A 62-year-old man with hypertension on atenolol for 3 years presents with acute onset severe bronchospasm and wheezing 2 hours after taking his morning dose. He has no prior history of asthma or COPD. Vital signs: BP 145/92 mmHg, HR 58/min, RR 28/min, SpO₂ 88% on room air. What is the most appropriate immediate next step in management?

Explanation

## Clinical Scenario Analysis This patient presents with acute bronchospasm temporally related to atenolol administration — a classic **Type B (Dose-Independent) Adverse Drug Reaction** manifesting as a known pharmacological side effect of non-selective beta-blockers. ## Mechanism of Beta-Blocker–Induced Bronchospasm **Key Point:** Non-selective beta-blockers (atenolol, propranolol) block β₂-adrenergic receptors on bronchial smooth muscle, removing the bronchodilatory effect of endogenous catecholamines and causing unopposed bronchoconstriction in susceptible individuals. ## Classification of This ADR | Feature | Type B Reaction | |---------|----------------| | **Dose-dependence** | No (occurs at therapeutic doses) | | **Predictability** | High (known pharmacological effect) | | **Mechanism** | Exaggerated pharmacological action | | **Timing** | Usually within hours of dose | | **Incidence** | 1–10% of patients on non-selective β-blockers | | **Management** | Drug withdrawal + symptomatic relief | ## Immediate Management Protocol 1. **Discontinue the offending agent** — atenolol must be stopped immediately; continued exposure worsens bronchospasm. 2. **Administer rapid-acting bronchodilator** — nebulized salbutamol (β₂-agonist) provides immediate relief by directly stimulating bronchial β₂-receptors, bypassing the blockade. 3. **Supportive care** — oxygen supplementation to maintain SpO₂ >92%. 4. **Future prevention** — switch to cardioselective beta-blocker (e.g., metoprolol, bisoprolol) or alternative antihypertensive class (ACE inhibitor, calcium channel blocker). **High-Yield:** The key distinction is that this is **NOT an allergy** (no IgE involvement, no prior sensitization required) and **NOT a dose-dependent toxicity** — it is a predictable, pharmacologically-mediated Type B reaction requiring immediate drug withdrawal and symptomatic treatment. **Clinical Pearl:** Cardioselective beta-blockers (β₁-selective at low doses) are safer in patients with reactive airway disease because they spare β₂-mediated bronchodilation; however, at higher doses they lose selectivity and can still cause bronchospasm. [cite:KD Tripathi 8e Ch 12]