Asthma Management Protocol
On this page
Direct answer
Salbutamol, a systemic corticosteroid, and reassessment at fixed intervals are the skeleton of every acute asthma protocol: oxygen to keep SpO2 at 93-95%, salbutamol 2.5-5 mg nebulised every 20 minutes in the first hour (or 4-10 puffs by inhaler and spacer, repeated), ipratropium 0.5 mg added every 20 minutes for three doses in severe attacks, and prednisolone 40-50 mg orally started within the first hour. Severity is graded clinically and by peak expiratory flow: 33-50% of predicted or best with inability to complete sentences marks severe asthma, and life-threatening features — silent chest, SpO2 below 90%, PEF below 33%, exhaustion, bradycardia, a normal or rising PaCO2, confusion — demand critical care involvement, intravenous magnesium sulphate 2 g over 20 minutes, and preparation for intubation with the long-expiratory-time, permissive-hypercapnia strategy.
What you must remember
- Severity map: moderate — PEF 50-75% of best or predicted, speaking in sentences; severe — PEF 33-50%, cannot complete sentences, respiratory rate 25 or more, heart rate 110 or more; life-threatening — PEF below 33%, silent chest, cyanosis, SpO2 below 90%, exhaustion, confusion, arrhythmia, and a normal or high PaCO2.
- The red flag of gases: a normal PaCO2 in a tiring asthmatic signals impending respiratory failure — hypocapnia is expected while the patient works hard.
- Bronchodilator regimen: salbutamol nebuliser 2.5-5 mg every 20 minutes for the first hour (thereafter 40-60 minutely per response); ipratropium 0.5 mg every 20 minutes for three doses in severe or life-threatening attacks; continuous nebulisation in refractory cases per protocol.
- Steroids early: prednisolone 40-50 mg orally daily for about 5-7 days (or equivalent intravenous hydrocortisone); benefit begins within hours and steroids prevent relapse — no taper needed for short courses.
- Second-line in severe attacks: intravenous magnesium sulphate 2 g over 20 minutes; aminophylline as a monitored infusion in selected units; helium-oxygen mixtures are special-situation adjuncts.
- Oxygen target: SpO2 93-95% — hyperoxia offers nothing and delays recognition of deterioration; titrate with pulse oximetry continuously.
- What to avoid: sedatives and anxiolytics (they mask fatigue), chest physiotherapy, unnecessary antibiotics, and repeated beta-agonist without potassium monitoring (hypokalaemia with repeated salbutamol).
- Ventilating severe asthma: low rate (6-10), long expiratory time (I:E 1:4 or more), small tidal volumes 6-8 mL/kg predicted weight, permissive hypercapnia, and active management of auto-PEEP (breath stacking causes hypotension — disconnect the circuit to let the lung empty).
One severe attack, worked as a timeline
A 24-year-old with a two-day exacerbation arrives speaking in phrases, RR 30, HR 120, PEF 35% of predicted, SpO2 91% on air. The first hour runs by protocol: oxygen to 94%, back-to-back salbutamol-ipratropium nebulisation at 0, 20 and 40 minutes, prednisolone 45 mg orally, and monitoring including potassium (2.9 mEq/L after the first two nebulisers — replaced). At 60 minutes she is phonating in full sentences, PEF has risen to 58%, and she steps down to hourly nebulisation. Had the first hour gone the other way — PEF stuck below 33%, silent chest on auscultation, drowsy with PaCO2 climbing from 32 to 46 — the same protocol pivots: magnesium 2 g intravenously, critical care referral, and intubation performed early and gently, because an asthmatic arrest is a hypoxic arrest of a tired bellows, and the ventilator is set for obstruction (rate 8, I:E 1:4 or longer, watching the auto-PEEP and the blood pressure).
Where students slip
Three errors recur in exams and wards alike. First, treating a "normal" PaCO2 as reassurance: in severe asthma the combative, hyperventilating patient should be hypocapnic, so a PaCO2 of 40 in that context is a deterioration, not a comfort — the classic single-best-answer trap. Second, oxygen left running at high flow indefinitely: the GINA-era target is 93-95%, and the exam expects the number. Third, nebulisation mechanics: driving the nebuliser with oxygen (not air) in a hypoxaemic patient, using a spacer-equivalent technique when nebulisers are unavailable, and documenting the response of PEF or FEV1 at fixed times — measurement is what turns a protocol from ritual into treatment. Indian viva additions worth quoting: salbutamol-driven hypokalaemia, the steroid dose in milligrams, and the ventilator's disconnect-and-let-it-exhale manoeuvre for breath-stacking hypotension.
Frequently asked questions
What features define a life-threatening asthma attack?
Silent chest, SpO2 below 90%, PEF below 33% of predicted, exhaustion, confusion, bradycardia or arrhythmia, cyanosis, and a normal or rising PaCO2.
What is the first-hour nebulisation regimen in severe acute asthma?
Salbutamol 2.5-5 mg every 20 minutes for three doses with ipratropium 0.5 mg at the same intervals, plus early systemic corticosteroid 40-50 mg prednisolone equivalent.
Why is a normal PaCO2 worrying in acute severe asthma?
A hyperventilating asthmatic should be hypocapnic — normalisation means fatigue and alveolar hypoventilation are overtaking the work of breathing.
What role does intravenous magnesium play?
Magnesium sulphate 2 g over 20 minutes is recommended in severe attacks not responding to initial nebulised therapy, as bronchodilation and stabilisation.
How is a ventilated asthmatic set up?
Low rate with prolonged expiration (I:E 1:4 or more), 6-8 mL/kg predicted weight, permissive hypercapnia, with active surveillance for auto-PEEP, breath stacking and its hypotension.