Class 1C Antiarrhythmics
- 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
Class 1C Antiarrhythmics
Subscribe to watch this premium Class 1C Antiarrhythmics mnemonic in the Antiarrhythmic Drugs (New) playlist.
Subscribe to watch this premium mnemonic
Summary
Class 1C antiarrhythmics include the drugs propafenone and flecainide.
Clinically, these drugs are antiarrhythmics that are used to treat SVT and are used for rhythm control in the treatment of A-Fib. They may also be used as last resort agents for the treatment of VTach.
The Class 1C drugs work by acting primarily on non-nodal tissue to strongly block sodium channels. This leads to a strong decrease in the slope of the phase 0 upstroke, which slows conduction in many different cells of the heart. The Class 1C drugs can increase the length of the ERP in the accessory bypass tracts and AV node, but leave the ERP unchanged in the Purkinje fibers and ventricles. Notably, the AP duration is usually unchanged in the ventricles.
The most important side effect of these drugs is their ability to cause arrhythmias. The risk of provoking arrhythmias is increased in patients with abnormal heart tissue, which is why these drugs are contraindicated in patients with MI, and in patients with structural heart defects.
Key Points
- Class 1C Antiarrhythmics
- Drugs
- Flecainide
- Propafenone
- Encainide
- Mechanism
- Strong Sodium (Na+) Channel blockade
- Strongest binding strength (slowest dissociation) among Class 1 AAs; Binding affinity for Na+ receptor is 1C > 1A > 1B
- Leads to strong use dependence
- Primarily acts in non-nodal heart tissue
- Phase 0 upstroke is mediated by calcium in nodal tissue, which is less affected by sodium channel blockade
- Strongly prolongs phase 0 depolarization
- Little to no effect on ERP
- in Purkinje fibers
- in Ventricles
- Unchanged AP duration in Ventricles
- Little effect on QT interval (low risk of Torsades de Pointes)
- Prolongs the ERP
- in AV node
- in accessory bypass tracts (e.g. bundle of Kent)
- Strong Sodium (Na+) Channel blockade
- Clinical Use
- Treats SVT (Supraventricular Tachycardia)
- Treats A-Fib (Atrial Fibrillation)
- Used for rhythm control in atrial fibrillation
- May be used for pharmacologic cardioversion or maintenance of normal heart rhythm after electrical cardioversion
- Used for rhythm control in atrial fibrillation
- Treats A-Fib (Atrial Fibrillation)
- Treats VTach (Ventricular Tachycardia)
- Used as a last resort
- e.g. for cases that do not respond to other treatments
- Used as a last resort
- Treats SVT (Supraventricular Tachycardia)
- Side Effects
- Causes Arrhythmias (Proarrhythmic)
- Contraindicated in ischemic heart disease
- especially after myocardial infarction
- Contraindicated in structural heart disease
- Contraindicated in ischemic heart disease
- Causes Arrhythmias (Proarrhythmic)
- Drugs