Neuroscience Research Australia (NeuRA), Sydney NSW, Australia.
School of Medical Sciences, University of New South Wales, Sydney NSW, Australia.
Sleep. 2018 Nov 1;41(11). doi: 10.1093/sleep/zsy160.
A negative intrathoracic pressure threshold is one commonly proposed mechanism for triggering respiratory-induced arousals in obstructive sleep apnea (OSA). If so, they should occur during inspiration, shortly after maximal negative pressure swings. Alternatively, respiratory-induced arousals may occur throughout the respiratory cycle if other mechanisms also contribute. However, arousal timing has been minimally investigated. This study aimed to (1) determine the temporal relationship between respiratory-induced arousals and breathing phase and (2) characterize neuromuscular and load compensation responses prior to arousal.
Fifty-one CPAP-treated OSA patients underwent a sleep physiology study with genioglossus and tensor palatini EMG, nasal mask/pneumotachograph, and epiglottic pressure. Transient CPAP reductions were delivered to induce respiratory-related arousals.
Of 354 arousals, 65(60-70)%[mean(CI)] occurred during inspiration, 35(30-40)% during expiration. Nadir epiglottic pressure occurred 68(66-69)% into inspiration while inspiratory arousals had a uniform distribution throughout inspiration. Expiratory arousals occurred predominantly in early expiration. CPAP reductions initially reduced minute ventilation by ~2.5 liter/min, which was restored immediately prior to expiratory but not inspiratory arousals. Duty cycle just prior to arousal was greater for inspiratory versus expiratory arousals [0.20(0.18-0.21) vs. 0.13(0.11-0.15)Δbaseline, p = 0.001]. Peak tensor palatini EMG was higher for expiratory versus inspiratory arousals during prearousal breaths [7.6(5.8-9.6) vs. 3.7(3.0-4.5)%Δbaseline, p = 0.001], whereas genioglossus and tonic tensor palatini EMG were similar between arousal types.
Over one third of respiratory-induced arousals occur during expiration. These findings highlight the importance of nonpressure threshold mechanisms of respiratory-induced arousals in OSA and suggest that expiratory arousals may be a novel marker of enhanced tensor palatini neuromuscular compensation.
胸腔内负压阈是阻塞性睡眠呼吸暂停（OSA）中触发呼吸相关觉醒的一个常用机制。如果是这样，它们应该发生在吸气过程中，最大负压波动后不久。或者，如果其他机制也有贡献，呼吸相关觉醒可能发生在整个呼吸周期中。然而，觉醒时间的研究很少。本研究旨在：（1）确定呼吸相关觉醒与呼吸相之间的时间关系；（2）在觉醒前描述神经肌肉和负荷补偿反应。
51 例 CPAP 治疗的 OSA 患者接受了一项睡眠生理研究，包括颏舌肌和腭帆提肌肌电图、鼻罩/气动计和会厌压。短暂的 CPAP 降低被用来诱发呼吸相关的觉醒。
在 354 次觉醒中，65%（60-70%）[平均值（CI）]发生在吸气期，35%（30-40%）发生在呼气期。吸气末会厌压发生在吸气的 68%（66-69%）时，而吸气性觉醒在整个吸气过程中均匀分布。呼气性觉醒主要发生在呼气早期。CPAP 降低最初使分钟通气量减少约 2.5 升/分钟，这在呼气前即刻得到恢复，但在吸气性觉醒时则没有。在觉醒前，呼吸周期比呼气性觉醒更大[0.20（0.18-0.21）比 0.13（0.11-0.15）Δ基线，p = 0.001]。在觉醒前呼吸中，与吸气性觉醒相比，呼气性觉醒的腭帆提肌肌电图峰值更高[7.6（5.8-9.6）比 3.7（3.0-4.5）%Δ基线，p = 0.001]，而颏舌肌和腭帆提肌的紧张性肌电图在觉醒类型之间相似。
超过三分之一的呼吸相关觉醒发生在呼气期。这些发现强调了 OSA 中呼吸相关觉醒的非压力阈值机制的重要性，并表明呼气性觉醒可能是腭帆提肌神经肌肉补偿增强的一个新标志物。
