Can metoprolol cause dyspnea, particularly in patients with asthma or chronic obstructive pulmonary disease?

Can Metoprolol Cause Shortness of Breath?

Yes, metoprolol can cause shortness of breath, particularly in patients with asthma or severe reactive airway disease, where it is absolutely contraindicated due to the risk of life-threatening bronchospasm. 1

Mechanism of Respiratory Compromise

Metoprolol blocks β₂-adrenergic receptors in bronchial smooth muscle, reducing bronchodilation and increasing airway resistance, which can precipitate acute respiratory failure in susceptible patients. 2 Although metoprolol is β₁-selective, this selectivity is dose-dependent and incomplete—at therapeutic doses, some β₂ antagonism occurs, especially at higher doses. 2

Absolute Contraindication: Active Asthma

Active asthma or severe reactive airway disease with current bronchospasm is an absolute contraindication to both oral and intravenous metoprolol, because β-blockade can precipitate life-threatening bronchospasm. 2 Historical case series from the 1980s demonstrated severe bronchospasm in young patients with severe asthma given high initial doses of β-blockers, forming the basis for this absolute contraindication. 2, 3, 4

• In one study, 7 of 15 asthma patients were withdrawn prematurely from metoprolol due to bronchoconstriction, with one patient developing severe symptoms after just the first 12.5 mg dose. 3
• The respiratory response to metoprolol in asthma patients is unpredictable—when wheezing occurred, it developed following small, potentially subtherapeutic doses. 4
• All non-selective beta-blockers (e.g., propranolol, nadolol, labetalol, carvedilol) are contraindicated in any obstructive airway disease due to the risk of bronchospasm. 5

Relative Contraindication: COPD

Beta-blockers are not absolutely contraindicated in COPD; cardioselective agents such as metoprolol are preferred when β-blockade is indicated (e.g., post-MI, heart failure). 2 However, patients must be carefully selected and monitored:

• Meta-analyses show that cardioselective β-blockers do not produce a clinically significant decline in FEV₁ in patients with mild-to-moderate COPD and are not linked to increased respiratory adverse events. 2
• Observational data suggest that cardioselective β-blockers may improve overall survival and potentially reduce COPD exacerbation frequency. 6, 2
• In stable COPD patients, metoprolol 200 mg daily did not significantly affect FEV₁ or forced vital capacity compared to placebo, though one patient experienced increased dyspnea without objective changes. 7

Important Distinction Between COPD and Asthma

Asthma is an absolute contraindication to any beta-blocker, whereas COPD represents a relative contraindication that can be safely managed with cardioselective agents. 5 The European Society of Cardiology designates bisoprolol as the only beta-blocker not contraindicated in COPD, though metoprolol is an acceptable alternative. 5

Clinical Recognition of Metoprolol-Induced Dyspnea

If respiratory compromise develops while the patient is receiving metoprolol:

• Stop metoprolol immediately to prevent worsening bronchospasm. 2
• Monitor for wheezing, prolonged expiration, increased work of breathing, and falling oxygen saturation; provide supplemental oxygen to keep SpO₂ > 92%. 2
• Administer inhaled β₂-agonists (e.g., albuterol) promptly, as they can reverse metoprolol-induced bronchospasm. 2, 8, 9
• Bronchospasm responds to inhaled isoprenaline or terbutaline in all documented cases. 4, 9

FDA Warning on Bronchospastic Disease

The FDA label explicitly states: "Patients with bronchospastic disease should, in general, not receive beta-blockers, including metoprolol." 1 The label continues: "Because beta₁ selectivity is not absolute, use the lowest possible dose of metoprolol and consider administering metoprolol in smaller doses three times daily, instead of larger doses two times daily, to avoid the higher plasma levels associated with the longer dosing interval. Bronchodilators, including beta₂ agonists, should be readily available or administered concomitantly." 1

Very Limited Exception for Non-Asthmatic Airway Disease

In older patients with mild wheezing or COPD (but no active asthma), a very low starting dose of metoprolol (≈12.5 mg) with close monitoring may be acceptable when a compelling cardiac indication exists (e.g., recent myocardial infarction, heart failure). 2 This cautious approach relies on:

• Immediate-release formulation for rapid reversal
• Ready availability of bronchodilators
• Vigilant observation for wheezing or prolonged expiration 2

Studies show that metoprolol in slow-release formulations produces lower peak plasma levels and less marked ventilatory effects compared to ordinary tablets in asthmatic patients. 9

Alternative Therapies When Metoprolol Causes Dyspnea

Replace metoprolol with non-dihydropyridine calcium-channel blockers (diltiazem or verapamil) for rate control when bronchospasm risk is present. 2 ACE inhibitors, ARBs, or dihydropyridine calcium-channel blockers can be used safely because they have no effect on bronchial smooth-muscle tone. 2

Common Pitfalls to Avoid

• Do not assume all β-blockers are equally safe; even cardioselective metoprolol can block β₂ receptors at therapeutic doses and remains contraindicated in active asthma. 2
• Do not continue metoprolol at lower doses when mild respiratory symptoms appear, because loss of selectivity can worsen bronchospasm. 2
• Do not use non-selective β-blockers (e.g., carvedilol, propranolol) in any patient with obstructive airway disease, as they markedly increase airway resistance. 5, 2
• Propranolol caused a significant reduction in FEV₁ and FVC compared with metoprolol in COPD patients, with two patients requiring IV theophylline therapy. 8