Medical Service, Sleep Medicine Section, John D. Dingell Veterans Affairs Medical Center , Detroit, Michigan.
Division of Pulmonary/Critical Care and Sleep Medicine, Department of Medicine, Wayne State University School of Medicine , Detroit, Michigan.
J Appl Physiol (1985). 2018 Jan 1;124(1):83-90. doi: 10.1152/japplphysiol.00125.2017. Epub 2017 Oct 12.
The reason for increased sleep-disordered breathing with predominance of central apneas in the elderly is unknown. We hypothesized that the propensity to central apneas is increased in older adults, manifested by a reduced carbon-dioxide (CO) reserve in older compared with young adults during non-rapid eye movement sleep. Ten elderly and 15 young healthy adults underwent multiple brief trials of nasal noninvasive positive pressure ventilation during stable NREM sleep. Cessation of mechanical ventilation (MV) resulted in hypocapnic central apnea or hypopnea. The CO reserve was defined as the difference in end-tidal CO ([Formula: see text]) between eupnea and the apneic threshold, where the apneic threshold was [Formula: see text] that demarcated the central apnea closest to the eupneic [Formula: see text]. For each MV trial, the hypocapnic ventilatory response (controller gain) was measured as the change in minute ventilation (V̇e) during the MV trial for a corresponding change in [Formula: see text]. The eupneic [Formula: see text] was significantly lower in elderly vs. young adults. Compared with young adults, the elderly had a significantly reduced CO reserve (-2.6 ± 0.4 vs. -4.1 ± 0.4 mmHg, P = 0.01) and a higher controller gain (2.3 ± 0.2 vs. 1.4 ± 0.2 l·min·mmHg, P = 0.007), indicating increased chemoresponsiveness in the elderly. Thus elderly adults are more prone to hypocapnic central apneas owing to increased hypocapnic chemoresponsiveness during NREM sleep. NEW & NOTEWORTHY The study describes an original finding where healthy older adults compared with healthy young adults demonstrated increased breathing instability during non-rapid eye movement sleep, as suggested by a smaller carbon dioxide reserve and a higher controller gain. The findings may explain the increased propensity for central apneas in elderly adults during sleep and potentially guide the development of pathophysiology-defined personalized therapies for sleep apnea in the elderly.
老年人睡眠呼吸障碍增多，以中枢性呼吸暂停为主，其原因尚不清楚。我们假设，与年轻人相比，老年人更容易发生中枢性呼吸暂停，表现在非快速动眼睡眠期间，二氧化碳（CO）储备减少。10 名老年健康人和 15 名年轻健康成年人在稳定的非快速动眼睡眠期间接受多次短暂的鼻无创正压通气试验。停止机械通气（MV）会导致低碳酸血症性中枢性呼吸暂停或低通气。CO 储备定义为呼吸末 CO（[Formula: see text]）与呼吸暂停阈值之间的差异，其中呼吸暂停阈值为[Formula: see text]，表示最接近呼吸暂停时的[Formula: see text]。对于每个 MV 试验，通过 MV 试验期间分钟通气量（V̇e）的变化来测量低碳酸血症性通气反应（控制器增益），对应于[Formula: see text]的相应变化。与年轻成年人相比，老年患者的静息[Formula: see text]显著降低。与年轻成年人相比，老年人的 CO 储备显著减少（-2.6±0.4 对-4.1±0.4 mmHg，P=0.01），控制器增益显著增加（2.3±0.2 对 1.4±0.2 l·min·mmHg，P=0.007），表明老年人的化学敏感性增加。因此，老年人在非快速动眼睡眠期间由于低碳酸血症化学敏感性增加而更容易发生低碳酸血症性中枢性呼吸暂停。新发现和值得注意的发现本研究描述了一个原创发现，即与健康年轻人相比，健康老年人在非快速动眼睡眠期间表现出呼吸不稳定增加，这表现在 CO 储备减少和控制器增益增加。这些发现可能解释了老年人在睡眠期间发生中枢性呼吸暂停的倾向增加，并可能为老年人睡眠呼吸暂停的病理生理学定义的个体化治疗提供指导。
