- 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, 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).
|Cardioselective beta blockers (β1 selective)||With ISA|
|Nonselective beta blockers (β1, β2, and β3 receptors)||With 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, 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.
Effects of β-adrenergic blockade
|Types of β receptors||Main site of action||Effects of β-adrenergic blockade|
|β2||Smooth muscle|| |
|Ciliary body of the eye|| |
|Pancreatic beta cells|
|Skeletal muscle|| |
|Lipoprotein lipase enzyme|
|β3||Adipose tissue|| |
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; there are 2 lungs - β2 blockers affect bronchial smooth muscles.
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
|Beta blocker adverse effects|
Nonselective beta blockers and cardioselective beta blockers
(β1-receptor and β2-receptor blockade)
Nonselective beta blockers
|Peripheral vasculature|| |
Beta blockers should be introduced gradually with slow increases in dosage and slowly tapered off when no longer needed.
- Caused by the sudden termination of beta blockers
- Clinical features: : tachycardia, tachyarrhythmia, hypertension, acute coronary syndrome,
- 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 the airways.
- Correct cardiovascular decompensation (hypotension, bradycardia, and cardiogenic shock).
- IV fluids and vasopressors (e.g., epinephrine)
- IV atropine: to correct bradycardia
- IV glucagon: antidote for beta-blocker poisoning
- IV calcium salts: to improve cardiac contractility
- IV 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).
We list the most important adverse effects. The selection is not exhaustive.
- (β 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 angiotensin-receptor blockers 
- : cardioselective β blockers (preferred) in combination with ACE-I/ARB and spironolactone (slows progression of CHF) 
- Atrial flutter/fibrillation, PSVT, VT, and premature ventricular contractions: β-blockers are class II (e.g., metoprolol, esmolol, propranolol).
Specific indications for propranolol
- prophylaxis 
- Hypertensive crises (e.g., malignant hypertension): IV labetalol (rapid onset of action)
- : topical β blockers (timolol, betaxolol)
- Pregnancy-induced hypertension: Labetalol is a first-line drug.
|Absolute contraindications||Relative contraindications|
We list the most important contraindications. The selection is not exhaustive.