Although occasional apneas and hypopneas during sleep may be normal, prolonged exposure to frequent apneas and hypopneas results in clinical problems that define the OSA syndrome. The clinical sequelae in OSA (
Fig. 67-3) are related to periodic nocturnal asphyxia and sleep disruption.
Excessive daytime sleepiness and related sequelae stem from chronically disrupted sleep patterns and possibly nocturnal asphyxia. Apneas and hypopneas are frequently terminated by brief arousals less than 15 seconds in duration. Patients are usually unaware of these events, despite markedly disrupted sleep architecture. In severe cases, patients never achieve sustained or deep sleep and experience the symptoms of chronic sleep disruption, which include depression, personality changes, cognitive impairment, decreased vigilance, and irresistible sleepiness (see
Fig. 67-3). These problems can compromise the individual’s quality of life, family relations, job performance, and safety. Public safety is also of concern. For example, OSA patients have a higher rate of motor vehicle accidents.
see Fig. 67-3) are related to repeated episodes of asphyxia and to fluctuations in intrathoracic pressure and autonomic activity during obstructed breaths. Sustained pulmonary and systemic hypertension and biventricular dysfunction may eventually develop. Several recent studies suggest that a strong causal relationship exists between OSA and systemic hypertension. OSA patients may be at increased risk for malignant cardiac arrhythmias. Sinus and atrial arrhythmias, atrioventricular blocks, and ventricular arrhythmias occur primarily during apneic spells. It is not known how often apnea-related cardiac arrhythmias are life threatening. The incidence of cerebrovascular accidents and myocardial infarction are reportedly increased in OSA patients. One retrospective study reported a higher mortality in OSA patients with more severe sleep-disordered breathing. In that study, effective treatment appeared to have a positive influence on cumulative survival rates. Large population studies of OSA morbidity and mortality, however, are not available.
Revision date: June 21, 2011
Last revised: by Jorge P. Ribeiro, MD