Sleep apnoea / polysomnography

SLEEP APNOEA / POLYSOMNOGRAPHY — 15 MARKS DEFINITIONS

Sleep apnoea–hypopnoea syndrome (SAHS) — repetitive episodes of complete or partial upper-airway obstruction during sleep producing intermittent hypoxaemia, hypercapnia, sympathetic surges and cortical arousals, with consequent daytime symptoms.

AASM event definitions: Apnoea = fall in airflow of 90% or more for 10 seconds or longer. Hypopnoea = fall in airflow of 30% or more for 10 seconds or longer with either a 3% or greater desaturation or an arousal. RERA = respiratory-effort-related arousal not meeting apnoea or hypopnoea criteria.

Indices: AHI = (apnoeas + hypopnoeas) per hour of sleep; RDI = AHI plus RERAs per hour; ODI = oxygen desaturations per hour; T90 = percentage of sleep time with saturation below 90%; hypoxic burden = area under the desaturation curve.

Types — obstructive (respiratory effort present, airflow absent), central (both effort and airflow absent — includes Cheyne–Stokes respiration in heart failure and stroke), mixed, and treatment-emergent central apnoea appearing on PAP therapy.

Severity: mild AHI 5–15, moderate 15–30, severe above 30 per hour. Diagnosis of OSA requires AHI 15 or more, or AHI 5 or more with symptoms or associated comorbidity.

OSA is the most common sleep-related problem in older adults. Development is age-dependent and male-dominant, and incidence is higher in the obese and in those with increased neck circumference. Prevalence of AHI 15 or more approaches 20–30% in those over 65, and the male-to-female ratio narrows sharply after the menopause. Sleep-disordered breathing is very common in heart failure.

India — urban adult prevalence is approximately 9–13% in men and 5–7% in women. Indians develop OSA at a lower BMI than Caucasians because of craniofacial morphology (shorter mandible, narrower airway) and central adiposity; therefore use Asian-Indian cut-offs — overweight BMI 23 kg/m², obesity 25 kg/m², waist circumference 90 cm in men and 80 cm in women.

Four contributing traits ("PALM"): Pcrit — anatomical collapsibility of the pharynx; Arousal threshold — a low threshold causes premature arousal and ventilatory instability; Loop gain — an unstable, over-responsive ventilatory control system; Muscle responsiveness — poor reflex recruitment of genioglossus and other dilators.

Age-related contributions — reduced upper-airway dilator tone and reflex responsiveness, increased pharyngeal fat deposition and airway length, loss of lung-volume tethering of the airway, increased loop gain, blunted arousal and chemoreflex responses, and reduced protective effect of oestrogen in women after the menopause.

Consequences of untreated OSA — nocturnal hypoxia with associated risk of cardiac arrhythmias and myocardial and cerebral infarction; resistant hypertension (a recognised secondary cause); heart failure, atrial fibrillation, pulmonary hypertension, type 2 diabetes and metabolic syndrome; excessive daytime sleepiness with driving and occupational risk; cognitive impairment and increased dementia risk; depression; and reduced olfactory identification and discrimination in proportion to severity (higher AHI and lower mean arterial oxygen saturation), thought to reflect central cholinergic dysfunction.

Nocturnal — loud, irregular snoring; witnessed apnoeas; choking or gasping arousals; waking sweating, anxious and tachycardic; excessive movement during sleep; nocturia; dry mouth. Daytime — morning headache, morning drowsiness, excessive daytime sleepiness, poor concentration, irritability, depressed mood, reduced libido.

Atypical presentation in older adults — sleepiness may be absent or attributed to age. Instead consider OSA in nocturia, nocturnal confusion or sundowning, falls, new or worsening cognitive impairment, refractory hypertension, recurrent atrial fibrillation and unexplained pulmonary hypertension. Obesity is less prominent than in younger patients. The bed-partner history is essential and is frequently unavailable in widowed or institutionalised elders — ask nursing staff instead.

Screening instruments — STOP-BANG (Snoring, Tiredness, Observed apnoea, blood Pressure, BMI over 35, Age over 50, Neck over 40 cm, Gender male; 3–4 intermediate risk, 5 or more high risk). Note that the age and gender items make almost every older man score positive, so specificity in geriatric practice is poor. Also the Epworth Sleepiness Scale (above 10 abnormal), the Berlin Questionnaire and NoSAS.

Attended, in-laboratory polysomnography is the gold standard. AASM levels of testing: Level 1 — attended, in-laboratory, full-channel PSG. Level 2 — unattended full-channel portable study. Level 3 — home sleep apnoea test (HSAT), limited channels: airflow, respiratory effort, oximetry, with or without ECG, heart rate and body position. Level 4 — one or two channels, usually oximetry alone.

Level-1 PSG channels:

Sleep staging — EEG (frontal, central and occipital derivations referenced to the contralateral mastoid: F4-M1, C4-M1, O2-M1), electro-oculogram (two channels) and submental EMG.

Airflow — nasal pressure transducer (for hypopnoea) and oronasal thermistor (for apnoea).

Respiratory effort — thoracic and abdominal respiratory inductance plethysmography belts.

Gas exchange — pulse oximetry, with transcutaneous or end-tidal carbon dioxide where hypoventilation is suspected.

Others — ECG, bilateral anterior tibialis EMG (limb movements), body-position sensor, snore microphone, and synchronised audio-video (essential for parasomnias and REM sleep behaviour disorder).

Scoring and report — scored in 30-second epochs as stages W, N1, N2, N3 and R. The report should include total sleep time, sleep efficiency, sleep-onset and REM latency, wake after sleep onset, percentage of each stage, arousal index, AHI overall and in supine and REM sleep separately, RDI, ODI, minimum and mean oxygen saturation, T90, periodic limb movement index, and cardiac rhythm.

Indications for PSG — suspected sleep apnoea; suspected periodic limb movement disorder; suspected REM sleep behaviour disorder or injurious parasomnia; suspected nocturnal seizures; narcolepsy (followed next day by the multiple sleep latency test); PAP titration; assessment of treatment failure or persistent symptoms despite therapy; and insomnia refractory to adequate treatment. PSG is not indicated for uncomplicated insomnia, uncomplicated circadian rhythm disorders, or restless legs syndrome, which is a clinical diagnosis.

Home sleep apnoea testing is acceptable in uncomplicated adults with a high pre-test probability of moderate-to-severe OSA. It is not appropriate where there is significant cardiorespiratory disease, suspected hypoventilation, neuromuscular disease, chronic opioid use, or suspicion of a non-OSA sleep disorder — all of which are common in geriatric practice. HSAT underestimates the AHI because total recording time rather than total sleep time is the denominator; therefore a negative or technically inadequate HSAT in a symptomatic patient must be followed by in-laboratory PSG.

Practical problems in older adults — the first-night effect, difficulty tolerating electrodes, mobility and transfer problems, nocturia interrupting the study, risk of delirium in an unfamiliar environment, and intrinsically fragmented sleep, all of which reduce the reliability of a single night's study.

General and behavioural — weight reduction; avoid evening alcohol, benzodiazepines and opioids, which worsen upper-airway collapse and blunt arousal; smoking cessation; treat nasal obstruction and hypothyroidism; positional therapy for supine-predominant disease; optimise heart failure; and give explicit driving advice — untreated OSA with sleepiness is a driving hazard and, in many jurisdictions, a reportable one.

Continuous positive airway pressure (CPAP) is first-line and the standard of care for moderate-to-severe OSA. Auto-titrating PAP is acceptable in uncomplicated disease; bilevel PAP for hypoventilation or pressure intolerance. CPAP improves sleepiness, quality of life, blood pressure and mood; adherence is the limiting factor (conventional target: at least 4 hours a night on at least 70% of nights). Older patients adhere at least as well as younger ones when adequately supported.

Oral appliances — mandibular advancement devices for mild-to-moderate OSA, CPAP intolerance or supine-predominant disease. They require adequate dentition, a major limitation in older adults, and are contraindicated in significant temporomandibular joint disease.

Surgery — uvulopalatopharyngoplasty, nasal surgery, tonsillectomy and maxillomandibular advancement; results are poorer and risks higher in the elderly, so surgery is reserved for carefully selected patients with a correctable obstruction. Hypoglossal nerve stimulation is an option for CPAP-intolerant patients within defined AHI and BMI limits and in the absence of complete concentric palatal collapse.

Central sleep apnoea and Cheyne–Stokes respiration — optimise heart-failure therapy first; consider nocturnal oxygen; adaptive servo-ventilation is contraindicated in symptomatic heart failure with an ejection fraction of 45% or less (SERVE-HF trial showed increased mortality); phrenic nerve stimulation is an option in selected patients.

Definition: repetitive complete (apnoea) or partial (hypopnoea) upper-airway obstruction in sleep causing intermittent hypoxaemia and arousals. Apnoea = 90% airflow fall for 10 s; hypopnoea = 30% fall for 10 s with 3% desaturation or arousal.

Severity: AHI mild 5–15, moderate 15–30, severe above 30. Diagnosis: AHI 15 or more, or 5 or more with symptoms.

Pathophysiology: PALM traits — airway collapsibility, low arousal threshold, high loop gain, poor dilator muscle responsiveness; ageing adds reduced muscle tone, pharyngeal fat, reduced lung-volume tethering and blunted chemoreflexes.

Features: loud irregular snoring, witnessed apnoeas, waking sweating and tachycardic, morning headache and drowsiness, daytime sleepiness. In older adults, presentation may instead be nocturia, nocturnal confusion, falls, refractory hypertension or cognitive decline.

Complications: arrhythmia, myocardial and cerebral infarction, resistant hypertension, heart failure, atrial fibrillation, pulmonary hypertension, diabetes, cognitive impairment, road-traffic risk.

Polysomnography: gold standard, Level 1 attended in-laboratory. Channels — EEG, EOG and submental EMG for staging; nasal pressure and thermistor for airflow; thoracoabdominal belts for effort; oximetry; ECG; tibialis EMG; position, snore and video. Scored in 30-second epochs; report AHI (total, supine, REM), RDI, ODI, arousal index, minimum and mean saturation, T90, PLM index. Level 3 home testing for uncomplicated high-probability cases only; it underestimates AHI.

Management: weight loss, avoid evening alcohol and sedatives, positional therapy, treat nasal obstruction, driving advice. CPAP first-line (adherence 4 h/night on 70% of nights); mandibular advancement device if mild-moderate or CPAP-intolerant and dentition adequate; selected surgery or hypoglossal nerve stimulation. ASV contraindicated if LVEF 45% or less. 3-point current update: (i) SURMOUNT-OSA (NEJM 2024) — tirzepatide reduced AHI by 25–29 events per hour with disease resolution in 43–51%, and on 20 December 2024 the FDA approved it as the first drug for moderate-to-severe OSA with obesity; CPAP remains first-line. (ii) The field is moving beyond the AHI to hypoxic burden and endotype-driven (PALM) therapy, with AASM Scoring Manual v3 (2023) updating event rules. (iii) FDA-cleared wearable sleep-apnoea notifications are increasing detection but require confirmatory HSAT or PSG; in India, use Asian BMI and waist cut-offs because OSA occurs at lower BMI. End of module — Elder abuse · Advance care planning · End-of-life care · Transitional care · Insomnia · Sleep apnoea Next in series: cardiovascular, respiratory and neurology (Parkinson's disease)