• Clinical science

Antiarrhythmic drugs

Summary

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.

Overview

Classes of antiarrhythmic drugs [1][2]
Class Drug group Mechanism of action Examples Use Adverse effects
Class IA antiarrhythmics
  • Fast sodium channel blockers
  • Reduce conduction velocity (negative dromotropy), particularly in depolarized tissue (e.g., during tachycardia)
  • Stabilize membrane
  • Categorized into 3 subgroups based upon their effects on the Na+ channel and the action potential (AP) duration
  • Moderate blockade of Na+ channels (intermediate association/dissociation)
  • Prolong AP duration (right shift)
  • Slow conduction velocity
  • Prolong effective refractory period (ERP)
  • Weak blockade of the K+ channel
Class IB antiarrhythmics
  • Weak blockade of Na+ channels (fast association/dissociation)
  • Shorten AP duration (left shift)
  • Slow conduction velocity
  • No effect on or slight prolongation of ERP
  • Strongest effect on ischemic myocardium
  • CNS: dizziness, nausea, seizures
  • Cardiovascular: AV conduction block, ventricular extrasystoles
Class IC antiarrhythmics
  • Strong blockade of Na+ channels (slow association/dissociation) → QRS prolongation
  • No to minimal effect on AP duration (no shift)
  • Slow conduction velocity
  • Prolong ERP in AV node and accessory tract
  • ERP unaffected in Purkinje and ventricular tissue
  • Proarrhythmogenic: contraindicated post-MI
Class II antiarrhythmic drugs
Class III antiarrhythmic drugs
  • Potassium channel blockers
Class IV antiarrhythmic drugs
  • Inhibit slow calcium channels
  • Decrease slope of phase 0 and 4slower conduction velocity → increased ERP
  • Prolong AV node repolarization
  • Prolong PR interval
Class V antiarrhythmic drugs
  • Variable mechanisms
  • See “Other antiarrhythmic drugs” below for details.
  • See below
  • See below

All antiarrhythmic drugs are also potentially proarrhythmic! Intravenous administration should only be performed with continuous cardiac monitoring!

References:[4][5][6][7][8]

Other antiarrhythmic drugs

Adenosine (drug) [1]

Avoid adenosine in patients with suspected pre-excitation tachycardia (e.g., WPW), because it may exacerbate the tachycardia via accessory pathway routes!

Digoxin

  • 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
  • Indications
  • See cardiac glycosides.

Magnesium sulfate [9][1]

If-channel blocker

References:[10][11][12][13][14][15][16][17][9]