A simplified method for determining phenotypic traits in patients with obstructive sleep apnea
A simplified method for determining phenotypic traits in patients with obstructive sleep apnea
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DOI：
10.1152/japplphysiol.00747.2012
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发表时间：
2013-04-01
影响因子：
3.3
通讯作者：
White, David P.
中科院分区：
文献类型：
--
作者：
Wellman, Andrew;Edwards, Bradley A.;White, David P.
阻塞性睡眠呼吸暂停综合征患者表型特征的简易测定方法J Appl Physiol 114：911-922，2013.首次发表于2013年1月24日; doi：10.1152/japplphysiol.00747.2012.-我们以前发表了一种方法，用于测量导致阻塞性睡眠呼吸暂停（OSA）的几个生理特征。然而，该方法的成功率相对较低（76%），并且需要数学建模，这可能限制了其应用。本文提出了一个实质性的修订，该技术。为了进行测量，在睡眠期间操纵持续气道正压通气（CPAP），以量化1）正常呼吸的通气需求，2）微觉醒开始发生时的通气水平，3）当咽部肌肉在睡眠期间被激活时关闭CPAP通气（鼻压= 0 cmH（2）O），以及4）当咽部肌肉相对被动时关闭CPAP通气。这些特征可以在所有13名参与者中确定（100%成功率）。个体在觉醒前能够耐受的通气量减少（通气#1和#2之间的差异范围为0.7至2.9升/分钟）和个体能够产生的代偿量（通气#3和#4之间的差异范围为-0.5至5.5升/分钟）存在显著的受试者间差异。重要的是，这些测量准确地反映了临床指标;通气#2和#3之间的差异，即必须克服以实现睡眠期间稳定呼吸的差距的测量，与呼吸暂停低通气指数相关（r = 0.9，P < 0.001）。该技术增加了一个额外的程序来测量回路增益（呼吸控制系统的灵敏度），这也允许量化唤醒阈值和上气道增益（上气道对增加呼吸驱动的反应）。值得注意的是，当在5个个体中的第二个晚上测量时，这些特征通常是可重复的。这项技术是一种相对简单的方法来定义潜在的OSA机制，并可能在临床环境中使用的个性化治疗。
A simplified method for determining phenotypic traits in patients with obstructive sleep apnea. J Appl Physiol 114: 911-922, 2013. First published January 24, 2013; doi:10.1152/japplphysiol.00747.2012.-We previously published a method for measuring several physiological traits causing obstructive sleep apnea (OSA). The method, however, had a relatively low success rate (76%) and required mathematical modeling, potentially limiting its application. This paper presents a substantial revision of that technique. To make the measurements, continuous positive airway pressure (CPAP) was manipulated during sleep to quantify 1) eupneic ventilatory demand, 2) the level of ventilation at which arousals begin to occur, 3) ventilation off CPAP (nasal pressure = 0 cmH(2)O) when the pharyngeal muscles are activated during sleep, and 4) ventilation off CPAP when the pharyngeal muscles are relatively passive. These traits could be determined in all 13 participants (100% success rate). There was substantial intersubject variability in the reduction in ventilation that individuals could tolerate before having arousals (difference between ventilations #1 and #2 ranged from 0.7 to 2.9 liters/min) and in the amount of ventilatory compensation that individuals could generate (difference between ventilations #3 and #4 ranged from -0.5 to 5.5 liters/min). Importantly, the measurements accurately reflected clinical metrics; the difference between ventilations #2 and #3, a measure of the gap that must be overcome to achieve stable breathing during sleep, correlated with the apnea-hypopnea index (r = 0.9, P < 0.001). An additional procedure was added to the technique to measure loop gain (sensitivity of the ventilatory control system), which allowed arousal threshold and upper airway gain (response of the upper airway to increasing ventilatory drive) to be quantified as well. Of note, the traits were generally repeatable when measured on a second night in 5 individuals. This technique is a relatively simple way of defining mechanisms underlying OSA and could potentially be used in a clinical setting to individualize therapy.