Diverse Properties & Uses of Beta-Blockers Materials

THE DIVERSE PROPERTIES AND USES OF BETA-BLOCKERS

Faculty:

The following continuing medical education team members were involved in the initial planning, development, and review of this activity:

L. Austin Fredrickson, MD, FACP 

L. Austin Fredrickson is an Associate Professor of Internal Medicine at Northeast Ohio Medical University, where he serves as core faculty and teaches diagnostics, therapeutics, clinical skills, and health humanities. He is board-certified in general internal medicine and practices rural primary care. 

Pamela Sardo, PharmD, BS

Pamela Sardo is a freelance medical writer, licensed pharmacist, and the founder/principal at Sardo Solutions. She received her BS from the University of Connecticut and a PharmD from the University of Rhode Island. Pam’s career spans many years in retail, clinics, hospitals, long-term care, Veterans Affairs, pharmaceutical manufacturing, and managed healthcare across broad therapeutic classes and disease states.

The following faculty members were involved in authoring and reviewing this activity:

Sandra Rogers, MD

Sandra Rogers is a primary care physician in Texas. She is board-certified through the American Board of Family Medicine and the American Board of Internal Medicine. She completed her dual residency at Eastern Virginia Medical School in Norfolk, Virginia. She has been practicing in Allen, Texas, for over 20 years.

Anna Shurtleff Smith, MPH, BSN-RN

Anna Shurtleff Smith is a graduate of the University of North Texas Health Science Center, School of Public Health, with a community health focus, and Texas Tech University School of Nursing. She has clinical experience in both inpatient and outpatient settings. Anna is passionate about patient education, health literacy, and health communications.

Steven Malen, PharmD, MBA

Dr. Steven Malen earned a dual degree, Doctor of Pharmacy (PharmD) and Master of Business Administration (MBA), from the University of Rhode Island. Throughout his career, he has worked as a clinical pharmacist in retail, specialty, and compounding settings. He specialized and taught on topics ranging from vaccines to veterinary compounding.

Topic Overview

Beta-blockers are essential in the treatment of many cardiovascular diseases, including congestive heart failure, myocardial infarction, and tachyarrhythmias. Beta-blockers are also used for migraine prophylaxis, performance anxiety, glaucoma, and various other conditions. They have notable side effects, contraindications, and warnings associated with their use. Healthcare professionals should be aware of these when determining the appropriateness of beta-blocker therapy. Additionally, healthcare professionals should note any potential drug interactions when beta-blocker therapy is initiated. This course will review the pharmacologic characteristics of beta-blockers, identify indications for beta-blocker therapy, and highlight adverse reactions, contraindications, warnings, and interactions associated with beta-blocker therapy. Finally, the management of beta-blocker overdose will be discussed.

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This activity was planned by and for the healthcare team, and learners will receive 3 Interprofessional Continuing Education (IPCE) credits for learning and change.

Joint Universal Activity Number: The Joint Accreditation Universal Activity Numbers assigned to this activity are:

Pharmacists: JA4008424-0000-25-015-H01-P

Pharmacy Technicians: JA4008424-0000-25-015-H01-T

Credits: 3 contact hour(s) (0.3 CEU(s)) of continuing education credit.

Credit Types:

IPCE Credits - 3 Credits

AAPA Category 1 Credit™️ - 3 Credits

AMA PRA Category 1 Credit™️ - 3 Credits

Pharmacy - 3 Credits

Type of Activity: Knowledge

Media: Computer-Based Training (i.e., online courses)

Estimated time to complete activity: 3 contact hour(s) (0.3 CEU(s)), including Course Test and course evaluation.

Release Date: January 5, 2026 Expiration Date: January 5, 2029

Target Audience: This educational activity is for Physicians, Physician Assistants, Pharmacists, and Pharmacy Technicians

How to Earn Credit: From January 5, 2026, through January 5, 2029, participants must:

Read the “learning objectives” and “author and planning team disclosures;”

Study the section entitled “educational activity;” and

Complete the Course Test and Evaluation form. The Course Test will be graded automatically. Following successful completion of the Course Test with a score of 70% or higher, a statement of participation will be made available immediately. (No partial credit will be given.)

CME Credit: Credit for this course will be uploaded to CPE Monitor^® for pharmacists. Physicians may receive AMA PRA Category 1 Credit™ and use these credits toward Maintenance of Certification (MOC) requirements. Physician Assistants may earn AAPA Category 1 CME credit, reportable through PA Portfolio. All learners should verify their individual licensing board's specific requirements and eligibility criteria.

Learning Objectives: Upon completion of this educational activity, participants should be able to:

Describe the mechanism of action of beta-blockers

Identify the uses for beta-blockers

Discuss side effects, interactions, warnings, and contraindications of beta-blocker therapy

Review the management of a beta-blocker overdose

Disclosures

The following individuals were involved in planning, developing, and/or authoring this activity: L. Austin Fredrickson, MD, FACP; Sandra Rogers, MD; Anna Shurtleff Smith, MPH, BSN-RN; Steven Malen, PharmD, MBA; and Pamela Sardo, PharmD, BS. None of the individuals involved in developing this activity has a conflict of interest or financial relationships related to the subject matter. There are no financial relationships or commercial or financial support relevant to this activity to report or disclose by RxCe.com or any of the individuals involved in the development of this activity. 

© RxCe.com LLC 2026: All rights reserved. No reproduction of all or part of any content herein is allowed without the prior, written permission of RxCe.com LLC.

Educational Activity

The Diverse Properties and Uses of Beta-Blockers

Introduction

Beta-blockers are essential in the treatment of many cardiovascular diseases, including congestive heart failure, myocardial infarction, and tachyarrhythmias. Beta-blockers are also used for migraine prophylaxis, performance anxiety, glaucoma, and various other conditions. They have notable side effects, contraindications, and warnings associated with their use. Healthcare professionals should be aware of these when determining the appropriateness of beta-blocker therapy. Additionally, healthcare professionals should note any potential drug interactions when beta-blocker therapy is initiated. This course will review the pharmacologic characteristics of beta-blockers, identify indications for beta-blocker therapy, and highlight adverse reactions, contraindications, warnings, and interactions associated with beta-blocker therapy. Finally, the management of beta-blocker overdose will be discussed.

History of Beta-blockers

The first commercially marketed beta-blocker was propranolol.^1,2 Propranolol’s effectiveness for the treatment of angina pectoris was quickly recognized, and not long after, its therapeutic effects on hypertension and arrhythmias were discovered.¹ Its inventor, physician, and scientist Sir James Black, was said to have revolutionized the management of angina with this discovery, earning him the Nobel Prize in 1988.^1,2 The discovery of how this beta-adrenergic receptor antagonist caused changes in the cardiovascular system is complex, but as a class, beta-blockers produce their therapeutic effects on the sympathetic branch of the autonomic nervous system.²

Beta-Blockers’ Pharmacological Profile and Mechanism of Action

The sympathetic nervous system regulates bodily functions by activating adrenergic receptors. These receptors include beta-adrenergic receptors in the heart that regulate cardiac contractility.³ Sympathetic nerve impulses are transmitted by catecholamines, primarily norepinephrine (noradrenaline) and epinephrine (adrenaline).³ These endogenous substances bind to alpha and beta-adrenergic receptors in the heart, lungs, liver, vascular smooth muscle, and many other areas within the body.³ While all subtypes of beta-adrenergic receptors are G-coupled protein receptors (GCRPs) that increase cyclic AMP, the response to beta receptor stimulation is determined by the ligand, as well as the receptor type and location.³ Catecholamine-receptor binding activates intracellular secondary messenger pathways, which alter cellular activity and can produce a measurable physiological response.³ For example, when epinephrine binds to adrenergic receptors in the heart, the physiological responses are increases in heart rate via the sinoatrial (SA) node, speed of impulse conduction through the atrioventricular (AV) nodal system, and the force of the contraction of the myocardium.³

Beta-blockers are a heterogeneous group of medications that differ in their receptor specificity, whose primary mechanism of action is to block adrenergic stimulation of beta-adrenergic receptors located in various parts of the body.³ There are three beta (ß) receptor subtypes: ß₁, ß₂, and ß₃.^3-5 A ligand, or signaling molecule, can be produced either endogenously or, in the case of a beta-blocker, synthetically.

Beta-1 receptors are primarily located in the heart and in the kidneys.^3,6 Within the heart, they mediate cardiac activity, with activation leading to increased heart rate, increased contractility, and increased AV node transmission.⁶ In the kidney, activation results in renin release.⁶

Beta-2 receptors are located in the lungs and peripheral vascular smooth muscle, and to a lesser extent in the heart. Upon activation, vasodilation and bronchodilation result.^3,6 In hepatic tissue, activation leads to glycogenolysis, which increases blood glucose.⁶

Finally, ß₃ receptors are located in adipose tissue and the bladder detrusor muscle, and activation of these receptors causes relaxation of the bladder detrusor and thermogenesis resulting from fat breakdown.^3-5

Beta-blockers are also classified as either non-selective or ß₁-selective.⁷ Non-selective agents bind ß₁ and ß₂ adrenoceptors.⁷ Beta-1 selective agents are considered cardioselective.⁷ The dose of the beta-blocker can cause changes in this relative selectivity, particularly when dosages are high.⁷ Additionally, some beta-blockers can also bind to alpha-adrenergic receptors.

Beta-1 receptor blockade results in decreased cardiac contractility, decreased heart rate, and decreased cardiac conduction times.⁷ Beta-2 receptor blockade results in vasoconstriction.⁸ Beta-3 β3-AR signaling regulates cardiac relaxation—notably through PKG-downstream signaling—and prevents hypertrophic remodeling, it recently appeared as a promising therapeutic target for HF with preserved ejection fraction (HFpEF).⁹

Beta-blockers may encompass several therapeutic categories, with many agents falling into more than one. Therapeutic categories include cardioselectivity, intrinsic sympathomimetic activity (ISA), membrane-stabilizing effects, partial agonist activity, lipophilicity, or vasodilation, all of which help determine the overall effects of each medication.¹⁰ Finally, some beta-blockers bind to serotonin receptors.¹¹

Cardioselectivity

Cardioselective beta-blockers include acebutolol, atenolol, betaxolol, bisoprolol, metoprolol, and nebivolol. Labetalol has both selective alpha-1-adrenergic and nonselective beta‑adrenergic receptor-blocking actions in a single substance.¹²

Intrinsic Sympathomimetic Activity

Some beta-blockers are not full antagonists but rather partial agonists.¹² Upon binding to a beta-adrenergic receptor, they partially activate the receptor while preventing catecholamines from binding and fully activating it.^7,8 As a result, normal or enhanced sympathetic activity is prevented.^7,8 The amount of beta stimulation is low grade while at rest, but when sympathetic activity is high, it acts as a typical beta-blocker.⁸ This is known as intrinsic sympathomimetic activity (ISA).^7,8 Beta-blockers that possess ISA do not lower resting heart rate or have as strong an effect on cardiac output as other beta-blockers without ISA.¹³ Acebutolol, penbutolol, and pindolol have ISA.⁸

Membrane-Stabilizing Activity

Certain beta-blockers have membrane-stabilizing activity that decreases the responsiveness of the myocardium (stabilizing it) to an action potential and prevents cardiac arrhythmias.¹⁰ It is at very high concentrations that membrane-stabilizing activity occurs; otherwise, it is not of much clinical significance.¹⁰ However, if an excessive amount of a beta-blocker that has membrane-stabilizing activity is ingested, e.g., in a deliberate overdose, this effect can lead to serious ventricular arrhythmias.¹⁴ Propranolol and carvedilol are the two most used beta-blockers that have membrane-stabilizing activity.¹⁵

Lipophilicity

A drug with high lipid solubility can easily cross cell membranes. Lipid solubility in a beta-blocker allows the drug to enter the central nervous system (CNS) by crossing the blood-brain barrier, potentially leading to increased CNS adverse effects.^16,17 Beta-blockers with high lipid solubility include carvedilol and propranolol.^8,15 Beta-blockers with moderate lipid solubility include metoprolol, labetalol, timolol, and pindolol.¹⁸ Bisoprolol has low to medium lipid solubility.¹⁸ Beta-blockers with low lipid solubility include atenolol, betaxolol, acebutolol, esmolol, nadolol, and sotalol.¹⁸

Vasodilatation

Traditional beta-blockers, both nonselective and selective, are vasoconstrictive due to unopposed α₁ activity; however, vasodilating beta-blockers are not associated with these negative metabolic effects.¹⁹

Serotonin Receptor Activity

Some beta-blockers, including propranolol, can bind to serotonin receptors.¹¹ This activity is a proposed mechanism of action as to why some beta-blockers have been effectively used as prophylactic treatments for migraine headaches.¹¹ A meta-analysis has demonstrated that propranolol is the most effective prophylactic treatment, while metoprolol is only likely effective. In contrast, atenolol, bisoprolol, and timolol had weak evidence of benefit, and acebutolol, alprenolol, and nadolol were ineffective.¹¹

Pharmacokinetics

Beta-blockers vary in their pharmacokinetic profiles.^10,20 Most beta-blockers undergo hepatic metabolism, except for nadolol and sotalol, which are not metabolized, esmolol, which is metabolized by red blood cell esterases, and atenolol, which is only metabolized to a limited extent. Beta-blockers are generally eliminated renally, and carvedilol, acebutolol, and unmetabolized atenolol are also partially eliminated in the feces. Half-life properties, metabolism, and elimination of beta-blockers vary and are included in the dosing section.^10,20

Beta-blocker Dosage Forms, Metabolism, and Half-lives

Beta-blockers are available for use as systemic (oral or intravenous) and ophthalmic (eye drop) preparations. Tables 1 through 4 below describe the dosage forms, metabolism, and half-lives of beta-blockers within the context of the labeled uses of specific medication brands. FDA-approved prescribing information should be referenced for safety, efficacy, indications, and specific dosing of each medication. Beta-blockers can be administered orally, intravenously, or ophthalmically, depending on the agent. Healthcare professionals are encouraged to regularly review current drug information on beta-blockers.

Table 1

Noncardioselective Agents Dosage Forms,

Metabolism and Half-Lives^21-25

Noncardioselective Agents
Nadolol t½: 10-24 hrs	Angina and hypertension Available orally Not metabolized. Renally eliminated as an unchanged drug.
Propranolol t½: 3-6 hrs (IR), 8-10 hrs (ER)	Acute myocardial infarction*, angina, atrial fibrillation, atrial flutter, hemangioma, hypertension, idiopathic hypertrophic subaortic stenosis, migraine prophylaxis, paroxysmal supraventricular tachycardia, pheochromocytoma, reduction of cardiovascular mortality, tremor Available orally (IR, ER, and oral solution) and IV Immediate-release tablets should be taken on an empty stomach. Extended-release capsules can be taken with or without food and should not be crushed or broken. Hepatic metabolism. Renal elimination.
Timolol t½: 1-4 hrs	Hypertension, migraine prophylaxis, myocardial infarction prophylaxis, ocular hypertension, open-angle glaucoma, and reduction of cardiovascular mortality Available orally and ophthalmically Hepatic metabolism. Renal elimination.
Sotalol t½: 12 hrs	Atrial fibrillation, atrial flutter, ventricular tachycardia Available as an IV solution, oral tablet, or oral solution Not metabolized. Renal elimination.

*FDA-approved indication was based on NHLBI-sponsored BHAT study of patients surviving the acute phase of MI, and when begun 5-21 days following infarction, was shown to reduce overall mortality up to 39 months. New 2024-2025 data: revised recommendations and debate the long-term benefits.

Table 2

Cardioselective Agents Dosage Forms

Metabolism and Half-Lives^26-33

Cardioselective Agents
Atenolol t½: 6-7 hrs	Acute myocardial infarction (STEMI), angina, hypertension, myocardial infarction prophylaxis, and reduction of cardiovascular mortality Available orally Little to no hepatic metabolism. Absorbed portion eliminated by renal excretion, with the rest of the dose excreted as unchanged drug in the feces
Betaxolol t½: approx. 15 hrs	Hypertension, ocular hypertension, open-angle glaucoma Available orally and ophthalmically Hepatic metabolism. Renal elimination.
Bisoprolol† t½: 9-12 hrs	Hypertension Available orally Hepatic metabolism. Renal elimination.
Esmolol t½: approx. 9 min	Atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia, perioperative hypertension, postoperative hypertension Available as an IV solution Infusion into small veins or through a butterfly catheter should be avoided, as it can cause thrombophlebitis Red blood cell esterase metabolism. Renal elimination.
Metoprolol tartrate, immediate-release Metoprolol succinate, extended-release t½: 3-7 hrs	Acute myocardial infarction (STEMI), angina, cardiomyopathy, heart failure, hypertension, and reduction of cardiovascular mortality Available as an IV solution or an oral tablet Hepatic metabolism. Renal elimination.
Nebivolol t½: 12 hrs in extensive metabolizers, 19 hours in poor metabolizers	Hypertension Available orally Hepatic metabolism. Renal and feces elimination.

^†now recommended in clinical guidelines for HFrEF

Table 3

Agents with Alpha-1 Antagonist Activity

Dosage Forms, Metabolism, and Half-Lives^34-36

Agents with alpha-1 antagonist activity
Carvedilol t½: 5-11 hrs	Acute myocardial infarction, cardiomyopathy, heart failure, hypertension, and reduction of cardiovascular mortality Available orally (IR and ER) Hepatic metabolism. Excreted in the bile and feces.
Labetalol‡ t½: 6-8 hrs	Hypertension Available as an IV solution and orally Hepatic metabolism. Excreted in the urine and feces.

^‡Hypertension in pregnancy increases the maternal risk for pre-eclampsia, gestational diabetes, premature delivery, and delivery complications, so it is recommended in these patients presenting with a need for urgent blood pressure control

Table 4

Agents with Intrinsic Sympathomimetic Activity (ISA)

Dosage Forms, Metabolism, and Half-Lives^37,38

Agents with intrinsic sympathomimetic activity (ISA)
Acebutolol t½: 3-4 hrs	Hypertension and premature ventricular contractions Available orally Hepatic metabolism. Excreted in urine and bile and via direct passage through the intestinal wall.
Pindolol t½: 3-4 hrs	Hypertension Available orally Hepatic metabolism. Renal elimination.

Recent Approvals (2025 Update)

Landiolol, an ultra-short-acting, highly selective β₁-blocker, received FDA approval in November 2024 for intravenous use.^39,40 In short-term use, it reduces the ventricular rate in adults with supraventricular tachycardia, including atrial fibrillation and atrial flutter.⁴¹ This agent has a half-life of approximately 4 minutes at steady state. Unlike longer-acting agents such as esmolol (half-life ~9 minutes), landiolol demonstrates superior cardioselectivity with minimal β₂ effects, reducing the risk of bronchospasm in patients with reactive airway disease.⁴¹ It expands options for short-term IV therapy, but it is not intended for chronic oral use.⁴¹

Table 5

Landiolol⁴¹

Agent	Selectivity	Half-Life	Primary Indication	Key Differentiation
Landiolol	B1-selective	~4 min (IV)	Acute tachyarrhythmias in critical care	Ultra-rapid onset; lower hypotension risk vs. esmolol

Labeled Uses

Beta-blockers are primarily used to treat cardiovascular diseases.²⁰ Labeled uses of systemic beta-blockers include angina pectoris, hypertension (alone or with other drugs), management of ventricular arrhythmias, management of hemodynamically stable patients with known or suspected MI to reduce morbidity and mortality, treatment of heart failure with reduced ejection fraction, migraine, essential tremor, and glaucoma (using ophthalmic preparations).²² Below are descriptions of the roles beta-blockers play for certain disease states.

Angina Pectoris

Angina pectoris, also known as stable angina, is a transient chest pain or pressure caused by myocardial ischemia.⁴² Myocardial ischemia is a result of an imbalance between myocardial oxygen demand and supply. For most patients, angina pectoris is typically caused by atherosclerotic heart disease.⁴² Angina pectoris is common, with approximately 10 million Americans suffering from the disease.⁴²

Improving the quality of life via a reduction in angina symptoms and preventing cardiovascular events (such as MI and death) are the primary goals of angina treatment.⁴² Beta-blockers decrease myocardial oxygen demand by decreasing heart rate, myocardial contractility, and stress on the left ventricle. It has been demonstrated that beta-blockers enhance exercise capacity, decrease the frequency of angina attacks, mitigate exercise-induced ST-segment depression, and reduce the requirement for sublingual nitroglycerin.^40,44,45

Beta-blockers can be effective for treating chronic angina, but β₁-selective agents are preferred. Non-selective beta-blockers may present with an increased risk of adverse effects.⁴⁴ Selection of a beta-blocker can be determined by factors such as patient comorbidities or dosing frequency. Beta-blockers are often preferred as initial therapy. The treatment goals when using beta-blockers for angina pectoris are to reduce the frequency and severity of anginal attacks, improve exercise tolerance, attain a resting heart rate of 50-60 bpm, decrease blood pressure, and heart rate during exercise. Use the lowest effective dose to avoid adverse effects. Beta-blockers should not be used in patients who have Prinzmetal angina (vasospastic angina), as use could lead to coronary vasospasm secondary to unopposed alpha activity.⁴⁶

Atrial Fibrillation 

Atrial fibrillation (AF) is the most common arrhythmia, characterized by ectopic atrial activity.^15,47 Beta-blockers are preferred agents for rate control in patients with atrial fibrillation.^15,47 Intravenous beta-blockers, such as metoprolol, propranolol, and esmolol, are useful for achieving acute control of ventricular rate.^15,47 Oral beta-blockers can then be used for chronic rate control, with metoprolol succinate, atenolol, and nadolol being once-daily options that can help improve compliance.^15,47

The 2024 European Society of Cardiology (ESC) AF Guidelines position beta-blockers as initial rate-control agents across ejection fractions, preferred over digoxin in younger patients or those with HFpEF (Heart Failure with Preserved Ejection Fraction), provided they are not in a state of acute decompensated HF. For rhythm control, they are used as adjuncts.⁴⁸

Heart Failure

Heart failure (HF) is a complex clinical syndrome with symptoms and signs that result from any structural or functional impairment of ventricular filling or ejection of blood.⁴⁹ Three agents — bisoprolol, carvedilol, and metoprolol succinate — have demonstrated efficacy in the management of heart failure with reduced ejection fraction (HFrEF).⁴⁹ Treatment with these beta-blockers can lessen the symptoms of HF, improve the patient’s clinical status, reduce the risk of death, and reduce the combined risk of death or hospitalization.⁴⁹ Beta-blocker therapy should be started at low doses and titrated up to the target dose, unless it is not tolerated.⁴⁹

The 2024-2025 updates from the European Society of Cardiology (ESC) and the American College of Cardiology (ACC) reinforce beta-blockers as a foundational therapy, titrated to target doses to reduce mortality. Guidelines now include SGLT2 inhibitors (e.g., canagliflozin) as preferred first-line, with foundational drug classes, including beta-blockers, started early, and can be added for those with tachycardia.⁵⁰

Hypertension

Hypertension is a leading cause of death and significantly increases the risk of developing atherosclerosis, heart disease, kidney disease, stroke, and retinal damage.^33,51 Blood pressure control is critically important for preventing hypertensive complications. Lifestyle changes like smoking cessation and weight loss can significantly lower blood pressure, but many people who have hypertension require treatment with antihypertensive medication.

Treatment of hypertension is a labeled use for beta-blockers, but they are not a first or second-line choice, as they may not be as effective as other classes in preventing stroke or cardiovascular events for patients with hypertension.^51,52 In addition, the beta-blockers are less effective for black patients, and their use increases the risk of glucose intolerance, the development of new-onset diabetes, fatigue, and sexual dysfunction.⁵¹ Beta-blockers can be added to the treatment regimen if there is a separate indication for these medications or if therapies and lifestyle modifications have not reduced blood pressure to the target level.^51,52

The 2024 ESC Guidelines recommend initiating beta-blockers as first-line or add-on therapy in patients with compelling indications, such as post-MI or HF, targeting systolic blood pressure (SBP) < 130 mm Hg for most adults (vs. prior < 140 mm Hg).⁴⁸ They stress combination therapy (e.g., beta-blocker + ACE inhibitor) for resistant cases and periodic reassessment of medications to reduce polypharmacy, when appropriate. Unlike U.S. guidelines, ESC prioritizes out-of-office monitoring and early detection via risk calculators.⁴⁸

Myocardial Infarction (MI)

Beta-blockers decrease oxygen demand, decrease the risk for ventricular fibrillation, have a beneficial effect on ventricular remodeling, decrease automaticity, reduce infarct size, and publications describe decreased risk of mortality.⁵³ Historical trials supporting the use of beta-blockers in patients post–MI were carried out before revascularization became common. The controversy about beta-blocker use in this population continues. Two studies presented at the ESC investigated patients with myocardial infarction but with an ejection fraction of >40% who were randomized to receive long-term β-blocker therapy or not, and the outcomes were very different.⁵⁴

While beta-blockers are strongly recommended for patients with MI and reduced left ventricular ejection fraction (LVEF), their role in patients with preserved or mildly reduced LVEF (≥40%) is less certain.⁵⁵ In the BETAMI-DANBLOCK study that included 5500 patients, among patients with a myocardial infarction and a left ventricular ejection fraction of at least 40%, beta-blocker therapy led to a lower risk of death or major adverse cardiovascular events than no beta-blocker therapy.⁵⁵

The REBOOT study, also presented at ESC, enrolled 4243 patients who were randomly assigned to receive beta-blocker therapy or none upon discharge after invasive care. This was a randomized, open-label clinical trial testing the benefits of β-blocker maintenance therapy in patients discharged after MI with or without ST-segment elevation. Patients were included if they had LVEF >40% and no history of HF. In this study, no reduction in all-cause death, reinfarction, or heart failure hospitalization was observed.⁵⁶

While the controversy continues, beta-blockers remain reasonable in patients with mildly reduced ejection fraction (EF) of 41 to 49.⁵⁴ Their role is uncertain in patients with a preserved (≥50%) left ventricular ejection fraction.⁵⁴

Ventricular Arrhythmias

Beta-blockers have been successfully used to prevent ventricular arrhythmias in patients who are having an acute coronary syndrome.⁵⁷ This is particularly well-researched in the arrhythmias of ventricular tachycardia and/or ventricular fibrillation.⁵⁷

Glaucoma and Ocular Hypertension

Topical beta-blockers, such as timolol and betaxolol, may be used to reduce intraocular pressure and are useful in patients with ocular hypertension and glaucoma. These beta blockers work by blocking the sympathetic nerve endings in the ciliary epithelium, which causes a fall in aqueous humor production.⁵⁸

Table 6

Key 2024-2025 Recommendation Changes^59-61

Condition	Recommendation	Preferred Agents	Target/Notes
Hypertension	Add-on with other classes for compelling indications(HFrEF); aim for SBP <130 mm Hg	Bisoprolol, nebivolol	Combine with lifestyle, reassess for de-escalation
HFrEF	Foundational; titrate to max tolerated dose	Carvedilol (preferred for subgroups)	Add to SGLT2i/ARNI; monitor EF
Post-MI (preserved EF)	Reassess and individualize regarding whether to discontinue after 1 year, if stable	N/A (de-escalate)	Focus on statins/anti- platelets

Off-Label Uses

Outside of managing cardiovascular conditions, systemic beta-blockers are used off-label to treat a variety of conditions, including cancer, Marfan syndrome, migraines, anxiety, agitation, and hyperthyroidism. Beta-blockers have also been prescribed for patients presenting with a variety of structural heart diseases, essential tremors, thoracic aneurysms, or portal hypertension in cirrhosis.

Oncology

Blocking beta-adrenergic signaling with beta-blockers inhibits the effects of stress.⁶² Beta-blocker use and breast cancer outcomes have been examined in previous studies with inconsistent results. In a population-based cohort of New Zealand women with breast cancer, in women with a subset of breast cancer (triple negative breast cancer), beta-blocker use was associated with a significantly longer recurrence-free interval.⁶²

Marfan Syndrome

Marfan syndrome is a hereditary connective tissue disorder caused by a mutation in the fibrillin‐1 gene.⁶³ It affects multiple body systems, most notably the cardiovascular, ocular, skeletal, dural, and pulmonary systems. Aortic root dilatation is the most frequent cardiovascular manifestation, and its complications, including aortic regurgitation, dissection, and rupture, are the leading cause of morbidity and mortality.⁶³ Beta-blockers have been used to treat this component of Marfan syndrome.⁶³

Migraines

As discussed above, some beta-blockers, including propranolol, can bind to serotonin receptors.¹¹ This activity is a proposed mechanism of action as to why some beta-blockers have been effectively used as prophylactic treatments for migraine headaches.

Anxiety

Performance anxiety is characterized by intense feelings of emotional distress before, during, or after performing in front of others.⁶⁴ Psychological interventions, such as cognitive behavioral therapy, should be considered the primary treatment.⁶⁴ Propranolol has been used with some reported effectiveness to prevent and treat competitive or performance anxiety in athletes.⁶⁴ A single dose taken approximately 60 minutes before an anticipated sports event has been shown to ameliorate or prevent anxiety symptoms.⁶⁴

Agitation

Beta-blockers have been used to treat agitation.^65,66 Beta-blockers, such as propranolol, may benefit individuals with behavioral and psychological symptoms of dementia.⁶⁶

Hyperthyroidism

Hyperthyroidism is defined as a syndrome of symptoms caused by excess thyroid hormone, characterized by HR acceleration, increased peripheral resistance, decreased cholesterol levels, increased metabolism, and tremor or neuropsychiatric symptoms.⁶⁷ Excess thyroid hormones are an important factor affecting the cardiovascular system. Untreated increased levels of thyroid hormones can cause atrial fibrillation (AF), embolic events, muscle weakness, and, in rare cases, cardiovascular collapse and even death.⁶⁷ In patients with symptomatic hyperthyroidism, the inclusion of β-blockers is recommended.⁶⁷

Contraindications and Warnings

Contraindications to beta-blockers include symptomatic bradycardia, cardiogenic shock, pulmonary hypertension, decompensated heart failure, and atrioventricular block.²⁰ Patients presenting with pulmonary hypertension or Type 1 AV block with Mobitz have rarely been prescribed beta-blockers with caution. Beta-blockers should be used with caution in patients with asthma or bronchospastic disease, as well as those with diabetes mellitus.⁴⁰ The use of beta-blockers in patients with asthma, COPD, or diabetes mellitus is discussed next.

Patients with Asthma or COPD

While beta-blockers are safe for most patients, they should be used cautiously in those with asthma and COPD.⁶⁸ These drugs, particularly the non-selective beta-blockers, can precipitate bronchial obstructions, increase airway reactivity, cause exacerbations, and block the receptors that agonists normally bind to, preventing the agonist from activating them.^12,69 Clinicians should avoid or carefully monitor the use of non-selective ß₁ and ß₂ antagonists (such as propranolol, nadolol, or timolol) in patients with severe or decompensated bronchospastic disease.^68,70 Cardioselective beta-blockers and beta-blockers with ISA can be used for patients with mild to moderate asthma or COPD after individualized risk-benefit assessment.^71-73 According to FAERS data, drugs like esmolol, metoprolol, and nebivolol (ß₁-selective), and nadolol, non-selective beta-blockers, may be safer for asthmatic patients, whereas betaxolol, bisoprolol (ß₁-selective), timolol, and propranolol, non-selective beta-blockers, should be individualized.⁷⁰

Diabetes Mellitus

The prescribing information about beta-blockers notes that these drugs should be used cautiously if a patient has diabetes, as hypoglycemia caused by beta-blockers is well-documented.^74-76 Blockade of ß₂ receptors can prevent catecholamines from increasing blood glucose in a hypoglycemic individual. It can also blunt the signs and symptoms of hypoglycemia (such as diaphoresis and tachycardia), putting patients at risk for severe hypoglycemia.³¹

The following points should be kept in mind:^31,74-76

Beta-blockers can cause hypoglycemia.

A case-by-case assessment of the risks and benefits of using beta-blockers in patients with diabetes is warranted.

Patients with diabetes who are prescribed a beta-blocker should be closely monitored, taught about the signs and symptoms of hypoglycemia, and informed that beta-blockers might blunt the signs and symptoms of hypoglycemia.

Withdrawal Warning

Prescribing information for beta-blockers includes a US boxed warning about abrupt discontinuation.^37,38 Abrupt discontinuation of a beta-blocker has been reported to cause tachycardia (sinus tachycardia, supraventricular or ventricular tachycardia), nervousness, anxiety, agitation, headache, sweatiness, tremor, nausea, and hypertensive crisis. In severe cases, complications may include angina, myocardial infarction, and sudden death.^21,31,37,77 This effect is thought to be due to the upregulation of beta receptors during beta-blocker therapy and increased receptor sensitivity to catecholamines.³⁸ Minor side effects may develop within 24 hours, but they generally develop within 3 days. Some are delayed 14 to 21 days.⁷⁷ In patients with acute withdrawal symptoms, beta-blockers should be reinitiated.⁷⁷

According to the prescribing information, discontinuing beta-blocker therapy should be done gradually over a period of 1 to 2 weeks to minimize side effects.^21,31,77 When tapering beta-blockers, monitor the patient and individualize the tapering based on the patient’s response. Developing a tapering regimen is also dependent on whether the patient is taking a short-acting or longer-acting drug and other factors, such as the patient having ischemic heart disease.^21,31 An example of a tapering regimen may be to reduce the daily dose by 50% per week until the lowest dose is reached.⁷⁷ Once the lowest dose is reached, maintain it for 1 week prior to discontinuation.⁷⁷

Adverse Reactions

Bradycardia, depression, exacerbation of heart failure, fatigue, hypotension, dizziness, dyspnea, headache, sexual dysfunction, and gastrointestinal distress are some of the most reported adverse effects associated with beta-blocker therapy.^37,78 In addition to these adverse events, Floppy Iris Syndrome has been observed during cataract surgery in some patients treated with alpha-1 blockers. Labetalol and carvedilol are alpha/beta blockers, and this warning is included in their prescribing information.^34,35 The use of beta-blockers may also be associated with hyperkalemia, ischemia, or Prinzmetal angina.³⁷

Drug Interactions

Drugs that affect blood pressure, heart rate, or the cardiac conduction system should be used cautiously when the patient is taking a beta-blocker.³⁷ Local and general anesthetics should also be used with caution in patients taking beta-blockers due to the risk of prolonged hypotension.³² Patients taking certain antidepressants and a beta-blocker can be at risk for adverse events³² such as bradycardia, hypotension, and falls, particularly with antidepressant drugs, which are inhibitors of cytochrome P450 2D6 liver enzymes (CYP2D6).⁷⁹ This inhibition would potentiate the plasma levels of the beta-blocker, increasing the beta-blocker effects.

Specific Populations

Pregnancy

Beta-blockers can cross the placenta.⁸⁰ Some beta-blockers have been associated with low birth weight, fetal bradycardia, hypoglycemia, and other adverse effects in neonates.^82-83 An individualized approach to treatment is warranted, with caution during pregnancy. A risk to a fetus from uncontrolled maternal hypertension must be considered. Labetalol has been prescribed for chronic hypertension in pregnant women and is often considered the first-line treatment.⁸¹

Lactation

Beta-blockers can be excreted in breast milk; however, the amount is largely determined by their protein binding, with those with low protein binding excreted in higher amounts.⁸² There is a low risk for the accumulation of beta-blockers such as propranolol, metoprolol, and labetalol in breast milk.³² Caution should be used with atenolol, nadolol, and sotalol as they are excreted in higher amounts in breast milk and may lead to the infant experiencing hypotension, bradycardia, and tachypnea.^81,84 Risk-benefit assessment and shared decision-making should be undertaken before use in women who are breastfeeding.

Renal Impairment

In patients with renal disease, beta-blockers that are not renally eliminated, such as labetalol, metoprolol, pindolol, and propranolol, have been prescribed.^85-87 Dosing may need to be adjusted if other beta-blockers are chosen for therapy in patients with impaired renal function.^86-88

Hepatic Impairment

Beta-blockers that are not hepatically eliminated, such as atenolol and nadolol, have been prescribed in patients with hepatic impairment.¹⁸ Dosing may need to be adjusted if other beta-blockers are chosen for therapy.⁸⁹

Beta-Blocker Poisoning

While the use of beta-blockers is generally considered safe when taken as prescribed, cases of overdose or poisoning can result in significant morbidity and mortality.^32,90 Healthcare professionals should be aware of the signs and symptoms of beta-blocker poisoning as well as management strategies.⁹¹ For example, a patient presented with undifferentiated shock, abdominal pain, hemodynamic instability with hypotension, and relative bradycardia.⁹² After ruling out other causes of hypotension, the patient was diagnosed with unintentional atenolol toxicity, with secondary mesenteric ischemia.⁹² This means that in patients with renal impairment, drug accumulation over time may predispose to unintentional beta-blocker poisoning.⁹²

Beta-blocker overdose causes excessive blockade of beta-adrenergic receptors, with receptor selectivity diminishing after overdose.⁹³ Overall, the toxicity following beta-blocker overdose will depend on both the agent and the dose ingested. Beta-blockers that have membrane-stabilizing activity appear to be more likely to cause arrhythmias.¹⁴

Beta-Blocker Overdose: Signs, Symptoms, and Treatment

The majority of patients who overdose on beta-blockers will display symptoms within 2 to 6 hours; however, if sustained-release formulations were ingested, signs and symptoms may be delayed up to 24 hours.⁹¹ Bradycardia and hypotension are the most common signs of beta-blocker overdose, with the risk of seizures also being possible.⁹¹ An overdose of sotalol can cause QT prolongation and torsade de pointes.⁹⁴ Bronchospasm and hypoglycemia can also result from beta-blocker overdose and may complicate its management.⁹⁵

Initial management of overdose includes stabilizing the patient and ensuring adequate oxygenation and circulation. Asymptomatic patients can often be observed and discharged unless other concerns remain. If it is suspected that the beta-blocker was ingested within the last hour, gastric lavage and activated charcoal are options for treatment, depending on the situation. IV access should be established, and continuous ECG monitoring should be started. The QT prolongation from sotalol can last three to four days.⁹⁴ Mildly symptomatic patients can receive boluses of an IV isotonic crystalloid for hypotension and atropine for bradycardia.⁹⁴ In many cases, these patients will require additional therapies that have been found to be beneficial in case reports, such as intravenous calcium salts, vasopressors, high-dose insulin, and lipid emulsion therapy.⁹⁶

Intravenous Glucagon

Glucagon is a recognized therapy for beta-blocker toxicity and acts as a cardiac stimulant to help treat bradycardia.^97-99 However, there is debate about glucagon’s place in beta-blocker toxicity therapy.^98,99

Glucagon bypasses beta receptors and increases cAMP levels, thereby increasing cardiac contractility and heart rate.^90,93 High doses of glucagon are recommended, with an initial dose of 50-150 mcg/kg in adults being administered over one to two minutes.^90,93 A transient effect should occur within approximately 5 minutes. If a benefit is observed, the initial dose should be followed by a continuous infusion at a rate of 2-5 mg/hour. While high-dose glucagon may be initially effective, the approach should be individualized, and an assessment should be made to determine whether the dose can be tapered as the patient improves.^90,93

Case Study Example

Mr. J, a 55-year-old male, is 14 months post-STEMI, with an EF of 48%. He is on bisoprolol 5 mg daily, aspirin, and atorvastatin. He is asymptomatic but concerned about fatigue and sexual dysfunction. His recent labs show normal renal function and no tachycardia.

Options:

1. Continue bisoprolol indefinitely. Rationale: traditional guideline adherence)¹²

2. Taper and discontinue. Rationale: 2025 REBOOT evidence for noninferiority in mildly reduced EF²⁵

3. Switch to carvedilol. Rationale: superior remodeling in subgroups

Feedback: Each choice above has evidentiary support. How do these options align with your practice?

Summary

Beta-blockers are a diverse class of medications primarily used to manage cardiovascular conditions. They have also demonstrated efficacy for numerous other conditions. Non-selective agents block ß₁ and ß₂ adrenoceptors. Beta-1 selective blockers are relatively selective for ß₁ adrenoceptors and are thus more cardioselective. While these medications share the same basic mechanisms of action, they have different properties, which makes knowledge of this class important for Healthcare professionals who manage or review patient therapies.

Course Test

Beta-blockers produce their therapeutic effect on which branch of the autonomic nervous system?

Enteric

Sympathetic

Parasympathetic

Somatic

The primary mechanism of action of beta-blockers is to prevent which of the following from binding to beta receptors?

Catecholamines

Acetylcholine

Amino acids

Cholestane

Which of the following options most accurately lists FDA-approved indications for the use of beta blockers?

Management of hemodynamically unstable MI, HIV-associated lipodystrophy, and heart failure

Migraine, essential tremor due to beta blocker use during breastfeeding, and tinnitus

Management of hemodynamically stable patients with MI, asthma, and glaucoma

Angina pectoris, hypertension, and management of ventricular arrhythmias

Reducing angina symptoms and preventing cardiovascular events is important. In patients presenting with angina, which of the following statements best describes the effects of beta-blockers?

Beta-blockers decrease myocardial oxygen demand by decreasing heart rate

Beta blockers have an unpredictable effect on myocardial contractility

Beta-blockers decrease exercise capacity and increase breaths per minute

Beta blockers increase the frequency of angina attacks

Compared with nonselective beta-blockers, cardioselective beta-blockers and beta-blockers with ISA can be used for patients with which of the following diseases?

Symptomatic bradycardia

Cardiogenic shock

Mild to moderate asthma or COPD

Decompensated heart failure

Which of the following is an appropriate step in the management of a beta-blocker overdose in a mildly symptomatic patient?

Immediate use of glucagon and vasopressors

Initially stabilizing the patient and ensuring adequate oxygenation and circulation

Beginning a lipid emulsion infusion at a rate of 2.5 mL/kg/min

Avoiding high-dose insulin therapy in hyperglycemic patients

Which of the following conditions are considered to be absolute contraindications to the use of beta-blockers?

Heart conduction abnormalities

Symptomatic bradycardia

Asthma

Diabetes mellitus

Which of the following actions is acceptable if an overdose of a beta blocker is identified?

Give bismuth salicylate if the beta-blocker was ingested in the last hour

Gastric lavage should occur if the overdose were from IV dosing

Activated charcoal should be administered after 12 hours

Asymptomatic patients can often be observed and discharged unless other concerns remain.

Patients taking a drug that inhibits cytochrome P450 2D6 liver enzymes (CYP2D6) and a beta blocker concurrently are at risk for which of the following adverse effects?

Exertional angina

Hypertension

Bradycardia

A hemostatic event

A patient who has asthma or COPD should particularly avoid which of the following beta-blockers?

All beta-blockers

Cardioselective (blockade of ß₁ adrenoceptors) beta-blockers

Beta-blockers with intrinsic sympathomimetic activity

Non-selective (blockade of both ß₁ and ß₂ adrenoceptors) beta-blockers

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