Class 3 Antiarrhythmics - Sotalol

Summary

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