Beta-adrenergic Blocking Agents (FETT)

BISOPROLOL

• Cardioselective beta blockers (β1 selective)

• Without instrinsic sympathomimetic activity (ISA)

• Selectively bind to and block β1 receptors, which are primarily found in the heart

• Decrease the heart rate, contractility, and AVN conductivity

• Nebivolol is the only beta blocker that causes NO-mediated vasodilation: it decreases vascular resistance by stimulating β3receptors and activating NO synthase in the vasculature

• Coronary heart disease

• Compensated heart failure

• Cardiac arrhythmias (e.g., atrial fibrillation, atrial flutter, PSVT)

• Bradycardia

• Bradyarrhythmia

• Cardioselectivity is dose-dependent: β2 receptor blocking activity increases with higher doses . [3]

• Generally do not cause bronchoconstriction or vasoconstriction

• Generally do not interfere with glycogenolysis; safe in diabetic patients

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

• 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) 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: activated charcoal/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

• Clinical features

  • Tachycardia, tachyarrhythmia

  • Hypertension

  • Acute coronary syndrome, sudden cardiac death

• Prevention: Taper dose over 7–10 days before discontinuing.

• Hypertension : beta blockers lower BP by ↓ cardiac output and ↓ renin secretion [30][31]

• Coronary artery disease

  • Acute myocardial infarction

    • Beta blockers should be initiated early in all patients (without contraindications) and continued long-term if tolerated.

    • Beta blockers decrease the size of the infarct and also reduce early and delayed mortality rates in patients with acute MI.

  • Angina pectoris: first-line treatment for stable angina pectoris in addition to ACE inhibitors or ARBs

• Heart failure: 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 class II antiarrhythmic agents; e.g., metoprolol, esmolol, propranolol)

Atenolol

Propranolol

Also b1 selective blocker without ISA.

Nonselective beta blocker (b1, b2) without ISA.

• Block β1, β2, and β3receptors

• Sotalol also blocks cardiac potassium channels (antiarrhythmic effect).

• Bronchoconstriction: may exacerbate asthma/COPD

• Vasoconstriction: avoid in patients with peripheral vascular disease

• Hypoglycemia and hyperglycemia

• Bradycardia and syncope

• Alternative to cardioselective beta blockers

• Propranolol

  • Essential tremor

  • Portal hypertension

  • Migraine prophylaxis

  • Thyroid storm

• Sotalol: cardiac arrhythmias

• Timolol: glaucoma

• Essential tremor

• Migraine prophylaxis

• Portal hypertension

• Hyperthyroidism and thyroid storm

• Infantile hemangioma

• Akathisia

• Hypertensive crises (e.g., malignant hypertension): IV labetalol (rapid onset of action)

• Glaucoma: topical beta blockers (timolol, betaxolol)

• Pregnancy-induced hypertension: Labetalol is the first-line drug.