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 assessment1.
  • 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 care1.
  • What narrows the airways: smooth muscle spasm, wall oedema and inflammation, and thick mucus plugs containing shed epithelium and eosinophils. Airways of all sizes are involved, and air trapping hyperinflates the lungs3,4.
  • Why patients are hypoxaemic: patchy narrowing causes ventilation-perfusion mismatch rather than true shunt, so supplemental oxygen corrects it readily3.
  • Status asthmaticus: an attack that goes on for hours or days despite bronchodilators, often with exhaustion, dehydration and marked tachycardia3.
  • In fatal asthma the lungs are overinflated and many airways are blocked by tenacious mucus plugs4.
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 1101.
  • 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 less1.
  • Life-threatening (any): drowsy, confused or collapsed; cyanosis; poor respiratory effort; silent chest; SpO2 below 92%; bradycardia or arrhythmia1.
  • 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.
  • Typical examination: anxious, upright patient using accessory muscles; hyperinflated chest; widespread wheeze; tachycardia; little, sticky sputum3,5.
  • Pulsus paradoxus explained: an inspiratory fall in systolic pressure of more than 10 mmHg. Breathing against obstructed airways creates big swings in intrathoracic pressure; on inspiration more blood is drawn into the right heart and lungs, so less reaches the left ventricle and stroke volume drops. In asthma it warns of impending respiratory failure, but it is hard to measure in a distressed patient, so do not rely on it5,6.
  • 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 breathing1.
  • Monitor for salbutamol toxicity: worsening tachycardia, metabolic acidosis, hypokalaemia1.
  • Chest X-ray: if pneumothorax, pneumonia or another cause is suspected, or the response is poor.
  • Gas pattern over time: early on the patient hyperventilates, so PaCO2 is low. A normal or rising PaCO2 in a breathless patient means fatigue and impending respiratory failure5.
  • The chest X-ray usually shows only hyperinflation; its value is finding pneumothorax or pneumonia3,5.
  • Spirometry pearl: in a very severe attack the airways may barely respond to a bronchodilator. During recovery FEV1 and FVC rise together, so the FEV1/FVC ratio stays low until the bronchospasm has largely settled3.
  • Differentials: anaphylaxis (treat with adrenaline), COPD exacerbation, pulmonary oedema, pulmonary embolism, pneumothorax, upper airway obstruction or vocal cord dysfunction, foreign body1.
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 hour1.
  • 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 hours1.
  • 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 care1.
  • 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 possible1.
  • 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 recommended1.
  • 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 bronchodilator1.
  • 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 presentations1.
  • 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 weeks1.
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 deterioration1.
  • 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 pigmentation1.
  • Neither bradycardia nor a rising PaCO2 is reassuring in a tired patient.
  • Avoid sedatives in acute asthma: they depress the respiratory drive a tiring patient depends on5.
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
  3. West JB. Pulmonary Pathophysiology: The Essentials. 8th ed. Philadelphia: Lippincott Williams & Wilkins; 2013. Chapter 4, Obstructive diseases.
  4. Kumar V, Abbas AK, Aster JC, editors. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Philadelphia: Elsevier Saunders; 2015. Chapter 15, The lung.
  5. Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. Chapter 254, Asthma.
  6. Dennis M, Bowen WT, Cho L. Mechanisms of Clinical Signs. Sydney: Elsevier Australia; 2012. Pulsus paradoxus.

Last updated from Sen’s notes on 22 October 2026.