Department of Electrical and Computer Engineering, University of Manitoba, Winnipeg, Manitoba, Canada.
Sleep. 2013 Jun 1;36(6):881-9. doi: 10.5665/sleep.2716.
Heart rate increases after obstructive events in patients with obstructive sleep apnea (OSA). This response is generally attributed to arousal from sleep. Opening of the obstructed airway, however, is associated with ventilatory and hemodynamic changes that could result in physiologic responses unrelated to arousal. Our objective was to determine the contribution of these physiologic responses to postevent tachycardia.
Analysis of data obtained during previous research protocols.
Academic sleep laboratory.
Twenty patients with severe OSA.
Patients were placed on a continuous positive airway pressure (CPAP) device. CPAP was reduced during sleep to different levels (dial-downs), producing obstructive events of varying severity. Some dial-downs with severe obstruction were maintained until spontaneous airway opening. In others, CPAP was increased after three obstructed breaths, terminating the events approximately 10 sec before spontaneous termination in long dial-downs.
Beat-by-beat heart rate (HR) was measured for 20 sec following airway opening. Spontaneous opening during sustained dial-downs occurred 21.9 ± 8.4 sec after dial-down, was associated with arousal, and resulted in the greatest postevent tachycardia (7.8 ± 4.0 min(-1)). However, deliberate termination of events (12.2 ± 2.6 sec after dial-down) was also followed by tachycardia that, in the absence of cortical arousal, showed a dose-response behavior, increasing with severity of obstruction and without apparent threshold. ΔHR following deliberately brief, severe obstruction (3.8 ± 3.0 min(-1)) was approximately half the ΔHR that followed spontaneous opening of equally severe obstructions despite the shorter duration and absence of cortical arousal.
Postevent tachycardia is due in large part to physiologic (arousal-unrelated) responses that occur upon relief of obstruction.
阻塞性睡眠呼吸暂停（OSA）患者在阻塞事件后心率会增加。这种反应通常归因于从睡眠中觉醒。然而，气道阻塞的开放与通气和血液动力学变化相关，这些变化可能导致与觉醒无关的生理反应。我们的目的是确定这些生理反应对事件后心动过速的贡献。
对之前研究方案中获得的数据进行分析。
学术睡眠实验室。
20 名严重 OSA 患者。
患者被放置在持续气道正压通气（CPAP）设备上。在睡眠期间，CPAP 被降低到不同的水平（下调），产生不同严重程度的阻塞事件。一些严重阻塞的下调持续到自发气道开放。在其他情况下，在三次阻塞呼吸后增加 CPAP，在自发终止前约 10 秒终止事件，在长下调中。
在气道开放后 20 秒测量逐拍心率（HR）。在持续下调过程中自发开放发生在下调后 21.9 ± 8.4 秒，与觉醒相关，并导致最大的事件后心动过速（7.8 ± 4.0 min(-1)）。然而，故意终止事件（下调后 12.2 ± 2.6 秒）也会导致心动过速，在没有皮质觉醒的情况下，心动过速呈剂量反应行为，随着阻塞的严重程度增加而增加，且没有明显的阈值。故意短暂、严重阻塞（3.8 ± 3.0 min(-1)）后的 ΔHR 大约是同等严重阻塞的自发开放后的 ΔHR 的一半，尽管持续时间较短且没有皮质觉醒。
事件后心动过速主要是由于阻塞缓解时发生的生理（与觉醒无关）反应引起的。
