Apnoea, adult

Apnoea is the absence of airflow at the nose and mouth for 10 seconds or more. In an adult it presents in two ways: as a witnessed pause in breathing, usually during sleep, reported by a bed partner; or as an acute event in which a person is found not breathing, which is a medical emergency until proved otherwise. This article covers both and gives the approach to a patient who has stopped, or is reported to have stopped, breathing.

Clinical relevance. Acute apnoea in an adult is cardiac arrest, opioid or sedative toxicity, airway obstruction, seizure, neuromuscular failure or brainstem catastrophe until excluded. Nocturnal apnoea is usually obstructive sleep apnoea, a treatable cause of hypertension, atrial fibrillation, stroke and road traffic collisions, but central apnoea and bradyarrhythmia pauses are less common and need a different response.

Classification.

• Obstructive: effort continues against a closed upper airway (sleep apnoea, laryngospasm, foreign body, anaphylaxis, epiglottitis).
• Central: effort is absent because of reduced drive (opioids, Cheyne-Stokes breathing in heart failure or after stroke, high altitude, brainstem lesion, primary central sleep apnoea).
• Mixed: begins central and ends obstructive.
• Severity of sleep-related events by the apnoea-hypopnoea index (AHI, events/hour): under 5 normal, 5 to 15 mild, 15 to 30 moderate, over 30 severe. A hypopnoea is a 30% or greater fall in airflow lasting 10 seconds or more with an oxygen desaturation of 3 to 4% or an arousal.

Mechanism.

• Obstructive: loss of pharyngeal dilator tone in sleep in a narrow airway (obesity, large neck, retrognathia, large tonsils or tongue, nasal obstruction); negative intrathoracic pressure swings, surges of sympathetic activity, repeated hypoxaemia and arousals.
• Central: ventilatory control instability (high loop gain) with overshoot of ventilation, hypocapnia under the apnoeic threshold and a pause (Cheyne-Stokes pattern: crescendo-decrescendo breathing with a cycle length of 60 seconds or more in heart failure); or direct depression of medullary respiratory neurones by opioids.

History.

• Who witnessed it, how long, how often, during sleep or wakefulness, and whether the person was rousable.
• Snoring, gasping or choking on waking, unrefreshing sleep, morning headache, nocturia, dry mouth, daytime sleepiness, memory and concentration problems, mood change, reduced libido.
• Heart failure, atrial fibrillation, stroke, hypertension, hypothyroidism, neuromuscular disease, previous head or neck surgery or radiotherapy.
• Drugs: opioids (including codeine and tramadol), benzodiazepines, zolpidem, gabapentin, pregabalin, alcohol, baclofen, sedating antipsychotics.
• Events suggesting alternative diagnoses: tongue bite, incontinence, post-event confusion (seizure); palpitations or collapse (arrhythmia); acid in the throat with choking (reflux); panic and fear (panic attack); violent limb movements with dream enactment (REM sleep behaviour disorder).

Examination.

• Body mass index, neck circumference (over 43 cm in men or over 41 cm in women is high risk), blood pressure.
• Upper airway: Mallampati class, tonsil size, retrognathia, nasal patency, macroglossia.
• Cardiovascular: rhythm, signs of heart failure, murmurs.
• Respiratory: cyanosis, signs of hypercapnia, chest wall deformity.
• Neurological: bulbar function, limb power, reflexes, cranial nerves.
• Endocrine: goitre, hypothyroid features, acromegalic features.

Red flags.

• Currently not breathing or agonal gasping (start resuscitation).
• Apnoea with cyanosis, collapse, or unresponsiveness.
• Pinpoint pupils and slow respiratory rate (opioid toxicity).
• Apnoea in a patient with neuromuscular disease, or associated with new bulbar or limb weakness.
• Witnessed pauses with syncope or documented heart rate under 30/minute (bradyarrhythmia).
• Daytime hypercapnia, new right heart failure, or oxygen saturation under 90% when awake.
• Drowsy driving, near miss or collision.
• Sudden onset after head injury, stroke or cervical spine disease.

• Acute, in a person found not breathing: cardiac arrest (ventricular fibrillation, asystole, pulseless electrical activity), opioid or sedative overdose, airway obstruction (choking, anaphylaxis, epiglottitis), post-ictal apnoea or status epilepticus, hypoglycaemia.
• Other acute causes: brainstem stroke, high cervical cord injury, drowning, electrocution, carbon monoxide or hydrogen sulphide exposure, neuromuscular crisis.
• Nocturnal, witnessed: obstructive sleep apnoea, central sleep apnoea (Cheyne-Stokes in heart failure, opioid related, treatment emergent after starting CPAP), obesity hypoventilation syndrome, bradyarrhythmia or sinus pauses of 3 seconds or more.
• Other nocturnal causes: nocturnal seizures, nocturnal gastro-oesophageal reflux with laryngospasm, nocturnal panic, REM sleep behaviour disorder with breath-holding, hypoglycaemia.
• Neuromuscular: motor neurone disease, myasthenia, Pompe disease, muscular dystrophy, phrenic nerve palsy.
• Structural: tonsillar hypertrophy, pharyngeal tumour, vocal cord paralysis, tracheal stenosis, retrognathia, acromegaly.

1. If the patient is not breathing: shout for help, check responsiveness and breathing for no more than 10 seconds, call the resuscitation team, and start the resuscitation sequence.
2. The sequence is chest compressions 30 then 2 rescue breaths for a non-breathing patient without a pulse; rescue breaths 10/minute if a pulse is present.
3. Reversible causes: capillary glucose (give 10% glucose 150 to 200 mL intravenously if under 4 mmol/L), pupil size and rate for opioids, temperature, rhythm, and an arterial or venous gas.
4. Awake and breathing but with a history of apnoea: structured sleep history with the Epworth Sleepiness Scale (0 to 24; over 10 is abnormal) and the STOP-BANG score (0 to 2 low, 3 to 4 intermediate, 5 to 8 high risk).
5. Baseline tests: full blood count (polycythaemia), urea and electrolytes, bicarbonate (venous bicarbonate of 27 mmol/L or more suggests hypoventilation), thyroid stimulating hormone, glucose or glycated haemoglobin, electrocardiogram.
6. Echocardiogram if heart failure or pulmonary hypertension is suspected; natriuretic peptide.
7. Home respiratory polygraphy (airflow, effort, oximetry, heart rate, position) for suspected uncomplicated obstructive sleep apnoea.
8. Attended polysomnography (electroencephalogram, electro-oculogram, chin electromyogram, leg movements, electrocardiogram) for suspected central apnoea, hypoventilation, neuromuscular disease, significant cardiorespiratory disease, parasomnia or non-diagnostic polygraphy.
9. Ambulatory electrocardiogram monitoring for 24 hours to 14 days, or an implantable loop recorder, when pauses with syncope are suspected.
10. Daytime blood gas, spirometry in sitting and lying positions (a fall in forced vital capacity of over 20% when supine suggests diaphragm weakness), maximal inspiratory pressure and sniff nasal pressure in neuromuscular disease.
11. Upper airway assessment (nasendoscopy) and brain or cervical imaging if a structural or central lesion is suspected.

Limits. A single night of polygraphy can miss mild disease (night to night variability of the AHI is up to 20 to 30%). It does not detect arousals or distinguish sleep from wake, so it underestimates the AHI.

The AHI correlates poorly with symptoms, and a low AHI does not exclude upper airway resistance syndrome. Central events can be scored incorrectly if effort belts are poorly placed.

Acute apnoea.

• Cardiac arrest: chest compressions at 100 to 120/minute, 5 to 6 cm depth, defibrillation for shockable rhythm.
• Give adrenaline 1 mg intravenously every 3 to 5 minutes (first dose immediately in non-shockable rhythms, after the third shock in shockable rhythms). Give amiodarone 300 mg after the third shock then 150 mg after the fifth.
• Opioid toxicity: open the airway, bag-mask ventilation with oxygen, naloxone 400 micrograms intravenously or 800 micrograms intramuscularly, repeating after 2 to 3 minutes to a total of 2 mg.
• If repeated naloxone doses are needed, infuse two thirds of the effective total dose each hour and monitor for at least 6 hours after the last dose. Buprenorphine and long acting opioids such as methadone can outlast naloxone, so observe for 12 hours or more.
• Benzodiazepine overdose: airway support is the treatment; flumazenil carries a seizure risk in dependence or mixed overdose and is not routine.
• Hypoglycaemia: 10% glucose 150 to 200 mL intravenously over 15 minutes, or glucagon 1 mg intramuscularly if there is no access.
• Anaphylaxis: adrenaline 0.5 mg intramuscularly (0.3 mg for 6 to 12 years), repeated every 5 minutes.
• Airway obstruction by a foreign body: back blows (5), abdominal thrusts (5), repeat; advanced airway if the patient becomes unresponsive.
• Seizure: lorazepam 4 mg intravenously (repeat once after 10 minutes) with airway support.

Obstructive sleep apnoea (after the acute phase).

• Lifestyle: weight loss (a 10% fall in body weight reduces the AHI by roughly 25 to 30%), avoid alcohol within 4 hours of bed, avoid sedatives, sleep on the side if the AHI is higher supine.
• CPAP for moderate and severe disease and for mild disease with symptoms or cardiovascular disease: auto-titrating 4 to 20 cmH2O; review adherence at 4 weeks (target at least 4 hours/night on 70% of nights).
• Mandibular advancement device for mild to moderate disease or CPAP intolerance.
• Surgery or hypoglossal nerve stimulation in selected anatomical cases after specialist assessment.

Central sleep apnoea. Optimise heart failure therapy first. For Cheyne-Stokes breathing: nocturnal oxygen or CPAP.

Adaptive servo-ventilation is contraindicated when the left ventricular ejection fraction is 45% or less with predominant central apnoea, because of increased cardiovascular mortality. For opioid related disease, reduce the opioid dose where possible.

Bradyarrhythmia. Pacing for symptomatic sinus pauses of over 3 seconds while awake, or over 6 seconds at night with symptoms, and for high grade atrioventricular block.

Monitoring. Continuous oximetry, capnography and rhythm monitoring after acute apnoea; adherence and efficacy download from CPAP (residual AHI under 5 events/hour); blood pressure at 3 months.

Referral and escalation. Resuscitation team and critical care for acute apnoea; sleep service for suspected sleep apnoea or any suspicion of central apnoea or hypoventilation; cardiology for pauses and heart failure; neurology for neuromuscular disease or seizures; ENT for structural airway causes; bariatric or weight management services when the BMI is 35 or more.

Admission or disposition. Admit anyone after a witnessed apnoeic event with cyanosis, collapse, bradyarrhythmia, hypercapnia or hypoxaemia when awake, and all opioid overdoses until observation criteria are met. Outpatient assessment is reasonable for stable, otherwise well patients with suspected obstructive sleep apnoea and no daytime hypoxaemia.

Safety netting. Advise not to drive or operate machinery while sleepy. The licensing authority must be informed when the condition causes sleepiness at the wheel, and driving may resume after symptom control is documented.

Carers should learn the recovery position and resuscitation steps. Return urgently for choking, collapse, daytime breathlessness, chest pain, new leg swelling, or any pause with loss of consciousness.

Special groups.

• Pregnancy: obstructive sleep apnoea is linked with hypertensive disorders and gestational diabetes; CPAP is safe.
• Perioperative: tell the anaesthetist; bring CPAP; minimise opioids and sedatives; prefer regional techniques and nurse semi-upright.
• Heart failure and atrial fibrillation: treat sleep apnoea, as untreated disease increases arrhythmia recurrence after cardioversion.
• Opioid prescribing: review the dose in patients with sleep apnoea; avoid combining opioids, gabapentinoids and benzodiazepines.