Anti-arrhythmic Drugs Overview

Anti-arrhythmic Drugs Overview

• Anti-arrhythmic drugs are classified into various classes based on their mechanisms and effects on cardiac physiology.

Class IB Sodium Channel Blockers

• Examples: Lidocaine, Flecainide, Propafenone
• Mechanism of Action:
  • Selectively inhibit Na+ channels with a low effect.
  • Do not change the QRS complex; shortens both repolarization and QT interval.
  • Act primarily in phase 0, suppressing depolarization.
  • Negative dromotropic effect causing slowed or blocked AV conduction, prolonging the PQ interval.
• Pharmacokinetics:
  • Administered parenterally.
  • Undergo high first-pass metabolism.
• Clinical Effects:
  • Effective for treating ventricular arrhythmias.
  • Suitable for patients with myocardial infarction (MI) and severe heart failure (HF).
  • Local anesthetic properties.
• Side Effects:
  • Risk of hypersensitivity reactions such as rash, fever, and angioedema.
  • Drug-drug interactions can increase digoxin toxicity.
  • Central nervous system effects like tinnitus, seizures, and drowsiness.
  • Amiodarone toxicity includes pulmonary fibrosis, thyroid abnormalities, and skin discoloration.

Class II B-Adrenoceptor Blockers

• Examples: Propranolol, Metoprolol
• Mechanism of Action:
  • Block K+ outflow during phase 3, resulting in prolonged repolarization and a longer QT interval.
  • Extend action potential duration.
• Pharmacokinetics:
  • Administered intravenously (IV) with high oral first-pass metabolism.
  • Metabolized by cytochrome P450 enzymes.

Class III K+ Channel Blockers

• Examples: Ibutilide
• Mechanism of Action:
  • Primarily functions as a potassium channel blocker, affecting cardiac repolarization, though specifics were not outlined in the provided details.