I’ve lost count of the number of patients who’ve come in saying “I have sleep apnea” as if it’s one condition. It’s not. Obstructive sleep apnea and central sleep apnea are fundamentally different diseases that happen to share a symptom — pauses in breathing during sleep. The causes, risk factors, diagnostic markers, and treatments are distinct, and confusing the two leads to real clinical harm.

The Plumbing vs The Wiring

The simplest way to understand the difference is this: obstructive sleep apnea is a plumbing problem. Central sleep apnea is a wiring problem.

Obstructive sleep apnea (OSA) occurs when the physical airway collapses during sleep. The muscles of the throat relax, the tongue falls back, and the airway narrows or closes completely. Your brain is sending the signal to breathe. Your chest and diaphragm are trying to breathe. But the air can’t get through. It’s a mechanical obstruction.

Central sleep apnea (CSA) occurs when the brain temporarily stops sending the signal to breathe. The airway is open. There’s no obstruction. The respiratory muscles simply don’t receive the command to contract. It’s a failure of respiratory drive.

On a polysomnogram, the difference is immediately visible. During an obstructive event, you see continued respiratory effort — the chest and abdomen moving as the patient tries to breathe against the closed airway. During a central event, all respiratory effort ceases. The breathing just stops.

Who Gets What

The risk factors diverge considerably:

OSA risk factors:

• Excess weight (the strongest modifiable risk factor)
• Large neck circumference
• Male sex (though women catch up post-menopause)
• Age
• Craniofacial anatomy — recessed jaw, large tongue, narrow palate
• Nasal obstruction
• Alcohol and sedative use
• Family history

CSA risk factors:

• Heart failure (this is the big one — up to 40% of heart failure patients have CSA)
• Stroke or brainstem lesions
• Opioid use (chronic opioid therapy is a major cause of CSA)
• High altitude
• Age
• Male sex

The American Academy of Sleep Medicine distinguishes several CSA subtypes, including Cheyne-Stokes respiration (the rhythmic crescendo-decrescendo breathing pattern seen in heart failure), treatment-emergent central apnea (central events that appear after starting CPAP for OSA), and high-altitude periodic breathing.

Why the Distinction Matters for Treatment

This is where the stakes get high. The frontline treatment for OSA — CPAP therapy — works by pneumatically splinting the airway open with continuous positive pressure. If the airway is collapsing, blowing air through it at the right pressure keeps it open. Logical, effective, well-proven.

But CPAP doesn’t treat central sleep apnea effectively in many cases. If the problem is that the brain isn’t sending the breathing signal, keeping the airway open doesn’t address the root cause. In some CSA patients, CPAP makes things worse by lowering CO2 levels below the apnoeic threshold, triggering more central events.

Treatment approaches for CSA include:

• Adaptive servo-ventilation (ASV). This is the most effective device therapy for many CSA patients. ASV monitors breathing patterns and provides variable pressure support — more when the patient’s breathing weakens, less when it’s strong. It essentially fills in the gaps left by inconsistent respiratory drive. However, ASV is contraindicated in heart failure patients with reduced ejection fraction due to findings from the SERVE-HF trial showing increased cardiovascular mortality.

• Treating the underlying cause. For CSA secondary to heart failure, optimising cardiac treatment often reduces central events. For opioid-induced CSA, reducing or eliminating the opioid (when clinically possible) can resolve the breathing disorder.

• Supplemental oxygen. Nocturnal oxygen therapy can stabilise breathing in some CSA patients by preventing the oxygen desaturation that triggers arousal and respiratory instability.

• Phrenic nerve stimulation. A newer approach, the Remede System is an implantable device that stimulates the phrenic nerve to maintain diaphragm activity during sleep. It’s approved for moderate-to-severe CSA and represents a fundamentally different treatment philosophy — directly driving respiration rather than supporting the airway.

The Overlap Problem

Things get complicated because many patients have both. Mixed sleep apnea — also called complex sleep apnea — involves obstructive and central events occurring together. Treatment-emergent central sleep apnea is particularly common: you start a patient on CPAP for their obstructive events, and central events appear that weren’t present on the diagnostic study.

This happens in roughly 5-15% of OSA patients starting CPAP. In most cases, the central events resolve spontaneously within a few weeks as the patient adapts. In some, they persist and require a switch to ASV or bilevel therapy.

Getting the Diagnosis Right

If you’ve been diagnosed with “sleep apnea” and your treatment isn’t working, it’s worth asking your sleep physician a direct question: is this obstructive, central, or mixed? The answer should be on your sleep study report. If nobody has explained the distinction to you, ask.

For OSA patients on CPAP whose AHI remains elevated despite good mask seal and adequate pressure, central events may be the culprit. Your CPAP machine’s data report should show the breakdown of obstructive vs central events.

They share a name, but obstructive and central sleep apnea are different conditions that demand different solutions. Getting that distinction right is the first step toward effective treatment.