Antiarrhythmic drugs are used to prevent recurrent arrhythmias and restore sinus rhythm in patients with cardiac arrhythmias. These drugs are classified based on their electrophysiological effect on the myocardium. Antiarrhythmic drugs do not improve the survival of patients with non-life-threatening arrhythmias and may increase mortality, particularly in patients with structural heart disease. They are associated with severe adverse effects, primarily due to their proarrhythmic effects on the myocardium. Patients who have received an intravenous antiarrhythmic should be monitored closely with serial ECGs. Several classes of antiarrhythmics, including beta blockers, calcium channel blockers, amiodarone, cardiac glycosides, and lidocaine, also have other medical uses, which are discussed in their respective articles.
|Classes of antiarrhythmic drugs |
|Class||Drug group||Mechanism of action||Examples||Use||Adverse effects|
Class IA antiarrhythmics
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|Class IB antiarrhythmics|| |
|Class IC antiarrhythmics|| |
|Class II antiarrhythmic drugs|| || || || |
|Class III antiarrhythmic drugs|| || |
|Class IV antiarrhythmic drugs|| |
|Class V antiarrhythmic drugs|| || |
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All antiarrhythmic drugs are also potentially proarrhythmic! Intravenous administration should only be performed with continuous cardiac monitoring!
“I am Ambivalent about the QUEEn PROofreading my DISsertation”: Class IA antiarrhythmic drugs are QUEEnidine, PROcainamide, DISopyramide.
“LInDO MEXIco Is the Best”: LIDOcaine and MEXIletine are class IB antiarrhythmic drugs.
“I Can't Fail, Please”: Class IC antiarrhythmics are Flecainide, Propafenone.
“I Am Sober, Doctor, for III days”: Ibutilide, Amiodarone, Sotalol, and Dofetilide are class III antiarrhythmic drugs.
Diltiazem and Verapamil Diminish conduction Velocity.
Class IB antiarrhythmic drugs work Best after myocardial infarction; class IC antiarrhythmic drugs are Contraindicated.
Adenosine (drug) 
- Mechanism of action: activates Gi protein → inhibition of adenylate cyclase → ↓ cAMP → deactivation of L-type Ca2+ channels and activation of K+ channels → ↓ Ca2+ and ↑ K+ efflux → hyperpolarization → transient (short-acting, ∼ 15 seconds) → acute termination of supraventricular tachycardia
- Rapid bolus IV (very short half-life: < 10 seconds) 
- May be administered repeatedly if the previous dose was unsuccessful
- Adverse effects 
- Interactions: Theophylline and caffeine weaken the effects of adenosine because they are adenosine receptor antagonists.
- Mechanism of action: inhibits Na+/K+-ATPases → higher intracellular Na+ concentration → reduced efficacy of Na+/Ca2+ exchangers → higher intracellular Ca2+ concentration → increased contractility, decreased heart rate
- Adverse effects: See “”.
Magnesium sulfate 
- Mechanism of action: decreases calcium influx → prevents early afterdepolarizations (EADs)
- Adverse effects
- Mechanism of action: selectively inhibits If channel in the pacemaker cells of the SA node → prolongs slow depolarization (phase 4) → slows heart rate
- Indications: symptomatic stable coronary heart disease and congestive heart failure (NYHA II-IV) in patients who cannot tolerate beta blockers
- Adverse effects
IVabradine slows depolarization in phase IV.