Sleep Apnea — Symptoms, Causes & Treatment | MyMedicPlus

Sleep apnoea (sleep apnea — US spelling) is a common sleep-disordered breathing (SDB) condition characterised by repeated episodes of partial (hypopnoea — 30% or greater reduction in airflow with 3% or greater oxygen desaturation) or complete (apnoea — cessation of airflow for 10 seconds or more) upper airway obstruction during sleep, causing cyclical oxygen desaturation (nocturnal hypoxaemia), arousal-induced sleep fragmentation, and autonomic nervous system surges. The most common type — obstructive sleep apnoea (OSA) — results from collapse or narrowing of the pharyngeal airway due to reduced muscle tone and anatomical predisposition. Central sleep apnoea (CSA) results from failure of central respiratory drive (no effort made to breathe) and is associated with heart failure, stroke, brainstem pathology, and opioid use. Complex or mixed sleep apnoea has features of both. The severity of OSA is measured by the apnoea-hypopnoea index (AHI) — the number of apnoea and hypopnoea events per hour of sleep: mild OSA is AHI 5–14 events/hour; moderate OSA is 15–29 events/hour; severe OSA is 30 or more events/hour. An estimated 1 billion adults globally have OSA of at least mild severity (AHI above 5), including 34% of men and 17% of women aged 30–70 in developed countries, with the majority undiagnosed. OSA is strongly associated with obesity, cardiovascular disease, type 2 diabetes, and premature mortality.

Obesity (BMI above 30) is the strongest modifiable risk factor for OSA — excess adipose tissue around the pharynx and in the parapharyngeal spaces narrows the upper airway lumen, and increased abdominal and truncal adiposity reduces functional residual capacity when supine (reducing respiratory drive). A 10% increase in weight is associated with a 32% increase in AHI. Anatomical predisposing factors: large neck circumference (above 40 cm in women, above 43 cm in men); retrognathia or micrognathia (recessed lower jaw — positions the tongue posteriorly, directly narrowing the retroglossal airway); large soft palate; crowded oropharynx; macroglossia (enlarged tongue — associated with acromegaly and hypothyroidism); adenotonsillar hypertrophy (the most common cause of OSA in children); nasal obstruction (deviated septum, nasal polyps — increases inspiratory effort and negative pharyngeal pressure, promoting collapse); and brachycephalic facial structure. Demographic and lifestyle risk factors: male sex (testosterone promotes pharyngeal fat deposition and reduces upper airway muscle tone — explaining the 2:1 male predominance, which narrows after the menopause when female risk rises); advancing age above 40 (progressive pharyngeal muscle atrophy); alcohol consumption within 3–4 hours of bedtime (profound dose-dependent pharyngeal muscle relaxation — increases AHI by 25% even in normal subjects); benzodiazepines, z-drugs, and opioids (reduce arousal threshold and pharyngeal muscle tone); smoking (upper airway mucosal inflammation and oedema); menopause (loss of progesterone, which stimulates respiratory drive); hypothyroidism (macroglossia, mucosal oedema, reduced respiratory drive); and acromegaly (IGF-1-driven macroglossia and craniofacial changes). Central sleep apnoea (CSA) causes: congestive heart failure with reduced ejection fraction (Cheyne-Stokes respiration from oscillating ventilatory drive); stroke or brainstem lesions; high-altitude residence; and chronic opioid use (opioids suppress the hypercapnic respiratory drive).

Nocturnal symptoms: loud, disruptive snoring (the most common presenting symptom and the most frequent reason a bed partner seeks medical advice); witnessed apnoeas — the bed partner observes the patient stop breathing for 10–30 seconds, then resume with a loud gasp, snort, or choking sound; nocturnal gasping, choking, or sensation of suffocation (sometimes waking the patient — though many patients are unaware of their own apnoeas); restless sleep (frequent positional changes driven by arousal events); nocturia (waking to urinate — caused by atrial natriuretic peptide release triggered by intrathoracic pressure swings, affecting up to 60% of OSA patients — a frequently missed clue to OSA diagnosis); night sweats; and in severe cases, nocturnal enuresis (bed wetting in children and occasionally adults). Daytime symptoms: excessive daytime sleepiness (EDS) — the most impactful symptom for quality of life; quantified with the Epworth Sleepiness Scale (ESS — scores of 10 or above indicate abnormal daytime somnolence); patients fall asleep during passive activities (watching TV, reading) and dangerously during active tasks (driving, conversations). Non-restorative sleep: patients wake feeling unrefreshed despite apparently adequate sleep duration — the hallmark of sleep fragmentation from OSA arousals. Morning headaches: from CO2 retention and intracranial vasodilation during apnoeic episodes — typically bilateral, worse in the morning, and resolve spontaneously within 1–2 hours of waking. Cognitive impairment: particularly in attention, processing speed, working memory, and executive function — chronic nocturnal hypoxaemia causes subtle white matter damage. Mood disturbance: irritability, anxiety, and clinical depression — comorbid with OSA in approximately 30–50%. Sexual dysfunction (erectile dysfunction and reduced libido in men — from vascular and hormonal effects of chronic hypoxaemia and sleep deprivation).

In-laboratory polysomnography (PSG — the gold standard): attended full overnight sleep study measuring EEG sleep staging, electrooculogram (eye movements), electromyogram (chin and limb muscles — periodic limb movements), airflow (thermistor and pressure transducer), respiratory effort (chest and abdominal plethysmography belts), oxygen saturation (SpO2 by pulse oximetry), ECG, body position, and snoring microphone; provides the AHI (events per hour) and a hypoxaemia index (T90 — percentage of total sleep time with SpO2 below 90%), as well as sleep architecture and efficiency data. AHI severity classification: 5–14 events/hour — mild OSA; 15–29 — moderate; 30 or above — severe; below 5 with symptoms — upper airway resistance syndrome (UARS). Home sleep apnoea testing (HSAT — type 3 portable device: measures airflow, respiratory effort, SpO2, heart rate, and body position without EEG or sleep staging): acceptable for uncomplicated suspected moderate-to-severe OSA (NICE NG202, AASM guidelines); less accurate in complex cases (heart failure, neuromuscular disease, suspected central apnoea); may underestimate AHI as it divides events by time in bed rather than total sleep time. Clinical screening tools: STOP-BANG questionnaire (8 questions — Snoring, Tired, Observed apnoeas, blood Pressure, BMI, Age, Neck, Gender — score 3 or above = high risk for moderate-severe OSA, sensitivity 93%); Epworth Sleepiness Scale (ESS — 8 situations rated 0–3; score 10 or above = excessive daytime sleepiness). Investigations: thyroid function tests (hypothyroidism as a secondary cause); FBC (polycythaemia as a marker of chronic hypoxaemia); fasting glucose and HbA1c (comorbid type 2 diabetes). Paediatric OSA: the diagnostic threshold is AHI above 1 event/hour (lower than adults, as any recurrent obstruction in a growing child is clinically significant).

CPAP (continuous positive airway pressure): the gold standard treatment for moderate-severe OSA and for mild OSA with significant symptoms. A motor unit delivers a continuous stream of pressurised air through a mask interface (nasal, full-face, or nasal pillow) at a set or auto-titrating pressure (APAP) typically 5–20 cmH2O — acts as a pneumatic splint to maintain upper airway patency throughout the respiratory cycle; reduces AHI by over 90% when used effectively; proven to reduce blood pressure (by 2–3 mmHg mean BP with 4+ hours/night use), improve daytime sleepiness (ESS reduction of 3–5 points), reduce cardiovascular event risk (meta-analyses of moderate-severe OSA), resolve nocturnal arrhythmias, improve glycaemic control, and reduce motor vehicle accident risk; NICE recommends CPAP as first-line for moderate-severe OSA (AHI above 15). Adequate adherence is defined as 4 or more hours per night on at least 70% of nights — average adherence is 50–65% without support; CPAP clinics with telemonitoring data download and adherence coaching significantly improve outcomes. Mandibular advancement device (MAD/oral appliance therapy): custom-fitted removable device worn during sleep that advances the lower jaw 5–10 mm anteriorly, enlarging the retroglossal and retropalatal airspace; indicated for mild-to-moderate OSA, positional-predominant OSA, CPAP-intolerant patients, and as a CPAP alternative in mild OSA; reduces AHI by approximately 50% (less effective than CPAP but often better tolerated); requires regular dental monitoring for temporo-mandibular joint effects. Weight loss: the most impactful long-term management strategy — a 10–15% reduction in body weight reduces AHI by 25–35%; bariatric surgery (Roux-en-Y gastric bypass or sleeve gastrectomy) resolves OSA in approximately 83–85% of obese patients. Positional therapy: for positional OSA (AHI predominantly in the supine position — defined as supine AHI at least twice the non-supine AHI) — vibrotactile positional devices (NightBalance, Sleepon), tennis ball technique, or positional pillow; effective in approximately 25–30% of OSA patients with clear positional predominance. Upper airway surgery: tonsillectomy and adenoidectomy (first-line for paediatric OSA from adenotonsillar hypertrophy — curative in 80%); uvulopalatopharyngoplasty (UPPP — removes excess pharyngeal soft tissue) in selected adult cases — moderate evidence. Hypoglossal nerve stimulation (Inspire — upper airway stimulator): implantable device that stimulates the hypoglossal nerve synchronously with inspiration, protracting the tongue to maintain airway patency; approved for moderate-severe OSA (AHI 15–65, without central apnoeas, BMI below 32) in CPAP-intolerant patients — significant benefit in 65–70% at 12 months.

Systemic hypertension: present in approximately 50% of OSA patients; OSA is the most common identifiable secondary cause of resistant hypertension (BP not controlled despite 3 or more antihypertensives); each apnoeic episode triggers sympathetic activation and catecholamine release causing blood pressure surges, and sustained overnight sympathetic overdrive leads to daytime hypertension. Atrial fibrillation (AF): 2–3-fold increased risk — nocturnal hypoxaemia triggers atrial stretch, inflammation, and arrhythmic foci; CPAP treatment reduces AF recurrence after cardioversion and ablation by approximately 40%. Coronary artery disease and myocardial infarction: approximately 2-fold elevated risk in untreated moderate-severe OSA — from combined effects of hypoxaemia, hypertension, sympathetic activation, and endothelial dysfunction. Ischaemic stroke: 2–3-fold elevated risk — OSA promotes atrial fibrillation, atherosclerosis, and thrombotic tendency. Type 2 diabetes: sleep fragmentation and intermittent hypoxaemia impair insulin sensitivity and glucose tolerance — OSA independently increases T2DM risk by approximately 2-fold even after controlling for obesity. Pulmonary hypertension (elevated pulmonary arterial pressure): in approximately 20–40% of patients with severe OSA from hypoxic pulmonary vasoconstriction; can lead to right heart failure in extreme cases. Motor vehicle accidents and occupational accidents: 3–7-fold elevated risk from excessive daytime somnolence — OSA is responsible for an estimated 10–25% of serious road traffic accidents; DVLA regulations in the UK require voluntary cessation of driving until effectively treated. Non-alcoholic fatty liver disease (NAFLD)/metabolic-associated steatotic liver disease (MASLD): nocturnal hypoxaemia promotes hepatic steatosis and fibrosis independently of obesity. Depression and anxiety: comorbid in 30–50%, bidirectionally worsening both conditions. Cognitive decline and dementia risk: emerging evidence links chronic OSA-associated intermittent hypoxaemia to accelerated amyloid accumulation and elevated dementia risk, partially reversible with CPAP.

Weight management: the most impactful long-term preventive measure — maintain a healthy BMI through a Mediterranean or calorie-controlled diet and regular aerobic exercise; even modest weight loss of 5–10% reduces AHI meaningfully. Bariatric surgery for severely obese OSA patients (BMI above 35 with comorbidities) resolves OSA in approximately 83–85% of cases; post-bariatric sleep study should confirm resolution before stopping CPAP. Alcohol and sedative restriction: avoid alcohol within 3–4 hours of bedtime — even moderate alcohol intake (2–3 units) significantly worsens OSA severity; avoid benzodiazepines, z-drugs (zopiclone, zolpidem), and opioids unless specifically monitored, as these reduce pharyngeal muscle tone and suppress arousal responses to apnoeic events. Positional strategies: for confirmed positional OSA, avoidance of supine sleep (vibrotactile devices, positional pillows, positional alarms) is a simple and highly effective intervention. Sleep hygiene: regular consistent sleep schedule, adequate sleep duration (7–9 hours for adults), darkened cool bedroom — reduce sleep debt, which worsens apnoea severity and increases accident risk. Smoking cessation: smoking causes upper airway mucosal oedema and inflammation, worsening OSA severity. Consistent CPAP adherence: aim for 4 or more hours of nightly CPAP use on at least 70% of nights — CPAP clinics use telemonitored adherence data to identify mask leaks, pressure needs, and usage patterns; auto-titrating PAP (APAP) improves comfort and adherence over fixed-pressure CPAP. Annual follow-up: OSA review at a sleep clinic annually — reassess weight, blood pressure, ESS, CPAP adherence, and AHI; repeat sleep study if clinical status changes significantly. Screen for and manage cardiovascular risk factors (hypertension, diabetes, dyslipidaemia) at each review — OSA-related cardiovascular risk is substantially reduced by effective CPAP use and weight management.

See your GP for assessment if: your bed partner or household member has witnessed you stop breathing, choking, or gasping during sleep — this is the most important symptom requiring same-day or next-day assessment; you feel excessively sleepy during the day even after 7-8 hours of sleep, especially if you drive or operate machinery — undiagnosed OSA is responsible for 10-25% of serious road traffic accidents; you have a high STOP-BANG score (3 or more positives: Snoring loudly, Tired/sleepy, Observed apnoeas, blood Pressure high, BMI over 35, Age over 50, Neck circumference over 40 cm, Gender male) — requires GP referral to sleep clinic; morning headaches on waking most days — a common but under-recognised symptom of nocturnal hypoxia. Attend Emergency Department if: you develop sudden onset irregular heartbeat (palpitations), chest pain, or breathlessness — OSA is strongly associated with atrial fibrillation, and acute presentation requires urgent cardiac assessment; a child has significant night-time snoring with observed breathing pauses or very restless sleep — paediatric OSA from adenotonsillar hypertrophy needs ENT assessment (tonsillectomy is usually curative). Do not drive if you are significantly sleepy from suspected OSA — DVLA in the UK requires voluntary cessation of driving until treated with effective CPAP if OSA causes excessive daytime sleepiness.