Central sleep apnea (CSA) affects roughly 0.9% of adults over age 40 in the general population, making it far less common than obstructive sleep apnea. In the largest sleep cohort study available, the Sleep Heart Health Study, 47.6% of participants had obstructive sleep apnea while only 0.9% had central sleep apnea. But that general number hides dramatic spikes in specific groups: up to 40% of people with heart failure have it, and about 24% of people on long-term opioid therapy develop it.
General Population Rates
In the Sleep Heart Health Study, which included 5,804 participants, the breakdown looked like this: about half had no sleep-disordered breathing at all, 47.6% had obstructive sleep apnea, 2.7% had mostly obstructive apnea with a central component mixed in, and 0.9% had central sleep apnea on its own. A related breathing pattern called Cheyne-Stokes respiration, where breathing gradually speeds up and slows down in cycles, showed up in just 0.4% of participants.
Those numbers mean that for every person diagnosed with central sleep apnea, there are roughly 50 people with the obstructive type. Central sleep apnea is genuinely rare in the broader population. The purely idiopathic form, meaning central sleep apnea with no identifiable underlying cause, is rarer still. Population estimates put idiopathic CSA at about 0.05% in men and 0.003% in women. Only about 11% of all CSA patients fall into this category, though researchers note that underlying causes aren’t always thoroughly ruled out before making that diagnosis.
Why Age Makes a Big Difference
Central sleep apnea becomes substantially more common with age. One large epidemiologic study found a prevalence of 1.7% in middle-aged adults compared to 12.1% in older adults. That sevenfold jump reflects real changes in how the aging brain controls breathing during sleep.
In younger adults, the brain can tolerate bigger shifts in carbon dioxide levels before breathing becomes unstable. In older adults, it takes much less of a shift to trigger a pause in breathing. Researchers have measured this directly: in older adults, a drop in CO2 of just 2.6 mmHg below normal was enough to cause central apneas, while younger adults needed a drop of about 4.1 mmHg before the same thing happened. On top of that instability, older adults are more likely to have conditions that independently raise CSA risk, including heart failure, irregular heart rhythms like atrial fibrillation, and thyroid problems.
Heart Failure Is the Biggest Risk Factor
Central sleep apnea shows up in approximately 40% of patients with congestive heart failure, making it the single most important associated condition. When researchers use a threshold of more than 15 breathing disruptions per hour, between 49% and 55% of heart failure patients qualify as having significant sleep-disordered breathing. In heart failure patients specifically, central sleep apnea is actually more common than the obstructive type.
The connection makes physiological sense. When the heart pumps inefficiently, it takes longer for blood to travel from the lungs to the brain. That delay means the brain gets outdated information about oxygen and carbon dioxide levels, so it overcorrects, creating a cycle of over-breathing and under-breathing. This produces the characteristic crescendo-decrescendo pattern of Cheyne-Stokes respiration, where breathing gradually gets deeper, then shallower, then pauses entirely before starting over. Each full cycle lasts 40 seconds or more. People over 60 with heart failure are at particularly high risk.
Opioid Use and Medication-Induced CSA
Long-term opioid therapy is the most well-recognized medication cause of central sleep apnea. Across studies, the average prevalence of CSA among chronic opioid users is 24%. For patients on methadone prescribed for pain management, rates climb to about 30%. Opioids suppress the brainstem’s breathing drive, which is particularly vulnerable during sleep when voluntary breathing control is already reduced.
This form of central sleep apnea behaves differently from the heart failure type. Rather than the rhythmic waxing and waning of Cheyne-Stokes respiration, opioid-related CSA tends to produce irregular, unpredictable pauses. It can develop at any point during chronic opioid therapy and doesn’t always resolve when dosages are adjusted.
Stroke and Neurological Conditions
Despite the brain’s central role in CSA, stroke turns out to be a less common trigger than you might expect. In a large population-based cohort of patients with recent ischemic stroke, only 1.4% met criteria for central sleep apnea. The median number of central apneas per hour was zero. Post-stroke sleep-disordered breathing is common overall, but it overwhelmingly takes the obstructive form rather than the central form.
High Altitude as a Temporary Trigger
One situation that causes central sleep apnea in nearly everyone is sleeping at high altitude. Periodic breathing during sleep at elevation is almost universal among people who normally live closer to sea level. The thin air triggers the same kind of breathing instability seen in other forms of CSA: the brain senses low oxygen, ramps up breathing, drops carbon dioxide too low, and then breathing pauses until CO2 builds back up.
This form persists even with acclimatization, and its severity is proportional to sleeping altitude. However, it doesn’t seem to worsen overall sleep quality as much as you’d expect. With acclimatization, the breathing cycles lengthen and average oxygen levels during sleep stay relatively stable. People who have lived at high altitude for generations show a blunted version of this response, suggesting their respiratory control systems have adapted over time.
How CSA Is Identified
Central sleep apnea is diagnosed through an overnight sleep study. The hallmark is pauses in breathing lasting at least 10 seconds where, unlike obstructive apnea, there’s no effort to breathe at all. Your chest and abdomen simply stop moving. A diagnosis requires at least 5 central apneas or shallow breaths per hour, with central events making up more than half of all breathing disruptions recorded.
There’s also a form called treatment-emergent central sleep apnea that appears only after someone starts using a CPAP machine for obstructive sleep apnea. In these cases, the obstructive events resolve with positive airway pressure therapy, but central apneas emerge or persist in their place. This is one reason sleep specialists sometimes recommend follow-up sleep studies after starting CPAP treatment.
Beyond the sleep study numbers, a diagnosis also requires at least one symptom of disrupted sleep: excessive daytime sleepiness, difficulty staying asleep, waking up short of breath, snoring, or a bed partner noticing pauses in breathing. The combination of objective measurements and real-world symptoms helps distinguish clinically meaningful CSA from the occasional central apneas that can show up on anyone’s sleep study without causing problems.