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病理生理学对阻塞性睡眠呼吸暂停综合征管理的影响。

Implications of pathophysiology for management of the obstructive sleep apnoea syndrome.

作者信息

McNicholas W T

机构信息

Dept of Respiratory Medicine, St. Vincent's Hospital, Dublin, Ireland.

出版信息

Monaldi Arch Chest Dis. 1998 Oct;53(5):524-9.

PMID:9861812
Abstract

The pathophysiology of obstructive sleep apnoea syndrome (OSAS) is complex and incompletely understood, but is principally based on an imbalance between the collapsing forces of the upper airway (UA) during inspiration and the counteracting dilating forces of the UA dilating muscles. A narrowed UA is very common among OSAS patients, which is usually due, in adults, to nonspecific factors such as fat deposition in the neck or abnormal bony morphology of the UA. Functional impairment of the UA dilating muscles is particularly important in the development of OSAS, and patients have a reduction in both tonic and phasic contraction of these muscles during sleep when compared to normal subjects. Arousal plays an important role in the termination of each apnoea, but may also contribute to the development of further apnoea because of a 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 obstructive sleep apnoea syndrome should help both in the choice of optimum therapy for each individual patient and also in the development of new therapeutic techniques.

摘要

阻塞性睡眠呼吸暂停综合征(OSAS)的病理生理学较为复杂且尚未完全明晰,但其主要基于吸气时上气道(UA)的塌陷力与UA扩张肌的对抗扩张力之间的失衡。UA狭窄在OSAS患者中非常常见,在成人中通常归因于非特异性因素,如颈部脂肪沉积或UA的异常骨骼形态。UA扩张肌的功能损害在OSAS的发展中尤为重要,与正常受试者相比,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。觉醒在每次呼吸暂停的终止中起重要作用,但也可能由于呼吸暂停后过度通气导致的低碳酸血症引起的呼吸驱动力降低而促成进一步呼吸暂停的发生。可能会出现反复阻塞性呼吸暂停的周期性模式。更好地理解阻塞性睡眠呼吸暂停综合征的综合病理生理学,应有助于为每个患者选择最佳治疗方法以及开发新的治疗技术。

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