Department of Pulmonary Medicine, ESI Hospital Basai Darpur, New Delhi.
Monaldi Arch Chest Dis. 2021 Nov 4;92(2). doi: 10.4081/monaldi.2021.1776.
The chronic obstructive pulmonary disease (COPD) patients could have respiratory failure during sleep without daytime overt arterial blood gas (ABG) abnormality. We undertook a study first of its kind to attempt in distinguishing the underlying pathophysiological mechanisms. It was a prospective observational study in stable COPD patients. The inclusion criterion was presence of day time PaO2>60 mmHg and PaCO2<45 mmHg. Twenty five out of 110 patients were excluded because of the ABG abnormality. The remaining 85 patients were subjected to overnight pulse oximetry and end-tidal (ET)-CO2 monitoring. The nocturnal oxygen desaturation was defined as per Fletcher's criteria. The nocturnal hypoventilation was defined as per American academy of sleep medicine (AASM) guidelines. Patients having saw-tooth pattern on pulse oximetry and/or snoring were subjected to polysomnography. 38/85(44.8%) patients had nocturnal gas exchange abnormality in absence of daytime respiratory failure and were identified into 3 different phenotypes: obstructive sleep apnoea (OSA), nocturnal hypoventilation and nocturnal oxygen desaturation. The isolated abnormality was seen in 24 patients: 10 patients had OSA, 9 had nocturnal hypoventilation and 5 had nocturnal oxygen desaturation. Overlap of two or more phenotypes was seen in 14 patients. As compared to the nocturnal hypoventilation and desaturation phenotypes, the OSA phenotype had a significantly higher BMI & FEV1. The nocturnal hypoventilation and the desaturation phenotypes did not have significant difference in FEV1 and BMI, but the daytime SpO2 and PaO2 differed significantly. Such parameters could help in identifying the three distinct COPD-sleep phenotypes (OSA, nocturnal hypoventilation and nocturnal oxygen desaturation). A phenotype based nocturnal management may help in delaying the process of overt respiratory failure in COPD.
慢性阻塞性肺疾病（COPD）患者在睡眠期间可能会发生呼吸衰竭，而白天动脉血气（ABG）并无异常。我们进行了一项首例此类研究，旨在尝试区分潜在的病理生理机制。这是一项在稳定期 COPD 患者中进行的前瞻性观察性研究。纳入标准为白天 PaO2>60mmHg 和 PaCO2<45mmHg。由于 ABG 异常，110 例患者中有 25 例被排除在外。其余 85 例患者接受了夜间脉搏血氧饱和度和呼气末（ET）-CO2 监测。夜间氧饱和度下降根据 Fletcher 标准定义。夜间通气不足根据美国睡眠医学学会（AASM）指南定义。脉搏血氧饱和度呈锯齿状模式和/或打鼾的患者进行多导睡眠图检查。38/85（44.8%）例患者在白天无呼吸衰竭的情况下存在夜间气体交换异常，并被分为 3 种不同表型：阻塞性睡眠呼吸暂停（OSA）、夜间通气不足和夜间低氧血症。24 例患者存在孤立性异常：10 例患者存在 OSA，9 例患者存在夜间通气不足，5 例患者存在夜间低氧血症。14 例患者存在两种或多种表型重叠。与夜间通气不足和低氧血症表型相比，OSA 表型的 BMI 和 FEV1 显著更高。夜间通气不足和低氧血症表型的 FEV1 和 BMI 无显著差异，但日间 SpO2 和 PaO2 有显著差异。这些参数有助于识别 COPD 的三种不同睡眠表型（OSA、夜间通气不足和夜间低氧血症）。基于表型的夜间管理可能有助于延缓 COPD 中显性呼吸衰竭的进程。
