Class 3 Antiarrhythmics - Sotalol
- Adenosine
- Class 3 Antiarrhythmics - Dofetilide & Ibutilide
- Class 1A Antiarrhythmics
- Class 1B Antiarrhythmics
- Class 1C Antiarrhythmics
- Class 2 Antiarrhythmics
- Sotalol
- Class 3 Antiarrhythmics - Amiodarone
- Class 4 Antiarrhythmics
- Digoxin
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)
- Used for rhythm control
- Treats Atrial Flutter
- Treats Ventricular tachycardia
- Treats A-Fib (atrial fibrillation)
- 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
- Primarily acts at non-nodal tissue
- 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
- Beta-blocker
- Class 3 Mechanisms
- 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
- Causes Long QT (Torsades de Pointes risk)
- Drug Class