Understanding How an Antiarrhythmic Drug Helps Control Irregular Heartbeats
Introduction
Cardiac arrhythmias are common medical conditions that nurses encounter in emergency, ICU and cardiac units. Understanding antiarrhythmic drugs is important not only for exam but also to improve patient care and clinical decision making.
In this blog we will explain arrhythmas, anti-arrhythmic drugs, their mechanism and classification with example
Definition of Arrhythmia
Arrhythmia is a condition in which the electrical activity of the heart and the rhythm of the heartbeat become abnormal. This means the heart will beat either too fast, too slow, or irregularly.
Definition of Anti-Arrhythmia / Antiarrhythmic-Drugs
An antiarrhythmic drug is a medication used to prevent, treat, or control abnormal heart rhythms (arrhythmias) by changing the electrical activity of the heart.
Mechanism of Arrhythmia (How does arrhythmia occur?)
Anti arrhythmic drugs work by controlling the electrical activity of the heart. Arrhythmias happen when electrical impulses move too fast, too slow, or irregularly. These drugs help restore normal rhythm by affecting ion channels, refractory period, and conduction speed.
The heart’s electrical cycle (action potential) has 5 phases:
- Phase 0 – Rapid depolarization (Na⁺ influx)
- Phase 1 – Early repolarization
- Phase 2 – Plateau (Ca²⁺ influx)
- Phase 3 – Repolarization (K⁺ efflux)
- Phase 4 – Resting phase
1.Class I – Sodium Channel Blockers (Phase 0 Action)
Mechanism:
These drugs block fast Na⁺ channels, slow depolarization, and decrease conduction velocity.
They reduce the excitability of cardiac cells.
Subtypes:
Class IA – Moderate Na⁺ block
Prolong action potential
Examples: Quinidine, Procainamide, Disopyramide
Class IB – Weak Na⁺ block
Shorten action potential
Examples: Lidocaine, Mexiletine
Class IC – Strong Na⁺ block
Markedly slow conduction
Examples: Flecainide, Propafenone
2.Class II – Beta Blockers (Phase 4 Action)
Mechanism:
They block beta-adrenergic receptors → slow SA and AV node conduction.
They decrease heart rate and reduce automaticity.
Examples: Metoprolol, Propranolol, Atenolol
Used for: SVT, AF rate control, palpitations
3.Class III – Potassium Channel Blockers (Phase 3 Action)
Mechanism:
Block K⁺ channels, prolong repolarization and action potential duration.
Increase refractory period → prevents re-entry arrhythmia.
Examples: Amiodarone, Sotalol, Dofetilide
Used for: Atrial fibrillation, ventricular tachycardia
4.Class IV – Calcium Channel Blockers (Phase 2 & AV Node)
Mechanism:
Block L-type Ca²⁺ channels → slow AV node conduction.
Reduce contractility and heart rate.
Examples: Verapamil, Diltiazem
Used for: SVT, atrial flutter, AF rate control
5.Class V – Miscellaneous Mechanisms
These drugs work through unique mechanisms.
Adenosine
- Slows AV node conduction
- “Resets” the heart in SVT
Digoxin
- Increases vagal tone
- Slows AV node rate (useful in AF)
Magnesium sulfate
- Stabilizes heart cell membranes
- Used in torsades de pointes
