In OSA patients, upper airway obstruction during sleep occurs in the pharynx behind the soft palate or tongue base. We do not fully understand why OSA patients experience frequent pharyngeal occlusion during sleep, whereas nonapneic individuals do not. OSA patients may have abnormalities in upper airway structure, nonstructural factors, or respiratory control mechanisms. For example, obstructive apneas and hypopneas may result from normal sleep-induced changes in the muscular control of pharyngeal patency in individuals with a small or excessively collapsible pharynx.

Small pharyngeal lumens have been demonstrated in OSA patients by several imaging techniques, although few well-controlled studies are available. Some OSA patients do have abnormal upper airway structure on physical examination. Nasal obstruction, large tonsils and adenoids, an elongated soft palate, micrognathia, and macroglossia have all been associated with OSA. These anatomic abnormalities result in airway narrowing, requiring greater effort to achieve adequate airflow. Collapse occurs when the fall in intraluminal pressure exceeds the dilating muscle forces. Surgical correction of these structural problems can improve OSA. However, visual inspection does not reveal specific upper airway abnormalities in many OSA patients.

Obesity may predispose to apnea via many mechanisms, which could include altered tissue compliance and muscle function from fatty infiltration, elastic loading by fatty tissue around the upper airway, and metabolic and endocrine changes that might affect upper airway mechanics during sleep.

The OSA syndrome involves the events illustrated in

Fig. 67-2. With the initial onset of sleep, the pharynx collapses and airflow decreases despite continued efforts to breathe. Hypoventilation causes progressive asphyxia, which stimulates breathing efforts. However, the airway often remains occluded until arousal occurs. With arousal, there is a surge in upper airway muscle activity, the upper airway opens, and airflow is restored. Hyperventilation in response to the accumulated hypercapnia and hypoxia initially follows restoration of airway patency. The subsequent hyperventilation-induced hypocapnia, along with sleep onset, is followed by a decrease in upper airway muscle activity and recurrent pharyngeal collapse. This sequence can occur hundreds of times a night in patients with severe OSA.