• D W Hudgel, R J Martin, M Capehart, B Johnson, and P Hill.
• J. Appl. Physiol. 1983 Sep 1;55(3):669-77.

AbstractThe purpose of this study was to determine whether hypoventilation contributes to the sleep hypoxemia observed in chronic obstructive pulmonary disease (COPD) patients and to examine breathing pattern and respiratory muscle electromyographic (EMG) activity during these episodes. Seven COPD patients who experienced at least a 10% decrease in arterial O2 saturation (SaO2) during rapid-eye-movement sleep (REM) sleep, six COPD patients with a minimal fall in SaO2, and five healthy subjects were studied. An inductance vest was used to quantitate ventilation. Skin electrodes were used to estimate diaphragmatic and intercostal electromyographic activity. Minute ventilation and EMG activity decreased in all three groups during sleep. Ventilation was irregular during REM sleep in the patients. During REM sleep, desaturating patients had longer episodes of hypopneic breathing [30 +/- 8 s (SE)] than nondesaturating patients (13 +/- 1 s, P less than 0.01). Desaturating patients spent a greater proportion of REM time hypopneic (53 +/- 5 vs. 28 +/- 5%, P less than 0.01) and had a greater decrease in functional residual capacity during hypopnea (P less than 0.05). SaO2 followed the hypopneic and hyperpneic breathing in REM sleep so that desaturating patients had more time for desaturation to occur. Thus hypoventilation appears to be a primary factor in sleep O2 desaturation in these patients. Because of the fall in lung volume, maldistribution of ventilation may also contribute.

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