Abstract Mkid 52

The pathophysiology of obstructive sleep apnoea (OSAS) is principally based on an imbalance of the collapsing forces of the upper airway (UA) during inspiration and the counteracting dilating forces of the UA dilating muscles. A narrowed UA is very common among OSAS patients, which is usually due in an adult to non-specific factors such as fat deposition in the neck, or abnormal bony morphology of the UA. Functional impairment of the UA dilating muscles is particularly important in the development of OSA, and patients have a reduction in both tonic and phasic contraction of these muscles during sleep when compared to normals. A variety of defective respiratory control mechanisms are found in OSA, including impaired chemical drive, defective inspiratory load responses, and abnormal UA protective reflexes. These defects may play an important role in the abnormal UA muscle responses found among patients with OSA. Local UA reflexes mediated by surface receptors sensitive to intrapharyngeal pressure changes appear to be important in this respect. A better understanding of the integrated pathophysiology of OSAS should help both in the choice of optimum therapy for each individual patient, and also in the development of new therapeutic techniques.