Xiao Si-Chang, He Bai-Ting, Steier Joerg, Moxham John, Polkey Michael I, Luo Yuan-Ming
State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, China.
Lane Fox Respiratory Unit, Sleep Disorders Centre, Guy's & St Thomas' NHS Foundation Trust, London, UK.
Sleep. 2015 Jun 1;38(6):941-9. doi: 10.5665/sleep.4746.
It has been hypothesized that arousals after apnea and hypopnea events in patients with obstructive sleep apnea are triggered when neural respiratory drive exceeds a certain level, but this hypothesis is based on esophageal pressure data, which are dependent on flow and lung volume. We aimed to determine whether a fixed threshold of respiratory drive is responsible for arousal at the termination of apnea and hypopnea using a flow independent technique (esophageal diaphragm electromyography, EMGdi) in patients with obstructive sleep apnea.
Sleep center of state Key Laboratory of Respiratory Disease.
Seventeen subjects (two women, mean age 53 ± 11 years) with obstructive sleep apnea/hypopnea syndrome were studied.
We recorded esophageal pressure and EMGdi simultaneously during overnight full polysomnography in all the subjects.
A total of 709 hypopnea events and 986 apnea events were analyzed. There was wide variation in both esophageal pressure and EMGdi at the end of both apnea and hypopnea events within a subject and stage 2 sleep. The EMGdi at the end of events that terminated with arousal was similar to those which terminated without arousal for both hypopnea events (27.6% ± 13.9%max vs 29.9% ± 15.9%max, P = ns) and apnea events (22.9% ± 11.5%max vs 22.1% ± 12.6%max, P = ns). The Pes at the end of respiratory events terminated with arousal was also similar to those terminated without arousal. There was a small but significant difference in EMGdi at the end of respiratory events between hypopnea and apnea (25.3% ± 14.2%max vs 21.7% ± 13.2%max, P < 0.05].
Our data do not support the concept that there is threshold of neural respiratory drive that is responsible for arousal in patients with obstructive sleep apnea.
有假说认为，阻塞性睡眠呼吸暂停患者呼吸暂停和呼吸浅慢事件后的觉醒是在神经呼吸驱动超过一定水平时触发的，但该假说基于食管压力数据，而食管压力数据依赖于气流和肺容量。我们旨在使用一种不依赖气流的技术（食管膈肌肌电图，EMGdi）来确定在阻塞性睡眠呼吸暂停患者中，呼吸驱动的固定阈值是否是呼吸暂停和呼吸浅慢终止时觉醒的原因。
呼吸疾病国家重点实验室睡眠中心。
对17名阻塞性睡眠呼吸暂停/低通气综合征患者（2名女性，平均年龄53±11岁）进行了研究。
在所有受试者整夜进行全多导睡眠监测期间，我们同时记录食管压力和EMGdi。
共分析了709次呼吸浅慢事件和986次呼吸暂停事件。在同一受试者的2期睡眠中，呼吸暂停和呼吸浅慢事件结束时，食管压力和EMGdi均存在很大差异。对于呼吸浅慢事件（最大幅度的27.6%±13.9% 对比 29.9%±15.9%，P = 无显著差异）和呼吸暂停事件（最大幅度的22.9%±11.5% 对比 22.1%±12.6%，P = 无显著差异），以觉醒结束的事件末期的EMGdi与未以觉醒结束的事件末期的EMGdi相似。以觉醒结束的呼吸事件末期的食管压力也与未以觉醒结束的呼吸事件末期的食管压力相似。呼吸浅慢和呼吸暂停事件末期的EMGdi存在微小但显著的差异（最大幅度的25.3%±14.2% 对比 21.7%±13.2%，P < 0.05）。
我们的数据不支持在阻塞性睡眠呼吸暂停患者中存在负责觉醒的神经呼吸驱动阈值这一概念。
