Sleep disorders - sleep apnoea
Description
Definitions
- Apnoea - >=90% airflow reduction for >=10 s
- Hypopnoea - >=30% airflow reduction for >=10 s + >=3% desaturation or arousal
- AHI = apnoeas + hypopnoeas per hour of sleep
- RDI = AHI + respiratory effort-related arousals
- ODI = >=3% or 4% desaturation dips per hour (the 4% ODI correlates best with cardiovascular outcome)
- T90 - % of sleep time with SpO2 <90% (hypoxic burden predicts cardiovascular risk better than AHI)
Types
| Effort | Mechanism | |
|---|---|---|
| Obstructive (OSA) | Present (paradoxical thoraco-abdominal movement) | Pharyngeal collapse despite drive |
| Central (CSA) | Absent | Absent or unstable respiratory output |
| Mixed | Central onset, obstructive end | Both |
| Obesity hypoventilation (OHS) | - | BMI >30 + awake PaCO2 >45 + no other cause |
Severity by AHI
| Normal | Mild | Moderate | Severe |
|---|---|---|---|
| <5 | 5-15 | 15-30 | >30 |
- *AHI correlates poorly with symptoms.* Treat the patient, not the number
Epidemiology
- Moderate-severe OSA in ~10-17% of men, 3-9% of women; most undiagnosed
- ~5-9% of Australian adults report a diagnosis; prevalence rising with obesity
- M>F ~2-3:1; the gap narrows after menopause
- Peak 40-70 yr
- Aboriginal and Torres Strait Islander peoples: higher prevalence and severity
- CSA: much less common; ~30-50% of chronic HFrEF, and prevalent in chronic opioid use
Aetiopathogenesis
OSA - the four endotypes (PALM), and why treatment differs
- Pcritical - anatomically collapsible pharynx (the dominant factor in most)
- Arousal threshold - low threshold -> wakes before airway recruitment, unstable sleep
- Loop gain - high -> overshoot/undershoot ventilatory control
- Muscle responsiveness - poor genioglossus recruitment
- This explains why some patients with mild AHI are very symptomatic and why non-PAP therapies work in selected patients
OSA risk factors
- Obesity (esp. central and neck fat), BMI >35, neck circumference >43 cm (M) / >41 cm (F)
- Male sex, age 40-70, postmenopausal
- Craniofacial: retrognathia/micrognathia, high arched palate, macroglossia, tonsillar hypertrophy, nasal obstruction
- Family history
- Alcohol, sedatives, opioids, smoking
- Endocrine: hypothyroidism, acromegaly, PCOS, Cushing
- Fluid shift (rostral fluid redistribution - heart failure, ESKD explains nocturnal worsening)
- Down syndrome, Marfan, neuromuscular disease
- Occupational relevance: commercial vehicle drivers, shift workers
Consequence cascade
- Repetitive collapse -> hypoxia-reoxygenation + arousals + large negative intrathoracic pressure swings
- -> sympathetic surge -> non-dipping BP, hypertension, arrhythmia
- -> oxidative stress, systemic inflammation, endothelial dysfunction, insulin resistance
- -> inc atrial stretch and transmural pressure -> AF
- -> sleep fragmentation -> daytime sleepiness, cognitive and mood impairment
CSA causes
- Cheyne-Stokes respiration in HFrEF - high sympathetic tone, prolonged circulation time, pulmonary congestion, chemoreceptor hypersensitivity -> high loop gain**
- Associated with lower LVEF, raised PCWP and higher mortality - a marker of HF severity
- Opioids (dose-related; ataxic/Biot breathing)
- Stroke and brainstem lesions, CNS disease (MS), neuromuscular disorders
- High altitude
- Idiopathic in older adults
- Treatment-emergent CSA - appears on CPAP for OSA; usually resolves with continued use
Diagnosis
Symptoms
- Nocturnal: loud irregular snoring, witnessed apnoeas, choking/gasping arousals, restless sleep, nocturia, sweating
- Daytime: unrefreshing sleep, sleepiness when sedentary, morning headache, dry mouth, poor concentration, irritability, low mood, reduced libido
- Epworth Sleepiness Scale >=11 = excessive daytime sleepiness
- Insensitive - many with severe OSA score normally, especially women, who present with fatigue, insomnia and mood symptoms rather than sleepiness
Examination
- BMI, neck circumference, waist
- Crowded oropharynx - Mallampati III-IV, tonsillar hypertrophy, macroglossia, low soft palate
- Retrognathia, nasal obstruction, deviated septum
- BP (often non-dipping and resistant), signs of pulmonary hypertension, RHF, obesity
- Look for acromegaly, hypothyroidism, Cushing
Screening tools
- STOP-BANG: Snoring, Tiredness, Observed apnoea, Pressure (BP), BMI >35, Age >50, Neck >40 cm, Gender male
- >=3 sensitive, >=5 high probability of moderate-severe OSA
- Screening tools rule out, they do not diagnose
Confirming the diagnosis
- Level 1 in-laboratory polysomnography - the reference standard
- Required if: suspected CSA, hypoventilation, significant cardiorespiratory or neuromuscular disease, other sleep disorder (narcolepsy, RBD, PLMD), or an equivocal home study
- Level 2-3 home sleep apnoea testing - acceptable for uncomplicated, high-probability OSA
- Underestimates AHI (denominator is recording time, not sleep time) - a negative study in a high-probability patient must be followed by PSG
Diagnostic criteria
- AHI >=5/h + >=1 attributable symptom or comorbidity (sleepiness, unrefreshing sleep, snoring/choking, insomnia, hypertension, mood disorder, cognitive dysfunction, IHD, AF, stroke, T2DM), OR
- AHI >=15/h regardless of symptoms
Additional tests
- ABG / venous bicarbonate - raised HCO3- is the cheapest screen for chronic hypercapnia and OHS
- TFT, HbA1c, lipids; echo if PH or HFrEF suspected
- Overnight oximetry has poor sensitivity; a normal oximetry does not exclude OSA
Differential for excessive daytime sleepiness
- Insufficient sleep (the commonest cause), shift work, circadian rhythm disorder
- Narcolepsy (cataplexy, sleep paralysis, hypnagogic hallucinations, short REM latency on MSLT)
- Periodic limb movement disorder / restless legs
- Depression, hypothyroidism, medication, chronic fatigue, poor sleep hygiene
Management
1. Behavioural and risk-factor modification - in everyone
- Weight loss - 10% weight loss reduces AHI by ~26%; sustained loss can be curative
- Avoid alcohol and sedatives in the evening, especially benzodiazepines and opioids
- Positional therapy if supine-predominant (AHI supine >=2x non-supine)
- Smoking cessation, sleep hygiene, treat nasal obstruction
- *Driving advice at diagnosis - Austroads Assessing Fitness to Drive*: report to the licensing authority; commercial drivers require documented treatment adherence and control before returning to duty
2. CPAP - first-line for moderate-severe and for symptomatic mild OSA
- Pneumatic splint of the upper airway
- Proven benefit: daytime sleepiness, quality of life, mood, cognition, driving performance, modest BP reduction (~2-3 mmHg; larger in resistant hypertension)
- *No RCT has shown a reduction in cardiovascular events or mortality (SAVE, RICCADSA, ISAACC)*
- Observational data suggest benefit; the trials were limited by poor adherence (~3 h/night) and by excluding sleepy patients
- Do not promise a cardiovascular benefit - treat symptoms and quality of life
- Adherence is everything: target >=4 h/night on >=70% of nights
- Troubleshoot: mask fit and type, humidification, nasal congestion, claustrophobia, pressure intolerance (auto-titrating or EPR), aerophagia, partner factors
- Auto-CPAP is appropriate for uncomplicated OSA; fixed pressure after titration if comorbid cardiorespiratory disease
3. Alternatives to CPAP
- Mandibular advancement splint - mild-moderate OSA, or CPAP-intolerant
- Less effective at reducing AHI but often better tolerated - the health outcomes are comparable
- Requires adequate dentition; side effects: TMJ pain, occlusal change
- Hypoglossal nerve stimulation - moderate-severe OSA, CPAP-failure, BMI limits, no concentric palatal collapse on drug-induced sleep endoscopy
- Substantial and durable AHI reduction with high adherence; newer bilateral systems broaden candidacy
- Surgery - tonsillectomy (large tonsils, especially in young adults), nasal surgery (improves CPAP tolerance), maxillomandibular advancement (highly effective in craniofacial disproportion)
- UPPP alone has poor and unpredictable results
- Bariatric surgery - severe obesity; often the definitive treatment
4. Pharmacotherapy - a genuinely new option
- Tirzepatide - moderate-severe OSA with obesity: AHI reduction ~25-29 events/h in SURMOUNT-OSA, with weight and cardiometabolic benefit
- The first drug with substantive OSA evidence; does not replace PAP in severe symptomatic disease, but changes the conversation in obesity-associated OSA
- Modafinil/armodafinil or solriamfetol for residual sleepiness despite adequate PAP adherence - only after re-checking adherence, pressure, and other causes of sleepiness
- No role for oxygen alone in OSA - it corrects saturation without relieving obstruction or arousals
5. Obesity hypoventilation syndrome
- Bilevel NIV (not CPAP) if awake hypercapnia persists or during acute decompensation
- Weight loss, bariatric surgery; treat coexisting OSA
6. Central sleep apnoea - treat by mechanism
| Mechanism | Treatment |
|---|---|
| Cheyne-Stokes in HFrEF (high loop gain) | Optimise heart failure therapy first - GDMT, CRT, decongestion. Trial of CPAP; nocturnal oxygen |
| Depressed drive with hypercapnia (opioids, neuromuscular, brainstem) | Bilevel NIV |
| Idiopathic CSA | CPAP or NIV; acetazolamide |
| Treatment-emergent CSA | Continue CPAP - usually resolves |
- *Adaptive servo-ventilation is CONTRAINDICATED in symptomatic HFrEF with LVEF <=45% and predominant CSA - SERVE-HF showed increased cardiovascular mortality*
- Reduce or cease opioids where possible
- Routine supplemental oxygen is not recommended in CSA outside the palliative setting
7. Perioperative
- Undiagnosed OSA is a major anaesthetic risk - screen with STOP-BANG preoperatively
- Minimise opioids and sedatives, regional technique where possible, monitored recovery, continue home PAP
Associations
(Odds ratios from observational data - association, not proven causation)
- Hypertension (OR ~1.4-2.9) - especially resistant and non-dipping hypertension
- Atrial fibrillation (OR ~4) - and a strong predictor of AF recurrence after cardioversion or ablation
- Heart failure (OR ~2.4); CSA/Cheyne-Stokes marks severity
- Stroke (OR ~1.6-4.3)
- Coronary artery disease (OR ~1.3)
- Type 2 diabetes and metabolic syndrome (OR ~1.2-2.6)
- Depression (OR ~2.6), anxiety, cognitive impairment
- Pulmonary hypertension - usually mild; more if OHS or coexisting lung disease
- MASLD, gout, glaucoma, nocturia, erectile dysfunction
- Motor vehicle accidents - 2-3x risk; the single most important medicolegal issue
- Obesity, PCOS, acromegaly, hypothyroidism, Cushing
- Chronic kidney disease and dialysis (fluid shift)
- COPD ("overlap syndrome") - worse nocturnal hypoxaemia, higher mortality
- Perioperative complications, difficult intubation
Natural history & complications
- Progressive with weight gain and ageing; improves with sustained weight loss
- Untreated severe OSA (AHI >30) - increased all-cause and cardiovascular mortality in cohort studies
- Symptomatic response to CPAP is often dramatic and rapid (days-weeks) when adherence is achieved
- If sleepiness persists on genuinely adherent CPAP, look for another cause
- ~30-50% abandon CPAP within the first year - the first weeks determine long-term adherence
Complications
- Cardiovascular: hypertension, AF and other arrhythmias (nocturnal bradyarrhythmia and asystole during apnoeas), IHD, HF, stroke
- Metabolic: insulin resistance, T2DM, MASLD
- Neurocognitive: sleepiness, impaired concentration and memory, depression
- Accidents - vehicular and occupational
- Chronic hypercapnic respiratory failure if OHS or overlap syndrome
- Cor pulmonale, secondary polycythaemia
- Relationship and quality-of-life impact
Monitor
- PAP download data - usage hours, residual AHI, leak (check at every review; residual AHI on device data is not a substitute for clinical assessment)
- Epworth, weight, BP
- Reassess after significant weight change - the sleep study and pressure requirement change with it
- Driving fitness at every review for commercial drivers
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