Respiratory emergencies

Acute severe asthma

Overview and approach

Severe asthma needs rapid clinical severity assessment and repeated response checks.

  • Classify on arrival as mild–moderate, severe or life-threatening using observation and pulse oximetry, because clinical signs may not match hypoxaemia. Start salbutamol while you complete the assessment (1).
  • Aim of the emergency clinician: prevent intubation. Near-fatal asthma is acute asthma with respiratory arrest or PaCO2 above 50 mmHg, with or without altered consciousness.
  • Check response after every bronchodilator dose and escalate early. Life-threatening asthma needs immediate transfer to higher-level care (1).
Assessment and clinical features

ABCDE, speech, work of breathing, saturation, pulse, mental state and air entry; peak flow only if feasible without delaying care.

  • Mild–moderate: can walk and speak whole sentences; SpO2 on room air above 94%; RR below 25, HR below 110 (1).
  • Severe (any): cannot complete a sentence in one breath; accessory muscle use or tracheal tug; obvious distress; SpO2 94% or less; RR 25 or more; HR 110 or more; FEV1 50% predicted or less (1).
  • Life-threatening (any): drowsy, confused or collapsed; cyanosis; poor respiratory effort; silent chest; SpO2 below 92%; bradycardia or arrhythmia (1).
  • End of the bed test: inability to speak in full sentences, accessory muscle use or tracheal tugging, cyanosis and sweating. Pulsus paradoxus is a sign of severity.
  • Complications to look for: pneumothorax, pneumomediastinum, arrhythmias, myocardial ischaemia, hypokalaemia, hypomagnesaemia, hypophosphataemia, lactic acidosis and hyperglycaemia.
  • Epidemiology: over 2.2 million Australians had current asthma and 406 deaths were attributed to asthma in 2006; the highest risk of death is in people over 70.
Differentials and investigations

Blood gas and imaging are selective; look for pneumothorax, infection and fatigue.

  • Blood gas in life-threatening asthma. PaCO2 above 50 mmHg, or a normal PaCO2 with low PaO2, means the patient is tiring. A metabolic acidosis may reflect high-dose salbutamol or work of breathing (1).
  • Monitor for salbutamol toxicity: worsening tachycardia, metabolic acidosis, hypokalaemia (1).
  • Chest X-ray: if pneumothorax, pneumonia or another cause is suspected, or the response is poor.
  • Differentials: anaphylaxis (treat with adrenaline), COPD exacerbation, pulmonary oedema, pulmonary embolism, pneumothorax, upper airway obstruction or vocal cord dysfunction, foreign body (1).
Management and follow-up

Immediate senior help, protocol bronchodilator/systemic steroid and oxygen care; escalation and ventilation decisions need experienced staff.

  • Oxygen: start if SpO2 is below 92% and titrate to 92–96% (88–92% if at risk of hypercapnia) (1)(2).
  • Mild–moderate: salbutamol 4–12 puffs (100 microg each) by pMDI and spacer, repeated every 20 minutes for the first hour (1).
  • Severe: salbutamol 12 puffs by spacer (or a 5 mg nebule if a spacer cannot be used) plus ipratropium 8 puffs (21 microg each) every 20 minutes for the first hour; repeat bronchodilators for 24 hours (1).
  • Life-threatening: continuous nebulised salbutamol (2 x 5 mg nebules, oxygen-driven) plus ipratropium 500 microg every 20 minutes for the first hour, and immediate transfer to higher-level care (1).
  • Steroids within 1 hour: prednisolone 37.5–50 mg orally, then each morning for a total of 5–10 days; no taper needed. Alternative: dexamethasone 16 mg daily for 2 days. Use IV hydrocortisone if oral is not possible (1).
  • Second line: IV magnesium sulfate 0.2 mmol/kg (maximum 10 mmol) over 20 minutes in severe or life-threatening asthma or a poor response. It does not replace inhaled beta agonists. Nebulised magnesium is not recommended (1).
  • Do not give oral or IV salbutamol. Use adrenaline if anaphylaxis is suspected, or if the patient is peri-arrest or cannot inhale bronchodilators; do not use it as the initial bronchodilator (1).
  • Consider admission if hypoxic at presentation, FEV1 below 60% predicted at 1 hour, unresolved distress at 1–2 hours, a previous ICU admission, a presentation within 4 weeks or frequent presentations (1).
  • Discharge: inhaled corticosteroid (medium-dose or higher, with a long-acting beta agonist) after a severe exacerbation, enough oral steroid to finish the course, an interim asthma action plan, GP review within 3 days and a comprehensive review in 2–4 weeks (1).
Red flags and clinical pearls

Silent chest, exhaustion, confusion or rising/normalising CO2 in a distressed patient is ominous. Do not delay escalation awaiting a peak-flow value.

  • Reduced wheeze alone is an unreliable sign of improvement: it can mean deterioration (1).
  • Near-fatal asthma has two phenotypes: slow-onset eosinophilic (80–85% of fatal events, over days to weeks in poorly controlled asthma) and rapid-onset neutrophilic.
  • Pulse oximetry can overestimate saturation in people with darker skin pigmentation (1).
  • Neither bradycardia nor a rising PaCO2 is reassuring in a tired patient.
References
  1. Australian Asthma Handbook: Managing acute asthma in adults and adolescents in the ED
  2. Australian Asthma Handbook: Managing acute asthma in primary care

Last updated from Sen’s notes on 9 October 2026.