Arterial Oxygen Desaturation during Sleep in Children with Asthma and Its Relation to Airway Obstruction and Ventilatory Drive

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Abstract
The possibility that arterial O2 saturation (SaO2) decreases during sleep in children with chronic bronchial asthma was investigated. The relationship between decreases in sleep SaO2 and airflow obstruction and ventilatory drives, as characterized by ventilatory and inspiratory muscle activity responses to hypoxia and hypercapnia, was also examined. Asthmatics, (16) on suboptimal bronchodilator therapy and 10 healthy children were studied. Both maximum decrease in SaO2 and number of desaturations (decrease in SaO2 .gtoreq. 4%) per hour during sleep were greater in the asthmatics than in the control subjects. Both maximum decrease in SaO2 and number of desaturations per hour asleep were correlated with change in FEV1 [1 s forced expiratory volume] and FEF25%-75% [forced expiratory fraction during 25-75% vital capacity] over the sleep period. Changes in SaO2 were unrelated to awake measurements of ventilatory drive. Of the asthmatics, 8 also were studied when on a more optimal medication regimen. On this program they had less airflow obstruction before and after sleep, and the number and extent of decreases in SaO2 did not differ from those of the control subjects. Decreases in SaO2 occurred during sleep in suboptimally-treated asthmatic children. SaO2 changes during sleep were related to the amount of airflow obstruction that developed during sleep. SaO2 changes during sleep were not related to ventilatory drive measured during wakefulness. A good therapeutic regimen eliminated abnormal amounts of sleep hypoxemia by improving airflow limitation. When their pulmonary status is unstable, asthmatic children may develop clinically significant hypoxemia during sleep.