COPD sleep phenotypes: Genesis of respiratory failure in COPD

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.