Obstructive sleep apnea is a multisystemic disorder with pathologic sequelae that become apparent after a number of years. Patients with obstructive sleep apnea generally present with hypersomnolence, and diagnosis is eventually established through observation of the patient during sleep. Patients with obstructive sleep apnea snore loudly and experience nocturnal oxygen desaturation and repetitive disruptions from sleep that eventually lead to daytime hypersomnolence. Numerous complex interactive pathophysiologic events occur during each obstructive episode, and it is important for the clinician to be aware of the cardiopulmonary, neurologic, and anatomic abnormalities associated with this condition. The anatomic configuration of the pharynx and the physiologic response to occlusion of the upper airway have a major role in the pathogenesis of this disorder. Alveolar ventilation during an apneic episode is immediately reduced to zero, and the metabolic demands for oxygen must be met by oxygen stores within the body. With repetitive episodes of obstruction, the oxygen stores within the lungs are diminished and the rate of arterial oxyhemoglobin desaturation increases. During apneic episodes, the systemic blood pressure increases while heart rate and cardiac output decrease. Bradydysrhythmias have been noted with the obstructive apneic episodes, and ventricular dysrhythmias are associated with episodes of severe oxyhemoglobin desaturation. Coexisting cardiopulmonary or neuromuscular disease in patients with obstructive sleep apnea contributes to the development of hypoventilation, serious gas exchange derangement, and general cardiovascular instability.