Acute severe asthma
"An exacerbation is a progressive worsening of airflow obstruction severe enough to change treatment. Two patterns exist: slow-onset (the majority — days of mucus-laden eosinophilic inflammation) and rapid-onset (a minority, neutrophilic, sometimes NSAID-triggered, that can kill within hours). The mainstays are inhaled β-agonists and early systemic steroids; the ventilation strategy is controlled hypoventilation."
Summarised from Irwin & Rippe's Intensive Care Medicine; with Marino's The ICU Book and Oh's Intensive Care Manual.Precipitants and who is at risk of dying
| Common triggers | Markers of near-fatal risk |
|---|---|
| Viral URTI (esp. rhinovirus) | Previous intubation/ICU for asthma |
| Allergen / irritant exposure | Hospital admission in the last year |
| Non-adherence to controllers | Heavy SABA use, poor controller use |
| NSAIDs / β-blockers | Prior near-fatal attack, brittle asthma |
| Smoking, pollution | Psychosocial factors, poor perception of severity |
Grade every attack — it drives the response
| Category | Features (any one escalates) |
|---|---|
| Moderate | PEF 50–75% best/predicted; talking in sentences; SpO₂ ≥92%; no features below |
| Acute severe | PEF 33–50%; can't complete sentences; RR ≥25; HR ≥110 |
| Life-threatening | PEF <33%; SpO₂ <92%; silent chest, cyanosis, poor effort; normal PaCO₂ (4.6–6.0); exhaustion, altered consciousness, arrhythmia, hypotension |
| Near-fatal | Raised PaCO₂ and/or needing mechanical ventilation with raised airway pressures |
A tachypnoeic asthmatic should be blowing off CO₂ (low PaCO₂). A "normal" or rising PaCO₂ signals exhaustion and impending respiratory arrest — it is a life-threatening/near-fatal sign, not reassurance.
Why the airway closes
- Bronchospasm + airway-wall oedema + mucus plugging on a background of eosinophilic (or, in rapid-onset, neutrophilic) inflammation → severe airflow limitation.
- Prolonged expiration → dynamic hyperinflation and auto-PEEP → increased work of breathing and impaired venous return.
- V/Q mismatch → hypoxaemia; muscle fatigue → the CO₂ that should be low starts to rise.
- High risk of barotrauma (pneumothorax, pneumomediastinum) once ventilated.
Stepwise management
Oxygen
Titrate to SpO₂ 94–98%. Unlike COPD, hypoxaemia is the immediate threat.
Bronchodilators — back-to-back
Salbutamol 5 mg nebulised, repeated/continuous, + ipratropium 0.5 mg 4–6 hourly. Oxygen-driven nebuliser.
Systemic steroids — early
Prednisolone 40–50 mg PO or hydrocortisone 100 mg IV. Give to all; continue for ~5 days.
Magnesium
MgSO₄ 2 g IV over 20 min (single dose) for life-threatening or poor initial response.
Escalate (ICU/HDU)
IV salbutamol or aminophylline (with levels); consider ketamine (bronchodilator); treat anaphylaxis with IM adrenaline. Get senior/ICU help early.
What does NOT help / harms: routine antibiotics (only if infection), sedatives in the unventilated patient, and aggressive IV fluids without indication. Reassess PEF and the patient after every step.
Intubate reluctantly, ventilate gently
"When ventilation is unavoidable, the preferred strategy is controlled hypoventilation with permissive hypercapnia — deliberately under-ventilating to minimise dynamic hyperinflation and barotrauma. Intubation is high-risk: peri-intubation collapse from gas trapping is a real danger."
Summarised from Irwin & Rippe; Marino.| Aspect | Approach |
|---|---|
| When to intubate | Exhaustion, silent chest, falling consciousness, rising PaCO₂, haemodynamic instability, arrest — a clinical decision |
| Induction | Ketamine (bronchodilator) is favoured; anticipate hypotension from hyperinflation — fluids/pressor ready |
| Ventilator settings | Low rate (8–12), low Vt (~6 mL/kg PBW), high inspiratory flow, long expiratory time (I:E 1:3–1:5) |
| Targets | Permissive hypercapnia; keep Pplat <30; monitor auto-PEEP |
| If sudden collapse | Disconnect and let the chest deflate; exclude tension pneumothorax (DOPE) |
| Rescue | Deep sedation ± neuromuscular blockade; volatile anaesthetic; ECMO/ECCO₂R for refractory cases |
Common mistakes
In a tiring asthmatic a normal/rising PaCO₂ is a pre-arrest sign — escalate, don't relax.
Steroids take hours to work — give them early to every acute severe attack.
High rates/volumes cause gas trapping, hypotension and barotrauma. Use controlled hypoventilation.
Life-threatening asthma needs MgSO₄ and early ICU involvement, not repeated single nebs alone.
Sedatives blunt drive and precipitate arrest — support ventilation instead.
Exam pearls
Q: Life-threatening features?
PEF <33%, SpO₂ <92%, silent chest, cyanosis, poor effort, bradycardia/hypotension, exhaustion, altered consciousness, and a normal PaCO₂.
Q: Why is a normal CO₂ ominous?
A distressed asthmatic hyperventilates and should have a low CO₂; a normal/rising CO₂ means the muscles are failing — impending arrest.
Q: First-line drugs?
Oxygen (SpO₂ 94–98%), back-to-back salbutamol + ipratropium, early systemic steroids, IV magnesium for severe/poor response.
Q: Ventilation strategy?
Controlled hypoventilation with permissive hypercapnia — low rate, low Vt, long expiration, Pplat <30, watch auto-PEEP; disconnect if hypotensive.
Q: Induction agent of choice?
Ketamine — a bronchodilator that also maintains blood pressure.
All the comparisons in one place
The distinctions examiners and the bedside both demand — gathered at the end.
Asthma vs COPD (acute)
| Feature | Asthma | COPD |
|---|---|---|
| Reversibility | Largely reversible | Largely fixed |
| Oxygen target | 94–98% | 88–92% |
| CO₂ in attack | Low early; rising = danger | Often chronically raised |
| NIV role | Limited/cautious | First line for acidosis |
Slow-onset vs Rapid-onset exacerbation
| Feature | Slow-onset (~80%) | Rapid-onset (~10–15%) |
|---|---|---|
| Time course | Hours–days/weeks | Minutes–hours |
| Inflammation | Eosinophilic, mucus plugging | Neutrophilic, less mucus |
| Triggers | Infection, poor adherence | Allergen, NSAIDs, stress |
| Course | Slower to respond | Can be fatal fast — but may reverse quickly |
Acute severe vs Life-threatening vs Near-fatal
| Marker | Acute severe | Life-threatening | Near-fatal |
|---|---|---|---|
| PEF | 33–50% | <33% | — |
| SpO₂ | ≥92% | <92% | — |
| PaCO₂ | Low | Normal | Raised / needs ventilation |
| Chest / effort | Distressed, HR ≥110 | Silent chest, exhaustion, ↓ GCS | Arrest risk |
References
- Irwin RS, Lilly CM, Mayo PH, Rippe JM (eds). Irwin & Rippe's Intensive Care Medicine. 9th ed. Wolters Kluwer; 2023.
- Marino PL. Marino's The ICU Book. 5th ed. Wolters Kluwer; 2025.
- Bersten AD, Handy JM (eds). Oh's Intensive Care Manual. Elsevier; 2026.
- Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention — 2026 Update.
- British Thoracic Society / SIGN. British Guideline on the Management of Asthma.
- Nair P, Milan SJ, Rowe BH. Addition of intravenous aminophylline to β2-agonists in adults with acute asthma. Cochrane Database Syst Rev.
- Powell C, Kolamunnage-Dona R, Lowe J, et al. Magnesium sulphate in acute severe asthma. Lancet Respir Med. 2013;1:301–308.