sleep apnea

Sleep Apnea Understand, identify and treat sleep apnea.

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Definition

Sleep apnea is a condition in which breathing stops for more than 10 seconds during sleep. Sleep apnea is a major, though often unrecognized, cause of daytime sleepiness.

Description

A sleeping person normally breathes continuously and uninterruptedly throughout the night. A person with sleep apnea, however, has frequent episodes (up to 400–500 per night) in which he or she stops breathing. This interruption of breathing is called "apnea." Breathing usually stops for about 30 seconds; then the person usually startles awake with a loud snort and begins to breathe again, gradually falling back to sleep.

There are two forms of sleep apnea. In obstructive sleep apnea (OSA), breathing stops because tissue in the throat closes off the airway. In central sleep apnea, (CSA), the brain centers responsible for breathing fail to send messages to the breathing muscles. OSA is much more common than CSA. It is thought that about 1–10% of adults are affected by OSA; only about one tenth of that number have CSA. OSA can affect people of any age and of either sex, but it is most common in middle-aged, somewhat overweight men, especially those who use alcohol.

— Richard Robinson

A temporary suspension of breathing occurring repeatedly during sleep that often affects overweight people or those having an obstruction in the breathing tract, an abnormally small throat opening, or a neurological disorder.

Definition

Sleep apnea, or sleep-disordered breathing, is a condition in which breathing is briefly interrupted or even stops episodically during sleep. Because repeated arousal or even full awakening when breathing stops disturbs sleep, individuals suffering from sleep apnea are often drowsy during the day. Complications from an insufficient amount of oxygen reaching the brain are serious and even potentially life threatening. Sleep apnea appears to be far more common than was initially realized when it was first described in 1965.

Description

The syndrome of sleep apnea is subdivided into two types: central and obstructive. Central sleep apnea, in which the brain does not properly signal respiratory muscles to begin breathing, is much less common than obstructive sleep apnea. In the latter condition, there are repeated episodes of upper airway obstruction during sleep, typically reducing blood oxygen saturation.

A distinctive form of obstructive sleep apnea is known as the Pickwickian syndrome, named after the protagonist in Charles Dickens' Pickwick Papers. Like that character, individuals with the Pickwickian syndrome are overweight, with large necks, fat buildup around the soft tissues of the neck, and loss of muscle tone with aging. When the neck muscles relax during sleep, these characteristics allow the windpipe to collapse during breathing, which usually causes loud snoring.

When the individual with obstructive sleep apnea attempts to inhale, this causes suction that collapses the windpipe and blocks air flow for 10–60 seconds. The resulting fall in blood oxygen level signals the brain to awaken the person enough to tighten the upper airway muscles and reopen the windpipe, resulting in a snort or gasp before snoring resumes. The entire cycle may occur repeatedly, as often as hundreds of times each night.

Demographics

Approximately 6–7% of the population of the United States, or 18 million Americans, are thought to have sleep apnea, but only 10 million have symptoms, and only 0.6 million have yet been diagnosed. In Americans aged 30–60 years, obstructive sleep apnea affects nearly one in four men and one in 10 women; men are twice as likely as women to have sleep apnea. As sleep apnea seldom occurs in premenopausal females, it is suggested that hormones may play some role in the disorder.

Other predisposing factors include age, as nearly 20–60% percent of the elderly may be affected; over-weight status or obesity; or use of alcohol or sedatives. Based on a 1995 study, elderly African Americans are more than twice as likely as elderly whites to suffer from sleep apnea. Some families appear to have increased incidence of sleep apnea.

Causes and symptoms

Causes of central sleep apnea include various severe and life-threatening lesions of the lower brainstem, which controls breathing. Examples include bulbar poliomyelitis, a form of polio affecting the brainstem; degenerative diseases; radiation treatment to the neck, damaging the lower brainstem; and severe arthritis of the cervical spine and/or base of the skull, putting pressure on the lower brainstem.

Symptoms of central sleep apnea include cessation of breathing during sleep, often causing frequent awakenings and complaints of insomnia. In central sleep apnea, breathing patterns may also be disrupted during wakefulness. Other symptoms may relate to the underlying neurological condition affecting the brainstem, and may include difficulty swallowing, change in voice, or limb weakness and numbness.

Normally, muscles in the upper throat keep this part of the airway open, allowing air to enter the lungs. Although these muscles relax somewhat during sleep, they retain enough tone to keep the passage open. If the passage is narrow, relaxation of throat muscles during sleep can obstruct, or block, the passage and hinder or prevent air from flowing into the lungs.

Individuals with obstructive sleep apnea may have airway obstruction because of excessive relaxation of throat muscles or because of an already narrowed passage.

Because many patients with obstructive sleep apnea have no major structural defects in the airway and are not obese, other factors such as disordered control of ventilation and changes in lung volume during sleep may play a role in causing the condition.

Soon after falling asleep, the patient with obstructive sleep apnea typically begins snoring heavily. The snoring continues for some time and may become louder before the apnea, during which breathing stops for 10–60 seconds. A loud snort or gasp ends the apnea, followed by more snoring in a recurrent pattern. Decreased oxygen level in the blood during the apneas may cause decreased alertness and other symptoms, while disturbance of the sleep pattern at night may cause daytime drowsiness.

Those with the Pickwickian syndrome have a large neck or collar size, nasal obstruction, a large tongue, a narrow airway, or certain shapes of the palate and jaw.

While patients with sleep apnea may not be aware of the problem, their spouse may seek medical assistance because they are frequently awakened by their partner's snoring, which may be described as loud, squeaky, or raspy. In other cases, the patient may seek help for fatigue, difficulty staying awake during the day, or falling asleep at inappropriate times.

Because of restless sleep and decreased oxygen supply to the brain, patients with sleep apnea may complain of impaired mental function, slowed reaction times, problems concentrating, memory loss, poor judgment, personality changes such as irritability or depression, morning headaches, and decreased interest in sex.

Additional symptoms may include excessive sweating during sleep, bedwetting, nightmares, dry mouth when awakening caused by sleeping with the mouth open, development of high blood pressure, and frequent upper respiratory infections. Young children with sleep apnea may have visible inward movement of the chest during sleep, learning problems, growth or developmental problems, and hyperactive behavior.

Drinking alcohol before bedtime or taking sleeping pills may increase the risk of apneic episodes, as may breathing through the mouth rather than the nose during sleep.

Severe obstructive sleep apnea may cause pulmonary hypertension, or increased pressure in lung arteries, eventually leading to heart failure. Other complications may include increased risk of cardiovascular disease, stroke, heart arrhythmias or irregular heartbeats, and disorders of immune function.

Diagnosis

Although sleep apnea has been more widely diagnosed in the past decade, experts estimate that at least 90–95% of cases remain undiagnosed. Reasons for this include vague, slowly developing symptoms that largely occur when the patient is sleeping; limited knowledge of the disease by physicians; and expensive, specialized testing needed for definitive diagnosis.

Talking to the patient and the spouse or parent is an important first step, but it may not be sufficient. Similarly, the physical examination often fails to reveal distinctive abnormalities. Helpful diagnostic aids may include a questionnaire asking about typical symptoms and sleep habits, and a detailed inspection of the mouth, neck, and throat. Arterial blood gases may reveal low oxygen or high carbon dioxide levels in the blood.

More recently, it has been recognized that obstructive sleep apnea can occur even in individuals of normal weight who lack the other distinctive features of the Pick-wickian syndrome. Up to 40% of people with obstructive sleep apnea are not obese.

When sleep apnea is suspected from characteristic symptoms and physical appearance, in many other cases, an overnight polysomnography (PSG) testing at a specialized sleep center may be suggested. During this test, breathing, brain waves, heartbeat, muscle tension, and eye movement are monitored through wires attached to the skin while the patient sleeps. Oxygen levels can be monitored through a device applied to a fingertip, and audio and/or video recordings may provide additional diagnostic information.

After the test, a physician trained in PSG testing analyzes the recordings to determine if sleep apnea or other conditions are present. In some cases, PSG can also be done at home after a sleep technologist attaches the wires and instructs the parent or other responsible adult on how to record sleep activity. Although portable PSG tests are less expensive and more convenient, they are subject to lost or inadequate recording, technical problems, and slightly lower diagnostic accuracy. Patients with inconclusive results on home studies and those with negative studies but persistent symptoms should have standard PSG testing in a sleep center.

Treatment team

The internist or family practitioner is often the first physician consulted because the earliest symptoms of sleep apnea are typically vague. If sleep apnea is suspected, the patient is usually referred to a neurologist or specialist in sleep disorders. Ear, nose, and throat specialists can help determine if there are characteristic abnormalities of the jaw or palate contributing to the problem, and in some cases they may perform corrective surgery if indicated. Lung specialists should manage severe cases of sleep apnea that result in pulmonary hypertension. Technicians involved in the diagnosis and treatment of sleep apnea may include PSG technicians and respiratory therapists.

Treatment

For mild cases of sleep apnea, simple measures may suffice, such as losing weight through a diet and exercise program, or preventing the person from sleeping on their back. More severe cases may need assisted breathing devices to wear at night or surgery to correct airway obstruction. Individuals with sleep apnea should avoid sedatives, sleeping pills, narcotics, and alcohol, especially at bedtime, as these central nervous system depressants can prevent them from awakening enough to keep breathing.

General suggestions to promote better sleep include good sleep habits, going to bed at a regular time each night, and arising at the same time each morning rather than sleeping late on weekends. Keeping the bedroom at a comfortable temperature is conducive to better sleep. Exercising 20–30 minutes each day, at least five to six hours before bedtime, may be helpful both for sleeping better and for weight loss.

Caffeine and related stimulants found in coffee, tea, chocolate, and some diet drugs and pain relievers should be avoided. Smoking disrupts sleep by causing early morning awakening in response to nicotine withdrawal. Alcohol reduces the amount of time spent in deep sleep and rapid eye movement (REM) sleep and proportionately increases time spent in the lighter stages of sleep, which are less refreshing.

To relax before bedtime, taking a warm bath, reading, or other restful bedtime ritual may be helpful. Sleeping until the sun rises helps the body's internal biological clock reset itself, as does daily exposure to an hour of morning sunlight. When unable to sleep despite these measures, it is better to read, watch television, or listen to soothing music rather than lying in bed awake, which can cause anxiety and worsen insomnia.

To keep the airway open during sleep, some individuals with obstructive sleep apnea need a device called nasal CPAP, or continuous positive airway pressure, which delivers air through a mask over the nose or over both the nose and mouth. This is considered to be the most effective and widely used therapy.

Complications of CPAP may include nasal congestion or dryness, discomfort related to wearing the mask, and feelings of claustrophobia. To relieve these problems, heated humidifiers to moisturize and warm the air, better fitting and more comfortable masks, or applying steroids within the nasal passages may be helpful. In patients who find it difficult to exhale against the increased pressure of CPAP, bilevel positive-pressure therapy may be equally effective.

Some investigators are studying mechanical devices inserted into the mouth during sleep to open the airway by moving the jaw forward. Although these oral appliances appear to prevent daytime sleepiness and sleep disordered breathing, they do not seem to be as effective as nasal CPAP. However, they may be a reasonable option for patients who are unwilling or unable to use nasal CPAP.

Obstructive sleep apnea in children may be caused by enlarged tonsils and adenoids and can be corrected by tonsillectomy. In adults, surgery to remove airway obstruction may be needed, depending on the anatomical structure. Excess tissue at the back of the throat may be removed in a procedure called an uvulopalatopharyngoplasty, or UPPP. Some cases may require repairing a deviated nasal septum, or other surgery to remove blockage of the nose or upper throat. Surgery to correct obstructive sleep apnea seems to be most effective when it is tailored to the individual's specific anatomical obstruction.

As a last resort, a tracheostomy can be performed, making an opening in the windpipe to bypass the obstructed airway during sleep. During the day, a valve over the opening is closed so the person can speak, and at night, the valve is opened to bypass the obstruction.

If brainstem injury or disease impairs respiratory drive, causing central sleep apnea, mechanical ventilation on a respirator may be needed to ensure continued breathing.

Medications being tested in sleep apnea include Provigil, a nonaddictive drug that improves daytime alertness. Side effects may include nausea and headaches. Decongestants may reduce airway obstruction related to nasal congestion. Results of a controlled trial published in November 2003 suggest that the cholinesterase inhibitor physostigmine may reduce apnea episodes.

Clinical trials

The National Institutes of Neurological Disorder and Stroke, the National Heart, Lung, and Blood Institute (NHLBI), and the National Institute on Aging all support sleep apnea research.

The National Institute of Child Health and Human Development (NICHD) is recruiting children and adolescents with obstructive sleep apnea or other obesity-related diseases for a trial of orlistat (Xenical, Hoffmann LaRoche). By preventing the action of digestive enzymes, this drug interferes with the absorption of approximately one-third of dietary fat. Study subjects may receive active medication or placebo, but all will be enrolled in a weight loss program, including nutrition education, behavioral self-monitoring strategies, and promotion of physical activity.

The APPLES study (apnea positive pressure long-term efficacy study), sponsored by the NHLBI, is recruiting patients with obstructive sleep apnea to determine the effectiveness of nasal CPAP therapy as compared with a similar-appearing control device that does not administer air delivered under positive pressure. Outcomes studied in this trial include mental function, mood, daytime sleepiness, and quality of life. Contact information is the office of study chair William C. Dement, MD, PhD, (650) 723-8131, or .

The NHLBI is also planning a study of the outcomes of sleep disorders in men aged 65 years and older. It will look at whether sleep disorders such as obstructive sleep apnea are associated with increased risk of cardiovascular disease, falls, decreased physical function, impaired mental function, decreased bone density, fractures, and death.

Prognosis

Treating sleep apnea by eliminating the obstruction usually prevents and reverses complications such as pulmonary hypertension, high blood pressure, and heart disease. Individuals with obstructive sleep apnea who are unable or unwilling to tolerate CPAP may suffer from abnormal heart rhythms, reduced alertness, and sleep deprivation.

Left untreated, sleep apnea can profoundly reduce daytime functioning, work performance, social relationships, and quality of life. If patients fall asleep while driving or engaging in another potentially hazardous activity during the day, sleep apnea may be fatal. Severe, untreated sleep apnea doubles or even triples the risk of automobile accidents compared with the general population. These individuals are also at risk of sudden death from respiratory arrest during sleep.

Children with unrecognized obstructive sleep apnea may experience problems with learning, development, and behavior, as well as failure to grow, heart problems, and high blood pressure. Daytime sleepiness may cause personality changes, poor school performance, and difficulties with interpersonal relationships. Lagging development may lead to frustration and even depression.

Until additional research is carried out, it remains unclear if there is a "safe" number of apnea episodes, or how sleep apnea interacts with other causes of lung or heart failure. It appears that most patients with sleep apnea and heart or lung failure also have underlying diseases such as obstructive lung disease caused by smoking or asthma, severe obesity, or coronary artery disease.

Central sleep apnea usually has a poor prognosis related to the underlying injury or disease affecting the brainstem. Most patients with central sleep apnea require prolonged mechanical ventilation, which can also lead to many serious complications.

Special concerns

Sleep apnea is difficult to diagnose without expensive testing, can aggravate or cause heart and lung problems, often reduces function and quality of life, and may require invasive surgical procedures or long-term use of nasal CPAP. For all these reasons, prevention of obstructive sleep apnea is a worthwhile goal.

Weight reduction in overweight individuals and decreasing intake of alcohol and sedatives have independent health benefits as well as reducing risk of developing obstructive sleep apnea. In children with enlargement of the tonsils and adenoids, corrective surgery may reduce upper respiratory infections while preventing sleep apnea.

In experiments in rats, intermittent decreases in blood oxygen levels during sleep, similar to those seen with obstructive sleep apnea, cause degenerative changes in the hippocampus, a brain region involved in memory and learning. These degenerative changes in the brain are associated with deficits in maze learning. If similar changes occur in obstructive sleep apnea, this might explain decreased mental function observed with this disorder. Brain degeneration related to episodic decreases in oxygen levels would be another important reason to ensure that obstructive sleep apnea is diagnosed and effectively treated.

Although it is well recognized that sleep apnea is more common in men than in women, a study in October 2003 also suggested that men are far more likely than women to seek treatment at a specialized sleep clinic. Research is ongoing to determine the cause of gender differences in sleep apnea and to increase referrals of women to sleep centers where they may obtain appropriate care.

Resources

PERIODICALS

Boyer, S., and V. Kapur. "Role of Portable Sleep Studies for Diagnosis of Obstructive Sleep Apnea." Current Opinion in Pulmonary Medicine 2003 Nov 9(6): 465–70.

Durand, E., F. Lofaso, S. Dauger, G. Vardon, C. Gaultier, and J. Gallego. "Intermittent Hypoxia Induces Transient Arousal Delay in Newborn Mice." Journal of Applied Physiology 96 (March 2004): 1216–1222.

Fitzpatrick, M. F., H. McLean, A. M. Urton, A. Tan, D. O'Donnell, and H. S. Driver. "Effect of Nasal or Oral Breathing Route on Upper Airway Resistance during Sleep." European Respiratory Journal 22, no. 5 (November 2003): 827–32.

Gozal, D., B. W. Row, et al. "Temporal Aspects of Spatial Task Performance during Intermittent Hypoxia in the Rat: Evidence for Neurogenesis." European Journal of Neuroscience 2003 Oct 18(8): 2335–42.

Hedner, J., H. Kraiczi, Y. Peker, and P. Murphy. "Reduction of Sleep-Disordered Breathing after Physostigmine." American Journal of Respiratory and Critical Care Medicine (2003) 168: 1246–1251.

Jordan, A. S., and R. D. McEvoy. "Gender Differences in Sleep Apnea: Epidemiology, Clinical Presentation and Pathogenic Mechanisms." Sleep Medicine Review 2003 Oct 7(5): 377–89.

Jordan, A. S., D. P. White, and R. B. Fogel. "Recent Advances in Understanding the Pathogenesis of Obstructive Sleep Apnea." Current Opinion in Pulmonary Medicine 2003 Nov 9(6): 459–64.

Kao, Y. H., Y. Shnayder, and K. C. Lee. "The Efficacy of Anatomically Based Multilevel Surgery for Obstructive Sleep Apnea." Otolaryngology Head Neck Surgery 2003 Oct 129(4): 327–35.

Lim, J., T. Lasserson, J. Fleetham, and J. Wright. "Oral Appliances for Obstructive Sleep Apnea." Cochrane Database Systems Review 2003 (4): CD004435.

Moyer, C. A., S. S. Sonnad, S. L. Garetz, J. I. Helman, and R. D. Chervin. "Quality of Life in Obstructive Sleep Apnea: A Systematic Review of the Literature." Sleep Medicine 2001 Nov 2(6): 477–91.

Qureshi, A., and R. D. Ballard. "Obstructive Sleep Apnea." Journal of Allergy and Clinical Immunology 2003 Oct 112(4): 643–51.

Wolk, R., A. S. Shamsuzzaman, and V. K. Somers. "Obesity, Sleep Apnea, and Hypertension." Hypertension 2003 Nov 10.

WEBSITES

Clinical Trials (March 2, 2004). http://www.clinicaltrials.gov/ct/action/GetStudy.

HealthFinder PO Box 1133, Washington, DC 20013-1133. (March 1, 2004). http://www.healthfinder.gov/search/default.asp?ct=HFDocs&so=Rank%5Bd%5D%2CDocTitle&doclang=1&page=1&q1=sleep&apnea.

National Institute of Neurological Disorders and Stroke NIH Neurological Institute. PO Box 5801, Bethesda, MD 20824. (800) 352-9424. (March 2, 2004). http://www.ninds.nih.gov/search.htm?Text2=%27Sleep+apnea%27&Text1=Sleep+apnea.

National Sleep Foundation. When You Can't Sleep: The ABCs of ZZZs. 2002. February 22, 2004 (March 2, 2004). http://www.sleepfoundation.org/publications/ZZZs.cfm

Stanford University Medical Center 300 Pasteur Drive, Stanford, CA 94305. (650) 723-4000. (March 2, 2004). http://www.stanford.edu/~dement/childapnea.html.

U.S. National Library of Medicine 8600 Rockville Pike, Bethesda, MD 20894. (March 2, 2004). http://www.nlm.nih.gov/medlineplus/ency/article/003997.htm.

OTHER

Apneos Corporation 2033 Ralston Avenue #41, Belmont, CA 94002. (650) 591-2895. (March 2, 2004). http://www.apneos.com.

ORGANIZATIONS

The American Lung Association. 61 Broadway, 6th Floor, New York, NY 10006. (212) 315-8700. (March 2, 2004). http://lungusa.org/diseases/sleepapnea.html.

The Sleep Apnea Society of Alberta. c/o 911-78 Avenue SW, Calgary, AB T2V0T7. (800) 817-5337. (March 2, 2004). http://www.sleep-apnea.ab.ca/prognosis.htm.

Laurie Barclay

A sleep disorder characterized by periods of an absence of attempts to breathe. The person is momentarily unable to move respiratory muscles or maintain airflow through the nose and mouth.

Definition

Sleep apnea is a condition in which breathing stops for more than ten seconds during sleep. Sleep apnea is a major, though often unrecognized, cause of daytime sleepiness. It can have serious negative effects on a person's quality of life, and is thought to be considerably underdiagnosed in the United States.

Description

A sleeping person normally breathes continuously and without interruption throughout the night. A person with sleep apnea, however, has frequent episodes (up to 400-500 per night) in which he or she stops breathing. This interruption of breathing is called "apnea." Breathing usually stops for about 30 seconds; then the person usually startles awake with a loud snort and begins to breathe again, gradually falling back to sleep.

There are two forms of sleep apnea. In obstructive sleep apnea (OSA), breathing stops because tissue in the throat closes off the airway. In central sleep apnea, (CSA), the brain centers responsible for breathing fail to send messages to the breathing muscles. OSA is much more common than CSA. It is thought that about 1–10% of adults are affected by OSA; only about one tenth of that number have CSA. OSA can affect people of any age and of either sex, but it is most common in middle-aged, somewhat overweight men, especially those who use alcohol.

Causes & Symptoms

Obstructive Sleep Apnea

Obstructive sleep apnea occurs when part of the airway is closed off (usually at the back of the throat) while a person is trying to inhale during sleep. People whose airways are slightly narrower than average are more likely to be affected by OSA. Obesity, especially obesity in the neck, can increase the risk of developing OSA, because the fat tissue tends to narrow the airway. In some people, the airway is blocked by enlarged tonsils, an enlarged tongue, jaw deformities, or growths in the neck that compress the airway. Blocked nasal passages may also play a part in some people's apnea.

When a person begins to inhale, expansion of the lungs lowers the air pressure inside the airway. If the muscles that keep the airway open are not working hard enough, the airway narrows and may collapse, shutting off the supply of air to the lungs. OSA occurs during sleep because the neck muscles that keep the airway open are not as active then. Congestion in the nose can make collapse more likely, since the extra effort needed to inhale will lower the pressure in the airway even more. Drinking alcohol or taking tranquilizers in the evening worsens this situation, because these substances cause the neck muscles to relax. These drugs also lower the "respiratory drive" in the nervous system, reducing breathing rate and strength.

People with OSA almost always snore heavily, because the same narrowing of the airway that causes snoring can also cause OSA. Snoring may actually help cause OSA as well, because the vibration of the throat tissues can cause them to swell. However, most people who snore do not go on to develop OSA.

Other risk factors for developing OSA include male sex; pregnancy; a family history of the disorder; and smoking. With regard to gender, it has been found that male sex hormones sometimes cause changes in the size or structure of the upper airway. The weight gain that accompanies pregnancy can affect a woman's breathing patterns during sleep, particularly during the third trimester. With regard to family history, OSA is known to run in families even though no gene or genes associated with the disorder have been identified as of 2002. Smoking increases the risk of developing OSA because it causes inflammation, swelling, and narrowing of the upper airway.

Some patients being treated for head and neck cancer develop OSA as a result of physical changes in the muscles and other tissues of the neck and throat. Doctors recommend prompt treatment of the OSA to improve the patient's quality of life.

Central Sleep Apnea

In central sleep apnea, the airway remains open, but the nerve signals controlling the respiratory muscles are not regulated properly. This loss of regulation can cause wide fluctuations in the level of carbon dioxide (CO₂) in the blood. Normal activity in the body produces CO₂, which is brought by the blood to the lungs for exhalation. When the blood level of CO₂ rises, brain centers respond by increasing the rate of respiration, clearing the CO₂. As blood levels fall again, respiration slows down. Normally, this interaction of CO₂ and breathing rate maintains the CO₂ level within very narrow limits. CSA can occur when the regulation system becomes insensitive to CO₂ levels, allowing wide fluctuations in both CO₂ levels and breathing rates. High CO₂ levels cause very rapid breathing (hyperventilation), which then lowers CO₂ so much that breathing becomes very slow or even stops. CSA occurs during sleep because when a person is awake, breathing is usually stimulated by other signals, including conscious awareness of breathing rate.

A combination of the two forms is also possible, and is called "mixed sleep apnea." Mixed sleep apnea episodes usually begin with a reduced central respiratory drive, followed by obstruction.

OSA and CSA cause similar symptoms. The most common symptoms are:

• daytime sleepiness
• morning headaches
• a feeling that sleep is not restful
• disorientation upon waking
• memory loss and difficulty paying attention
• poor judgment
• personality changes

Sleepiness is caused not only by the frequent interruption of sleep, but by the inability to enter long periods of deep sleep, during which the body performs numerous restorative functions. OSA is one of the leading causes of daytime sleepiness, and is a major risk factor for motor vehicle accidents. Headaches and disorientation are caused by low oxygen levels during sleep, from the lack of regular breathing.

Other symptoms of sleep apnea may include sexual dysfunction, loss of concentration, memory loss, intellectual impairment, and behavioral changes including anxiety and depression.

Sleep apnea is also associated with night sweats and nocturia, or increased frequency of urination at night. Bedwetting in children is also linked to sleep apnea.

Sleep apnea can also cause serious changes in the cardiovascular system. Daytime hypertension (high blood pressure) is common. An increase in the number of red blood cells (polycythemia) is possible, as is an enlarged left ventricle of the heart (cor pulmonale), and left ventricular failure. In some people, sleep apnea causes life-threatening changes in the rhythm of the heart, including heartbeat slowing (bradycardia), racing (tachycardia), and other types of arrhythmias. Sudden death may occur from such arrhythmias. Patients with the Pickwickian syndrome (named after a Charles Dickens character) are obese and sleepy, with right heart failure, pulmonary hypertension, and chronic daytime low blood oxygen (hypoxemia) and increased blood CO₂ (hypercapnia).

Diagnosis

Excessive daytime sleepiness is the complaint that usually brings a person to see the doctor. A careful medical history will include questions about alcohol, tobacco, or tranquilizer use; family history; snoring (often reported by the person's partner); and morning headaches or disorientation. A physical examination will include examination of the mouth, nose and throat to look for narrowing or obstruction, or unusual size or shape of the tonsils or adenoids. Blood pressure is also measured. Measuring heart rate or blood levels of oxygen and CO₂ during the daytime will not usually be done, since these are abnormal only at night in most patients.

In some cases the person's dentist may suggest the diagnosis of OSA on the basis of a dental checkup or evaluation of the patient for oral surgery.

Confirmation of the diagnosis usually requires making measurements while the person sleeps. These tests are called a polysomnography study, and are conducted during an overnight stay in a specialized sleep laboratory. Important parts of the polysomnography study include measurements of:

• heart rate
• airflow at the mouth and nose
• respiratory effort
• sleep stage (light sleep, deep sleep, dream sleep, etc.)
• oxygen level in the blood, using a noninvasive probe (ear oximetry)

Simplified studies done overnight at home are also possible, and may be appropriate for people whose profile strongly suggests the presence of obstructive sleep apnea; that is, middle-aged, somewhat overweight men, who snore and have high blood pressure. The home-based study usually includes ear oximetry and cardiac measurements. If these measurements support the diagnosis of OSA, initial treatment is usually suggested without polysomnography. Home-based measurements are not used to rule out OSA, however, and if the measurements do not support the OSA diagnosis, polysomnography may be needed to define the problem further.

Treatment

Treatment of obstructive sleep apnea begins with reducing the use of alcohol or tranquilizers in the evening, if these have been contributing to the problem. Quitting smoking is recommended for a number of health concerns in addition to OSA. Weight loss is also effective, but if the weight returns, as it often does, so does the apnea. Changing sleeping position may be effective. Snoring and sleep apnea are both most common when a person sleeps on his back. Turning to sleep on the side may be enough to clear up the symptoms. Raising the head of the bed may also help.

There are few reports of OSA being treated by alternative and complementary approaches. In 2002, however, some Japanese researchers reported on the case of a 44-year-old male who was successfully treated for OSA by taking a Kampo extract, or traditional Japanese herbal formulation.

Allopathic Treatment

Opening of the nasal passages can provide some relief for sleep apnea sufferers. There are a variety of nasal devices such as clips, tapes, or holders which may help, though discomfort may limit their use. Nasal decongestants may be useful, but should not be taken for sleep apnea without the consent of the treating physician. Supplemental nighttime oxygen can be useful for some people with either central and obstructive sleep apnea. Tricyclic antidepressant drugs such as protriptyline (Vivactil) may help by increasing the muscle tone of the upper airway muscles, but their side effects may severely limit their usefulness.

For moderate to severe sleep apnea, the most successful treatment is nighttime use of a ventilator, called a CPAP machine. CPAP (continuous positive airway pressure) blows air into the airway continuously, preventing its collapse. CPAP requires the use of a nasal mask. The appropriate pressure setting for the CPAP machine is determined by polysomnography in the sleep lab. Its effects are dramatic; daytime sleepiness usually disappears within one to two days after treatment begins. CPAP is used to treat both obstructive and central sleep apnea.

CPAP is tolerated well by about two-thirds of patients who try it. Bilevel positive airway pressure (BiPAP), is an alternative form of ventilation. With BiPAP, the ventilator reduces the air pressure when the person exhales. This form of treatment is more comfortable for some.

Another approach to treating OSA involves the use of oral appliances intended to improve breathing either by holding the tongue in place or by pushing the lower jaw forward during sleep to increase the air volume in the upper airway. The first type of oral appliance is known as a tongue retaining device or TRD. The second type is variously called an oral protrusive device (OPD) or mandibular advancement splint (MAS), because it holds the mandible, or lower jaw, forward during sleep. These oral devices appear to work best for patients with mild-to-moderate OSA, and in some cases can postpone or prevent the need for surgery. Their rate of patient compliance is about 50%; most patients who stop using oral appliances do so because their teeth are in poor condition. TRDs and OPDs can be fitted by dentists; however, most dentists work together with the patient's physician following a polysomnogram rather than prescribing the device by themselves.

Surgery can be used to correct obstructions in the airway. The most common surgery is called UPPP, for uvulopalatopharynoplasty. This surgery removes tissue from the rear of the mouth and top of the throat. The tissues removed include parts of the uvula (the flap of tissue that hangs down at the back of the mouth), the soft palate, and the pharynx. Tonsils and adenoids are usually removed as well. This operation significantly improves sleep apnea in slightly more than half of all cases. More recently, oral surgeons have been performing region-specific surgery for OSA, which grew out of the recognition that obstructions may exist in more than one level of the patient's upper airway. Region-specific surgery has a cure rate of over 90%, though it may involve more than one surgical operation.

A modified tracheotomy may also be performed to treat OSA. This procedure involves the surgical placement of a tiny breathing tube that fits in a 2 mm incision in the throat.

Reconstructive surgery is possible for those whose OSA is due to constriction of the airway by lower jaw deformities. Genioplasty, which is a procedure that plastic surgeons usually perform to reshape a patient's chin to improve his or her appearance, is now being done to reshape the upper airway in patients with OSA.

Expected Results

Appropriate treatment enables most people with sleep apnea to be treated successfully, although it may take some time to determine the most effective and least intrusive treatment. In many cases consultation and cooperation between the person's physician and dentist help in finding the best treatment option. Polysomnography testing is usually required after beginning a treatment to determine how effective it has been.

Prevention

For people who snore frequently, weight control, smoking cessation, avoidance of evening alcohol or tranquilizers, and adjustment of sleeping position may help reduce the risk of developing obstructive sleep apnea.

Resources

Books

"Disorders of the Oral Region." Section 9, Chapter 105 in The Merck Manual of Diagnosis and Therapy, edited by Mark H. Beers, MD, and Robert Berkow, MD. Whitehouse Station, NJ: Merck Research Laboratories, 1999.

Pascualay, Ralph, and Sally Warren Soest. Snoring and Sleep Apnea, 2nd ed. New York, NY: Demos Vermande, 1996.

"Sleep Disorders." Section 14, Chapter 173 in The Merck Manual of Diagnosis and Therapy, edited by Mark H. Beers, MD, and Robert Berkow, MD. Whitehouse Station, NJ: Merck Research Laboratories, 1999.

Periodicals

Chasens, E. R., and M. G. Umlauf. "Nocturia: A Problem That Disrupts Sleep and Predicts Obstructive Sleep Apnea" Geriatric Nursing 24 (March-April 2003): 76–81, 105.

Chung, S. A., S. Jairam, M. R. Hussain, and C. M. Shapiro. "How, What, and Why of Sleep Apnea. Perspectives for Primary Care Physicians." Canadian Family Physician 48 (June 2002): 1073–1080.

Edwards, N., P. G. Middleton, D. M. Blyton, and C. E. Sullivan. "Sleep Disordered Breathing and Pregnancy." Thorax 57 (June 2002): 555–558.

Hisanaga, A., T. Itoh, Y. Hasegawa, et al. "A Case of Sleep Choking Syndrome Improved by the Kampo Extract of Hange-Koboku-To." Psychiatry and Clinical Neuro-science 56 (June 2002): 325–327.

Kapur, V., K. P. Strohl, S. Redline, et al. "Underdiagnosis of Sleep Apnea Syndrome in U.S. Communities." Sleep and Breathing 6 (June 2002): 49–54.

Koliha, C. A. "Obstructive Sleep Apnea in Head and Neck Cancer Patients Post Treatment … Something to Consider?" ORL—Head and Neck Nursing 21 (Winter 2003): 10–14.

Neill, A., R. Whyman, S. Bannan, et al. "Mandibular Advancement Splint Improves Indices of Obstructive Sleep Apnoea and Snoring but Side Effects Are Common." New Zealand Medical Journal 115 (June 21, 2002): 289–292.

Rose, E., R. Staats, J. Schulte-Monting, et al. "Long-Term Compliance with an Oral Protrusive Appliance in Patients with Obstructive Sleep Apnoea." [in German] Deutsche medizinische Wochenschrift 127 (June 7, 2002): 1245–1249.

Shiomi, T., A. T. Arita, R. Sasanabe, et al. "Falling Asleep While Driving and Automobile Accidents Among Patients with Obstructive Sleep Apnea-Hypopnea Syndrome." Psychiatry and Clinical Neuroscience 56 (June 2002): 333–334.

Stanton, D. C. "Genioplasty." Facial Plastic Surgery 19 (February 2003): 75–86.

Umlauf, M. G., and E. R. Chasens. "Bedwetting—Not Always What It Seems: A Sign of Sleep-Disordered Breathing in Children." Journal for Specialists in Pediatric Nursing 8 (January-March 2003): 22–30.

Veale, D., G. Poussin, F. Benes, et al. "Identification of Quality of Life Concerns of Patients with Obstructive Sleep Apnoea at the Time of Initiation of Continuous Positive Airway Pressure: A Discourse Analysis." Quality of Life Research 11 (June 2002): 389–399.

Viera, A. J., M. M. Bond, and S. J. Yates. "Diagnosing Night Sweats." American Family Physician 67 (March 1, 2003): 1019–1024.

Organizations

American Academy of Otolaryngology, Head and Neck Surgery, Inc. One Prince Street, Alexandria, VA 22314-3357. (703) 836-4444. .

American Dental Association. 211 East Chicago Avenue, Chicago, IL 60611. (312) 440-2500. .

American Sleep Apnea Association. 1424 K Street NW, Suite 302, Washington, DC 20005. (202) 293-3650. Fax: (202) 293-3656. .

Canadian Coordinating Office for Health Technology Assessment. .

National Sleep Foundation. 1522 K Street, NW, Suite 500, Washington, DC 20005. .

Other

American Sleep Apnea Association (ASAA). Considering Surgery for Snoring?.

National Heart, Lung, and Blood Institute (NHLBI). Facts About Sleep Apnea. NIH Publication No. 95-3798. .

[Article by: Paula Ford-Martin; Rebecca J. Frey, PhD]

For more information on sleep apnea, visit Britannica.com.

1. temporary cessation of breathing.
2. asphyxia.

• sleep a. — transient attacks of failure of autonomic control of respiration, becoming more pronounced during sleep and resulting in acidosis and pulmonary arteriolar vasoconstriction and hypertension.

This article needs additional citations for verification. Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (November 2008)

Sleep apnea
Classification and external resources
ICD-10	G47.3
ICD-9	780.57
eMedicine	ped/2114
MeSH	D012891

Sleep apnea (or sleep apnoea in British English) is a sleep disorder characterized by pauses in breathing during sleep. Each episode, called an apnea (Greek: ἄπνοια (ápnoia), from α- (a-), privative, πνέειν (pnéein), to breathe), lasts long enough so that one or more breaths are missed, and such episodes occur repeatedly throughout sleep.^[1] The standard definition of any apneic event includes a minimum 10 second interval between breaths, with either a neurological arousal (a 3-second or greater shift in EEG frequency, measured at C3, C4, O1, or O2), a blood oxygen desaturation of 3-4% or greater, or both arousal and desaturation. Sleep apnea is diagnosed with an overnight sleep test called a polysomnogram, or a "Sleep Study".

Clinically significant levels of sleep apnea are defined as five or more episodes per hour of any type of apnea (from the polysomnogram). There are three distinct forms of sleep apnea: central, obstructive, and complex (i.e., a combination of central and obstructive) constituting 0.4%, 84% and 15% of cases respectively.^[2] Breathing is interrupted by the lack of respiratory effort in central sleep apnea; in obstructive sleep apnea, breathing is interrupted by a physical block to airflow despite respiratory effort. In complex (or "mixed") sleep apnea, there is a transition from central to obstructive features during the events themselves.

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 (sequelae). Symptoms may be present for years (or 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.

Contents 1 History 2 Prevalence and costs 3 Obstructive sleep apnea 3.1 Symptoms, signs and sequelae 4 Central sleep apnea 4.1 Laboratory findings 4.2 Clinical details 4.2.1 Section references 5 Mixed apnea and complex sleep apnea 6 Treatment 6.1 Benefits and risks for treatment by surgery 6.2 Surgery and anesthesia in patients with sleep apnea 7 See also 8 References 8.1 General references 9 External links

History

The first reports in the medical literature of what is now called obstructive sleep apnea date only from 1965, when it was independently described by French and German investigators. However, the clinical picture of this condition has long been recognized as a character trait, without an understanding of the disease process. The term “Pickwickian syndrome” that is sometimes used for the syndrome was coined by the famous early 20th century physician, William Osler, who must have been a reader of Charles Dickens. The description of Joe, "the fat boy" in Dickens's novel, The Pickwick Papers, is an accurate clinical picture of adult obstructive sleep apnea syndrome.

The early reports of obstructive sleep apnea in the medical literature described individuals who were very severely affected, often presenting with severe hypoxemia, hypercapnia and congestive heart failure. Tracheostomy was the recommended treatment and, though it could be life-saving, post-operative complications in the stoma were frequent in these very obese and short-necked individuals.

The management of obstructive sleep apnea was revolutionized with the introduction of continuous positive airway pressure (CPAP), first described in 1981 by Colin Sullivan and associates in Sydney, Australia. The first models were bulky and noisy but the design was rapidly improved and by the late 1980s CPAP was widely adopted. The availability of an effective treatment stimulated an aggressive search for affected individuals and led to the establishment of hundreds of specialized clinics dedicated to the diagnosis and treatment of sleep disorders. Though many types of sleep problems are recognized, the vast majority of patients attending these centers have sleep disordered breathing.

Prevalence and costs

It is estimated that 20 million Americans are affected by sleep apnea. That is nearly 1 in 15 Americans; making sleep apnea as prevalent as asthma or diabetes. It is also estimated that 85-90 percent of individuals affected are undiagnosed and untreated.^[3] The Wisconsin Sleep Cohort Study found that nine percent of women and 24 percent of men had sleep apnea.^[4]

The costs of untreated sleep apnea reach further than just health issues. It is estimated that the average untreated sleep apnea patient's health care costs $1,336 more than an individual without sleep apnea. If approximations are correct, 17 million untreated individuals account for $22,712,000,000 in unnecessary health care costs.^[5]

Obstructive sleep apnea

Main article: Obstructive sleep apnea

Obstructive sleep apnea (OSA) is the most common category of sleep-disordered breathing. The muscle tone of the body ordinarily relaxes during sleep and at the level of the throat the human airway is composed of collapsible walls of soft tissue which can obstruct breathing 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 low blood oxygen (hypoxemia), sleep deprivation, and other complications. The most serious complication is a severe form of congestive heart failure called cor pulmonale.

Individuals with low muscle tone and 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. The elderly are more likely to have OSA than young people. Men are more typical sleep apnea sufferers than women and children, although it is not uncommon in the latter two.

Common symptoms include loud snoring, restless sleep, and sleepiness during the daytime. Diagnostic tests include home oximetry or polysomnography in a sleep clinic.

Some treatments involve lifestyle changes, such as avoiding alcohol or muscle relaxants, losing weight, and quitting smoking. Many people benefit from sleeping at a 30 degree elevation of the upper body^[6] or higher, as if in a recliner. Doing so helps prevent the gravitational collapse of the airway. Lateral positions (sleeping on a side), as opposed to supine positions (sleeping on the back), are also recommended as a treatment for sleep apnea,^[7][8][9] largely because the gravitational component is smaller in the lateral position. Some people benefit from various kinds of oral appliances to keep the airway open during sleep. "Breathing machines" like the continuous positive airway pressure (CPAP) may help. There are also surgical procedures to remove and tighten tissue and widen the airway.

Symptoms, signs and sequelae

As already mentioned, snoring is almost a uniform finding in an individual with this syndrome. Snoring is the turbulent sound of air moving through the back of the mouth, nose, and throat. Although not everyone who snores is experiencing difficulty breathing, "snoring" in combination with other conditions such as overweight and obesity has been found to be highly predictive of OSA risk. ^[10] The loudness of the snoring is not indicative of the severity of obstruction, however. If the upper airways are tremendously obstructed, there may not be enough air movement to make much sound. Even the loudest snoring does not mean that an individual has sleep apnea syndrome. The sign that is most suggestive of sleep apneas occurs if snoring stops. If it does, along with breath, while the persons' chest and body tries to breathe - that is literally a description of an event in obstructive sleep apnea syndrome. When breathing starts again, there is typically a deep gasp, and then the resumption of snoring.

Other indicators include (but are not limited to): hypersomnolence, obesity BMI >30, large neck circumference (16” in women, 17” in men), enlarged tonsils and large tongue volume, micrognathia morning headaches, irritability/mood-swings/depression, learning and/or memory difficulties, and sexual dysfunction.

The term "sleep disordered breathing" is commonly used in the US to describe the full range of breathing problems during sleep in which not enough of air reaches the lungs (hypopnea and apnea). Sleep disordered breathing is associated with an increased risk of cardiovascular disease, stroke, high blood pressure, arrhythmias, diabetes, and accidents.^{[11][12][13][14]} 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.^[15] Stroke is associated with obstructive sleep apnea.^[16] Sleep apnea sufferers also have a 30% higher risk of heart attack or premature death than those unaffected.^[17]

On June 27, 2008, edition of the journal Neuroscience Letters, researchers revealed that people with OSA show tissue loss in brain regions that help store memory, thus linking OSA with memory loss.^[18] Using magnetic resonance imaging (MRI), the scientists discovered that sleep apnea patients' mammillary bodies were nearly 20 percent smaller, particularly on the left side. One of the key investigators hypothesized that repeated drops in oxygen lead to the brain injury.^[19]

Central sleep apnea

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 does 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 malfunction and fail to give the signal to inhale, causing the individual to miss one or more cycles of breathing. If the pause in breathing is long enough, the percentage of oxygen in the circulation will drop to a lower than normal level (Hypoxaemia) and the concentration of carbon dioxide will build to a higher than normal level (hypercapnia). In turn, these conditions of hypoxia and hypercapnia will trigger additional effects on the body. Brain cells need constant oxygen to live, and, if the level of blood oxygen goes low enough for long enough, the consequences of brain damage and even death will occur. Fortunately, central sleep apnea is more often a chronic condition that causes much milder effects than sudden death. The exact effects of the condition will depend on how severe the apnea is, and the individual characteristics of the person having the apnea. Several examples are discussed below, and more about the nature of the condition is presented in the section on Clinical Details.

In any person, hypoxia and hypercapnia have certain common effects on the body. The heart rate will increase, unless there are such severe co-existing problems with the heart muscle itself or the autonomic nervous system that makes this compensatory increase impossible. The more translucent areas of the body will show a bluish or dusky cast from cyanosis, which is the change in hue that occurs due to lack of oxygen in the blood ("turning blue"). Overdoses of drugs that are respiratory depressants (such as heroin, and other opiates) kill by damping the activity of the brain's respiratory control centers. In central sleep apnea, the effects of sleep alone can remove the brain's mandate for the body to breathe. Even in severe cases of central sleep apnea, the effects almost always result in pauses that make breathing irregular, rather than cause the total cessation of breathing.

• Normal Respiratory Drive: After exhalation, the blood level of oxygen decreases and that of carbon dioxide increases. Exchange of gases with a lungful of fresh air is necessary to replenish oxygen and rid the bloodstream of built-up carbon dioxide. Oxygen and carbon dioxide receptors in the blood stream (called chemoreceptors) send nerve impulses to the brain, which then signals reflex opening of the larynx (so that the opening between the vocal cords enlarges) and movements of the rib cage muscles and diaphragm. These muscles expand the thorax (chest cavity) so that a partial vacuum is made within the lungs and air rushes in to fill it.
• Physiologic effects of central apnea: During central apneas, the central respiratory drive is absent, and the brain does not respond to changing blood levels of the respiratory gases. No breath is taken despite the normal signals to inhale. The immediate effects of central sleep apnea on the body depend on how long the failure to breathe endures. At worst, central sleep apnea may cause sudden death. Short of death, drops in blood oxygen may trigger seizures, even in the absence of epilepsy. In people with epilepsy, the hypoxia caused by apnea may trigger seizures that had previously been well controlled by medications. In other words, a seizure disorder may become unstable in the presence of sleep apnea. In adults with coronary artery disease, a severe drop in blood oxygen level can cause angina, arrhythmias, or heart attacks (myocardial infarction). Longstanding recurrent episodes of apnea, over months and years, may cause an increase in carbon dioxide levels that can change the pH of the blood enough to cause a metabolic acidosis.

Laboratory findings

AHI	Rating
<5	Normal
5-15	Mild
15-30	Moderate
>30	Severe

Polysomnography of sleep apnea shows pauses in breathing that are followed by drops in blood oxygen and increases in blood carbon dioxide. In adults, a pause must last 10 seconds to be scored as an apnea. However in young children, who normally breathe at a much faster rate than adults, the pause may be many seconds shorter and still be considered apnea. The cessation of airflow in central sleep apnea has an association with no physical attempts to breathe. On polysomnograms, there is an absence of rib cage and abdominal movements while airflow ceases at the nose and lips. Obstructive sleep apnea shows pauses in breathing for at least 10 seconds causing a decrease in blood oxygen and associates with physical attempts to breathe.

Hypopneas in adults are defined as a 50% reduction in air flow for more than ten seconds, followed by a 4% desaturation, and/or arousal. The Apnea-Hypopnea Index (AHI) is expressed as the number of apneas and hypopneas per hour of sleep.

Clinical details

Any individual, no matter how healthy, who is given enough of a central respiratory depressant drug will develop apnea on a central basis. Generally, drugs that are central respiratory depressants also have sedative effects, and so the individual taking a toxic dose of such a drug is likely to be asleep, or at least in an altered state of consciousness, when breathing becomes irregular. Alcohol is such a central respiratory depressant in large doses, so are opiates, barbiturates, benzodiazepines, and many other tranquilizers. Some individuals have abnormalities that predispose them to central sleep apnea. The treatment for the condition depends on its specific cause.

Similarly, in any person who has some form of sleep apnea (including obstructive sleep apnea), breathing irregularities during sleep can be dangerously aggravated by taking one of these drugs. Quantities that are normally considered safe may cause the person with chronic sleep apnea to stop breathing altogether. Should these individuals have general anesthesia, for example, they require prolonged monitoring after initial recovery, as compared to a person with no history of sleep apnea, because apnea is likely to occur with even low levels of the drugs in their system.

Premature infants with immature brains and reflex systems are at high risk for central sleep apnea syndrome, even if these babies are otherwise healthy. Fortunately, those premature babies who have the syndrome will generally outgrow it as they mature, providing they receive careful enough monitoring and supportive care during infancy to survive. Because of the propensity toward apnea, medications that can cause respiratory drive depression are either not given to premature infants, or given under careful monitoring, with equipment for resuscitation immediately available. Such precautions are routinely taken for premature infants after general anesthesia. Caffeine has been found to help reduce apnea in preterm infants and to aid in care after general anesthesia.^[20]

Sudden infant death syndrome is sometimes theorized to be attributable to sleep apnea.

Congenital Central Hypoventilation Syndrome: This rare, inborn condition involves a specific gene, PHOX2B. This homeobox gene guides maturation of the autonomic nervous system, and loss-of-function mutations lead to the failure of the brain to effectively control breathing during sleep in patients with the syndrome. There may be a pattern of recognizable facial features among individuals affected with this syndrome.^[21]

Once almost uniformly fatal, congenital hypoventilation ("abnormally low ventilation") syndrome is now treatable. The children who have it must have tracheotomies and access to mechanical ventilation on respirators while sleeping, but most do not need to use a respirator while awake. The use of a diaphragmatic pacemaker may offer an alternative for some patients. When pacemakers have enabled some children to sleep without the use of a mechanical respirator, reported cases still required the tracheotomy to remain in place, because the vocal cords did not move apart with inhalation. This form of central sleep apnea has been called Ondine's curse. Now that some children with the syndrome have grown up, there is particular need for their avoidance of adolescent behaviors, such as alcohol use, which can easily be lethal.^[22]

Adults suffering from congestive heart failure are at risk for a form of central sleep apnea called Cheyne-Stokes respiration. This is periodic breathing with recurrent episodes of apnea alternating with episodes of rapid breathing. In those who have it, Cheyne-Stokes respirations occur while both awake and asleep. There is good evidence that replacement of the failed heart (heart transplant) cures central apnea in these patients. The use of some medications that are respiratory stimulants decrease the severity of apnea in some patients.

Section references

This section may need to be wikified to meet Wikipedia's quality standards. Please help by adding relevant internal links, or by improving the section's layout. (April 2009)

1) Macey PM. Macey KE. Woo MA. Keens TG. Harper RM. Aberrant neural responses to cold pressor challenges in congenital central hypoventilation syndrome.[see comment]. [Journal Article] Pediatric Research. 57(4):500-9, 2005 Apr.

2) Bradley TD. Floras JS. Sleep apnea and heart failure: Part II: central sleep apnea. [Review] [55 refs] [Journal Article. Review] Circulation. 107(13):1822-6, 2003 April 8.

3) Mansfield DR. Solin P. Roebuck T. Bergin P. Kaye DM. Naughton MT. The effect of successful heart transplant treatment of heart failure on central sleep apnea.[see comment]. [Journal Article] Chest. 124(5):1675-81, 2003 Nov.

4)Javaheri S. Acetazolamide improves central sleep apnea in heart failure: a double-blind, prospective study. [Clinical Trial. Journal Article. Randomized Controlled Trial] American Journal of Respiratory & Critical Care Medicine. 173(2):234-7, 2006 Jan 15. 7 oclock and all's crap

Mixed apnea and complex sleep apnea

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.^{[citation needed]}

Complex sleep apnea has recently been described by researchers as a novel presentation of sleep apnea. Patients with complex sleep apnea exhibit OSA, but upon application of positive airway pressure, the patient exhibits persistent central sleep apnea. This central apnea is most commonly noted while on CPAP therapy, after the obstructive component has been eliminated. This has long been seen in sleep laboratories, and has historically been managed either by CPAP or BiLevel therapy. Adaptive servo-ventilation modes of therapy have been introduced to attempt to manage this complex sleep apnea. Studies have demonstrated marginally superior performance of the adaptive servo ventilators in treating Cheyne-Stokes breathing, however, no longitudinal studies have yet been published, nor have any results been generated which suggest any differential outcomes versus standard CPAP therapy. At the AARC 2006 in Las Vegas, NV, researchers reported successful treatment of hundreds of patients on Adapt SV therapy, however these results have not been reported in peer reviewed publications as of July, 2007.

An important finding by Dernaika, et al., (Chest 2007, 132) suggests that transient central apnea produced during CPAP titration (the so called "complex sleep apnea") is "... transient and self-limited." The central apneas may in fact be secondary to sleep fragmentation during the titration process. As of July 2007, there has been no alternate convincing evidence produced that these central sleep apnea events associated with CPAP therapy for obstructive sleep apnea are of any significant pathophysiologic import.

Research is ongoing, however, at the Harvard Medical School, including adding dead space to positive airway pressure for treatment of complex sleep-disordered breathing. (Sleep Med. 2005 Mar; 6(2): 177-8PMID 15716223).

Treatment

The most common treatment and arguably the most consistently effective treatment for sleep apnea is the use of a continuous positive airway pressure (CPAP) device^[23] , which 'splints' the patient's airway open during sleep by means of a flow of pressurized air into the throat. However the CPAP machine only assists inhaling whereas a BiPAP machine assists with both inhaling and exhaling, and is used in more severe cases.^{[citation needed]}

In addition to CPAP, a dentist specializing in sleep disorders can prescribe Oral Appliance Therapy (OAT). The oral appliance is a custom made mouthpiece that shifts the lower jaw forward which opens up the airway. OAT is usually successful in patients with mild to moderate obstructive sleep apnea. OAT is a relatively new treatment option for sleep apnea in the United States, but it is much more common in Canada and Europe.

CPAP and OAT are effective only for obstructive sleep apnea, not for central or mixed cases.

In mild cases of obstructive sleep apnea, use of a specially shaped pillow or shirt may reduce sleep apnea episodes, usually by causing users to sleep on the side instead of on the back or in a reclining position instead of flat.

For patients who do not tolerate or fail non-surgical measures, surgical treatment to anatomically alter the airway is available. Several levels of obstruction may be addressed, including the nasal passage, throat (pharynx), base of tongue, and facial skeleton. Surgical treatment for obstructive sleep apnea needs to be individualized in order to address all anatomical areas of obstruction. Often correction of the nasal passages needs to be performed in addition to correction of the oropharynx passage. Septoplasty and turbinate surgery may improve the nasal airway. Tonsillectomy and uvulopalatopharyngoplasty (UPPP or UP3) is available to address pharyngeal obstruction. Base of tongue advancement by means of advancing the genial tubercle of the mandible may help with the lower pharynx. A myriad of other techniques are available, including hyoid bone myotomy and suspension and various radiofrequency technologies. For patients who fail these operations, the facial skeletal may be advanced by means of a technique called maxillo-mandibular advancement, or two-jaw surgery (upper and lower jaws). Technically, this is accomplished by a surgery similar to orthognathic surgeries addressing an abnormal bite. The surgery involves a Lefort type one osteotomy and bilateral sagittal split mandibular osteotomies.

Possibly due to changes in pulmonary oxygen stores, sleeping on one's side (as opposed to on one's back) has been found to be helpful for central sleep apnea with Cheyne Stokes respiration (CSA-CSR)^[9].

Medications like Acetazolamide^[24][25] lower blood pH and encourage respiration. Low doses of oxygen are also used as a treatment for hypoxia but are discouraged due to side effects.^[25][26][27]

A 2005 study in the British Medical Journal found that learning and practising the didgeridoo helped reduce snoring and sleep apnea, as well as daytime sleepiness. This appears to work by strengthening muscles in the upper airway, thus reducing their tendency to collapse during sleep.^[28]

Benefits and risks for treatment by surgery

CPAP is functional in sleep apnea and it is cost-efficient for the health care system, but it is a symptomatic therapy and does not cure the disease ^[29]. In contrast, although not well known, surgery is more expensive and can cure sleep apnea: The Stanford Center for Excellence in Sleep Disorders Medicine achieved a 95% cure rate of sleep apnea patients by surgery ^[30]. Maxillomandibular advancement (MMA) is considered the most effective surgery for sleep apnea patients^[31], because it increases the posterior airway space (PAS) ^[32]. The main benefit of the operation is that the oxygen saturation in the arterial blood increases^[32]. In a study published 2008 93.3.% of surgery patients achieved a successful quality of life based on the Functional Outcomes of Sleep Questionnaire (FOSQ)^[32]. Surgery lead to a significant increase in general productivity (P = .0003), social outcome (P = .0020), activity level (P = .0008), vigilance (P = .0028), intimacy and sex (P = .0039), and the total score (P = .0002) postoperatively ^[32]. Overall risks of MMA surgery are low: The Stanford University Sleep Disorders Center found 4 failures in a series of 177 patients ^[33].

Surgery and anesthesia in patients with sleep apnea

This section needs additional citations for verification. Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (July 2009)

Several inpatient and outpatient procedures use sedation. Many drugs and agents used during surgery to relieve pain and to depress consciousness remain in the body at low amounts for hours or even days afterwards. In an individual with either central, obstructive or mixed sleep apnea, these low doses may be enough to cause life-threatening irregularities in breathing or collapses in a patient’s airways.^[34]

Use of analgesics and sedatives in these patients postoperatively should therefore be minimized or avoided.

Surgery on the mouth and throat, as well as dental surgery and procedures, can result in postoperative swelling of the lining of the mouth and other areas that affect the airway. Even when the surgical procedure is designed to improve the airway, such as tonsillectomy and adenoidectomy or tongue reduction - swelling may negate some of the effects in the immediate postoperative period. Once the swelling resolves and the palate becomes tightened by postoperative scarring however, the full benefit of the surgery may be noticed.

Individuals with sleep apnea generally require more intensive monitoring after surgery for these reasons. Sleep apnea patients undergoing any medical treatment must make sure his or her doctor and/or anesthetist are informed about their condition. Alternate and emergency procedures may be necessary to maintain the airway of sleep apnea patients. If an individual suspects he or she may have sleep apnea, communication with their doctor about possible pre-procedure screening may be in order.

See also

• Obstructive sleep apnea
• Obesity hypoventilation syndrome
• Marfan syndrome
• Ondine's curse
• Sleep medicine

References

1. ^ "Sleep Apnea 101
2. ^ Mayo Clinic Discovers New Type Of Sleep Apnea
3. ^ Young, T, et al., “Epidemiology of obstructive sleep apnea: a population health perspective.” Am J Respir Crit Care Med 165 (2002): 1217-1239.
4. ^ Young, Terry, et al., "The Occurrence of Sleep-Disordered Breathing among Middle-Aged Adults." The New England Journal of Medicine. 328, no. 17 (1993): 1230-1235.
5. ^ Kapur, MD, Vishesh, et al., "The Medical costs of Undiagnosed Sleep Apnea". Sleep. 22, no. 6 (1999): 749-755.
6. ^ Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea - Neill et al. 155 (1): 199 - American Journal of Respiratory and Critical Care Medicine
7. ^ The Study Of The Influence Of Sleep Position On Sleep Apnea
8. ^ Positioner-a method for preventing sleep apnea
9. ^ ^{a b} Lateral sleeping position reduces severity of cent...[Sleep. 2006] - PubMed Result
10. ^ Morris, LG; A. Kleinberger, K. Lee, L. Liberatore, O. Burschtin (November 2008). "Rapid risk stratification for obstructive sleep apnea, based on snoring severity and body mass index". Otolaryngol Head Neck Surg (Elsevier) 139 (5): 615–618. doi:10.1016/j.otohns.2008.08.026. 
11. ^ Yan-fanga, Shi; Yu-ping, Wang (January 2009). "Sleep-disordered breathing: Impact on functional outcome of ischemic stroke patients". Sleep Medicine (Elsevier) Article in Press, Corrected Proof: 324. doi:10.1016/j.pcad.2008.06.002. 
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15. ^ Grigg-Damberger M. (2006-02). "Why a polysomnogram should become part of the diagnostic evaluation of stroke and transient ischemic attack". Journal of Clinical Neurophysiology 23 (1): 21–38. doi:10.1097/01.wnp.0000201077.44102.80. PMID 16514349. 
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General references

• Maninder Kalra; Ranajit Chakraborty (March 2007). "Genetic susceptibility to obstructive sleep apnea in the obese child". Sleep Medicine 8 (2): 169–175. doi:10.1016/j.sleep.2006.09.003. PMID 17275401. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17275401&query_hl=4&itool=pubmed_docsum. 
• American Academy of Sleep Medicine Task Force (1999). "Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research.". Sleep 22 (5): 667–89. PMID 10450601. 
• Bell, R. B.; Turvey, T. A. (2001). "Skeletal advancement for the treatment of obstructive sleep apnea in children". Cleft Palate-Craniofacial Journal 38 (2): 147–54. doi:10.1597/1545-1569(2001)038<0147:SAFTTO>2.0.CO;2. 
• Caples S, Gami A, Somers V (2005). "Obstructive sleep apnea.". Ann Intern Med 142 (3): 187–97. doi:10.1001/archinte.142.1.187. PMID 15684207. 
• Cohen, M. M. J.; Kreiborg, S. (1992). "Upper and lower airway compromise in the Apert syndrome". American Journal of Medical Genetics 44: 90–93. doi:10.1002/ajmg.1320440121. 
• de Miguel-Díez J, Villa-Asensi J, Alvarez-Sala J (2003). "Prevalence of sleep-disordered breathing in children with Down syndrome: polygraphic findings in 108 children." (PDF). Sleep 26 (8): 1006–9. PMID 14746382. http://www.annals.org/cgi/reprint/142/3/187.pdf. 
• Mathur R, Douglas N (1994). "Relation between sudden infant death syndrome and adult sleep apnoea/hypopnoea syndrome.". Lancet 344 (8925): 819–20. doi:10.1016/S0140-6736(94)92375-2. PMID 7916096. 
• Mortimore I, Douglas N (01 September 1997). "Palatal muscle EMG response to negative pressure in awake sleep apneic and control subjects.". Am J Respir Crit Care Med 156 (3 Pt 1): 867–73. PMID 9310006. http://ajrccm.atsjournals.org/cgi/content/full/156/3/867. 
• Perkins, J. A.; Sie, K. C. Y., Milczuk, H., & Richardson, M. A. (1997). "Airway management in children with craniofacial anomalies". Cleft Palate-Craniofacial Journal 34 (2): 135–40. doi:10.1597/1545-1569(1997)034<0135:AMICWC>2.3.CO;2. 
• Sculerati N.; Gottlieb MD. Zimbler MS. Chibbaro PD. McCarthy JG. (December 1998). "Airway management in children with major craniofacial anomalies.". Laryngoscope 108 (12): 1806–12. doi:10.1097/00005537-199812000-00008. 
• Shepard, J. W.; Thawley, S. E. (1990). "Localization of upper airway collapse during sleep in patients with obstructive sleep apnea". American Review of Respiratory Disorders 141: 1350–55. 
• Sher, A. (1990). Obstructive sleep apnea syndrome: a complex disorder of the upper airway. Otolaryngologic Clinics of North America, 24, 600.
• Shott S, Amin R, Chini B, Heubi C, Hotze S, Akers R (2006). "Obstructive sleep apnea: Should all children with Down syndrome be tested?". Arch Otolaryngol Head Neck Surg 132 (4): 432–6. doi:10.1001/archotol.132.4.432. PMID 16618913. 
• Shouldice RB, O'Brien LM, O'Brien C, de Chazal P, Gozal D, Heneghan C (2004). "Detection of obstructive sleep apnea in pediatric subjects using surface lead electrocardiogram features". Sleep 27 (4): 784–92. PMID 15283015. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15283015&dopt=Citation. 
• Slovis B. & Brigham K. (2001). "Disordered Breathing". in ed Andreoli T. E.. Cecil Essentials of Medicine. Philadelphia: W.B. Saunders. pp. pp210–211. 
• Strollo P, Rogers R (1996). "Obstructive sleep apnea.". N Engl J Med 334 (2): 99–104. doi:10.1056/NEJM199601113340207. PMID 8531966. 
• Sullivan C, Issa F, Berthon-Jones M, Eves L (1981). "Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares.". Lancet 1 (8225): 862–5. doi:10.1016/S0140-6736(81)92140-1. PMID 6112294. 

External links

• American Sleep Association
• American Academy of Sleep Medicine
• British Snoring & Sleep Apnoea Association
• Mayo Clinic Discovers New Type of Sleep Apnea, Mayo Clinic, September 1, 2006.
• National Heart, Lung, and Blood Institute: Your Guide To Healthy Sleep
• UK Sleep Apnoea Trust Association
• Merck: Sleep Apnea
• American Academy of Dental Sleep Medicine

v • d • e Pathology of the nervous system, primarily CNS (G00–G47, 320–349) Brain/ encephalopathy Inflammatory Encephalitis (Viral encephalitis, Herpesviral encephalitis) · Cavernous sinus thrombosis · Brain abscess (Amoebic) Degenerative Extrapyramidal and movement disorders Basal ganglia disease: Parkinsonism (Parkinson's disease, Postencephalitic parkinsonism)  · Neuroleptic malignant syndrome  · Pantothenate kinase-associated neurodegeneration · Progressive supranuclear palsy · Striatonigral degeneration · Hemiballismus · Huntington's disease · Olivopontocerebellar atrophy Dyskinesia: Dystonia (Spasmodic torticollis, Meige's, Blepharospasm) · Chorea (Choreoathetosis)  · Myoclonus (Myoclonic epilepsy) Essential tremor  · Restless legs  · Stiff person Dementia Alzheimer's (Early-onset)  · Frontotemporal dementia/Frontotemporal lobar degeneration (Pick's, Dementia with Lewy bodies) · Multi-infarct dementia Mitochondrial disease Leigh's Demyelinating autoimmune (Multiple sclerosis, Neuromyelitis optica, Schilder's disease) · hereditary (Adrenoleukodystrophy, Alexander, Canavan, Krabbe, ML, Pelizaeus-Merzbacher, VWM, MFC, CAMFAK syndrome) · Central pontine myelinolysis · Marchiafava-Bignami disease  · Alpers' Episodic/ paroxysmal Seizure/epilepsy Focal  · Generalised  · Status epilepticus  · Myoclonic epilepsy Headache Migraine (Familial hemiplegic)  · Cluster  · Vascular  · Tension Vascular Transient ischemic attack (Amaurosis fugax, Transient global amnesia) Cerebrovascular disease  · Stroke (MCA, ACA, PCA, Foville's, Millard-Gubler, Lateral medullary, Weber's, Lacunar stroke) Sleep disorders Insomnia  · Hypersomnia  · Sleep apnea (Obstructive, Ondine's curse)  · Narcolepsy  · Cataplexy  · Kleine-Levin  · Circadian rhythm sleep  · Delayed sleep phase  · Advanced sleep phase CSF Intracranial hypertension (Hydrocephalus/Normal pressure, Idiopathic intracranial hypertension) · Cerebral edema · Intracranial hypotension Other Brain herniation · Reye's  · Hepatic encephalopathy  · Toxic encephalopathy Spinal cord/ myelopathy Inflammatory Myelitis: Poliomyelitis · Demyelinating disease (Transverse myelitis) · Tropical spastic paraparesis Other Syringomyelia · Syringobulbia · Morvan's syndrome · Vascular myelopathy (Foix-Alajouanine syndrome) · Spinal cord compression Both/either Inflammatory Encephalomyelitis (Acute disseminated) Meningitis/Arachnoiditis: Bacterial (Tuberculous, Haemophilus, Pneumococcal) · Viral (Herpesviral) · Fungal (Cryptococcal) · Aseptic (Drug-induced) Meningoencephalitis Systemic atrophies SA Friedreich's ataxia · Ataxia telangiectasia MND UMN only: PLS · PP · HSP LMN only: PMA · PBP (Fazio-Londe, Infantile progressive bulbar palsy) · SMA (SMN-linked, Kennedy disease, SMAX2, DSMA1) both: ALS see also congenital, tumors

v • d • e Sleep Sleep stages Rapid eye movement sleep · Non-rapid eye movement sleep · Slow-wave sleep Brain waves Alpha wave · Beta wave · Gamma wave · Delta wave · Theta rhythm · K-complex Sleep disorders Advanced sleep phase syndrome · Automatic behavior · Circadian rhythm sleep disorder · Delayed sleep phase syndrome · Dyssomnia · Hypersomnia · Insomnia · Narcolepsy · Night eating syndrome · Night terror · Nocturia · Nocturnal emission · Nocturnal myoclonus · Non-24-hour sleep-wake syndrome · Obesity hypoventilation syndrome · Ondine's curse · Parasomnia · Sleep apnea · Sleep deprivation · Sleeping sickness · Sleepwalking · Somniloquy Benign phenomena Dream · Exploding head syndrome · False awakening · Hypnagogia · Hypnic jerk · Lucid dream · Nightmare · Sleep paralysis · Somnolence Related topics Bed (Bunk bed, Four poster bed, Futon, Hammock, Mattress) · Bed bug · Bedding · Bedroom · Bedtime · Bedtime toy · Bedtime story · Caffeine nap · Chronotype · Dream journal · Jet lag · Lullaby · Nap · Nightwear · Polyphasic sleep · Polysomnography · Power nap · Siesta · Sleep and creativity · Sleep and learning · Sleep debt · Sleep diary · Sleep inertia · Sleep medicine · Sleeping while on duty · Sleepover · Snoring · Excessive daytime sleepiness

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