## Beta-Blockers and Bronchospasm Risk **Key Point:** Non-selective β-blockers block both β₁ (cardiac) and β₂ (bronchial) receptors, causing unopposed α-adrenergic activity in airways and triggering bronchospasm. ### Mechanism of Bronchospasm 1. **β₂-receptor blockade** → loss of bronchodilatory effect of endogenous catecholamines 2. **Unopposed α-adrenergic activity** → bronchoconstriction 3. **Increased airway resistance** → clinical bronchospasm, especially in patients with reactive airway disease **High-Yield:** Non-selective beta-blockers (propranolol, labetalol, nadolol) are absolutely contraindicated in asthma and COPD. Cardioselective β₁-blockers (metoprolol, atenolol) have lower risk but should still be used with caution. ### Beta-Blocker Selectivity Comparison | Agent | Selectivity | Asthma/COPD Risk | Notes | | --- | --- | --- | --- | | Propranolol | Non-selective | **High** | Contraindicated | | Labetalol | Non-selective | **High** | Contraindicated (despite α-blocking activity) | | Metoprolol | β₁-selective | Low | Relatively safer; still use cautiously | | Atenolol | β₁-selective | Low | Relatively safer; still use cautiously | | Carvedilol | Non-selective + α-blocking | **High** | Contraindicated | **Warning:** Even cardioselective β-blockers lose selectivity at higher doses and can cause bronchospasm in susceptible patients. **Clinical Pearl:** In hypertensive patients with asthma or COPD, preferred alternatives include ACE inhibitors, ARBs, calcium channel blockers, or alpha-2 agonists. [cite:Harrison 21e Ch 297]
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