Medicine & USMLE

Class 3 Antiarrhythmics - Sotalol

Antiarrhythmic Drugs (New)
  1. Adenosine
  2. Class 3 Antiarrhythmics - Dofetilide & Ibutilide
  3. Class 1A Antiarrhythmics
  4. Class 1B Antiarrhythmics
  5. Class 1C Antiarrhythmics
  6. Class 2 Antiarrhythmics
  7. Sotalol
  8. Class 3 Antiarrhythmics - Amiodarone
  9. Class 4 Antiarrhythmics
  10. Digoxin


Sotalol is an antiarrhythmic drug that is unique for having both Class 2 and Class 3 antiarrhythmic properties. That said, the class 3 effects predominate at normal doses of the drug.

As a class 3 drug, sotalol acts primarily on non-nodal tissue to block potassium channels. This markedly prolongs the repolarization of heart cells, increases the length of the ERP, prolongs the AP duration, and increases the QT interval.

As a class 2 drug, sotalol is a beta blocker that slows pacemaking at the SA node and slows conduction at the AV node.

As an antiarrhythmic, sotalol is clinically used to treat Atrial Flutter as well as A-Fib, in which it is primarily used for rhythm control. Sotalol can also be used to treat ventricular arrhythmias.

Side effects of sotalol include excessive beta blockade and a risk of causing Torsades de Pointes.

Key Points

  • Sotalol
    • Drug Class
      • Class 2 Antiarrhythmic
      • Class 3 Antiarrhythmic
        • Class 3 effects predominate at normal therapeutic doses
    • Clinical Use
      • Treats A-Fib (atrial fibrillation)
        • Used for rhythm control
          • May be used for pharmacologic cardioversion (rare) as well as maintenance of normal sinus rhythm after electrical cardioversion (common)
        • While sotalol has some rate control effects, it is not administered for this purpose. Sotalol is rarely ever used in isolation for rate control (pure class 2 beta blockers like metoprolol are preferred)
      • Treats Atrial Flutter
      • Treats Ventricular tachycardia
    • Mechanism
      • Class 3 Mechanisms
        • Primarily acts at non-nodal tissue
          • As a beta blocker, sotalol has nodal effects, but it’s primary action is on non-nodal cardiomyocytes
        • Blocks Potassium (K+) channels
          • This is a class 3 antiarrhythmic effect
        • Markedly prolongs repolarization
        • Increases effective refractory period (ERP)
        • Increases AP duration
        • Prolongs QT interval
          • Creates risk for early after-depolarizations and Torsades de Pointes
      • Class 2 Mechanisms
        • Beta-blocker
          • Blocks beta-1 receptors
          • Reduces cAMP and calcium influx, primarily at nodal tissue
        • Slows SA node pacemaker function
        • Slows AV node conduction
    • Side Effects
      • Causes Long QT (Torsades de Pointes risk)
        • All drugs that increase QT interval increase the risk of early after-depolarizations causing ventricular arrhythmias like Torsades de Pointes
        • Avoid in patients with congenital or acquired long QT syndrome
      • Excessive beta-blockade