Nonapneic mechanisms of arterial oxygen desaturation during rapid-eye-movement sleep

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Abstract
Alveolar hypoventilation and deterioration of gas exchange were proposed as mechanisms causing HbO2 desaturation during rapid-eye-movement (REM) sleep in subjects with chronic obstructive pulmonary disease (COPD). By measuring minute ventilation with a respiratory inductive plethysmograph and simultaneous arterial and mixed venous blood O2 and CO2 contents, the change was observed in minute ventilation, blood respiratory quotient, alveolar O2 tension (PAO2), arterial CO2 and O2 tension (PaCO2 and PaO2, respectively), venous admixture (.ovrhdot.Qva/.ovrhdot.QT), and alveolar-arterial O2 gradient (AaDO2) from non-REM to REM sleep in 6 of 7 COPD subjects. Mean minute ventilation decreased (26%, P < 0.05) as did PaO2 (51-44 Torr, P < 0.001) and PAO2 (81-74 Torr, P < 0.02) during 19 episodes of REM sleep-related desaturations. Mean .ovrhdot.Qva/.ovrhdot.QT increased (0.322-0.472, P < 0.001), while AaDO2 did not change significantly. Although alveolar hypoventilation contributed, deterioration of gas exchange accounted for the largest part of the observed REM hypoxemia. Respiratory effort, estimated from changes in inspiratory pleural pressure, decreased during REM sleep as did arteriovenous O2 content difference (4.7-4.1 ml/ml, P < 0.005). Since thermodilution cardiac output measurements did not change significantly, there is apparently a detectable decrease in O2 utilization by respiratory muscles concomitant with decreased ventilatory effort during REM sleep.