血症会使呼吸驱动力降低。可能会出现反复阻塞性呼吸暂停的周期性模式。更好地理解OSA的综合病理生理学应该有助于开发新的治疗技术。

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