Defined as the lack of breathing through the nose and mouth for at least ten seconds, sleep apnea can be obstructive or central or mixed. Obstructive sleep apnea (OSA) occurs when tissues in the throat collapse and block airflow in the lungs during sleep, although efforts to breathe continue. This is manifest as inspiratory snoring. Central apnea occurs when the brain fails to send appropriate signals to the body to initiate breathing. There is neither airflow nor chest wall movement. Patients with neuromuscular weakness may have movements during sleep that may be too little to be measured and be misdiagnosed as central sleep apnea. True central sleep apnea (Ondine’s curse; Locked-in Syndrome after massive strokes) is uncommon. Severe heart failure can be associated with Cheyne-Stokes respiration where hyperventilation is regularly alternated with apneas.
In sleep apnea, breathing ceases, oxygen in the blood decreases, arousal occurs, sleep ends, and breathing resumes. The individual then drifts back to sleep and another apnea occurs with this cycle continuing throughout the night, resulting in hundreds of arousals from sleep. (People without neuromuscular disorders may experience up to five apneas per hour of sleep and not be considered to have significant sleep apnea.) That person may arise in the morning unrefreshed, fatigued, and may be sleepy during the day.
Associated findings of OSA include loud snoring, obesity, positive family history of apnea and snoring, daytime sleepiness, and when very severe, right-sided heart failure (see Diastolic Heart Failure), and hypo-ventilation (see Underventilation). OSA occurs most frequently when individuals sleep on their backs, but eventually apneic episodes are present with any sleep position. Many factors can make snoring and apnea worse, such as nasal obstruction from a bad cold. Smoking causes the lining of the upper airway to swell, alcohol and sedative drugs cause the muscles in the back of the upper airway to relax, and excessive weight decreases the size of the upper airway along with compressing the lungs from increased abdominal girth.
Many polio survivors have abnormal breathing during sleep, including both OSA and hypoventilation. OSA is probably more severe in polio survivors than in people without other medical problems. OSA also was found to be more common in obese survivors with normal lung function, whereas hypoventilation was found to be more common in those survivors with scoliosis, restrictive lung function, and a history of more diffuse neurological problems during the acute phase of polio (Hsu & Staats, 1998). Needing an iron lung during the acute phase is a predictor of future hypoventilation.
Sleep apnea is diagnosed by polysomnography in an overnight sleep study, generally performed in a sleep laboratory by experienced technicians. The test monitors sleep stages, eye movements, snoring, airflow at the nose and mouth, heartbeat, chest wall breathing motion, and oxygen saturation. Oxygen saturation can be monitored easily in the home by nocturnal oximetry and serves as an adequate screen for severe OSA.
Medical treatment of OSA includes weight loss if obese, relief of nasal obstruction if present, avoidance of alcohol and sedative drugs, and sleep positioning on one’s stomach or side instead of back. If apnea is more severe (15 to 20 apneas per hour of sleep or more), nocturnal noninvasive ventilation, such as nasal continuous positive airway pressure (CPAP)—when there is little respiratory muscle weakness—or bi-level pressure support, is prescribed (see Ventilators). The upper airway in OSA is most vulnerable to closure during REM sleep (Ellis et al., 1987), and CPAP gently “splints” the airway open and stabilizes it. Obstructed breathing during sleep is relieved as long as nocturnal ventilation is used. Compliance with nasal masks has proven to be a problem in some people, particularly those with claustrophobia and those with OSA which is not very severe. These individuals do not have severe symptoms (sleepiness and fatigue), and they may not be convinced that nocturnal ventilation helps them (Hsu & Staats, 1998). Upper airway surgery to remove excessive tissue in the tonsils and soft palate areas, known as uvulopalatopharyngoplasty, is more effective to eliminate snoring than to cure apnea, but it is inadvisable in polio survivors who depend upon frog breathing (Alba, 1985). This procedure can also weaken speech and swallowing.
References
Alba, A. (1985). Recognition of need for respiratory support. In G. Laurie & J. Raymond (Eds.), Proceedings of Gazette International Networking Institute's Third International Post-Polio and Independent Living Conference (pp. 17-18). Saint Louis, MO: Gazette International Networking Institute.
Ellis, E.R., Bye, P.T.P., Bruderer, J.W., & Sullivan, C.E. (1987). Treatment of respiratory failure during sleep in patients with neuromuscular disease. American Review of Respiratory Disease, 135, 148-152.
Hsu, A., & Staats, B. (1998). "Postpolio" sequelae and sleep-related disordered breathing. Mayo Clinic Proceedings, 73, 216-224.