Coexistence of OSA may compensate for sleep related reduction in neural respiratory drive in patients with COPD.

He, Bai-Ting; Lu, Gan; Xiao, Si-Chang; Chen, Rui; Steier, Joerg; Moxham, John; Polkey, Michael I; Luo, Yuan-Ming · Thorax · 2017

cross_sectional · Level IV

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Abstract

The mechanisms underlying sleep-related hypoventilation in patients with coexisting COPD and obstructive sleep apnoea (OSA), an overlap syndrome, are incompletely understood. We compared neural respiratory drive expressed as diaphragm electromyogram (EMG<sub>di</sub>) and ventilation during stage 2 sleep in patients with COPD alone and patients with overlap syndrome. EMG<sub>di</sub> and airflow were recorded during full polysomnography in 14 healthy subjects, 14 patients with OSA and 39 consecutive patients with COPD. The ratio of tidal volume to EMG<sub>di</sub> was measured to indirectly assess upper airway resistance. Thirty-five patients with COPD, 12 healthy subjects and 14 patients with OSA completed the study. Of 35 patients with COPD, 19 had COPD alone (FEV<sub>1</sub> 38.5%±16.3%) whereas 16 had an overlap syndrome (FEV<sub>1</sub> 47.5±16.2%, AHI 20.5±14.1 events/hour). Ventilation (V<sub>E</sub>) was lower during stage 2 sleep than wakefulness in both patients with COPD alone (8.6±2.0 to 6.5±1.5 L/min, p<0.001) and those with overlap syndrome (8.3±2.0 to 6.1±1.8 L/min). Neural respiratory drive from wakefulness to sleep decreased significantly for patients with COPD alone (29.5±13.3% to 23.0±8.9% of maximal, p<0.01) but it changed little in those with overlap syndrome. The ratio of tidal volume to EMG<sub>di</sub> was unchanged from wakefulness to sleep in patients with COPD alone and healthy subjects but was significantly reduced in patients with OSA or overlap syndrome (p<0.05). Stage 2 sleep-related hypoventilation in COPD alone is due to reduction of neural respiratory drive, but in overlap syndrome it is due to increased upper airway resistance.

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