Search

Seven patients with chronic obstructive lung disease (COLD) were monitored during their overnight sleep to determine the occurrence of disordered breathing and oxygen desaturation. Nasal and oral airflows were sensed by thermistor probes, chest wall movement by impedance pneumography and arterial oxygen saturation by ear oximetry. These variables were correlated with electroencephalographic and electrooculographic tracings. The subjects had a mean base line oxygen saturation of 89.2 per cent and slept an average of 218 minutes. Six of these seven subjects had one to 30 episodes of oxygen desaturation (decrease more than 4 per cent), 4 seconds to 30 minutes in duration, with declines in saturation as great as 36 per cent. In two subjects, saturation dropped to less than 50 per cent. Breathing was disordered in five of the seven subjects and included apnea and hypopnea. Subjects experienced from nine to 37 episodes of disordered breathing. Disordered breathing caused 42 per cent of the episodes of desaturation, all of which were less than 1 minute in duration. The mean maximum decline in saturation was 7.6 per cent. All episodes of desaturation lasting longer than 5 minutes occurred in rapid eye movement (REM) sleep and were not caused by disordered breathing. The mean maximal decrease in saturation was 22 per cent. This study reveals that disordered breathing is common in subjects with COLD and often causes desaturation but that it cannot explain all episodes of sleep desaturation.

Twenty-one postmenopausal women were monitored for sleep-disordered breathing and nocturnal oxygen desaturation to evaluate the contribution of progestational hormones to the occurrence of these sleep events. For approximately one month 11 subjects received 30 mg of medroxyprogesterone (MPG) daily, and 10 received placebo tablets in a randomized, double-blind controlled study. Respiration, saturation and electroencephalography were monitored during one night of sleep before and one night after therapy. Contrasted with the low incidence of disordered breathing and desaturation in premenopausal women, 71 percent of the postmenopausal women had such events. In the placebo-treated group, all measured variables of sleep and breathing were identical on the two nights, which suggested that the findings of a single night of sleep monitoring may be representative of other nights of sleep. Although several subjects appeared to show improvement with MPG, only the maximum duration of apnea was significantly reduced the second night (p less than 0.03).

Twenty postmenopausal women were monitored for disordered breathing (apnea and hypopnea) and oxygen desaturation during one night's sleep. These women were compared with 18 premenopausal women previously reported to have a low incidence of sleep-disordered breathing and nocturnal oxygen desaturation. Twelve of the 20 postmenopausal women had 102 episodes of sleep-disordered breathing and 118 episodes of oxygen desaturation, compared with only six episodes of apnea in two premenopausal women (P less than 0.01). Premenopausal women did not become desaturated. Of the postmenopausal women, 11 became desaturated; and in five of them saturation decreased to less than 85 per cent. Duration of sleep, and increased age and weight: height ratios, correlated significantly with the incidence of desaturation (P less than 0.01--P less than 0.05). Postmenopausal women resemble men with respect to disordered breathing during sleep and nocturnal oxygen desaturation. Protection from these sleep events in premenopausal women might be afforded by the respiratory stimulant effects of circulating progesterone.

Using standard sleep techniques, we performed a placebo-controlled and randomized study to assess the effect of alcohol ingestion (2 ml/kg of body weight) on breathing and oxygen saturation during sleep. Twenty asymptomatic men volunteered for the two-night study: 11 were given a placebo on night 1, and alcohol on night 2 (group A); nine were given alcohol on night 1 and a placebo on night 2 (group B). We compared the incidence of sleep events (apnea, hypopnea and arterial oxygen disaturation) during the nights the subjects received alcohol and during the nights they received the placebo. Alcohol was associated with significant increases in the occurrence of the following: the number of sleep events (207 to 383,p less than 0.01), the events of arterial oxygen disaturation (118 to 226, p less than 0.01) and the number of apneic events (20 to 110, p less than 0.01). Alcohol had no significant effects on the number of times hypopnea occurred. Values obtained during sleep on the control night after alcohol ingestion also showed that the episodes of arterial oxygen desaturation remained statistically increased over control values before the ingestion of any alcohol (p = 0.01). These results show that in asymptomatic men alcohol ingestion increases the incidence of arterial oxygen desaturation and disordered breathing during sleep and that the increase in arterial oxygen desaturation persists for an additional night, even when no alcohol is consumed.