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COPD and obstructive sleep apnoea (OSA), two highly prevalent disorders,1 are both associated with substantial sleep-related hypoventilation.2 Sleep-related hypoventilation in these patients is of greater magnitude than that recorded in healthy subjects. These observations raise the possibility that patients concurrently affected by COPD and OSA, also known as overlap syndrome, may develop worse sleep-related hypoventilation than patients with COPD or OSA alone. When sufficiently severe, sleep-related hypoventilation can reset the chemoreceptor threshold with resultant daytime hypercapnia.3 This (hypothetical) chain of events could explain why, despite less severe airway obstruction, the prevalence of daytime hypercapnia in patients with overlap syndrome is greater than that in patients with COPD4 or OSA alone.5 More profound hypercapnia and nocturnal hypoxaemia might also explain the reported increase in mortality in overlap syndrome compared with COPD.6
He et al7 advance our understanding of the mechanisms of sleep-related hypoventilation in overlap syndrome. Specifically, and for the first time, the investigators compare the neural respiratory drive and ventilation during non-rapid eye movement (NREM) sleep in overlap syndrome against drive and ventilation in COPD alone, OSA alone and in healthy subjects. Neural respiratory drive was quantified as the amplitude of the diaphragm electromyogram signal (EMGdi) recorded with oesophageal electrodes.8 To assess upper airway resistance, the investigators computed the ratio of tidal volume to EMGdi.9
As expected, minute ventilation during sleep decreased in all participants: 10% in healthy subjects, 24% in COPD, 21% in OSA and ‘only’ 27% in patients with overlap syndrome. This lack of synergy between COPD and OSA in worsening sleep hypoventilation resulted from the unique response …
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