Ventilatory responses during wakefulness in children with obstructive sleep apnea

The pathophysiology of the obstructive sleep apnea syndrome (OSAS) is not fully understood. In children, airway obstruction secondary to tonsilloadenoidal hypertrophy is the leading cause of OSAS. However, not all children with tonsilloadenoidal hypertrophy develop OSAS. Thus, other factors, including abnormalities in ventilatory control, may contribute to the etiology of OSAS. To test this, we performed polysomnography and hypercapnic and hypoxic ventilatory response testing in 20 children and adolescents with OSAS (mean age, 8 ± 3 [SD] yr) and 19 control subjects. Only two children with OSAS were obese. Children with OSAS had an apnea index of 16 ± 20, peak PET(CO₂) of 54 ± 5 mm Hg, and Sa(O₂) nadir of 84 ± 13% during polysomnography. Ventilatory responses were performed by rebreathing techniques. The slope of the hypercapnic ventilatory responses, corrected for body surface area, was 1.74 ± 0.79 L/min/m²/mm Hg PET(CO₂) in children with OSAS and 1.45 ± 0.58 L/min/m²/mm Hg PET(CO₂) in control subjects (NS). Hypoxic ventilatory responses, corrected for body surface area, were - 0.94 ± 0.49 L/min/m²/% Sa(O₂) in children with OSAS and -0.95 ± 0.45 L/min/m²/% Sa(O₂) in control subjects (NS); however, the sample size was small. There was a weak inverse correlation between the slope of the hypercapnic ventilatory response and the duration of hypoventilation during polysomnography (r = -0.44, p < 0.05). We conclude that children with OSAS have normal ventilatory responses to hypercapnia, and they may have normal ventilatory responses to hypoxia. We speculate that abnormal central ventilatory drive plays little if any role in the pathogenesis of pediatric OSAS. Furthermore, we speculate that the diminished ventilatory responses seen in adults with OSAS are acquired secondary to chronic hypoxemia and hypercapnia.