Central Sleep Apnea

What is central sleep apnea (CSA)?

It refers to repetitive failure to initiate efforts to breathe.

Can central sleep apneas cause excessive drops in blood oxygen levels?

Yes. Although severe oxygen desaturations are more common with obstructive apneas, they sometimes do occur to surprisingly (and dangerously) low levels in conjunction with central apneas: even in some non-obese patients without concurrent lung disorders or pre-existing heart problems.

What are the causes of central sleep apnea?

There are many possible causes. A discussion of all of them is beyond the purpose of this web site. Instead, we will focus on those causes that are both common and likely to be causing serious problems for patients who visit The Sleep Site.

Repeated Arousals From Sleep and Sensitivity to Low Blood Carbon Dioxide Tensions

-The control of breathing during sleep differs from that during full wakefulness. When we inhale, we take in oxygen, and when we exhale, we breathe out carbon dioxide which is a waste product of our body’s metabolism. During sleep, especially non-REM sleep, even minor increases in the carbon dioxide levels in our blood stimulate us to take another breath. In similar fashion, even small decreases in blood carbon dioxide levels (which can result from our breathing more deeply or rapidly) will result in pauses in breathing (central apneas).

-when we first doze off, it is normal to experience brief pauses in breathing. Once we are soundly asleep, breathing tends to stabilize and become regular.

-if patients are unduly arousable, each of these normal pauses in breathing may trigger an arousal or brief awakening with a sudden, transient increase in breathing that drops carbon dioxide levels–which then results in another pause in breathing as the patient begins to doze off again, which in turn triggers yet another arousal…and so on. This phenomenon is reminiscent of a “slipping clutch”. If afflicted patients could simply get into a sound sleep, their breathing would stabilize and become regular, but they “can’t get there”.

-Obviously, anything that triggers arousals or awakenings in such patients might result in their “getting stuck” in this frustrating cycle of dozing and arousing. Some specific circumstances that can precipitate the triggering of CSAs via this basic mechanism:


This is a MAJOR CAUSE OF CSA that recently was termed “COMPLEX SLEEP APNEA” (the emergence of central apneas promptly upon institution of treatment of obstructive sleep apnea with positive airway pressure).

THIS PROBLEM CAUSES MANY PATIENTS WITH OBSTRUCTIVE SLEEP APNEA TO ABANDON TREATMENT…unless something is done to address their central sleep apneas.

WHY? Because patients with complex sleep apnea cannot achieve and maintain sound sleep when using CPAP or bilevel PAP. They find that they either cannot fall into a sound sleep when using their equipment, or that their sleep is light and fragmented by arousals.


In some but not all cases, bed partners observe that the patients are having pauses in breathing, even though all snoring may have been eliminated.
Some (but not all) patients awaken with feelings of breathlessness or with gasping.
Some note that they do not feel as well during the day as they expected.

I HAVE ALWAYS FELT THAT IT IS CRUCIAL TO DEAL WITH THIS PROBLEM OF CENTRAL APNEAS THAT EMERGE WHEN POSITIVE AIRWAY PRESSURE IS FIRST STARTED. I find it vital to ensure that patients are able to sleep comfortably through the night with their equipment in place. Attention to every detail is extremely important. Otherwise, sleep apnea victims will never be able to get used to using positive airway pressure, such that they will either abandon treatment entirely or turn to therapeutic alternatives with much lower success rates. I suspect that the fact that many sleep centers do not treat central apneas may help explain why national CPAP compliance rates are so low.

HOW CAN ONE TREAT THE PROBLEM OF CENTRAL SLEEP APNEAS RESULTING FROM INSTITUTION OF CPAP OR BILEVEL PAP? Until now, the options were limited and not predictably helpful. Fortunately, a better answer has just emerged.

USE OF BILEVEL PAP WITH A “BACK-UP RATE” (INTERMITTENT MANDATORY VENTILATION OR IMV). These units sense when patients fail to initiate breathing and then respond with delivery of bursts of air at pre-set rates and pressure levels, much like a demand ventilator by way of the nose. However, they often were poorly tolerated by patients who would report inability to synchronize their breathing with the machine, and the less than subtle way that they would intervene at the time of breathing pauses would often trigger arousals and set up a cycle of repeated central apneas–thereby making the problem even worse.

DELIVERY OF SUPPLEMENTAL OXYGEN VIA THE CPAP OR BILEVEL PAP UNIT. This strategy sometimes stabilizes breathing but not in many cases. Also, oxygen therapy has its own problems. Oxygen concentrators are heavy and not travel friendly. Their ongoing rental is very expensive. They also are frequently noisy and many of them generate heat: both of which can worsen the sleep of patients and their bed partners alike!
ADAPTIVE SERVO-VENTILATION (ASV). Here is the good news! At last, a treatment has been developed that is far more comfortable than bilevel PAP with IMV, that is virtually always effective and that typically renders use of supplemental oxygen unnecessary. Click here for more information on this important breakthrough in sleep medicine: adaptive servo-ventilation (ASV).


As described elsewhere on The Sleep Site, this common syndrome involves repeated jerks in the lower extremities–and in some cases, in the arms. It usually does not cause symptoms–such that treatment is often unnecessary. However, in patients prone to central sleep apnea, repeated arousals triggered by PLMS may result in precipitation of repeated pauses in breathing that then may perpetuate themselves, as the patient experiences inability to return to sound sleep.

3. ANY OTHER FACTORS–WHETHER INHERENT IN THE PATIENT OR ENVIRONMENTAL, SUCH AS NOISE can trigger the onset of repeated central apneas in predisposed patients.

Heart Failure and/or Atrial Fibrillation

-The brain continuously monitors the carbon dioxide levels in the blood and increases or decreases our rate and depth of breathing correspondingly.

-HEART FAILURE means that the heart is functioning poorly and that it is not pumping blood as vigorously as it should. This phenomenon results in a delay in delivery of blood to the brain (“delayed circulation time”), such that the brain’s control of breathing is chronically based on outdated information about the current levels of carbon dioxide in the blood. The consequence is a waxing and waning of breathing effort (“overshooting and undershooting”), with intervening pauses in breathing, in a crescendo-decrescendo fashion: a pattern called Cheyne Stokes breathing. It is important to note that in some patients, the upper airway may be sucked shut during the crescendo increases in breathing: resulting in mixed (central followed by obstructive) apneas. Some studies have shown that half of patients with heart failure have sleep apnea, typically with a significant number of central apneas.

-ATRIAL FIBRILLATION is a relatively common type of abnormal heart rhythm. Normally, the upper chambers of the heart (atria) that receive blood are activated in a relatively stable fashion at a reasonable rate, and the larger lower, pumping chambers (ventricles) are then activated in a coordinated fashion to push the received blood out to the body and lungs: a well-synchronized mechanism somewhat reminiscent of the skilled milking of a cow. Patients with atrial fibrillation instead experience an uncoordinated quivering activation of the upper chambers at rates of over 300 contractions per minute. Only a fraction of these activations are allowed to get through to the ventricles, and such occurs in a relatively random fashion such that the ventricles often pump blood at times that very low blood volumes have been squeezed into them from the atria. The result is a drop in the total volume of blood pumped by the heart and a consequent delayed circulation time, such as occurs in heart failure. Thus, some (but not all) patients with atrial fibrillation develop Cheyne Stokes breathing.

There are additional mechanisms that enter into the development of Cheyne Stokes breathing in patients with heart failure and atrial fibrillation. However, a knowledge of the phenomenon of delayed circulation time facilitates an understanding of this important abnormal breathing pattern.

Also, it is important to realize that many patients with heart failure and atrial fibrillation also have obstructive sleep apneas.

-CENTRAL SLEEP APNEA IS AN OMINOUS FINDING IN HEART FAILURE PATIENTS–AND IT ALSO MAY ACCELERATE PROGRESSIVE DETERIORATION IN THEIR HEART FUNCTION. increased death rates and shortening of survival times in heart failure patients are strongly associated with Cheyne Stokes breathing. Furthermore, factors such as the resulting repeated drops in blood oxygen levels during central apneas can further damage the heart and render treatments for heart failure ineffective.


Failure to respond well to treatments for heart failure. Studies have shown that untreated sleep apnea can render heart failure virtually untreatable.
In some but not all cases, bed partners observe that the patients are having pauses in breathing, even though all snoring may have been eliminated.
Some (but not all) patients awaken with feelings of breathlessness or with gasping.
Increased daytime fatigue.


CPAP, BILEVEL PAP WITH INTERMITTENT MANDATORY VENTILATION AND OXYGEN sometimes help, but they frequently are ineffective.
ADAPTIVE SERVO-VENTILATION (ASV). This revolutionary new treatment typically eliminates central apneas and normalizes breathing in heart failure patients. Click here for more information on adaptive servo-ventilation (ASV).


–There are many other causes of central apneas that are less common–many of which can also cause inadequate depth of breathing (hypoventilation) during sleep. The following examples arise from damage to either the nervous system’s breathing control mechanisms or inadequate function of the muscles used for breathing. A number of these disorders may involve elevations in blood carbon dioxide tensions with failure of the patient’s breathing drive to respond normally to such build-ups in carbon dioxide levels.

Brainstem tumors, strokes, encephalitis and malformations such as Arnold-Chiari syndrome, Leigh’s syndrome, multiple sclerosis.
Autonomic (“automatic”) nervous system dysfunction–for example, in Shy Drager syndrome, Riley-Day syndrome and diabetic autonomic neuropathy.
Phrenic nerve palsies (damage to the nerves that activate the diaphragms).
Post-polio syndrome, amyotrophic lateral sclerosis (ALS), myasthenia gravis and Duchenne’s muscular dystrophy.

–Treatment of these other causes must be tailored to the individual patient.

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