- Clinical science
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|
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.
|Types of β receptors||Main site of action||Effects of β adrenergic stimulation||Effects of β adrenergic blockade|
|β3|| || |
Beta blockers competitively inhibit adrenergic substances (such as adrenaline, noradrenaline) at β receptors!
General side effects
|Inhibited receptor||Affected system||Adverse effects|
|Both β1 and β2||Cardiac|
|Peripheral vasculature|| |
Beta blocker withdrawal
- Caused by sudden termination of β blockers
- Clinical features: : tachycardia, tachyarrhythmia, hypertension, acute coronary syndrome, sudden cardiac death
- Prevention: : taper dose over 7–10 days before discontinuing
- Clinical features: : bradycardia/bradyarrhythmia, cardiogenic shock (hypotension; cold, clammy extremities), hypoglycemia, hyperkalemia, wheezing (bronchoconstriction), neurological symptoms (seizure, delirium, coma)
- Secure airway
- Correct hypotension: IV fluids and vasopressors (epinephrine)
- Correct bradycardia: IV atropine
- Treat cardiogenic shock: IV glucagon ; IV calcium salts (improves cardiac contractility)
- Correct hypoglycemia: IV high-dose insulin with glucose
- Prevent further absorption of β blocker: activated charcoal/gastric lavage ; IV lipid emulsions (esp. useful in lipophilic β blocker overdose)
We list the most important adverse effects. The selection is not exhaustive.
- Acute myocardial infarction: β blockers should be initiated early in all patients (without contraindications) and continued long-term if tolerated.
- : first-line treatment for stable angina pectoris in addition to ACE inhibitors or angiotensin-receptor blockers
- : as an adjunct with ACE-I/ARB and spironolactone (cardioselective β blockers are preferred)
- : all patients with atrial flutter/fibrillation, PSVT, VT, and premature ventricular contractions
Specific indications for propranolol
- Hypertensive crises; (e.g., malignant hypertension; ): IV labetalol (rapid onset of action)
- : topical β blockers (timolol, betaxolol)
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.