Beta Blockers

Article Author:
Khashayar Farzam
Article Editor:
Arif Jan
10/27/2018 12:31:25 PM
PubMed Link:
Beta Blockers


Beta blockers are medications that are used to treat various cardiovascular conditions and other pathologies.[1]

Beta receptors exist throughout the body in three distinct forms: beta-1 (B1), beta-2 (B2), beta-3 (B3). Beta-1 receptors mediate cardiac activity and associated cardiovascular markers. Beta-2 receptors control various aspects of metabolic activity and induce smooth muscle relaxation. Beta 3 receptors induce the breakdown of fat cells and are less clinically relevant. Blockage of these receptors with beta-blockers is used to treat a broad range of illnesses.[1]

Beta blockers are indicated and FDA approved for the treatment of tachycardia, hypertension, myocardial infarction, congestive heart failure, cardiac arrhythmia, angina, hyperthyroidism, essential tremor, aortic dissection, portal hypertension, glaucoma, migraine prophylaxis, and other conditions. It is also used to treat less common conditions such as long QT syndrome and hypertrophic obstructive cardiomyopathy. Beta blockers are available in three main forms: oral, intravenous, and ophthalmic. In the outpatient setting, patients will be prescribed beta blockers in oral form. Emergency room and in-patient settings warrant intravenous usage, particularly for the acute control of pathology.

Congestive heart failure patients are treated with beta blockers if it’s in a compensated state. Specifically, the beta blockers bisoprolol, carvedilol, and metoprolol succinate are used.

Athletes and musicians use beta blockers for their anxiolytic effect as well as their negative effects on the sympathetic nervous system. They are not FDA approved for the treatment of anxiety-related disorders; however, they have a potent anxiolytic effect. Combined with a reduction in tremor, they can lead to improved accuracy in sports such as archery and improvement in stage performance.

Mechanism of Action

There are two main classes of beta receptors: B1 and B2. Beta-3 receptors also exist. Two neurotransmitters, epinephrine, and norepinephrine, bind to B1 receptors and increase cardiac automaticity as well as conduction velocity. B1 receptors also induce renin release, and this leads to an increase in blood pressure. Binding to B2 receptors causes relaxation of the smooth muscles along with increased metabolic effects such as glycogenolysis. Some beta blockers also bind to alpha receptors to some degree. This allows them to induce a different clinical outcome when used in certain settings.

Once beta blockers bind to the B1 and B2 receptors, they inhibit these effects. Therefore, the chronotropic and inotropic effects on the heart are inhibited and the heart rate slows down. Beta blockers also decrease blood pressure via several theoretical mechanisms, including decreased renin and reduced cardiac output. The negative chronotropic and inotropic effects lead to a decreased oxygen demand; that is how angina improves after beta-blocker usage. These medications also prolong the atrial refractory periods and have a potent antiarrhythmic effect.

Beta blockers are classified as non-selective and beta-1 selective. There also exists B2 selective and B3 selective medications, neither has a known clinical purpose. Non-selective agents bind to both B1 and B2 receptors, antagonize them, and induce antagonizing effects via both receptors. Examples include propranolol, carvedilol, sotalol, and labetalol. B1 selective beta blockers only bind to the B1 receptors. They are cardio-selective. Examples include atenolol, bisoprolol, metoprolol, and esmolol.[2][3][4]

Beta blockers lower the secretion of melatonin and hence may cause insomnia and sleep changes in some patients.[5]

Alpha-1 receptors induce vasoconstriction and increased cardiac chronotropy. This means agonism at the alpha-1 receptors leads to a higher blood pressure and a higher heart rate. In contrast, antagonism at the alpha-1 receptor leads to vasodilation and negative chronotropy which leads to a lower blood pressure and lower heart rate. Some beta blockers, such as carvedilol, labetalol, and bucindolol, have additional alpha-1 receptor blockage activity in addition to their non-selective beta receptor blockage. This property is clinically useful because beta blockers that also block the alpha-1 receptor have a greater clinical effect on treating hypertension.[6]


Beta blockers are available in oral, intravenous, or ophthalmic form and can be injected intramuscularly.

Dosages are available in various ranges, depending on the specific medication.

Adverse Effects

Beta receptors are found all over the body and induce a broad range of physiologic effects. Blockage of these receptors with beta-blocker medications can lead to many adverse effects. Bradycardia and hypotension are two adverse effects that may be commonly seen. Fatigue, dizziness, nausea, and constipation are also commonly reported. Some patients report sexual dysfunction and erectile dysfunction.

Less commonly, bronchospasm is seen in patients on beta blockers. Asthmatic patients are at a higher risk.[7] Patients with Raynaud syndrome are also at risk of exacerbation. Beta blockers can induce both hypoglycemia and mask the hemodynamic signs usually seen in a hypoglycemic patient, such as tachycardia.

Some patients report insomnia, sleep changes and nightmares while using beta blockers. This effect is more pronounced with beta blockers that can cross the blood-brain barrier.

Carvedilol may increase edema in some patients.[8]

Sotalol blocks the potassium channels in the heart and thereby induces QT prolongation. It increases the risk of torsades de pointes.[9]

All beta blockers, especially in patients with cardiac risk factors, carry a risk of heart block.


Traditionally, beta blockers have been considered to be contraindicated in asthmatic patients. However, recommendations have aligned for allowing cardio-selective beta blockers, also known as B1 selective, in asthmatics but not non-selective beta blockers.

Beta blockers should not be used in patients who have cocaine-induced coronary vasospasm. There is a significant risk of unopposed alpha receptor activity which would worsen the vasospasm. Agonist activity at the alpha receptor leads to increased vasoconstriction and increased cardiac chronotropy.[10]

Patients who have either acute or chronic bradycardia and/or hypotension are relatively contraindicated when it comes to beta-blocker usage.

Specific beta blockers are contraindicated depending on the patient's past medical history. Patients diagnosed with long QT syndrome or who have had torsades de pointes in the past should not use the drug sotalol. Patients with Raynaud phenomenon should avoid beta blockers due to the risk of exacerbation.[11][9]


Heart rate and blood pressure should be monitored while using beta blockers. Some patients should also be monitored for electrocardiogram (ECG) changes.


The antidote for beta-blocker overdose is glucagon. It is especially useful in beta-blocker-induced cardiotoxicity. The second line of treatment is cardiac pacing if glucagon fails.