Obstructive sleep apnea (OSA) is a physical blockage of the airway, while central sleep apnea (CSA) is a communication failure between the brain and the muscles that control breathing. Both cause repeated pauses in breathing during sleep, but they arise from completely different problems and affect different populations. OSA accounts for roughly 97% of sleep apnea cases, while CSA makes up about 1% to 2%, with the remainder being mixed presentations.
How Each Type Disrupts Breathing
Your upper airway is essentially a muscular tube without any bone or cartilage holding it open. During sleep, the muscles that keep this tube from collapsing naturally relax. In obstructive sleep apnea, the airway physically collapses or narrows so much that air can’t pass through, even though your body is actively trying to breathe. The diaphragm contracts, the chest and abdomen strain against the blocked passage, and oxygen levels drop until the brain jolts you into partial wakefulness to reopen the airway.
Central sleep apnea looks entirely different. The airway stays open, but the brain’s respiratory control center, a cluster of neurons in the brainstem, temporarily stops sending the signal to inhale. Your chest and abdomen simply don’t move. There’s no effort, no straining, just a pause in breathing until the brain restarts the cycle. The distinction is visible during a sleep study: in OSA, the chest and abdomen move out of sync as they push against a closed airway, while in CSA, both go completely still.
Who Gets Obstructive Sleep Apnea
OSA is overwhelmingly tied to anatomy and body composition. Excess weight is the single biggest modifiable risk factor. A BMI of 30 or above increases the odds of moderate to severe sleep apnea by more than six times compared to a healthy weight. Obesity enlarges the soft tissues around the throat and increases fat deposits in the tongue itself, physically narrowing the space air has to travel through. A neck circumference over 40 cm (about 16 inches) is another well-established marker.
Beyond weight, structural features of the face, jaw, and throat matter. A smaller jaw, enlarged tonsils, or a naturally narrow airway all raise risk. Men are affected more often than women, and risk climbs after age 35. Alcohol relaxes the airway muscles further, roughly quadrupling the odds of OSA in heavy drinkers. Smoking, high blood pressure, and diabetes are also consistently linked. About 30% of people with OSA have pharyngeal muscles that respond poorly to the negative pressure created when they inhale, meaning their airway is slower to stiffen and reopen on its own.
Who Gets Central Sleep Apnea
CSA is driven by underlying medical conditions rather than physical anatomy. Heart failure is the most common culprit. Roughly 40% of people with congestive heart failure develop central sleep apnea. In these patients, changes in blood carbon dioxide levels destabilize the brain’s breathing rhythm, causing it to oscillate between overbreathing and not breathing at all, a pattern called Cheyne-Stokes respiration.
Other conditions that can trigger CSA include stroke, kidney failure, and neurological disorders that damage the brainstem. Opioid medications are another well-known cause, as they suppress the brainstem’s respiratory drive. Unlike OSA, central sleep apnea is not strongly associated with obesity or neck size, and it tends to appear in people who are already managing a serious health condition.
Symptoms That Overlap and Diverge
Both types cause fragmented sleep, daytime fatigue, and morning headaches. Both lead to drops in blood oxygen that, over time, strain the heart and cardiovascular system. The overlap is significant enough that you can’t reliably tell them apart based on how you feel during the day.
The clearest difference is snoring. OSA almost always involves loud, irregular snoring because air is being forced through a partially collapsed airway. Gasping or choking sounds are common as the airway reopens. CSA, on the other hand, is often relatively quiet. A bed partner might notice long pauses in breathing without the dramatic snoring that characterizes OSA. People with CSA are also more likely to report waking up short of breath rather than waking with a snort or gasp.
How Each Type Is Diagnosed
A sleep study, or polysomnography, is the only way to definitively distinguish between the two. Sensors track airflow through the nose and mouth, chest and abdominal movement, blood oxygen, brain waves, and heart rhythm throughout the night.
The key diagnostic difference comes down to effort. During an obstructive event, the airflow signal flatlines while chest and abdominal belts show the body straining to breathe, often moving in opposite directions (the chest pulls in while the abdomen pushes out). During a central event, airflow, chest movement, and abdominal movement all stop simultaneously. In obstructive episodes, each successive breath attempt tends to grow more forceful until the sleeper partially wakes. Central episodes show a gentler, more gradual pattern of breathing that fades out and then slowly fades back in.
Treating Obstructive Sleep Apnea
Continuous positive airway pressure, known as CPAP, is the first-line treatment for OSA at all severity levels. The device delivers a steady stream of pressurized air through a mask, acting as a pneumatic splint that holds the airway open. It’s effective for nearly everyone who can tolerate wearing it consistently.
For people with mild to moderate OSA who find CPAP difficult to use, a mandibular advancement device is a common alternative. This custom-fitted oral appliance pushes the lower jaw forward, which pulls the tongue away from the back of the throat and increases the airway’s diameter. It works best for people with a BMI under 30 and good dental health.
A newer option is hypoglossal nerve stimulation, a small implanted device that works like a pacemaker for the tongue. It stimulates the nerve that controls tongue position, pushing the tongue forward to keep the airway clear. In clinical studies, it reduced breathing disruptions by 68%, from about 29 events per hour down to 9. Candidates need a BMI under 32, and not all airway collapse patterns respond to it. Weight loss, positional therapy (staying off your back), and avoiding alcohol before bed also play supporting roles for many people.
Treating Central Sleep Apnea
Because CSA stems from a brain signaling problem rather than a physical blockage, treatment starts with addressing the underlying condition. For heart failure patients, optimizing cardiac medications can sometimes reduce or eliminate central apneas on its own.
When device therapy is needed, adaptive servo-ventilation (ASV) is the most targeted option. ASV monitors your breathing pattern in real time and delivers just enough pressure support to smooth out the pauses, backing off when you’re breathing normally and stepping in when your drive to breathe fades. It’s effective at eliminating central events, but carries an important restriction: a major clinical trial published in the New England Journal of Medicine found that ASV increased cardiovascular mortality in heart failure patients with a severely weakened heart (ejection fraction of 45% or below). For that group, ASV is contraindicated, and other approaches like supplemental oxygen or certain medications are used instead.
When Both Types Occur Together
Some people start out with a clear OSA diagnosis, begin CPAP therapy, and then develop central apneas that weren’t present before. This is called treatment-emergent central sleep apnea, previously known as complex sleep apnea. The physical obstruction is resolved, but central events appear, likely because removing the obstruction unmasks an underlying instability in the brain’s breathing control.
The good news is that this often resolves on its own. In one large study, central apneas disappeared in about 80% of affected patients within five to six weeks of continued CPAP use. For the roughly 4% of CPAP users who develop persistent central events, a switch to ASV or a different pressure delivery mode is typically the next step. If you’re tolerating CPAP well and your symptoms are improving, a brief course of treatment-emergent central apneas doesn’t necessarily mean you need a new device.