Arousal-Induced Hypocapnia Does Not Reduce Genioglossus Activity in Obstructive Sleep Apnea

Arousal-Induced Hypocapnia Does Not Reduce Genioglossus Activity in Obstructive Sleep Apnea
复制标题

DOI:
10.1093/sleep/zsx057
复制
发表时间:
2017-06-01
期刊:
影响因子:
5.6
通讯作者:
Jordan, Amy S.
Jordan, Amy S.
中科院分区:
医学2区
文献类型:
--
作者:
Cori, Jennifer M.;Thornton, Therese;Jordan, Amy S.

文献摘要

被引文献

相似文献

研究目的:确定终止阻塞性睡眠呼吸暂停 (OSA) 中阻塞性事件的唤醒是否 (1) 引起低碳酸血症,以及 (2) 随后在恢复睡眠后减少颏舌肌活动。方法:31 名未经治疗的 OSA 患者在睡眠时配备睡眠分期电极、鼻罩和呼吸速度描记器、呼气末 CO2 监测和肌肉注射。 颏舌肌电极。监测呼气末 CO2,并为呼吸唤醒分配一个唤醒末 CO2 变化值(最后一次唤醒呼吸时的 PET CO2 减去每个人的清醒时 PET CO2)。该变化值与正常睡眠相关的 PET CO2 增加相结合,用于确定觉醒是否会引起低碳酸血症,以及觉醒末 CO2 变化是否与恢复睡眠后呼吸时的颏舌肌活动相关。 结果:24 名参与者提供了 1137 次可用的觉醒。平均 +/- SD 唤醒末期 CO2 变化为 -0.2 +/- 2.4 mm Hg(低于清醒状态),表明低碳酸血症通常在唤醒期间发生。恢复睡眠后,颏舌肌活动并未降至觉醒前水平以下,并且在前两次呼吸中有所升高。唤醒末期 CO2 变化和颏舌肌活动呈负相关,即末期唤醒 CO2 减少 1 mm Hg 与恢复睡眠后呼吸时峰值和强直颏舌肌活动增加 2% 类似。 结论:唤醒引起的低碳酸血症不会导致恢复睡眠后扩张肌活动减少,因此低碳酸血症可能不会导致进一步的扩张。 通过这种机制的障碍。觉醒后扩张肌活动升高可能是由非 CO2 相关刺激驱动的。
Study Objectives: To determine whether arousals that terminate obstructive events in obstructive sleep apnea (OSA) (1) induce hypocapnia and (2) subsequently reduce genioglossus muscle activity following the return to sleep.Methods: Thirty-one untreated patients with OSA slept instrumented with sleep staging electrodes, nasal mask and pneumotachograph, end-tidal CO2 monitoring, and intramuscular genioglossus electrodes. End-tidal CO2 was monitored, and respiratory arousals were assigned an end-arousal CO2 change value (PET CO2 on the last arousal breath minus each individual's wakefulness PET CO2). This change value, in conjunction with the normal sleep related increase in PET CO2, was used to determine whether arousals induced hypocapnia and whether the end-arousal CO2 change was associated with genioglossus muscle activity on the breaths following the return to sleep.Results: Twenty-four participants provided 1137 usable arousals. Mean +/- SD end-arousal CO2 change was -0.2 +/- 2.4 mm Hg (below wakefulness) indicating hypocapnia typically developed during arousal. Following the return to sleep, genioglossus muscle activity did not fall below prearousal levels and was elevated for the first two breaths. End-arousal CO2 change and genioglossus muscle activity were negatively associated such that a 1 mm Hg decrease in end-arousal CO2 was associated with an similar to 2% increase in peak and tonic genioglossus muscle activity on the breaths following the return to sleep.Conclusions: Arousal-induced hypocapnia did not result in reduced dilator muscle activity following return to sleep, and thus hypocapnia may not contribute to further obstructions via this mechanism. Elevated dilator muscle activity postarousal is likely driven by non-CO2-related stimuli.