Adrenaline (Epinephrine) Is Not Recommended for COPD Exacerbations
Adrenaline has no role in the treatment of acute COPD exacerbations and should not be used. The evidence provided addresses asthma management, not COPD, and major COPD guidelines make no mention of epinephrine as a therapeutic option 1, 2, 3, 4.
Why Epinephrine Is Not Used in COPD Exacerbations
Guideline-Recommended Bronchodilator Therapy
Short-acting β2-agonists (SABAs) such as albuterol/salbutamol are the first-line bronchodilators for acute COPD exacerbations, typically combined with short-acting anticholinergics like ipratropium 1, 2.
The combination of nebulized salbutamol 2.5–5 mg plus ipratropium 0.25–0.5 mg every 4–6 hours provides superior bronchodilation lasting 4–6 hours compared with either agent alone 2.
Selective β2-agonists are preferred because they target bronchial smooth muscle with minimal cardiac effects, whereas epinephrine is a non-selective adrenergic agonist that stimulates α, β1, and β2 receptors, causing significant cardiovascular side effects (tachycardia, arrhythmias, hypertension) 1.
Evidence Base Is for Asthma, Not COPD
The systematic review comparing epinephrine to selective β2-agonists was conducted exclusively in asthma patients, not COPD patients 1.
Even in asthma, the evidence showed that epinephrine and selective β2-agonists have similar efficacy (pooled OR 0.99), with no advantage for epinephrine 1.
International asthma guidelines recommend against epinephrine except in anaphylaxis or angioedema 1.
Standard Evidence-Based Treatment for COPD Exacerbations
Immediate Pharmacologic Management
Administer combined nebulized salbutamol 2.5–5 mg plus ipratropium 0.25–0.5 mg every 4–6 hours during the acute phase 2.
Give oral prednisone 30–40 mg once daily for exactly 5 days starting immediately; this regimen improves lung function, shortens recovery time, and reduces treatment failure by >50% 2, 3, 4.
Prescribe antibiotics for 5–7 days when sputum purulence is present together with either increased dyspnea or increased sputum volume (two of three cardinal symptoms) 2, 4.
Respiratory Support
Target oxygen saturation of 88–92% using controlled delivery devices (Venturi mask 24–28% or nasal cannula 1–2 L/min) to avoid CO2 retention 2.
Initiate non-invasive ventilation (NIV) immediately as first-line therapy when acute hypercapnic respiratory failure (PaCO2 >45 mmHg) with acidosis (pH <7.35) persists >30 minutes after standard medical treatment; NIV reduces intubation rates by ~50% and improves survival 2, 5.
Medications to Avoid
Intravenous methylxanthines (theophylline/aminophylline) should be avoided because they increase adverse effects without clinical benefit 1, 2.
Epinephrine has no established role and would add unnecessary cardiovascular risk without proven benefit in COPD 1.
Key Clinical Distinction
The pathophysiology of COPD exacerbations differs fundamentally from acute asthma. COPD involves fixed airway obstruction with mucus plugging and inflammation, whereas asthma involves reversible bronchospasm 6, 7. The selective β2-agonists combined with anticholinergics address both bronchospasm and secretion management in COPD without the systemic α-adrenergic and β1-cardiac effects of epinephrine 2, 8.
In summary: Use selective β2-agonists (albuterol) combined with anticholinergics (ipratropium), systemic corticosteroids, and antibiotics when indicated—never epinephrine—for COPD exacerbations 1, 2, 4.