Guide — Sleep Medicine
Central Sleep Apnea & Cheyne-Stokes Respiration
Central sleep apnea is fundamentally different from its obstructive counterpart: the airway is open, but the brain stops sending the signal to breathe. This guide covers the major subtypes, the distinctive Cheyne-Stokes crescendo–decrescendo pattern in heart failure, critical ASV contraindications from the SERVE-HF trial, and the RT’s priorities for each presentation.
10 min read · Sleep Medicine
Written by Apex Respiratory Editorial Team
Educational use only. This material supports respiratory therapy education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional protocols, or physician orders. Always follow facility policies and current provider orders, and verify calculations independently before clinical use.
Overview
Central sleep apnea (CSA) is the cessation or reduction of airflow caused by absent or reduced central respiratory drive. The defining feature is that apneas occur without respiratory effort — no thoracoabdominal movement is detected on the respiratory inductance plethysmography (RIP) effort belts during the event. This absence of effort is what separates CSA from obstructive sleep apnea, where the airway collapses but the chest and abdomen continue to labor against the obstruction.
CSA is not a single disease but a group of disorders united by impaired ventilatory drive or unstable ventilatory control. Common clinical associations include heart failure, atrial fibrillation, stroke, chronic opioid therapy, renal failure, and high altitude. Symptoms often overlap with obstructive sleep apnea — fragmented sleep and daytime sleepiness — but CSA typically presents without loud snoring, with witnessed pauses that lack effort, and in heart failure patients, with nocturnal dyspnea and frequent arousals.
Key Concepts — Types of Central Sleep Apnea
CSA is broadly divided by whether PaCO₂ is elevated (hypercapnic, reduced-drive forms) or normal to low (nonhypercapnic, high-loop-gain forms). Understanding the mechanism guides treatment selection.
| Type | Mechanism | CO₂ Trend | Key Notes |
|---|---|---|---|
| Hypercapnic CSA | Reduced central drive — brainstem lesions, chronic opioid use, neuromuscular disease | High / normal-high PaCO₂ | Tends toward hypoventilation; may need BiPAP-ST |
| Cheyne-Stokes Respiration | Prolonged circulation time + high loop gain — crescendo-decrescendo tidal volume with interposed central apneas | Often low PaCO₂ (hyperventilation phases) | Classic in HFrEF and stroke; optimize heart failure therapy first |
| Treatment-Emergent (Complex) CSA | Central apneas appear or persist once CPAP relieves obstructive events | Variable | Often self-resolves with continued PAP over weeks |
| Opioid-Induced CSA | Opioids suppress central drive; may produce ataxic / Biot breathing pattern | Variable; often hypercapnic | Reduce or eliminate opioids when clinically feasible |
| High-Altitude Periodic Breathing | Hypoxia-driven hyperventilation creates oscillating ventilatory control at altitude | Low PaCO₂ | Resolves with descent or acclimatization |
Cheyne-Stokes Respiration — closer look
Cheyne-Stokes respiration (CSR) is characterized by acrescendo–decrescendo (waxing-and-waning) tidal-volume pattern with interposed central apneas or hypopneas. It is classically seen in heart failure with reduced ejection fraction (HFrEF) and after stroke. The mechanism is a prolonged lung-to-chemoreceptor circulation time combined with high loop gain: by the time CO₂ rises enough to trigger a breath, the body overshoots and then undershoots, creating the oscillating cycle. Recognizing the waxing-and-waning morphology on the polysomnogram is essential for distinguishing CSR from other central apnea patterns.
Assessment & Findings
Diagnosis requires an attended polysomnogram (PSG) or attended cardiorespiratory sleep study. Key findings:
- Predominantly central events — commonly more than 50% of scored events are central, with a central apnea index (CAI) or central AHI ≥5 events/hour.
- Absent effort on RIP belts — the thoracic and abdominal effort channels are flat during events; this is the key distinguishing feature from obstructive events, where effort waveforms persist (often with paradoxical movement).
- Cheyne-Stokes morphology — when present, the flow channel shows the characteristic sinusoidal waxing-and-waning pattern rather than an abrupt onset/termination.
- ABG findings — in hypercapnic CSA forms, an ABG may show elevated PaCO₂, confirming reduced baseline ventilatory drive. In high-loop-gain forms, PaCO₂ is often normal to low during wakefulness.
- Clinical context — obtain a full history including cardiac function (echocardiogram, LVEF), opioid medications, neurological history, and altitude of residence. A patient with HFrEF and a Cheyne-Stokes pattern is a different clinical problem than a patient on long-term opioids with hypercapnic CSA.
RT Priorities & Interventions
- Treat the underlying condition first. Optimizing guideline-directed medical therapy for heart failure often reduces or eliminates CSR. For opioid-induced CSA, reducing or eliminating opioids when clinically feasible is the primary intervention. These upstream steps may make PAP therapy unnecessary or far more effective.
- CPAP for coexisting OSA; supplemental oxygen. In patients with mixed events or treatment-emergent CSA, CPAP remains the first-line approach. Supplemental oxygen (nocturnal) helps some CSA patients, particularly at altitude and in mild heart failure presentations, by blunting the hypoxic ventilatory oscillation.
- ASV (adaptive servo-ventilation) — effective but with a critical contraindication. ASV delivers variable pressure support with an automatic backup rate, targeting a set average ventilation to stabilize breathing. It is effective for CSR and CSA in patients without severe systolic heart failure. However, ASV is contraindicated in patients with symptomatic chronic heart failure with reduced LVEF ≤45% and predominant central sleep apnea — the SERVE-HF trial (Cowie et al., 2015) demonstrated increased cardiovascular mortality and all-cause mortality in this population. This is one of the most clinically important safety contraindications in sleep medicine and must be confirmed before any ASV prescription is initiated.
- BiPAP with backup rate (BiPAP-ST) for hypercapnic CSA. Patients with hypercapnic CSA — from brainstem lesions, neuromuscular disease, or opioid suppression — require guaranteed minute ventilation. BiPAP in spontaneous-timed (ST) mode ensures a minimum respiratory rate and supports tidal volume, addressing the hypoventilation directly.
- Cheyne-Stokes in HFrEF — optimize heart failure therapy. Because ASV is contraindicated in symptomatic HFrEF with LVEF ≤45%, the primary treatment approach is guideline-directed heart failure management. Supplemental nocturnal oxygen is an adjunct. Involve cardiology early; PAP titration in this group requires close coordination.
Common Pitfalls
- Treating CSA like OSA with straight CPAP. CPAP may be ineffective for pure CSA or may unmask more central events (treatment-emergent CSA). Understand the predominant event type before selecting the PAP modality.
- Prescribing ASV in heart failure with reduced EF. Patients with symptomatic HFrEF (LVEF ≤45%) and predominant CSA must NOT receive ASV — this is harmful per SERVE-HF. Always verify the echocardiographic LVEF before any ASV initiation.
- Missing chronic opioids as a cause. Opioid-induced CSA is common and underrecognized. A thorough medication history — including chronic pain regimens, methadone, and buprenorphine — is essential in any new CSA workup.
- Mislabeling effort-absent events as obstructive. Without careful review of the RIP belt tracings, central events can be misscored as obstructive, leading to inappropriate therapy. A flat (absent) effort signal during the event is the defining criterion for a central classification.
Board Exam Pearls
- Central apnea = NO airflow AND NO effort. Obstructive apnea = no airflow WITH continued effort (chest/abdomen moving). This distinction drives the entire management algorithm.
- Cheyne-Stokes = crescendo–decrescendo tidal volume, think heart failure. The classic association is HFrEF or stroke. The waxing-and-waning morphology on the flow channel is the key diagnostic finding.
- ASV is contraindicated in symptomatic HFrEF (EF ≤45%) with predominant CSA (SERVE-HF). This trial result is high-yield. Know the ejection fraction threshold (45%) and the word “symptomatic” — it applies to chronic heart failure with reduced ejection fraction, not preserved EF.
- Treatment-emergent (complex) CSA often self-resolves on CPAP. When central events appear after obstructive events are eliminated by CPAP, continue PAP therapy — the pattern typically resolves over several weeks without changing the device.
FAQ
How is central sleep apnea different from obstructive?
In central apnea there is no airflow AND no respiratory effort, because the drive to breathe pauses. In obstructive apnea the airway collapses but effort continues — the chest and abdomen keep moving against a blocked airway.
What causes Cheyne-Stokes breathing?
A waxing-and-waning breathing pattern with central pauses, most often from heart failure with reduced ejection fraction or stroke, related to slow circulation time and an unstable (high-loop-gain) control system.
Why is ASV not used in some heart failure patients?
The SERVE-HF trial found higher cardiovascular and all-cause mortality when ASV was used in symptomatic chronic heart failure with an ejection fraction of 45% or less and predominant central apnea, so ASV is contraindicated in that group.
Can CPAP cause central apneas?
Yes — treatment-emergent (complex) central apneas can appear once CPAP relieves the obstructive events. They often resolve with continued CPAP over several weeks.
Practice with real values
CSA workup often involves ABG review — especially in hypercapnic forms. Run values through the ABG interpreter to practice classifying the acid-base and oxygenation status you’d see in a sleep patient with chronic hypoventilation or heart failure.
Open the ABG Interpreter →Related Resources
Sources
- Kacmarek RM, Stoller JK, Heuer AJ. Egan's Fundamentals of Respiratory Care. 12th ed. Elsevier; 2021.
- Aurora RN, Chowdhuri S, Ramar K, et al. The treatment of central sleep apnea syndromes in adults: practice parameters with an evidence-based literature review and meta-analyses. Sleep. 2012;35(1):17-40.
- Cowie MR, Woehrle H, Wegscheider K, et al. Adaptive servo-ventilation for central sleep apnea in systolic heart failure (SERVE-HF). N Engl J Med. 2015;373(12):1095-1105.