Central sleep apnea is a condition where your brain temporarily stops sending signals to the muscles that control breathing during sleep. Unlike the more common obstructive sleep apnea, where tissue physically blocks the airway, central sleep apnea involves an open airway with no effort to breathe at all. It affects roughly 0.9% of adults over 40, making it far less common than obstructive sleep apnea, but it can be serious, particularly when linked to heart failure or neurological conditions.
How Central Sleep Apnea Works
Breathing during sleep depends on automatic signals from the brainstem. These signals tell the diaphragm and other respiratory muscles when to contract. In central sleep apnea, that signaling cycle breaks down. The result is a pause in breathing, typically lasting at least 10 seconds, during which no air moves in or out and the body makes no attempt to inhale.
The key player is carbon dioxide (CO2), the waste gas your body exhales. Your brain uses CO2 levels in the blood as a thermostat for breathing. When CO2 rises, the brain triggers a breath. When it drops too low, the brain’s drive to breathe can shut off entirely. In central sleep apnea, CO2 levels frequently dip below the threshold needed to trigger the next breath, especially during the transition between wakefulness and sleep or after a brief arousal. The breathing pause continues until CO2 climbs back above that threshold, at which point the brain kicks the respiratory muscles back into action, often with a burst of rapid, deep breaths that overshoots the mark and drives CO2 too low again. This creates a repeating cycle of over-breathing followed by no breathing.
How It Differs From Obstructive Sleep Apnea
In obstructive sleep apnea, the throat muscles relax and collapse inward, physically blocking airflow. Your chest and diaphragm are still trying to breathe; they just can’t get air past the obstruction. In central sleep apnea, the airway stays open, but the respiratory muscles receive no command to move. A sleep study can distinguish the two by measuring chest and abdominal effort: obstructive events show effort against a closed airway, while central events show no effort at all.
Some people have both types simultaneously, a condition called complex or treatment-emergent central sleep apnea. This sometimes appears when someone being treated for obstructive sleep apnea with a standard CPAP machine begins experiencing central events once the airway obstruction is resolved.
Common Causes and Risk Factors
Heart Failure
Heart failure is the most significant driver of central sleep apnea. Among people with heart failure, the prevalence jumps to about 4.8%, roughly five times the rate in the general population. The mechanism is well understood: a weakened heart leads to fluid buildup in the lungs. That congestion stimulates nerve receptors in the lung tissue, which trigger chronic over-breathing and push CO2 levels lower than normal. When you lie down at night, blood from your legs shifts toward the chest, worsening the congestion and intensifying the cycle. A brief awakening during sleep causes a small burst of extra ventilation, enough to push CO2 below the breathing threshold and trigger a central apnea. This specific pattern of gradually rising and falling breathing effort, punctuated by pauses, is called Cheyne-Stokes breathing.
Opioid Use
Chronic opioid medications directly suppress the brainstem’s respiratory center, including the cluster of neurons responsible for setting breathing rhythm and pace. Opioids dampen the brain’s sensitivity to rising CO2, meaning it takes a higher-than-normal CO2 level to prompt a breath. They also reduce breathing rate and disrupt the regularity of the breathing pattern. The result is often chaotic, irregular breathing during sleep with frequent central pauses. For a formal diagnosis of opioid-related central sleep apnea, a sleep study needs to show more than 5 central events per hour without periodic breathing, or more than 10 per hour if periodic breathing is present.
Stroke and Neurological Conditions
Damage to the brainstem from a stroke, tumor, or degenerative disease can directly impair the respiratory control centers. Because the brainstem houses the automatic breathing circuitry, even small areas of injury in the right location can destabilize the signaling to respiratory muscles during sleep, when voluntary control of breathing is absent.
High Altitude
Healthy people with no underlying conditions can develop central sleep apnea at high elevations, generally above about 3,500 feet. Lower oxygen levels at altitude trigger over-breathing, which drives CO2 down and creates the same threshold problem seen in other forms of central sleep apnea. This typically resolves after descending or acclimatizing.
Who Gets It
Central sleep apnea is strongly skewed by age and sex. The median age at diagnosis is 69, and men are affected at roughly nine times the rate of women (1.8% versus 0.2% in population studies). Beyond heart failure and opioid use, other risk factors include kidney failure, atrial fibrillation, and living at high altitude.
Symptoms to Recognize
The symptoms overlap significantly with obstructive sleep apnea, which is one reason central sleep apnea often goes unrecognized. You or a bed partner may notice repeated pauses in breathing during sleep, but without the loud snoring and gasping typical of obstructive events. Common daytime symptoms include excessive sleepiness, morning headaches, difficulty concentrating, and waking up feeling unrefreshed. Some people wake during the night feeling short of breath, which can be particularly pronounced in the heart failure form.
Because the symptoms are nonspecific, a sleep study (polysomnography) is the only way to confirm the diagnosis. The study measures airflow, blood oxygen, and respiratory effort simultaneously, allowing clinicians to classify each breathing pause as central or obstructive. A diagnosis requires at least 5 central events per hour of sleep, with more than half of all events being central rather than obstructive.
Treatment Options
Treating the Underlying Cause
When central sleep apnea stems from heart failure, optimizing heart failure treatment often reduces or eliminates the breathing pauses. Reducing fluid overload, improving cardiac output, and managing blood pressure can lower pulmonary congestion enough to stabilize the breathing cycle. For opioid-induced cases, reducing the opioid dose or switching medications (when medically possible) is the most direct intervention.
Adaptive Servo-Ventilation
Adaptive servo-ventilation (ASV) is a specialized breathing machine designed specifically for central sleep apnea. Unlike a standard CPAP, which delivers a constant stream of air, ASV monitors your breathing pattern in real time and adjusts its support breath by breath. When it detects a pause or slowing, it increases airflow to keep you breathing. When your breathing is steady, it backs off or stops delivering air entirely. This makes it effective at smoothing out the cycling pattern of over-breathing and apnea.
There is one critical exception. The landmark SERVE-HF trial found that ASV increased the risk of cardiovascular death by 33.5% in heart failure patients whose hearts pumped poorly (ejection fraction of 45% or below). The absolute risk was significant: 10% annual cardiovascular death rate with ASV compared to 7.5% without it, and the risk worsened as heart function declined further. ASV is now contraindicated in this specific group. It remains an option for central sleep apnea from other causes, including opioid use, primary central sleep apnea, and heart failure with preserved heart function, though the evidence in that last group is less definitive.
Phrenic Nerve Stimulation
For people who cannot use or tolerate mask-based therapy, an implantable device that stimulates the phrenic nerve offers an alternative. The phrenic nerve controls the diaphragm. A small stimulator, implanted similarly to a cardiac pacemaker, sends electrical signals through the nerve during sleep to trigger diaphragm contractions and maintain breathing. In a meta-analysis of clinical studies, patients’ breathing disruption index dropped from a median of 40 events per hour to 18 events per hour. Unlike positive pressure machines, this approach creates natural negative-pressure breathing, closer to how the body breathes on its own.
Supplemental Oxygen
Nighttime supplemental oxygen can help in some cases by preventing the drops in blood oxygen that worsen the breathing instability cycle. It does not directly address the signaling problem, but it reduces the severity of oxygen desaturation during apneas and can decrease the frequency of events, particularly in heart failure patients for whom ASV is not safe.
Living With Central Sleep Apnea
Central sleep apnea is a chronic condition for most people, particularly when tied to heart failure or neurological disease. Treatment can dramatically improve sleep quality and daytime function, but it typically requires ongoing use. If you use an ASV machine or oxygen therapy, regular follow-up sleep studies help confirm the treatment is still effective, since the underlying condition may change over time. For the high-altitude form, the condition resolves once you return to lower elevation or after several nights of acclimatization, and no long-term treatment is needed.