Propranolol-Associated Asthma Exacerbation
Patient Background
Mr. Tom is a 62-year-old male with a medical history significant for essential tremor, mild persistent asthma, hypertension, and hyperlipidemia. His asthma had been well controlled for several years with fluticasone/salmeterol 100/50 mcg one inhalation twice daily, and albuterol metered-dose inhaler (MDI) as needed, which he reported using less than once per week. He had no recent asthma exacerbations or hospitalizations prior to the events described.
Clinical Presentation
Mr.Tom presented to his primary care provider with progressively worsening hand tremors that were interfering with fine motor tasks such as writing and eating. To address his essential tremor, propranolol immediate-release 10 mg twice daily was initiated. Although partial tremor improvement was noted, functional impairment persisted, prompting dose titration to 20 mg three times daily over the following weeks.
Approximately two weeks after the dose increase, Mr. Tom developed increasing shortness of breath, wheezing, and nocturnal cough. He attributed these symptoms to seasonal allergies and increased his use of albuterol to several times per day. Despite this escalation in rescue therapy, his respiratory symptoms continued to worsen.
He subsequently presented to the emergency department with acute dyspnea and wheezing and was admitted for management of an asthma exacerbation. During hospitalization, he required frequent nebulized bronchodilator therapy (albuterol/ipratropium), systemic corticosteroids, and supplemental oxygen. His home medications, including propranolol, were continued during admission.
At discharge, Mr. Tom was prescribed higher-dose inhaled corticosteroid/long-acting beta-agonist therapy (fluticasone/salmeterol 250/50 mcg twice daily) along with a prednisone taper. Propranolol was continued at 20 mg three times daily without reassessment of its potential role in the exacerbation.
At follow-up two weeks later, Mr. Tom reported improved baseline breathing but continued daily reliance on rescue inhaler therapy. His tremor remained well controlled, and propranolol therapy was continued.
Clinical Issue Identified
Nonselective beta-blockers such as propranolol inhibit both β₁- and β₂-adrenergic receptors. In patients with asthma, β₂ receptor blockade in bronchial smooth muscle can precipitate bronchospasm and asthma exacerbations, even at relatively low doses. The risk increases with dose escalation, which amplifies β₂ antagonism.
In this case, the temporal association between propranolol dose escalation and worsening respiratory symptoms, combined with increased reliance on rescue bronchodilator therapy, strongly suggests propranolol-induced asthma exacerbation. Failure to recognize the medication-related cause resulted in intensification of asthma therapy rather than addressing the underlying trigger.
Pharmacist Intervention and Clinical Management
Medication Review and Causality Assessment
- Identify propranolol as a likely contributor to asthma destabilization.
- Recognize increased short-acting beta-agonist use as an early warning sign of worsening control.
- Differentiate medication-induced disease worsening from allergic or infectious triggers..
Therapeutic Modification
- Discontinue propranolol to remove the precipitating factor for bronchospasm.
- Avoid nonselective beta-blockers in patients with known reactive airway disease.
Alternative Tremor Management
- Consider primidone as a first-line alternative for essential tremor.
- If beta-blocker therapy is deemed necessary, cautiously consider a β₁-selective agent (e.g., metoprolol) with close pulmonary monitoring, recognizing residual risk.
Asthma Optimization and Monitoring
- Reassess the need for sustained high-dose inhaled corticosteroid therapy once the offending agent is removed.
- Monitor rescue inhaler use, symptom frequency, and lung function.
- Educate the patient on recognizing early signs of asthma deterioration.
Documentation and Follow-Up
- Clearly document the adverse drug reaction to propranolol to prevent re-exposure.
- Coordinate care between primary care, pulmonology, and pharmacy as needed
Clinical Rationale and Ramifications
This case highlights the significant risk of nonselective beta-blockers in patients with asthma, even when the disease has been previously well controlled. Failure to recognize medication-induced disease exacerbation led to a cascade of additional therapies, including higher-dose inhaled corticosteroids and systemic steroids, exposing the patient to avoidable adverse effects.
By addressing the root cause—propranolol-induced bronchospasm—rather than escalating asthma therapy, clinicians could have prevented hospitalization, reduced symptom burden, and avoided unnecessary intensification of treatment. This case underscores the importance of reviewing comorbid conditions and medication mechanisms before initiating therapy and reassessing medications when disease control deteriorates unexpectedly.
Regular medication review and awareness of pharmacologic contraindications are essential to preventing avoidable harm and optimizing outcomes in patients with chronic respiratory disease.