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低海拔地区慢性阻塞性肺疾病患者在海拔 2590 米处的夜间脑组织氧合作用:一项随机试验的数据。

Nocturnal cerebral tissue oxygenation in lowlanders with chronic obstructive pulmonary disease travelling to an altitude of 2,590 m: Data from a randomised trial.

机构信息

Pulmonary Division and Sleep Disorders Center, University Hospital of Zurich, Zurich, Switzerland.

出版信息

J Sleep Res. 2021 Dec;30(6):e13365. doi: 10.1111/jsr.13365. Epub 2021 Apr 26.

Abstract

Altitude exposure induces hypoxaemia in patients with chronic obstructive pulmonary disease (COPD), particularly during sleep. The present study tested the hypothesis in patients with COPD staying overnight at high altitude that nocturnal arterial hypoxaemia is associated with impaired cerebral tissue oxygenation (CTO). A total of 35 patients with moderate-to-severe COPD, living at <800 m (mean [SD] age 62.4 [12.3] years, forced expiratory volume in 1 s [FEV ] 61 [16]% predicted, awake pulse oximetry ≥92%) underwent continuous overnight monitoring of pulse oximetry (oxygen saturation [SpO ]) and near-infrared spectroscopy of prefrontal CTO, respectively, at 490 m and 2,590 m. Regression analysis was used to evaluate whether nocturnal arterial desaturation (COPD , SpO <90% for >30% of night-time) at 490 m predicted CTO at 2,590 m when controlling for baseline variables. At 2,590 m, mean nocturnal SpO and CTO were decreased versus 490 m, mean change -8.8% (95% confidence interval [CI] -10.0 to -7.6) and -3.6% (95% CI -5.7 to -1.6), difference in change ΔCTO-ΔSpO 5.2% (95% CI 3.0 to 7.3; p < .001). Moreover, frequent cyclic desaturations (≥4% dips/hr) occurred in SpO and CTO, mean change from 490 m 35.3/hr (95% CI 24.9 to 45.7) and 3.4/hr (95% CI 1.4 to 5.3), difference in change ΔCTO-ΔSpO -32.8/hr (95% CI -43.8 to -21.8; p < .001). Regression analysis confirmed an association of COPD with lower CTO at 2,590 m (coefficient -7.6%, 95% CI -13.2 to -2.0; p = .007) when controlling for several confounders. We conclude that lowlanders with COPD staying overnight at 2,590 m experience altitude-induced hypoxaemia and periodic breathing in association with sustained and intermittent cerebral deoxygenation. Although less pronounced than the arterial deoxygenation, the altitude-induced cerebral tissue deoxygenation may represent a risk of brain dysfunction, especially in patients with COPD with nocturnal hypoxaemia at low altitude.

摘要

海拔暴露会导致慢性阻塞性肺疾病(COPD)患者缺氧,尤其是在睡眠期间。本研究在夜间在高海拔地区过夜的 COPD 患者中测试了这一假说,即夜间动脉缺氧与脑组织氧合受损(CTO)有关。共有 35 名中重度 COPD 患者(居住在<800m 处,平均[SD]年龄 62.4[12.3]岁,1 秒用力呼气量[FEV]占预计值的 61[16]%,清醒脉搏血氧饱和度[SpO]≥92%)分别在 490m 和 2590m 处进行了过夜连续脉搏血氧监测(氧饱和度[SpO])和前额叶 CTO 的近红外光谱监测。回归分析用于评估 490m 时夜间动脉血氧饱和度下降(COPD,夜间 SpO<90%的时间>30%)是否在控制基线变量后预测 2590m 时的 CTO。在 2590m 处,与 490m 相比,夜间平均 SpO 和 CTO 下降,平均变化-8.8%(95%置信区间[CI] -10.0 至-7.6)和-3.6%(95% CI -5.7 至-1.6),变化差异 ΔCTO-ΔSpO 为 5.2%(95% CI 3.0 至 7.3;p<.001)。此外,SpO 和 CTO 中频繁出现周期性血氧饱和度下降(≥4%下降/小时),从 490m 处的平均变化为 35.3/hr(95% CI 24.9 至 45.7)和 3.4/hr(95% CI 1.4 至 5.3),变化差异 ΔCTO-ΔSpO 为-32.8/hr(95% CI -43.8 至-21.8;p<.001)。回归分析证实,当控制多个混杂因素时,COPD 与 2590m 处较低的 CTO 存在关联(系数为-7.6%,95% CI -13.2 至-2.0;p=0.007)。我们得出结论,在 2590m 处过夜的低地 COPD 患者会经历海拔引起的缺氧和周期性呼吸,与持续和间歇性脑缺氧有关。虽然不如动脉缺氧明显,但海拔引起的脑组织缺氧可能代表大脑功能障碍的风险,尤其是在夜间低海拔缺氧的 COPD 患者中。

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