Department of Otorhinolaryngology, Teikyo University Chiba Medical Center, 3426-3 Anesaki, Ichihara, Chiba 299-0111, Japan.
Auris Nasus Larynx. 2022 Jun;49(3):313-321. doi: 10.1016/j.anl.2021.10.007. Epub 2021 Nov 9.
The pathogenesis of obstructive sleep apnea (OSA) is characterized not only by obstruction of the pharynx, but also by repeated obstruction. OSA onset is thought to involve four phenotypic traits: pharyngeal muscle responsiveness, respiratory center instability (loop gain), arousal threshold, and anatomical factors. Patients with lower muscle responsiveness are likely to have OSA, whereas those with higher responsiveness are not. When the loop gain is relatively high, reaction and suppression of the respiratory drive are repeated, decreasing ventilation and pharyngeal muscle activity and leading to mixed or central apnea events. Patients with a low arousal threshold tend to have frequent respiratory events and less severe respiratory efforts, whereas those with a high arousal threshold tend to have fewer respiratory events and more severe respiratory efforts. Pharyngeal muscle activity, as well as respiratory drive, increases during apnea and decreases after its release. Patients with a low arousal threshold have lower muscle responsiveness and instability of the respiratory center control, whereas those with a high arousal threshold have higher muscle responsiveness and relatively stable respiratory control. The overshoot and undershoot responses of the chemical drive and pharyngeal muscle tone characterize the periodic repetition of obstructive events, which are enhanced by the arousal response. The presence of certain anatomical factors is prerequisite for the onset of OSA. Also, not only volume and flow, but also stiffness and elasticity may contribute to the pathogenesis of OSA. Mouth breathing also plays an important role in the mechanism of pharyngeal collapse. These four factors influence each other, with the first three-muscle responsiveness, loop gain, and arousal threshold-in particular in a trinity. The era is already close in which not only anatomical treatment, but also treatments for other traits can be selected and combined according to the individual pathophysiological condition of each patient with OSA.
阻塞性睡眠呼吸暂停（OSA）的发病机制不仅表现为咽部阻塞，还表现为反复阻塞。OSA 的发病机制被认为涉及四个表型特征：咽部肌肉反应性、呼吸中枢不稳定性（环路增益）、觉醒阈值和解剖因素。肌肉反应性较低的患者可能患有 OSA，而肌肉反应性较高的患者则不会。当环路增益相对较高时，呼吸驱动的反应和抑制会反复发生，从而降低通气和咽部肌肉活动，导致混合性或中枢性呼吸暂停事件。觉醒阈值较低的患者往往会出现频繁的呼吸事件和较轻的呼吸努力，而觉醒阈值较高的患者则往往会出现较少的呼吸事件和更严重的呼吸努力。在呼吸暂停期间，咽部肌肉活动和呼吸驱动增加，在呼吸暂停释放后减少。觉醒阈值较低的患者肌肉反应性较低，呼吸中枢控制不稳定，而觉醒阈值较高的患者肌肉反应性较高，呼吸控制相对稳定。化学驱动和咽部肌肉张力的超调与欠调反应特征是阻塞性事件的周期性重复，这种重复会被觉醒反应增强。某些解剖因素的存在是 OSA 发病的前提条件。此外，不仅体积和流量，而且刚度和弹性也可能有助于 OSA 的发病机制。口呼吸在咽部塌陷的机制中也起着重要作用。这四个因素相互影响，其中前三个因素——肌肉反应性、环路增益和觉醒阈值——尤其在一个三联体中相互作用。现在已经接近这样一个时代，不仅可以根据每个 OSA 患者的个体病理生理状况进行解剖治疗，还可以选择和组合针对其他特征的治疗方法。
