Sleep arterial oxygen desaturation and chemical control of breathing during wakefulness in COPD.
Recent studies have demonstrated that oxygen desaturation occurs during sleep in some patients with chronic obstructive pulmonary disease (COPD). The degree of sleep hypoventilation in COPD may be related to an inadequate chemical control of ventilation. To investigate this relationship, we compared maximal sleep changes in arterial oxygen saturation (SaO2) with the hypercapnic and hypoxic ventilatory control during wakefulness in 24 patients with COPD. Both hypercapnic and hypoxic ventilatory responses were inversely correlated with the degree of maximal sleep desaturation in rapid-eye-movement (REM) sleep. Furthermore, the level of baseline SaO2 during wakefulness was also negatively related to the magnitude of sleep desaturation. Patients with insufficient chemical control of breathing appear to have larger falls in SaO2, particularly if they have lower baseline SaO2.
D000328:Adult; D000368:Aged; D005260:Female; D006801:Humans; D006935:Hypercapnia / Q000097:blood / Q000503:physiopathology; D007040:Hypoventilation / Q000097:blood / Q000503:physiopathology; D000860:Hypoxia / Q000097:blood / Q000503:physiopathology; D008173:Lung Diseases, Obstructive / Q000097:blood* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood*; D012119:Respiration; D012129:Respiratory Function Tests; D012890:Sleep / Q000502:physiology*; D014851:Wakefulness / Q000502:physiology*
D010100:Oxygen