Patients with COPD may show slow, progressive deteriorations in arterial blood gases during the night, particularly during rapid eye movement (REM) sleep. This is mainly due to hypoventilation, while a deterioration of ventilation/perfusion mismatch plays a minor role. The severity of gas exchanges alterations is proportional to the degree of impairment of diurnal pulmonary function tests, particularly of partial pressure of oxygen (PaO2) and of carbon dioxide (PaCO2) in arterial blood, but correlations between diurnal and nocturnal blood gas levels are rather loose. Subjects with diurnal PaO2 of 60-70 mmHg are distinguished in "desaturators" and "nondesaturators" according to nocturnal oxyhemoglobin saturation behavior. The role of nocturnal hypoxemia as a determinant of alterations in sleep structure observed in COPD is dubious. Effects of the "desaturator" condition on pulmonary hemodynamics, evolution of diurnal blood gases, and life expectancy are also controversial. Conversely, it is generally accepted that occurrence of sleep apneas in COPD is associated with a worse evolution of the disease. Nocturnal polysomnographic monitoring in COPD is usually performed when coexistence of sleep apnea ("overlap syndrome") is suspected, while in most other cases nocturnal oximetry may be enough. Nocturnal oxygen attenuates sleep desaturations among stable patients, without increases in PaCO2 of clinical concern. Nocturnal treatment with positive pressure ventilators may give benefit to some stable hypercapnic subjects and patients with the overlap syndrome.