Sleep apnea is a sleep disorder characterized by pauses in breathing during sleep. Each episode, called apneas, lasts long enough so that one or more breaths are missed, and occurs repeatedly throughout sleep. The standard definition of any apneic event includes a minimum 10 second interval between breaths, with either a neurological arousal, a blood oxygen desaturation of 3-4% or greater, or both arousal and desaturation. Sleep apnea is diagnosed with an overnight sleep test.
Regardless of type, the individual with sleep apnea is rarely aware of having difficulty breathing, even upon awakening. Sleep apnea is recognized as a problem by others witnessing the individual during episodes or is suspected because of its effects on the body. Symptoms may be present for years, even decades without identification, during which time the sufferer may become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance.
Obstructive sleep apnea (OSA) is the most common category of sleep-disordered breathing (84% of the cases). Since the muscle tone of the body ordinarily relaxes during sleep, and since, at the level of the throat, the human airway is composed of walls of soft tissue, which can collapse, it is easy to understand why breathing can be obstructed during sleep. Mild, occasional sleep apnea, such as many people experience during an upper respiratory infection, may not be important, but chronic, severe obstructive sleep apnea requires treatment to prevent sleep deprivation and other complications. The most serious complication is a severe form of congestive heart failure.
Individuals with decreased muscle tone, increased soft tissue around the airway (e.g., due to obesity), and structural features that give rise to a narrowed airway are at high risk for obstructive sleep apnea. Older people are more likely to have OSA than younger people. Men are more typical sleep apnea sufferers, although the condition is not unusual in women or children.
Common symptoms include loud snoring, restless sleep, and sleepiness during the daytime. Diagnostic tests include home oximetry or polysomnography in a sleep clinic. Sometimes, elevated arterial pressure (commonly called high blood pressure) is a sequela of obstructive sleep apnea syndrome. When high blood pressure is caused by OSA, it is distinctive in that, unlike most cases of high blood pressure (so-called essential hypertension), the readings do not drop significantly when the individual is sleeping. Stroke is associated with obstructive sleep apnea. Sleep apnea sufferers also have a 30% higher risk of heart attack or death than those unaffected.
In pure central sleep apnea or Cheyne-Stokes respiration, the brain's respiratory control centers are imbalanced during sleep. Blood levels of carbon dioxide, and the neurological feedback mechanism that monitors it do not react quickly enough to maintain an even respiratory rate, with the entire system cycling between apnea and hyperpnea, even during wakefulness. The sleeper stops breathing, and then starts again. There is no effort made to breathe during the pause in breathing: there are no chest movements and no struggling. After the episode of apnea, breathing may be faster (hyperpnea) for a period of time, a compensatory mechanism to blow off retained waste gases and absorb more oxygen.
While sleeping, a normal individual is "at rest", as far as cardiovascular workload is concerned. Breathing is regular in a healthy person during sleep, and oxygen levels and carbon dioxide levels in the bloodstream stay fairly constant. The respiratory drive is so strong that even conscious efforts to hold one's breath do not overcome it. Any sudden drop in oxygen or excess of carbon dioxide (even if tiny) strongly stimulates the brain's respiratory centers to breathe. In central sleep apnea, the basic neurological controls for breathing rate malfunctions and fails to give the signal to inhale, causing the individual to miss one or more cycles of breathing.
Some people with sleep apnea have a combination of both types. When obstructive sleep apnea syndrome is severe and longstanding, episodes of central apnea sometimes develop. The exact mechanism of the loss of central respiratory drive during sleep in OSA is unknown, but is most commonly related to acid-base and CO2 feedback malfunctions stemming from heart failure. There is a constellation of diseases and symptoms relating to body mass, cardiovascular, respiratory, and occasionally, neurological dysfunction that have a synergistic effect in sleep-disordered breathing. The presence of central sleep apnea without an obstructive component is a common result of chronic opiate use (or abuse), due to the characteristic respiratory depression caused by large doses of narcotics.
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