The pathogenesis of obstructive sleep apnea.
The pathogenesis of obstructive sleep apnea.
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DOI：
10.3978/j.issn.2072-1439.2015.07.28
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发表时间：
2015-08
影响因子：
2.5
通讯作者：
L. Pham;A. Schwartz
中科院分区：
文献类型：
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作者：
L. Pham;A. Schwartz
阻塞性睡眠呼吸暂停（OSA）是心血管疾病发病率和死亡率的一个主要来源，并且对医疗保健资源造成越来越大的负担。了解 OSA 的潜在致病机制最终将有助于制定合理的治疗策略。在本文中，我们回顾了有关 OSA 发病机制的当前概念。具体来说，我们考虑了上呼吸道在 OSA 发病机制中起主要作用的证据，并提供了一个框架来模拟其生物力学特性和睡眠期间塌陷的倾向。还讨论了调节上气道阻塞的解剖学和神经肌肉因素。最后，我们考虑周期性呼吸模型，并详细阐述上呼吸道阻塞破坏睡眠期间呼吸模式稳定的普遍机制。在我们的模型中，上呼吸道阻塞会引发通气供应和需求之间的不匹配。在此模型中，维持睡眠稳定性或通气之间的权衡可以解释 OSA 疾病的严重程度和表现的全部范围。反复的唤醒和气道通畅性的短暂增加可能会恢复睡眠期间的通气，而神经肌肉和对上气道阻塞的唤醒反应的改变可能会在通气仍处于次优水平的情况下改善睡眠稳定性。
Obstructive sleep apnea (OSA) is a major source of cardiovascular morbidity and mortality, and represents an increasing burden on health care resources. Understanding underlying pathogenic mechanisms of OSA will ultimately allow for the development of rational therapeutic strategies. In this article, we review current concepts about the pathogenesis of OSA. Specifically, we consider the evidence that the upper airway plays a primary role in OSA pathogenesis and provide a framework for modelling its biomechanical properties and propensity to collapse during sleep. Anatomical and neuromuscular factors that modulate upper airway obstruction are also discussed. Finally, we consider models of periodic breathing, and elaborate generalizable mechanisms by which upper airway obstruction destabilizes respiratory patterns during sleep. In our model, upper airway obstruction triggers a mismatch between ventilatory supply and demand. In this model, trade-offs between maintaining sleep stability or ventilation can account for a full range of OSA disease severity and expression. Recurrent arousals and transient increases in airway patency may restore ventilation between periods of sleep, while alterations in neuromuscular and arousal responses to upper airway obstruction may improve sleep stability at still suboptimal levels of ventilation.