Anti-Arrhythmic Drugs

Anti-arrhythmic drugs correct irregular heartbeats by altering cardiac impulses to restore normal rhythm and heart function.

  • Anti-arrhythmic drugs are medications used to treat and prevent abnormal heart rhythms (arrhythmias).
  • These drugs work by modifying the electrical activity of the heart to restore and maintain a normal heart rhythm, thereby ensuring efficient blood circulation throughout the body.
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Pathophysiology of Arrhythmias

  • Arrhythmias occur due to disturbances in the normal electrical conduction system of the heart. These disturbances can result from:
  • Enhanced Automaticity: Increased spontaneous depolarization of cardiac cells.
  • Triggered Activity: Abnormal depolarizations during or after repolarization.
  • Reentrant Circuits: Circular electrical pathways that perpetuate abnormal rhythms.
  • Anti-arrhythmic drugs aim to correct these disturbances by targeting various aspects of cardiac electrophysiology.

Classification of Anti-Arrhythmic Drugs

  • Anti-arrhythmic drugs are primarily classified according to the Vaughan Williams Classification, which categorizes these medications based on their primary mechanism of action on cardiac cells.
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Classification of Anti-Arrhythmic Drugs

  1. Class I: Sodium Channel Blockers

      • These drugs inhibit sodium (Na⁺) channels, reducing the rate of rise of the action potential (phase 0) in cardiac cells. They are further subdivided into:
    • Class IA
      • Mechanism: Moderate blockade of Na⁺ channels; also block potassium (K⁺) channels, prolonging action potential duration and refractory period.
      • Drugs:
      • Uses: Atrial and ventricular arrhythmias.
      • Side Effects: Prolonged QT interval, torsades de pointes, hypotension.
    • Class IB
    • Class IC
      • Mechanism: Potent blockade of Na⁺ channels with minimal effect on action potential duration.
      • Drugs:
      • Uses: Atrial and ventricular arrhythmias.
      • Side Effects: Bradycardia, hypotension, proarrhythmic effects.
  2. Class II: Beta Blockers

      • These drugs block beta-adrenergic receptors, decreasing the effects of sympathetic stimulation on the heart.
      • Mechanism: Reduce heart rate, myocardial contractility, and conduction velocity through the atrioventricular (AV) node.
      • Drugs:
      • Uses: Atrial fibrillation, ventricular arrhythmias, prevention of arrhythmic recurrence.
      • Side Effects: Bradycardia, hypotension, fatigue, bronchoconstriction.
  3. Class III: Potassium Channel Blockers

    • These drugs primarily block K⁺ channels, leading to prolonged repolarization and extended action potential duration.
    • Mechanism: Prolong the QT interval and the refractory period without affecting Na⁺ or Ca²⁺ channels significantly.
    • Drugs:
    • Uses: Atrial fibrillation, ventricular tachycardia, ventricular fibrillation.
    • Side Effects: Pulmonary fibrosis, thyroid dysfunction, liver toxicity, corneal deposits.
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Class Mechanism Drugs Uses Side Effects
Class I: Sodium Channel Blockers (IA) Moderate Na⁺ & K⁺ blockade; prolongs action potential and refractory period Quinidine, Procainamide, Disopyramide Atrial and ventricular arrhythmias Prolonged QT interval, torsades de pointes, hypotension
Class I: Sodium Channel Blockers (IB) Mild Na⁺ blockade; shortens action potential duration and refractory period Lidocaine, Phenytoin, Tocainide Ventricular arrhythmias, especially post-MI CNS toxicity (seizures, tremors), numbness
Class I: Sodium Channel Blockers (IC) Potent Na⁺ blockade; minimal effect on action potential duration Mexiletine, Lorcainide Atrial and ventricular arrhythmias Bradycardia, hypotension, proarrhythmic effects
Class II: Beta Blockers Beta-adrenergic receptor blockade; reduces heart rate and AV node conduction Sotalol Atrial fibrillation, ventricular arrhythmias Bradycardia, hypotension, fatigue, bronchoconstriction
Class III: Potassium Channel Blockers K⁺ channel blockade; prolongs QT interval and refractory period Amiodarone Atrial fibrillation, ventricular tachycardia, ventricular fibrillation Pulmonary fibrosis, thyroid dysfunction, liver toxicity, corneal deposits

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