VENTILATORY RESPONSES DURING WAKEFULNESS IN CHILDREN WITH OBSTRUCTIVESLEEP-APNEA

The pathophysiology of the obstructive sleep apnea syndrome (OSAS) is not fully understood. In children, airway obstruction secondary to ton silloadenoidal hypertrophy is the leading cause of OSAS. However, not all children with tonsilloadenoidal hypertrophy develop OSAS, Thus, ot her factors, including abnormalities in ventilatory control, may contr ibute to the etiology of OSAS. To test this, we performed polysomnogra phy and hypercapnic and hypoxic ventilatory response testing in 20 chi ldren and adolescents with OSAS (mean age, 8 +/- 3 [SD] yr) and 19 con trol subjects. Only two children with OSAS were obese. Children with O SAS 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 res ponses were performed by rebreathing techniques. The slope of the hype rcapnic ventilatory responses, corrected for body surface area, was 1. 74 +/- 0.79 L/min/m(2)/mm Hg PET(CO2) in children with OSAS and 1.45 /- 0.58 L/min/m(2)/mm Hg PET(CO2) in control subjects (NS). Hypoxic ve ntilatory responses, corrected for body surface area, were -0.94 +/- 0 .49 L/min/m(2)/% Sa(O2) in children with OSAS and -0.95 +/- 0.45 L/min /m(2)/% Sa(O2) in control subjects (NS); however, the sample size was small. There was a weak inverse correlation between the slope of the h ypercapnic ventilatory response and the duration of hypoventilation du ring polysomnography (r = -0.44, p < 0.05). We conclude that children with OSAS have normal ventilatory responses to hypercapnia, and they m ay have normal ventilatory responses to hypoxia. We speculate that abn ormal central ventilatory drive plays little if any role in the pathog enesis of pediatric OSAS. Furthermore, we speculate that the diminishe d ventilatory responses seen in adults with OSAS are acquired secondar y to chronic hypoxemia and hypercapnia.