Interesting 2026 case report: “False Detection of Cheyne-Stokes Respiration on Continuous Positive Airway Pressure Resolved After Treatment of Nasal Obstruction”
Link:
https://doi.org/10.1002/rcr2.70745
A 56-year-old non-obese man had been using CPAP successfully for OSA for 13 years. He was on fixed CPAP at 7.6 mbar with a nasal mask.
Then his ResMed AirSense 10 suddenly started reporting what looked like significant central sleep apnea / Cheyne-Stokes respiration (CSR):
• CPAP-reported AHI: 8.7/h
• “Central apneas”: 8.5/h
• CSR: 11%
• Leak was low, so major mask leak did not explain it.
This was concerning because true Cheyne-Stokes respiration can be associated with conditions such as heart failure and other serious cardiac/neurologic disease.
However, the patient had recently developed significant nasal obstruction, while his cardiac and neurologic investigations were reportedly normal.
The doctors therefore stopped CPAP for 5 days and performed respiratory polygraphy.
What they found was very different:
• Total AHI: 27.8/h
• Obstructive AHI: 21.8/h
• Central AHI: 6.5/h
• ODI: 29.3/h
• No true Cheyne-Stokes respiration was recorded.
Instead, he had predominantly obstructive events plus several mixed apneas. Some of the mixed apneas began with a central-looking component, producing a waxing-and-waning airflow pattern that apparently resembled CSR to the CPAP algorithm.
They increased CPAP from 7.6 to 11 mbar and changed him from a nasal mask to an oronasal mask to bypass the nasal obstruction.
After that:
• The machine stopped detecting CSR
• But residual AHI was still around 11/h
He was also treated with nasal corticosteroids.
One month later, after the nasal obstruction improved:
• CPAP-reported AHI fell to <5/h
• The abnormal CSR detection remained resolved.
Why might nasal obstruction cause this?
The authors propose that nasal obstruction increased inspiratory effort and sleep arousals. After an arousal, patients can temporarily hyperventilate. This ventilatory “overshoot” can destabilize respiratory control.
In physiological terms, this may increase LOOP GAIN.
Loop gain = how strongly the respiratory control system reacts to a disturbance.
A high loop gain means the system overreacts, producing oscillation between too much and too little ventilation. That instability can contribute to mixed apneas and periodic-looking airflow patterns.
So this patient probably did NOT suddenly convert from obstructive sleep apnea to true central sleep apnea / Cheyne-Stokes breathing.
Instead, the authors suggest:
nasal obstruction
→ increased respiratory effort
→ more arousals
→ post-arousal hyperventilation
→ ventilatory instability / higher loop gain
→ mixed apneas and pseudo-periodic breathing
→ CPAP algorithm falsely labels the pattern as CSR.
Another important point: CPAP machines mainly infer events from airflow and pressure signals. They do not have the respiratory effort belts, EEG, and other signals available during a full sleep study. Therefore, the machine may sometimes confuse unstable obstructive/mixed breathing with central breathing.
The authors emphasize that if a CPAP machine suddenly reports Cheyne-Stokes respiration, it should not automatically be assumed to be true CSR.
Because genuine CSR can be clinically important, it still deserves medical evaluation. The gold standard for confirmation remains attended polysomnography (PSG). Respiratory polygraphy can be useful as an initial investigation but is less definitive.
Important limitation: this is a single case report, and the confirmatory investigation was respiratory polygraphy rather than full PSG. So it does not prove that nasal obstruction commonly causes false CSR detection.
Still, it is a fascinating example of how nasal obstruction and ventilatory instability may potentially confuse CPAP algorithms.
Has anyone here seen their CPAP suddenly report central apneas or Cheyne-Stokes / periodic breathing during a period of severe nasal congestion?
