Central Sleep Apnoea
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Direct answer
Absence of respiratory effort — not a blocked airway — is what separates central sleep apnoea from the obstructive variety: the polysomnogram shows pauses in airflow with no diaphragmatic and intercostal movement, and the diagnosis requires an apnoea-hypopnoea index of five or more per hour with at least half the respiratory events central in origin. The most exam-relevant pattern is Cheyne-Stokes respiration with central sleep apnoea in heart failure with reduced ejection fraction, a high-loop-gain instability in which vigorous chemoreflex control of breathing repeatedly overshoots. Management treats the underlying disease first: optimise heart failure therapy, withdraw opioids and sedatives, and only then choose PAP. Adaptive servo-ventilation is contraindicated in central sleep apnoea with heart failure and an ejection fraction of 45 per cent or less, because the SERVE-HF trial showed excess cardiovascular mortality.
What you must remember
- Definition: AHI of 5 or more per hour with at least 50 per cent of events central; a central event has absent effort in both airflow and respiratory muscle channels, whereas obstructive events show continued or increased effort against a closed airway.
- Classification: Cheyne-Stokes respiration with heart failure; idiopathic central sleep apnoea; high-altitude periodic breathing; opioid-induced central apnoea; and treatment-emergent central sleep apnoea appearing when CPAP unmasks central events in a predominantly obstructive patient.
- Loop gain concept: heart failure prolongs circulation time and heightens chemosensitivity, so the CO2 set point oscillates around the apnoeic threshold — breathing waxes past normal, then stops entirely, in a crescendo-decrescendo cycle with an arousal at the peak.
- Heart failure first: ACE inhibitor or ARNI, beta-blocker, MRA and SGLT2 inhibitor optimisation, plus cardiac resynchronisation in appropriate patients, can attenuate Cheyne-Stokes respiration before any PAP device is chosen.
- The SERVE-HF rule: adaptive servo-ventilation increased cardiovascular and all-cause mortality in heart failure with ejection fraction of 45 per cent or below, so ASV is contraindicated there; CPAP is the first device tried, and ASV is reserved for persistent central events with preserved ejection fraction.
- Opioid-induced disease: manage by reducing the opioid wherever possible, since positive-pressure therapy often fails when the drive is pharmacologically suppressed; the same logic applies to benzodiazepine and narcotic-weaning advice.
- Pharmacological fallbacks: acetazolamide (a carbonic anhydrase inhibitor that induces mild metabolic acidosis, lowering the apnoeic threshold) and cautious theophylline have evidence in selected patients but are third-line.
- Device nuance: adaptive servo-ventilation delivers breath-by-breath back-up rate that tracks the patient's recent ventilation, damping the oscillation — elegant in physiology, dangerous in the low-EF heart.
Reading a polysomnogram in heart failure
A 70-year-old man with ischaemic cardiomyopathy, ejection fraction 28 per cent, reports poor sleep and daytime sleepiness; his study shows a crescendo-decrescendo breathing pattern with central apnoeas at the nadir, cycle length around 60 seconds, and an arousal at each peak — Cheyne-Stokes respiration with central sleep apnoea, AHI 32 with over 80 per cent central events. The correct sequence is not a machine. First confirm he is on maximally tolerated guideline-directed therapy, check for atrial fibrillation and diuretic status, and screen his medications for opioids. A trial of CPAP follows: it splints the upper airway and raises functional residual capacity, abolishing any obstructive component and, in a proportion of patients, the central events too. If central apnoea persists despite weeks of compliant CPAP and the ejection fraction remains 28 per cent, ASV is prohibited — that is the SERVE-HF lesson, and the alternatives are nocturnal oxygen, acetazolamide, or phrenic nerve stimulation where available. Contrast a second patient on long-term methadone with non-periodic central apnoeas: no device will fix chemoreceptor suppression, and the answer is opioid de-escalation under supervision.
Where students slip
The trap is applying CPAP logic to every sleep apnoea: CPAP can precipitate or worsen central events in a heart failure patient, and ASV — the intuitive fix for periodic breathing — killed more patients than placebo-level care in SERVE-HF. Second, examinees describe Cheyne-Stokes breathing as "apnoea then deep breathing"; marks go for the crescendo-decrescendo pattern with a cycle length of about a minute, driven by prolonged circulation time. Third, the "50 per cent of events central" criterion is what converts a mixed picture into a central diagnosis — a favourite single-best-answer discriminator.
Frequently asked questions
How does central sleep apnoea differ from obstructive on polysomnography?
Central events show absent airflow with absent respiratory effort, while obstructive events show absent airflow with continued or increasing effort against a collapsed upper airway.
Why does adaptive servo-ventilation harm patients with low ejection fraction?
The SERVE-HF trial found increased cardiovascular and all-cause mortality when ASV was used in central sleep apnoea with heart failure and ejection fraction of 45 per cent or less, so it is contraindicated in that group.
What is the first therapeutic step in Cheyne-Stokes respiration with heart failure?
Optimisation of guideline-directed heart failure therapy — ARNI or ACE inhibitor, beta-blocker, MRA, SGLT2 inhibitor — before any positive-airway-pressure device, since better cardiac function itself dampens periodic breathing.
Which drugs cause central sleep apnoea?
Long-acting opioids are the classic cause, with benzodiazepines and other sedatives contributing; management centres on withdrawal or dose reduction rather than device therapy.
What is loop gain in the context of central sleep apnoea?
The gain of the ventilatory control system: a high loop gain means small disturbances in carbon dioxide produce exaggerated ventilatory overshoot and undershoot, the physiological basis of periodic breathing.