Heiniger Grégory, Peci Arton, Marchi Nicola Andrea, Solelhac Geoffroy, Imler Théo, Waeber Adrien, Bradley Brian, Lecciso Gianpaolo, Wellman Andrew, Lovis Alban, Monney Pierre, Auberson Denise, Heinzer Raphael
Center for Investigation and Research in Sleep, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.
Division of Sleep and Circadian Disorders, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
J Sleep Res. 2025 Aug;34(4):e14429. doi: 10.1111/jsr.14429. Epub 2024 Dec 1.
Central sleep apneas (CSA) can occur de novo at high-altitude in individuals without sleep-disordered breathing at low altitude. These apneas are usually brief, lasting only 5-15 s. This report presents the first documented case of a man experiencing extreme altitude-induced CSA lasting more than 100 s in the absence of any sleep breathing disorder in normoxia. A 23-year-old male with no pre-existing health conditions was recruited for a study examining the work of breathing during sleep at a simulated altitude of 3500 m (FiO:13%). A lowland polysomnography was first conducted to exclude moderate to severe sleep-disordered breathing and showed an apnea-hypopnea index (AHI) of 7.6/h, an oxygen desaturation index (ODI) of 4.8/h, and a mean pulse oximetry-based oxygen saturation (SpO) of 93.9%. During the recording in the hypoxic chamber, the participant experienced prolonged CSA lasting up to 1 min and 49 s. These apneas were associated with significant oxygen desaturations (nadir: 44%). To investigate the origin of these atypical CSA, the participant underwent a new low-altitude polysomnography with transcutaneous CO measurement (mean PaCO:46 mmHg) and diurnal arterial blood gas analysis (pH: 7.42, pCO: 35.1 mmHg, pO: 79.9 mmHg, HCO : 22.4 mmol/L). These results indicated no signs of chronic hypercapnia or hypocapnia. A hypoxia tolerance test (FiO: 11.5%) demonstrated a good ventilatory response to hypoxia during exercise (1.004 L/min/kg). A rebreathing test according to the Read protocol in hyperoxia demonstrated an impaired ventilatory response to CO (<0.6 L/min/mmHg). This report documents a rare form of extreme hypoxia-induced CSA, potentially caused by impaired CO chemoreceptor sensitivity and an increased arousal threshold.
中枢性睡眠呼吸暂停(CSA)可在高海拔地区新发于低海拔时无睡眠呼吸障碍的个体。这些呼吸暂停通常很短暂,仅持续5 - 15秒。本报告介绍了首例有记录的病例,一名男子在常氧状态下无任何睡眠呼吸障碍,却经历了持续超过100秒的极端海拔诱导的CSA。一名23岁无既往健康问题的男性被招募参加一项研究,该研究在模拟海拔3500米(吸入氧分数:13%)的环境下检查睡眠期间的呼吸功能。首先进行了一次低海拔多导睡眠监测以排除中度至重度睡眠呼吸障碍,结果显示呼吸暂停低通气指数(AHI)为7.6次/小时,氧饱和度下降指数(ODI)为4.8次/小时,基于脉搏血氧饱和度的平均氧饱和度(SpO)为93.9%。在低氧舱记录期间,该参与者经历了长达1分49秒的长时间CSA。这些呼吸暂停与显著的氧饱和度下降相关(最低点:44%)。为了研究这些非典型CSA的起源,该参与者再次进行了低海拔多导睡眠监测,并进行了经皮二氧化碳测量(平均动脉血二氧化碳分压:46 mmHg)和日间动脉血气分析(pH:7.42,动脉血二氧化碳分压:35.1 mmHg,动脉血氧分压:79.9 mmHg,碳酸氢根:22.4 mmol/L)。这些结果表明没有慢性高碳酸血症或低碳酸血症的迹象。低氧耐受试验(吸入氧分数:11.5%)显示运动期间对低氧有良好的通气反应(1.004升/分钟/千克)。在高氧状态下根据里德方案进行的重复呼吸试验显示对二氧化碳的通气反应受损(<0.6升/分钟/毫米汞柱)。本报告记录了一种罕见的极端低氧诱导的CSA形式,可能是由二氧化碳化学感受器敏感性受损和觉醒阈值升高引起的。