A primary characteristic of obstructive sleep apnea (OSA) is chronic exposure to intermittent hypoxia (IH) due to repeated upper airway obstruction. Chronic IH exposure is believed to increase OSA severity over time by enhancing the acute ventilatory response to hypoxia (AHVR), thus promoting ventilatory overshoot when apnea ends and perpetuation of apnea during sleep. Continuous positive airway pressure (CPAP), the gold-standard treatment of OSA, reduces the AHVR, believed to result from correction of IH. However, CPAP also corrects ancillary features of OSA such as intermittent hypercapnia, negative intrathoracic pressure and surges in sympathetic activity, which may also contribute to the reduction in AHVR. Therefore, the objective of this study was to investigate the impact of nocturnal oxygen therapy (to remove IH only) and CPAP (to correct IH and ancillary features of OSA) on AHVR in newly diagnosed OSA patients. Fifty-two OSA patients and twenty-two controls were recruited. The AHVR was assessed using a 5 min iscopanic-hypoxic challenge before, and after, treatment of OSA by nocturnal oxygen therapy and CPAP. Following baseline measurements, OSA patients were randomly assigned to nocturnal oxygen therapy (Oxygen, n = 26) or no treatment (Air; n = 26). The AHVR was re-assessed following two weeks of oxygen therapy or no treatment, after which all patients were treated with CPAP. The AHVR was quantified following ~4 weeks of adherent CPAP therapy (n = 40). Both nocturnal oxygen and CPAP treatments improved hypoxemia (p < 0.05), and, as expected, nocturnal oxygen therapy did not completely abolish respiratory events (i.e., apneas/hypopneas). Averaged across all OSA patients, nocturnal oxygen therapy did not change AHVR from baseline to post-oxygen therapy. Similarly, the AHVR was not altered pre- and post-CPAP (p > 0.05). However, there was a significant decrease in AHVR with both nocturnal oxygen therapy and CPAP in patients in the highest OSA severity quartile (p < 0.05). Nocturnal oxygen therapy and CPAP both reduce the AHVR in patients with the most severe OSA. Therefore, IH appears to be the primary mechanism producing ventilatory instability in patients with severe OSA via enhancement of the AHVR.

阻塞性睡眠呼吸暂停 (OSA) 的一个主要特征是由于反复上呼吸道阻塞而长期暴露于间歇性缺氧 (IH)。人们认为，慢性 IH 暴露会随着时间的推移增强对缺氧的急性通气反应 (AHVR)，从而增加 OSA 的严重程度，从而在呼吸暂停结束时促进通气过度并在睡眠期间持续呼吸暂停。持续气道正压通气 (CPAP) 是 OSA 的金标准治疗方法，可降低 AHVR，据信是 IH 矫正的结果。然而，CPAP 还可以纠正 OSA 的辅助特征，例如间歇性高碳酸血症、胸内负压和交感神经活动激增，这也可能有助于降低 AHVR。所以，本研究的目的是调查夜间氧疗（仅去除 IH）和 CPAP（纠正 IH 和 OSA 的辅助特征）对新诊断 OSA 患者 AHVR 的影响。招募了 52 名 OSA 患者和 22 名对照者。在通过夜间氧疗和 CPAP 治疗 OSA 之前和之后，使用 5 分钟等浓度低氧刺激评估 AHVR。在基线测量后，OSA 患者被随机分配接受夜间氧气治疗（氧气、n  = 26）或不处理（空气；n  = 26）。在氧疗或不治疗两周后重新评估 AHVR，之后所有患者均接受 CPAP 治疗。在持续约 4 周的 CPAP 治疗后对 AHVR 进行量化（n  = 40）。夜间吸氧和 CPAP 治疗都改善了低氧血症（p  < 0.05），并且正如预期的那样，夜间吸氧并没有完全消除呼吸事件（即呼吸暂停/呼吸不足）。平均所有 OSA 患者，夜间氧疗没有改变 AHVR 从基线到氧疗后。同样，在 CPAP 前后，AHVR 没有改变（p > 0.05）。然而，在 OSA 严重程度最高的四分位数患者中，夜间氧疗和 CPAP 均显着降低了 AHVR（p  < 0.05）。夜间氧疗和 CPAP 均可降低最严重 OSA 患者的 AHVR。因此，IH 似乎是通过增强 AHVR导致重度 OSA 患者呼吸不稳定的主要机制。