- Clinical science
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 learning cards.
|Classes of antiarrhythmic drugs |
|Class||Drug group||Mechanism of action||Examples||Use||Adverse effects|
|Class IA antiarrhythmics|| || |
|Class IB antiarrhythmics|
|Class IC antiarrhythmics|| || |
|Class II antiarrhythmic drugs|| || || |
|Class III antiarrhythmic drugs|| |
|Class IV antiarrhythmic drugs|| |
|Class V antiarrhythmic drugs|| || || || |
All antiarrhythmic drugs are also potentially proarrhythmic! Intravenous administration should only be performed with continuous cardiac monitoring!
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+ entry → hyperpolarization → transient AV node block → acute termination of supraventricular tachycardia
- Adverse effects
Avoid adenosine in patients with suspected pre-excitation tachycardia (e.g., WPW), because it may exacerbate the tachycardia via accessory pathway routes!
- 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
- See .
Magnesium sulfate 
- Mechanism of action: decreases calcium influx → prevents early afterdepolarizations (EAPs)
- Refractory ventricular tachyarrhythmias (e.g., polymorphic VT)
- Loss of reflexes
- Respiratory depression
- Drug: ivabradine
- 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
- Vision changes