Beta-blockers, as a class of drugs, are primarily used to treat cardiovascular diseases and other conditions.[1]

Beta receptors exist in three distinct forms: beta-1 (B1), beta-2 (B2), and beta-3 (B3). Beta-1 receptors located primarily in the heart mediate cardiac activity. Beta-2 receptors with their diverse location in many organ systems 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 at present. Blockade of these receptors by beta-blocking medicines are used to treat a broad range of illnesses.[1] Beta-blockers, as a class of medications, are essential drugs and are first-line treatments in many acute and chronic conditions.

Beta-blockers are indicated and have FDA approval for the treatment of tachycardia, hypertension, myocardial infarction, congestive heart failure, cardiac arrhythmias, coronary artery disease, hyperthyroidism, essential tremor, aortic dissection, portal hypertension, glaucoma, migraine prophylaxis, and other conditions. They are also used to treat less common conditions such as long QT syndrome and hypertrophic obstructive cardiomyopathy. Beta-blockers are available for administration in three main forms: oral, intravenous, and ophthalmic, and the route of administration often depends on the acuity of the illness (parenteral use in arrhythmias), disease type (topical use in glaucoma) and chronicity of the disease. 

Congestive heart failure patients are treated with beta-blockers if they are in a compensated state. Specifically, the beta-blockers bisoprolol, carvedilol, and metoprolol succinate are the agents chosen.

Athletes and musicians may use beta-blockers for their anxiolytic effect as well as their inhibitory 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 may lead to improved stage performance.  

The catecholamines, 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. In contrast, binding to B2 receptors causes relaxation of the smooth muscles along with increased metabolic effects such as glycogenolysis.

Beta-blockers vary in their specificity towards different receptors, and accordingly, the effects produced depend on the type of receptor(s) blocked as well as the organ system involved. Some beta-blockers also bind to alpha receptors to some degree, allowing them to induce a different clinical outcome when used in specific settings.

Once beta-blockers bind to the B1 and B2 receptors, they inhibit these effects. Therefore, the chronotropic and inotropic effects on the heart undergo inhibition, and the heart rate slows down as a result. Beta-blockers also decrease blood pressure via several 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 classify as either non-selective and beta-1 selective. There are also beta-2, and beta-3 selective drugs; neither has a known clinical purpose to date. Non-selective agents bind to both beta-1 and beta-2 receptors and induce antagonizing effects via both receptors. Examples include propranolol, carvedilol, sotalol, and labetalol. Beta-1 receptor-selective blockers like atenolol, bisoprolol, metoprolol, and esmolol only bind to the beta-1 receptors; therefore, they are cardio-selective.[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 higher blood pressure and an increased heart rate. In contrast, antagonism at the alpha-1 receptor leads to vasodilation and negative chronotropic, which leads to lower blood pressure and decreases 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 more pronounced clinical effect on treating hypertension.[6]

Beta-blockers are available in oral, intravenous, or ophthalmic forms and are also injectable intramuscularly.

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

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

Less commonly, bronchospasm presents 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 hyperglycemia 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 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 contraindicated in asthmatic patients. However, recommendations have aligned for allowing cardio-selective beta-blockers, also known as beta-1 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 have relatively contraindication 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]