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Effects of obstructive sleep apnea on autonomic cardiac control during sleep.

机译:阻塞性睡眠呼吸暂停对睡眠期间自主性心脏控制的影响。

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INTRODUCTION: The present study investigated whether autonomic control of the heart for persons with low and high levels of sleep apnea/hypopnea differed between sleep stages and across the sleep period. DISCUSSION: Electrocardiography and impedance cardiography of 24 patients referred to polysomnography were recorded through the night. A mixed repeated-measures and between-subjects, quasi-experimental design was utilized. Heart period, high frequency heart rate variability, and pre-ejection period were computed, respectively, as measure of heart rate and estimates of parasympathetic and sympathetic control. The cardiac and autonomic measures for participants with low apnea-hypopnea indices were compared to those of patients with high rates of apnea-hypopnea across the sleep period and sleep stages. Cardiac rates of the two groups decreased incrementally through the sleep period. Cardiovascular measures during sleep from the group with high rates of apnea-hypopnea indicated larger parasympathetic activation in relation to wake baseline for epochs without arousals than from the group with low apnea-hypopnea rates. Parasympathetic activation during nonrapid-eye movement (non-REM) sleep (sleep stage 2) was significantly greater than during REM sleep. Higher levels of apnea-hypopnea seem to be associated with increased parasympathetic control, especially during lighter, non-REM sleep. A possible explanation for this phenomenon is a compensatory response to oxygen desaturation caused by disturbed breathing.
机译:引言:本研究调查了睡眠阶段低和高水平睡眠呼吸暂停/呼吸不足的人的心脏自主控制在睡眠阶段之间和整个睡眠期间是否有所不同。讨论:夜间记录了多导睡眠图检查的24例患者的心电图和阻抗心电图。采用了混合重复测量和受试者之间的准实验设计。计算心率,高频心率变异性和射血前时间,作为心率的度量以及副交感和交感控制的估计。将呼吸暂停低通气指数低的参与者的心脏和自主神经测量值与整个睡眠期和睡眠阶段呼吸暂停低通气率高的患者的心脏和自主性指标进行了比较。两组的心率在睡眠期间逐渐降低。呼吸暂停低通气发生率高的组在睡眠期间的心血管测量结果表明,与无呼吸暂停低通气发生率的组相比,无唤醒时期相对于唤醒基线的副交感神经激活更大。非快速眼动(non-REM)睡眠(第2阶段睡眠)期间的副交感神经激活明显大于REM睡眠期间的副交感神经激活。呼吸暂停低通气水平升高似乎与副交感神经控制的增强有关,尤其是在较轻的非快速眼动睡眠期间。对此现象的可能解释是对呼吸不畅引起的氧饱和度的补偿性反应。

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