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In the common form of sleep apnoea the throat closes while the brain keeps trying to breathe. Central sleep apnoea is the opposite: the airway is open, but the brain briefly stops sending the signal, so no effort is made at all. It shows up as pauses in breathing during sleep, often in a rising-and-falling pattern, along with broken sleep, waking short of breath, and daytime tiredness. It is much less common than the obstructive form, and it is usually a consequence of something else — most often heart failure, strong pain medicines such as opioids, sleeping at altitude, or a stroke. Because of that, treatment is aimed first at the underlying cause, and the machine used for ordinary sleep apnoea is not always the right answer here.
Definition
Central sleep apnoea is repeated cessation or reduction of breathing during sleep caused by absent or reduced respiratory drive, with no accompanying effort to breathe. This is the defining distinction from obstructive sleep apnoea, in which effort continues against a closed upper airway. The two frequently coexist, and the mix can change during a single night and with treatment.
The main types
| Type | Setting | Key point |
|---|---|---|
| Cheyne–Stokes breathing | Heart failure, sometimes stroke | Crescendo–decrescendo pattern with a long cycle; marks disease severity |
| Opioid-related | Long-term opioid therapy | Irregular, ataxic breathing; dose-related |
| Treatment-emergent | Appears when CPAP is started for obstructive apnoea | Usually settles within weeks on continued therapy |
| High-altitude periodic breathing | Sleeping above roughly 2,500 m | A normal physiological response, not a disease |
| Disease of the brainstem | Stroke, tumour, Chiari malformation, neurodegenerative disease | Uncommon; the control centre itself is affected |
| Idiopathic | No cause found | Rare |
Pathophysiology
An unstable control loop
Breathing during sleep is governed by a feedback system that senses carbon dioxide and adjusts ventilation. Its stability depends on how strongly it responds to a change (loop gain) and how long the information takes to travel. Where the response is too strong, or the circulation too slow, the system overshoots: the patient over-breathes, carbon dioxide falls below the level that triggers a breath, and breathing stops until it rises again. That oscillation is central apnoea, and it is a control problem rather than a mechanical one.
Why heart failure produces the classic pattern
A failing heart circulates blood slowly, so information about carbon dioxide reaches the brain late; pulmonary congestion simultaneously increases the ventilatory response. The combination of high gain and long delay produces the long, regular crescendo–decrescendo cycle of Cheyne–Stokes breathing. The severity of the pattern tracks the severity of the cardiac disease, which is why it is best understood as a marker of the heart failure rather than as an independent condition.1
Why opioids are different
Opioids suppress the brainstem respiratory centres directly, blunting rather than destabilising the response to carbon dioxide. The result is irregular, ataxic breathing rather than a regular cycle, and the answer is the opioid dose rather than a ventilator setting.
Co-morbidities
- Heart failure — the dominant association; central apnoea is common in reduced ejection fraction and correlates with severity.
- Atrial fibrillation — frequently coexists; see atrial fibrillation.
- Stroke — both a cause, through brainstem involvement, and an association.
- Chronic opioid therapy — dose-dependent, and often unrecognised in chronic pain populations.
- Obstructive sleep apnoea — coexistence is the rule rather than the exception.
- Chronic kidney disease — through fluid shifts and altered chemosensitivity.
- Deconditioning and daytime fatigue — the functional consequence, and the one most amenable to physiotherapy.
Prevalence
Central sleep apnoea accounts for a small minority of sleep-disordered breathing in the general population, but the picture changes entirely in specific groups. It is found in a substantial proportion of patients with symptomatic heart failure with reduced ejection fraction, and in a meaningful share of patients on long-term high-dose opioids. Treatment-emergent central apnoea appears in a small proportion of patients starting CPAP for obstructive apnoea and resolves spontaneously in most of them.2
Causes
- Heart failure — the commonest, through slow circulation and heightened ventilatory response.
- Opioids and other respiratory depressants — long-acting opioids in particular; benzodiazepines and gabapentinoids can compound the effect.
- Stroke and brainstem disease — direct involvement of respiratory control.
- Altitude — a normal response in almost everyone sleeping high enough.
- Kidney failure — particularly around dialysis.
- Starting CPAP — treatment-emergent central apnoea, usually transient.
- Congenital central hypoventilation — rare, presenting in childhood.
Symptoms
What is noticed
- Witnessed pauses in breathing during sleep — frequently reported by a partner rather than the patient.
- Waking suddenly short of breath, or with a sense of choking.
- Frequent awakenings and unrefreshing sleep.
- Daytime sleepiness and fatigue — though notably less prominent than in obstructive apnoea, and sometimes absent altogether.
- Poor concentration and low mood.
- In heart failure, worsening breathlessness lying flat and reduced exercise tolerance.
Snoring is typically absent or mild, which is a useful distinguishing feature: a patient with witnessed apnoeas who does not snore should raise the question of a central mechanism.
Warning signs
Diagnosis
How it is diagnosed
Diagnosis requires a sleep study that measures respiratory effort as well as airflow — the absence of effort during a pause is what defines a central event. Simple oximetry cannot distinguish central from obstructive apnoea. In-laboratory polysomnography is preferred where central apnoea is suspected, because home studies are less reliable at making the distinction and at characterising the pattern.
What else is assessed
- Cardiac assessment — echocardiography and heart failure review, because the sleep finding frequently reveals inadequately treated cardiac disease.
- Medication review — opioid dose and formulation, plus sedatives that compound the effect.
- Neurological assessment — where the pattern, history or examination suggests brainstem disease.
- Renal function, and a review of fluid status where relevant.
The distinction that matters
Establishing the proportion of central to obstructive events changes treatment fundamentally. Treating predominantly central apnoea as though it were obstructive, or vice versa, is the commonest management error — and in one specific circumstance it is dangerous, as below.
Management
Treat the cause first
This is the principle that distinguishes central from obstructive apnoea. Optimising heart failure therapy — the disease-modifying medications, device therapy where indicated, fluid management — reduces or abolishes Cheyne–Stokes breathing in many patients. Reducing or rotating opioids resolves opioid-related apnoea. Neither is a sleep intervention, and both work better than one.
Positive airway pressure
CPAP is used where obstructive events coexist, and improves some patients with heart failure-related central apnoea. Adaptive servo-ventilation (ASV) is a more sophisticated device that varies support breath by breath to smooth out the oscillation, and it is highly effective at suppressing the events.
Other options
Supplemental oxygen at night can stabilise breathing in selected patients with heart failure. Transvenous phrenic nerve stimulation, an implanted device that paces the diaphragm during sleep, is available in some centres for moderate to severe central apnoea. Acetazolamide is used occasionally, and is the standard approach for altitude-related periodic breathing. Treatment-emergent central apnoea usually needs nothing beyond continuing CPAP and reassessing.
Living with central sleep apnoea
It is usually part of something larger
Most people with this diagnosis also have heart failure or chronic pain, and the sleep problem is one component of a bigger picture. Managing the underlying condition well is what improves both, and it is worth framing it that way rather than as two separate problems.
Sleep habits
Regular timing, sleeping more upright where breathlessness is worse flat, avoiding alcohol and sedatives, and treating nasal congestion all help. None substitutes for treating the cause.
Living with the machine
Where a device is prescribed, early problems with mask fit, pressure tolerance and dryness are common and almost always solvable — but only if reported. Most people who abandon therapy do so in the first few weeks over problems that had a straightforward fix.
Prognosis
The outlook is largely determined by the underlying condition. In heart failure, the presence and severity of Cheyne–Stokes breathing marks more advanced disease and is associated with worse outcomes — but the evidence indicates it is primarily a marker rather than an independent driver, which is why suppressing it with ASV did not improve survival. Opioid-related apnoea improves as the dose falls. Altitude-related periodic breathing resolves on descent, and treatment-emergent apnoea resolves in most patients within weeks.
Role of the physiotherapist
Recognising it
Physiotherapists in cardiac rehabilitation and chronic pain services see the two highest-risk populations regularly, and often at greater length than the referring clinician. Witnessed apnoeas without snoring, waking short of breath, unrefreshing sleep and disproportionate daytime fatigue are all worth asking about directly — and worth referring on.
Exercise training
Exercise training improves exercise capacity in heart failure and, in several small studies, reduces the severity of sleep-disordered breathing — plausibly by improving cardiac function and circulatory delay. It is one of the few interventions that addresses the mechanism rather than the symptom. Prescribe within heart failure guidelines, monitor for signs of decompensation, and progress on symptoms. See cardiac rehabilitation.
Inspiratory muscle training
Has a supporting role in heart failure where inspiratory muscle weakness is demonstrated, improving capacity and breathlessness. Its effect specifically on central apnoea is unproven. See inspiratory muscle training.
Adherence and education
Where a device has been prescribed, ask about it at every visit. Practical barriers — mask leak, dryness, claustrophobia, pressure intolerance — are the usual reasons for abandonment, and a therapist who asks is often the person who gets them fixed. Reinforce that the cardiac medication and the sleep therapy are working on the same problem.
Part 1 · References
- Naughton MT. Cheyne–Stokes respiration: friend or foe? Thorax 2012;67(4):357–360.
- 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.
References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.
This is confirmed with a sleep study, and a home study can be arranged without a specialist appointment first.
Clinical evidence
Part 1 covers the same condition without the technical detail. What follows is the evidence base behind it, written for clinicians — the literature, the reasoning and the gaps.
For clinicians: this summary supports clinical reasoning and is not a protocol. Check current guidelines and local policy before applying it, and read it alongside the key references and guidelines directory.
Framing. Central sleep apnoea in heart failure is the standing example of a surrogate endpoint misleading a whole field. The apnoea–hypopnoea index is reliably reduced by adaptive servo-ventilation; mortality went up.1 The prevailing interpretation is that Cheyne–Stokes breathing in heart failure is largely a marker of circulatory delay and heightened chemosensitivity — and may be partly compensatory — rather than an independent cause of harm. Treatment is therefore directed at the heart, the opioid, or the brainstem lesion, and only then at the breathing pattern.2
Treatment evidence
- SERVE-HF randomised ASV in patients with HFrEF (EF ≤45%) and predominantly central apnoea. The AHI fell substantially; all-cause and cardiovascular mortality rose. ASV is now contraindicated in this population — the single most important fact in the field, and one that must be checked before any device referral.1
- CANPAP tested CPAP against control in heart failure with central apnoea. It improved ejection fraction, nocturnal oxygenation and six-minute walk distance but showed no transplant-free survival benefit, and was stopped early. A post-hoc analysis suggested benefit confined to those in whom the AHI was actually suppressed below 15 — hypothesis-generating only, and never confirmed prospectively.3
- ADVENT-HF, testing peak-flow-triggered ASV in a broader heart failure population including patients with obstructive-predominant disease, did not show harm but also did not demonstrate a survival benefit — leaving ASV without a positive outcome trial in any heart failure phenotype.4
- Transvenous phrenic nerve stimulation reduced AHI and improved quality of life in the remedē System randomised trial, with sustained effect in follow-up. The trial was powered on AHI, not on mortality — which, after SERVE-HF, is the obvious limitation.5
- Optimising heart failure therapy reduces central apnoea. Guideline-directed medical therapy, cardiac resynchronisation and management of congestion all lower the AHI, and this is the intervention with the strongest outcome rationale because its benefit is established independently.2
- Opioid reduction is the treatment for opioid-related central apnoea, with a demonstrated dose–response relationship between morphine-equivalent dose and central event frequency. Device therapy in this group has little evidence and does not address the mechanism.6
- Exercise training reduces sleep-disordered breathing severity in small heart failure trials, plausibly by improving cardiac output and reducing circulatory delay. Effects are modest and the trials are small, but the mechanism is the right one and the intervention has independent benefit.7
Clinical reasoning
- Check ejection fraction before any ASV referral. EF ≤45% with predominantly central apnoea is a contraindication. This is the highest-consequence single check in the management of these patients.
- Effort channels are required. Oximetry and most home studies cannot distinguish central from obstructive events. Where a central mechanism is suspected, laboratory polysomnography with respiratory effort measurement is the appropriate study.
- Absent snoring with witnessed apnoeas is the most useful bedside discriminator, and sleepiness is often less prominent than in obstructive disease — so an Epworth score in the normal range does not exclude it.
- Loop gain explains the treatment logic. High controller gain plus long circulatory delay produces instability; interventions that lower gain (oxygen, acetazolamide) or shorten delay (improved cardiac output) stabilise breathing, whereas pressure support alone addresses neither.
- Distinguish the phenotypes before choosing therapy. Cheyne–Stokes in heart failure, ataxic opioid-related breathing, treatment-emergent apnoea and brainstem disease share a label and share almost nothing else. Treatment-emergent apnoea in particular usually resolves on continued CPAP and should not trigger a device change.
- A new central pattern warrants a cardiac question. Emergence of Cheyne–Stokes breathing in a known heart failure patient often signals decompensation before symptoms declare it.
- Physiotherapy contribution is case-finding and mechanism-directed exercise, not device management. Cardiac rehabilitation and persistent-pain services see the two at-risk populations routinely and are well placed to ask the three questions that matter: witnessed pauses, waking short of breath, and unrefreshing sleep.
Evidence gaps
- No therapy directed at central apnoea has improved survival in any population. Whether any phenotype benefits from suppression remains unknown, and the CANPAP post-hoc suppression hypothesis has never been tested prospectively.
- The mechanism of harm in SERVE-HF is unexplained — proposed candidates include reduced preload, arrhythmia and loss of a compensatory function — and without it, extrapolation to other devices is guesswork.
- Central apnoea in HFpEF is largely unstudied despite the prevalence of that phenotype.
- Opioid-related central apnoea has no randomised treatment evidence; dose reduction is reasoned rather than trialled.
- Phrenic nerve stimulation has no mortality data, in a field where a device that improved the AHI has already been shown to increase mortality.
- Exercise training trials are small, short and heterogeneous, and none has been designed with sleep-disordered breathing as its primary endpoint.
References for the clinical evidence summary
- 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.
- Naughton MT. Cheyne–Stokes respiration: friend or foe? Thorax 2012;67(4):357–360.
- Bradley TD, Logan AG, Kimoff RJ, et al. Continuous positive airway pressure for central sleep apnea and heart failure (CANPAP). N Engl J Med 2005;353(19):2025–2033.
- Bradley TD, Logan AG, Lorenzi Filho G, et al. Adaptive servo-ventilation for sleep apnoea in heart failure (ADVENT-HF): a multicentre, randomised, parallel-group, open-label trial. Lancet Respir Med 2024;12(2):153–166.
- Costanzo MR, Ponikowski P, Javaheri S, et al. Transvenous neurostimulation for central sleep apnoea: a randomised controlled trial. Lancet 2016;388(10048):974–982.
- Correa D, Farney RJ, Chung F, et al. Chronic opioid use and central sleep apnea: a review of the prevalence, mechanisms, and perioperative considerations. Anesth Analg 2015;120(6):1273–1285.
- Yamamoto U, Mohri M, Shimada K, et al. Six-month aerobic exercise training ameliorates central sleep apnea in patients with chronic heart failure. J Card Fail 2007;13(10):825–829.
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