Understanding Central Sleep Apnea: Causes, Types, Symptoms, Diagnosis, and Treatment
Sleep Medicine • Cardiology • Pulmonology
Understanding Central Sleep Apnea (CSA)
Central sleep apnea is characterised by reduced or absent respiratory drive during sleep leading to diminished airflow and disrupted sleep architecture. Unlike obstructive sleep apnea, CSA stems from a failure of central respiratory control or chemoreception. Early identification guides targeted therapy and reduces morbidity.
Pathophysiology — brief
CSA results from reduced central respiratory drive, instability of ventilatory control (high loop gain), or impaired chemoreceptor function. This leads to cyclical decreases in ventilation, hypoxaemia and sleep fragmentation. Underlying causes vary—cardiac failure, opioid therapy, neurologic disease and high‑altitude exposure are common contributors.
Types of CSA
- Cheyne–Stokes respiration (CSR): associated with heart failure and stroke—crescendo‑decrescendo breathing with central apneas/hypopneas.
- Opioid‑related CSA: chronic opioid therapy can blunt respiratory drive and produce central apneas.
- High‑altitude periodic breathing: transient CSA occurring at altitude due to hypoxic ventilatory responses.
- Primary (idiopathic) CSA: rare, no clear cause identified after evaluation.
- CSA due to medical/neurologic disorders: e.g., stroke, brainstem lesions, neuromuscular disease, or hypothyroidism in some cases.
Clinical features & consequences
- Typical symptoms: excessive daytime sleepiness, unrefreshing sleep, nocturnal awakenings, witnessed apneas, morning headache and cognitive impairment.
- Cheyne–Stokes variant: paroxysmal nocturnal dyspnoea, orthopnoea may coexist; CSA worsens heart failure outcomes if untreated.
- Long‑term consequences: cardiovascular morbidity, impaired quality of life, increased hospitalization risk in heart failure, and neurocognitive decline in severe cases.
Assessment checklist
- History: ask about daytime sleepiness, witnessed apneas, nocturnal dyspnoea, opioid use, neurologic disease, altitude exposure, and heart failure symptoms.
- Examination: cardiovascular and neurological exam, BMI, neck circumference; assess signs of heart failure (peripheral oedema, JVP) and pulmonary disease.
- Review medications: opioids, sedatives, certain antidepressants and anti‑seizure drugs.
- Screening tools: Epworth Sleepiness Scale for sleepiness; assess heart failure severity (NYHA class) and recent cardiac investigations.
Investigations
- Overnight polysomnography (PSG): diagnostic test—shows absent respiratory effort during apneic events, cyclical pattern in CSR, oxygen desaturations and arousals. Differentiate from obstructive events by lack of respiratory effort.
- Cardiac evaluation: ECG, echocardiography (LVEF), BNP/NT‑proBNP in suspected heart failure.
- Medication/toxicology review: confirm opioid exposure and consider tapering where appropriate.
- Neurologic imaging/testing: brain imaging if focal neurological signs or suspected structural lesion.
Management principles
- Treat underlying cause: optimise heart failure management (ACEi/ARB, beta‑blocker, diuretics, device therapy), cease or reduce opioids where possible, and address reversible metabolic contributors.
- Positive airway pressure (PAP): CPAP may help some patients—especially when mixed obstructive disease coexists. Adaptive servo‑ventilation (ASV) can normalise ventilation in many CSA phenotypes but is contraindicated in patients with symptomatic heart failure with reduced ejection fraction (LVEF ≤45%) and predominant central events—review latest cardiology guidance and individualise care.
- Supplemental oxygen: may reduce central events and improve oxygenation in select patients (e.g., high‑altitude CSA, some heart failure patients) but does not stabilise ventilatory control long‑term.
- Pharmacologic options: acetazolamide may stabilise breathing in altitude‑related periodic breathing; theophylline or respiratory stimulants have limited evidence. Address opioid therapy with supervised taper and consider non‑opioid analgesics and multimodal pain strategies.
- Multidisciplinary care: coordinate sleep medicine, cardiology, pulmonology, pain specialists and neurology as needed for complex cases.
Special considerations & cautions
- ASV and heart failure: recent trials showed harm in certain heart failure populations (reduced LVEF) — avoid ASV in these patients and consult cardiology for device decisions.
- Opioid‑related CSA: consider opioid dose reduction or rotation, naloxone not indicated for chronic CSA; involve pain team for safe opioid tapering.
- High‑altitude CSA: descent or acetazolamide often effective; prophylactic measures for susceptible climbers/workers.
- Monitoring: reassess after optimization of heart failure or opioid reduction as CSA severity may change; repeat PSG when management changes significantly.
Red flags — urgent escalation
- Severe nocturnal hypoxaemia, syncope, unexplained heart failure decompensation, or recurrent nocturnal arrhythmias — urgent cardiology and sleep medicine review.
- Rapidly progressive neurological signs suggesting brainstem lesion — urgent neuroimaging and specialist referral.
- Opioid overdose risk or signs of misuse — urgent addiction/pain services and safety planning.
Case vignette
Patient: M., 68, with ischemic cardiomyopathy (LVEF 35%), NYHA class II breathlessness and daytime sleepiness. PSG showed Cheyne–Stokes respiration with central AHI 28/h and significant desaturations. Management: optimise heart failure therapy, avoid ASV given reduced LVEF, trial of oxygen at night and consider CPAP as bridging therapy; cardiology and sleep medicine follow‑up arranged to reassess after medical optimisation.
தமிழில் — சுருக்கம்
மைய தூக்கமின்மை (CSA) என்பது தூக்கத்தின் போது மத்திய சுவாச உந்துதல் குறையுமால் ஏற்படும். இதற்கான காரணங்கள் பலவகை—இதரமூலம் இருதய நோய், ஓபியோய்ட்கள் மற்றும் உயர்ந்த உயரம் அடங்கும். அடையாளம் காண்தல் மற்றும் காரணம் சரிசெய்தல் முதன்மை.
Key takeaways
- Suspect CSA when PSG shows apneas without respiratory effort or cyclical breathing patterns; consider cardiac, opioid and neurologic causes.
- Treat underlying disorders (optimise heart failure, reduce opioids); use PAP, supplemental oxygen or pharmacologic measures selectively with specialist input.
- Consult cardiology before ASV in heart failure patients; provide multidisciplinary care and repeat testing after major management changes.