ABSTRACT
Obstructive sleep apnea is a common disorder linked to the increasing prevalence of obesity in Western society, leading to recurrent oxyhemoglobin desaturations and arousals from sleep. Obstructive sleep apnea is caused by episodes of upper airway obstruction during sleep, and has been associated with increased morbidity and mortality [1-4] stemming from neurocognitive [5-8], cardiovascular [9-12], and respiratory dysfunction [13-18]. Upper airway obstruction is largely related to an increased propensity of the upper airway to collapse during sleep through a loss of neuromuscular tone. Sedatives and anesthetic agents can mimic the effects of natural sleep, thus increasing the risk for upper airway obstruction by blunting neuromuscular reflex and arousal responses that restore upper airway patency. This chapter will focus on the clinical and epidemiologic risk factors for upper airway obstruction, the pathophysiology of upper airway obstruction, and its implications for monitoring and treatment.
