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Central sleep apnea (CSA) occurs when the brain does not send the signal to breathe to the muscles of breathing. This usually occurs in infants or in adults with heart disease, cerebrovascular disease, or congenital diseases, but it also can be caused by some medications and high altitudes.

Central sleep apnea may occur in premature infants (born before 37 weeks of gestation) or in full term infants. It is defined as apneas lasting more than 20 seconds, usually with a change in the heart rate, a reduction in blood oxygen, or hypotonia (general relaxation of the body’s muscles). These children often will require an apnea monitor that sounds an alarm when apneas occur. Central sleep apnea in children is not the same thing as sudden infant death syndrome (SIDS).

Under normal circumstances, the brain monitors several things to determine how often to breathe. If it senses a lack of oxygen or an excess of carbon dioxide in the blood it will speed up breathing. The increase in breathing increases the oxygen and decreases the carbon dioxide in blood. Some people with heart or lung disease have an increase in carbon dioxide in their blood at all times.

When there is a chronic (long term) increase in blood carbon dioxide, the brain starts to ignore the oxygen level and monitors the blood carbon dioxide level to determine when to take the next breath. The control of breathing also becomes slower to respond to changes in carbon dioxide levels; so when a person takes more or deeper breaths and "blows off" carbon dioxide the drive to breathe decreases and the rate of breathing decreases. As a result of slower rate of breathing, the carbon dioxide builds back up in the blood and the rate of breathing increases again. The brain, slow to adjust, continues to signal for more rapid breathing until the carbon dioxide level drops too low. Breathing then slows down or stops until the carbon dioxide level rises again. This pattern of abnormal breathing is called Cheyne-Stokes breathing (after the men who described it). It is characterized by repetitive cycles of fast breathing followed by slow breathing and apnea. This breathing pattern happens when the person is awake or asleep, but becomes more of a problem when asleep. Some patients with heart failure have central sleep apnea associated with a Cheyne-Stokes pattern of breathing.

Central sleep apnea usually occurs in adults with other medical problems. In infants, it usually occurs with prematurity or other congenital disorders. In both patient groups it is usually suspected by the primary care doctor. Central sleep apnea can be diagnosed with a sleep study or overnight monitoring while the patient is in the hospital.

In infants, central sleep apnea is treated with an apnea alarm. This alarm monitors the infant’s breathing with sensors and sounds a loud noise when the infant experiences an apnea. The alarm usually wakes the infant and the parents. Most infants usually "out-grow" the central apnea episodes, so the alarm monitoring is stopped after the episodes resolve. In infants with other congenital problems, apnea monitoring may be needed for a longer period.

In adults with central sleep apnea, the apneas are treated by treating the underlying heart disease, medication interaction, high altitude, or other primary problem.

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Sleep Apnea (cont.)

What is obstructive sleep apnea and what causes it?

In obstructive sleep apnea (OSA), apneas have four components.

First, the airway collapses or becomes obstructed.
Second, an effort is made to take a breath, but it is unsuccessful.
Third, the oxygen level in the blood drops as a result of unsuccessful breathing.
Finally, when the amount of oxygen reaching the brain decreases, the brain signals the body to wake up and take a breath. (This is what the bed partner hears as a silence followed by a gasp for air.)
First, it is necessary to describe a "normal breath." A normal breath of air passes through the nasal passages, behind the soft palate and uvula (part of the soft palate), then past the tongue base, through the throat muscles, and between the vocal cords into the lungs. An obstruction to the flow of air at any of these levels may lead to apnea. The following are some examples:

airflow can become diminished if a person has a deviated septum (the middle wall of the nose that separates the two nostrils). A septum can be deviated to one or both sides narrowing the air passages;
there are filters in the nose called turbinates that can obstruct airflow when they become swollen;
if the palate and uvula (the part of soft palate that hangs down in the back of the throat) are long or floppy, they can fall backwards and close the area through which air flows;
the back of the tongue can also fall backwards and obstruct breathing especially when individuals lay flat on their backs; or
the side walls of the throat can fall together to narrow or close the airway.
To break it down even further:

the muscles of breathing work to expand the chest and lower the diaphragm to degenerate a negative pressure between the airways of the lungs and outside;
this negative pressure literally sucks air into the lungs;
the nasal passages, palate, tongue, and pharyngeal tissues can all contribute to narrowing of the airway;
if during an attempt to breathe the airway collapses or is obstructed the tissues of the airway are sucked together by the negative pressure;
the harder the chest tries to pull air in the greater the negative pressure and the more the tissues of the airway are sealed together; and
finally, when the oxygen in the blood stream decreases the person wakes up or the level of sleep becomes more shallow in order to more consciously take a breath.
People with obstructive sleep apnea have an airway that is more narrow than normal, usually at the base of the tongue and palate. When lying flat, the palate is above the air passage. When the pharyngeal muscles (muscles of the pharynx or throat ) relax the palate can fall backwards and this can obstruct the airway.

The genioglossus muscle is located where the base of the tongue attaches to the jawbone in front. Most people have enough space behind the tongue to take a breath without needing to pull the tongue forward. However, when obstructive sleep apnea patients are awake, this muscle needs to be active to pull the base of the tongue forward to open the airway. During sleep, most muscles including the genioglossus relax. During the stage of rapid eye movement (REM), the muscles completely relax. Relaxation of the genioglossus muscle during sleep allows the base of the tongue to fall backwards and the airway closes.

Patients with obstructive sleep apnea often don’t report waking up during the night with each episode of apnea. Frequently, during the apnea the brain only awakens from a deep sleep (stages 3, 4, or REM) to a shallow level of sleep. The genioglossus muscle then contracts and pulls the tongue forward so that a breath can be taken. The patient may remain asleep, but the deep sleep that is important to be fully rested the following day is disrupted