Asthma
A chronic inflammatory airway disease causing reversible bronchospasm and mucosal swelling that narrows the airways episodically, so triggers, variability and reversibility (not fixed obstruction) define both the symptoms and the treatment ladder.
In a nutshell
Trigger exposure activates mast cells and eosinophils, causing reversible smooth muscle spasm, mucosal oedema and mucus plugging. Because the obstruction is functional and inflammatory rather than structural, it varies over time and largely reverses with treatment, which is why control is judged by variability and inhaled corticosteroid is the foundation of therapy.
Classic presentation
A patient with an atopic history and episodic wheeze, chest tightness and a nocturnal cough, provoked by exercise, allergens or cold air, with more than 20% variability in peak flow.
Key points
- Obstruction is caused by three reversible processes together: smooth muscle spasm, mucosal oedema and mucus plugging, unlike the fixed structural damage of COPD.
- Symptoms vary diurnally and with triggers because the inflammation driving them waxes and wanes; this variability is the diagnostic fingerprint.
- A silent chest in an acute attack means too little air is moving to generate wheeze, not that the attack has improved; it is a pre-terminal sign.
- A normal or rising PaCO2 in a breathless asthmatic indicates exhaustion and impending respiratory failure, because hyperventilation should otherwise lower it.
- Treatment targets both processes: inhaled corticosteroid for the underlying inflammation, bronchodilator for the acute spasm; relying on a reliever alone leaves inflammation untreated.
- Severe and life-threatening attacks need oxygen, nebulised bronchodilators and early systemic corticosteroid, with senior escalation for silent chest or exhaustion.
First-line investigation
Spirometry with bronchodilator reversibility, supported by FeNO for eosinophilic inflammation and serial peak flow for diurnal variability.
First-line management
Regular low-dose inhaled corticosteroid, typically combined with a fast-acting beta-agonist in a single inhaler for maintenance and relief, stepped up according to control.
Exam traps
- A silent chest is not reassuring; it means obstruction is so severe that airflow is too low to wheeze, and is a marker of a life-threatening attack.
- A 'normal' PaCO2 in a tachypnoeic asthmatic is abnormal: it should be low from hyperventilation, so normalisation signals fatigue.
- Peak flow below 33% of best/predicted, exhaustion, hypotension or bradycardia are life-threatening features requiring urgent escalation, not stepwise reassessment.
- Over-reliance on a short-acting beta-agonist without inhaled corticosteroid is a recognised risk factor for fatal asthma.
Educational content pending clinical review. Not medical advice.