Obstructive sleep apnea (OSA) is a serious and chronic condition affecting as many as 15–20 million American adults. Resulting sleep deprivation has been linked to motor vehicle and workplace accidents. The incidence of OSA is increasing with the obesity epidemic, and it is increasingly recognized as a mediator of cardiovascular disease including atrial fibrillation, stroke, myocardial infarction, and sudden cardiac death. The importance of appropriate diagnosis and timely treatment thus cannot be overstated.

Obstructive sleep apnea manifests by repeated episodes of apnea or hypopnea during sleep. During deeper levels of sleep, especially that characterized by rapid eye movement (REM), there is loss of the normal tone of the pharyngeal and tongue muscles that keep the pharynx open, resulting in collapse of the oropharyngeal and nasopharyngeal airway. In the majority of the population this decrease in airway diameter is clinically insignificant. However, in OSA patients the varied degree of airway obstruction can have clinical consequences. Narrowing of the airway causes increased velocity of inspiratory airflow in the pharynx, causing decreased intraluminal pressure, further tissue collapse, and increased airway obstruction (Bernoulli's principle). In instances of complete airway obstruction, the patient will experience apnea, a cessation of breathing for at least 10 seconds. Incomplete obstruction may result in hypopnea, a reduction in airflow with associated oxygen desaturation, which is more common. Each apnea or hypopnea episode continues until the patient awakens to a more shallow level of sleep, which results in a recovery of pharyngeal muscle tone and recovery of airway integrity. The more frequent the apnea and hypopnea, the more fragmented the sleep, which results in greater sleep deprivation due to the lack of adequate REM activity.