Transient hypoxemia during sleep in chronic obstructive pulmonary disease is not a sleep apnea syndrome.

We measured ear oxygen saturation (SaO2), chest wall movement, and oronasal air flow, and took electroencephalographic tracings during nocturnal sleep in 20 healthy subjects and 20 similarly aged patients with chronic obstructive pulmonary disease (COPD), none of whom was obese. Thirteen of the patients with COPD were persistently hypoxemic and hypercapnic when awake ("blue and bloated", Type B); the remaining 7 maintained relatively normal arterial gas tensions when awake despite equally severe airways obstruction ("pink and puffing", Type A). Hypoxemic episodes (HE) (SaO2 falls of greater than 10%) occurred during sleep in all the blue bloaters but in only 3 of 7 pink puffers and 3 of 20 normal subjects. However, the maximal change in arterial oxygen tension (PaO2) (calculated from SaO2 values assuming normal pH) was similar in all 3 groups, averaging 24 mmHg. Furthermore, the cumulative duration of apnea and hypopnea was the same in each group. Only one patient COPD had more than 2 apneas per night, and obstructive apnea was seen only in the healthy subjects. Sleep apnea syndromes thus appear to be rare in nonobese patients with COPD. Of the 40 HE in patients with COPD, 29 occurred during periods of hypoventilation. In 10 blue bloaters whose arterial blood was sampled during sleep, the measured fall in PaO2 during the HE (mean, 11.2 mmHg) was greater than the rise in PaCO2 (mean, 4.2 mmHg). Although these changes in arterial gas tensions could be produced by an increase in ventilation-perfusion imbalance during the HE, it is suggested that unsteady-state gas exchange during transient hypoventilation could provide an alternative explanation.