Biomechanics of the upper S. M. Susarla 1, R. J. Thomas2,

://Obstructive sleep apnea (OSA) is a well-recognized disorder that affects at least 4 % of the population in the USA36,99. It is characterized by repetitive collapse of the upper airway, commonly defined as the soft tissue region bounded by the nasopharynx superiorly, the epiglottis inferiorly, the maxillomandibular com-plex anteriorly and the spinal column pos-teriorly. Collapse of the upper airway decreases its intra-luminal diameter and increases airway resistance, in accordance with Pouiseille’s Law (Fig. 1). This increased resistance to flow results in reductions in ventilation (hypopneas) or complete cessation of ventilation (apneas), with corresponding metabolic disturbances (respiratory acidosis due to hypoventilation) and sleep fragmentation. Compensation for metabolic disturbances occurs primarily in the form of alterations in respiratory effort, which is the primary determinant of arousals from sleep. While brief transitions to the wake state provide ventilator compensation to correct blood gas abnormalities, this comes at the cost of further destabilizing respiratory control at the sleep–wake interface. Concomitant activation of the sympathetic nervous sys-tem results in increases in blood pressure, which, over the long term, have been linke to increased risk for sudden death, stroke and myocardial infarction5,12,19,49,58,59,95. Sleep-event related arousals produce fragmentation of sleep patterns, resulting in excessive daytime somnolence, neu-rocognitive impairment and increased risk for accidents related to sleep deprivation36,38,61,98