Beta blockers are a group of drugs that inhibit the sympathetic activation of β-adrenergic receptors. Cardioselective blockers (e.g., atenolol, bisoprolol) primarily block β1 receptors in the heart, causing decreased heart rate, cardiac contractility, cardiac workload, and AVN conduction. Nonselective beta blockers (e.g., pindolol, propranolol) inhibit all β receptors and may cause bronchoconstriction, peripheral vasoconstriction, and metabolic imbalances (e.g., hypoglycemia and hyperglycemia, hypertriglyceridemia) in addition to cardiac effects. Cardioselective beta blockers have a lower side-effect profile and are preferred in the management of coronary heart disease, compensated heart failure, acute coronary syndrome, and certain types of arrhythmias. Propranolol, a nonselective beta blocker, is the first-line drug in the management of essential tremor, portal hypertension, migraine prophylaxis, and thyroid storm. Beta blockers are contraindicated in patients with symptomatic bradycardia, AV block, decompensated heart failure, and asthma. Initiation and cessation of beta-blocker therapy should always be gradual to avoid side effects or symptoms of withdrawal (e.g., rebound tachycardia, hypertension, acute cardiac death).
|Characteristics of beta blockers|
|Cardioselective beta blockers (β1 selective)||With intrinsic sympathomimetic activity (ISA)|| || |
|Without ISA|| |
|Nonselective beta blockers (β1, β2, and β3receptors)||With ISA|| |
|Without ISA|| |
|With additional α-blocking action|| |
With the exception of nebivolol, all cardioselective beta blockers begin with the letters A to M (B1 = first half of the alphabet). Except for beta blockers with alpha-blocking action (labetalol, bucindolol, carvedilol), all noncardioselective beta blockers begin with the letters N to Z (B2 = second half of the alphabet).
Beta blockers competitively bind to and block β-adrenergic receptors, thereby inhibiting sympathetic (adrenergic and/or noradrenergic) stimulation of β receptors. See “” for details regarding the effects of β-adrenergic stimulation.
|Overview of β-adrenergic blockade |
|Types of β receptors||Main site of action||Effects of|
Beta blockers competitively inhibit adrenergic substances (e.g., adrenaline, noradrenaline) at β receptors.
A rule to remember the main effector organs for β receptors: There is 1 heart (β1 blockers act on the heart) and 2 lungs (β2 blockers affect bronchial smooth muscles).
Intrinsic sympathomimetic activity (ISA) 
Mechanism of action: partial agonist activity
- Beta blockers with ISA bind to and stimulate the β-adrenergic receptor (agonistic effect) while competitively inhibiting the binding of epinephrine and norepinephrine to β-adrenergic receptors (antagonistic effect).
- Produce partial sympathetic activity while inhibiting the normal and activated sympathetic activity
- Cause less bradycardia and less peripheral vasoconstriction because of their mild agonistic action
- Have a favorable effect on lipid profile (esp. pindolol and acebutolol): preferred in patients with metabolic syndrome 
- Not recommended in patients with congestive heart failure, ischemic heart disease, and tachyarrhythmias 
- Agents: pindolol, acebutolol, carteolol, alprenolol 
|Pharmacokinetics of beta blockers|
|Lipophilic agents||Hydrophilic agents||Mixed|
|Beta blockers adverse effects|
|Type of beta blockers||Organ system||Effects|
Nonselective beta blockers and cardioselective beta blockers
Nonselective beta blockers
Beta blockers should be introduced gradually with slow increases in dosage and slowly tapered off when no longer needed.
A number of beta blockers (e.g., metoprolol, carvedilol) are metabolized by CYP2D6. Genetic polymorphisms of CYP2D6 (e.g., ultra-rapid metabolization, poor metabolization) can influence adverse effects and tolerated doses. 
- Clinical features 
- Secure the airways.
- Correct cardiovascular decompensation (hypotension, bradycardia, and cardiogenic shock) via IV access:
- Fluids (saline) and vasopressors (e.g., epinephrine)
- Atropine: to correct bradycardia
- Glucagon: antidote for beta-blocker poisoning
- Calcium salts: to improve cardiac contractility
- High-dose insulin with glucose: If cardiovascular decompensation is refractory to all of the above-mentioned agents, high-dose insulin is given for its positive inotropic effect.
- Prevent further absorption of beta blocker: /gastric lavage , IV lipid emulsions (esp. useful in lipophilic beta-blocker overdose).
- Poisoning with hydrophilic beta blockers (e.g., atenolol, nadolol) may require hemodialysis for removal of the drug from circulation. 
Caused by the sudden termination of beta blockers
- Clinical features
- Prevention: Taper dose over 7–10 days before discontinuing. 
We list the most important adverse effects. The selection is not exhaustive.
- : beta blockers lower BP by ↓ cardiac output and ↓ renin secretion 
Coronary artery disease
- Acute myocardial infarction 
- : first-line treatment for stable angina pectoris in addition to ACE inhibitors or ARBs 
- : cardioselective beta blockers (preferred) in combination with ACE inhibitors/ARBs and spironolactone (slows progression of CHF) 
- Arrhythmias: atrial flutter, atrial fibrillation, PSVT, VT, and premature ventricular contractions (beta-blockers are ; e.g., metoprolol, esmolol, propranolol) 
Specific indications for propranolol
- prophylaxis 
|Contraindications to beta blockers|
|Absolute contraindications||Relative contraindications|
We list the most important contraindications. The selection is not exhaustive.