Mechanism of hemoglobin desaturation during rapid-eye-movement sleep in normal subjects and in patients with cystic fibrosis.
To assess the mechanism of the decrease in hemoglobin O2 saturation during rapid-eye-movement sleep, we studied 5 normal subjects 22 to 30 yr of age and 20 patients with cystic fibrosis 9 to 29 yr of age. The largest decrease in arterial O2 saturation, as monitored with an ear oximeter during sleep, occurred during rapid-eye-movement sleep, with a mean +/- SEM decrease of 2 +/- 0.31% in the normal subjects and 7.4 +/- 1.3% in the patients in both groups. Rapid-eye-movement sleep was associated with a significant loss of intercostal and diaphragmatic tonic muscle activity (p < 0.01), as monitored with surface electrodes, and a decrease in the baseline position of the rib cage and abdomen, as recorded by magnetometers (p < 0.01). This suggests a decrease in functional residual capacity, which was accompanied by a consistently lower arterial O2 saturation during rapid-eye-movement sleep. Short periods (< 20 s) of inhibition of phasic respiratory muscle activity during rapid-eye-movement sleep were followed by further decreases in arterial O2 saturation. We conclude that the desaturation during rapid-eye-movement sleep in all subjects was mainly due to a decrease in functional residual capacity, leading to airway closure in the dependent lung regions. The hemoglobin desaturation was further aggravated by transient periods of hypoventilation.
D000293:Adolescent; D000328:Adult; D002648:Child; D003550:Cystic Fibrosis / Q000097:blood* / Q000503:physiopathology; D003964:Diaphragm / Q000502:physiology / Q000503:physiopathology; D004576:Electromyography; D005260:Female; D006454:Hemoglobins / Q000378:metabolism*; D006801:Humans; D007366:Intercostal Muscles / Q000502:physiology / Q000503:physiopathology; D008297:Male; D010092:Oximetry; D010100:Oxygen / Q000097:blood*; D012890:Sleep / Q000502:physiology; D012895:Sleep, REM / Q000502:physiology*
D006454:Hemoglobins; D010100:Oxygen