The factors implicated in the pathophysiology of OSAS in obese children include soft tissues restricting the upper airway size such as fat pads in the soft palate, lateral pharyngeal wall and at the base of the tongue. However, despite the anatomic evidence predisposing obese children to OSAS there are also alterations in functional mechanisms that lead to increased airway collapsibility predisposing these children to OSAS. Specifically, obesity is associated with significant alterations in body composition that could affect chest wall mechanics by weighting the chest wall and reducing lung compliance. Functional residual capacity is diminished to abdominal visceral fat impinging on the chest cavity. Such a reduction in functional residual capacity and compliance increases the risk for sleep disordered breathing by mechanisms of hypoventilation, atelectasis and ventilation perfusion mismatch all increasing the work of breathing and fatigue. Moreover, hypoventilation in itself may reduce upper airway motor tone. Further, ventilator responses may be altered as studies focusing on obese adults have shown that morbidly obese subjects are more susceptible to decreased ventilatory responses to both hypoxia and hypercapnia.