• Clinical science

Beta blockers (Beta antagonists)


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 and cardiac contractility, slower AVN conduction, and decreased cardiac workload. Nonselective β blockers (e.g., pindolol, propranolol) inhibit all β receptors and may cause bronchoconstriction, peripheral vasoconstriction, and metabolic imbalances (e.g., hypo- and hyperglycemia, hypertriglyceridemia) in addition to cardiac effects. Cardioselective β blockers have a lower side effect profile and are preferred in the management of coronary heart disease, compensated heart failure, acute coronary syndrome, and in certain types of arrhythmias. Propranolol, a nonselective β 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 β blocker therapy should always be gradual to avoid side effects or symptoms of withdrawal (rebound tachycardia, hypertension, acute cardiac death).


Nonselective beta blockers Cardioselective beta blockers (β1 selective) Nonselective beta blockers with additional α blocking action
With ISA (intrinsic sympathomimetic activity) Without ISA With ISA Without ISA
  • Acebutolol
  • Celiprolol
Specific effects
  • Selectively bind to and block β1 receptors, which are primarily found in the heart
  • Do not cause bronchoconstriction or vasoconstriction
  • Do not interfere with glycogenolysis; safe in diabetics
  • Cardioselectivity is dose-dependent

All cardioselective beta blockers begin with the letters A to M (B1 = first half of the alphabet). All non-cardioselective beta blockers with the exception of carvedilol begin with the letters N to Z.



Beta blockers competitively bind to and block β-adrenergic receptors, thereby inhibiting sympathetic (adrenergic and/or noradrenergic) stimulation of β receptors.

Types of β receptors Main site of action Effects of β adrenergic stimulation Effects of β adrenergic blockade
  • Heart
    • Anti-ischemic effect
      • β1 blockadeheart rate and ↓ cardiac contractility↓ BP and ↓ oxygen consumption by the heartanti-ischemic effect
    • Antiarrhythmic effect
      • β1 blockade ↓ AVN conduction, ↑ AVN refractory time, and heart rate → anti-arrhythmic effect
    • Anti-remodeling effect
  • Kidneys: renin releaseangiotensin II conversion → ↓ H2O resorption↓ BP
  • Lipolysis with weight gain

Beta blockers competitively inhibit adrenergic substances (such as adrenaline, noradrenaline) at β receptors!

Side effects

General side effects

Inhibited receptor Affected system Adverse effects
Both β1 and β2 Cardiac


  • Drowsiness, sleep disorders, nightmares
  • Fatigue/lethargy
  • Depression, hallucinations
Cholesterol levels
β2 Pulmonary
  • Bronchoconstriction (esp. patients with asthma and reactive airway disease)
Peripheral vasculature

Beta blocker withdrawal

Beta blocker overdose


We list the most important adverse effects. The selection is not exhaustive.


Cardiovascular indications

Specific indications for propranolol


Beta blockers should be introduced gradually with slow increases in dosage, and slowly tapered off and stopped when their use is no longer needed!


Absolute contraindications Relative contraindications


We list the most important contraindications. The selection is not exhaustive.

last updated 10/18/2019
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