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Antiarrhythmic drugs

Last updated: March 4, 2021

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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 [1][2]
Class Drug group Mechanism of action Examples Use Adverse effects

Class IA antiarrhythmics

  • Reduce or even block conduction (negative dromotropy), particularly in depolarized tissue (e.g., during tachycardia)
  • State-dependent: the faster the heart rate (e.g., tachycardia), the greater the effect
    • Shorter diastole
    • Sodium channels spend less time in resting state
  • Decreases the slope of phase 0 depolarization
  • Stabilize membrane
  • Categorized into 3 subgroups based upon their effects on the Na+ channel and the action potential (AP) duration
  • Moderate blockage of Na+ channels (intermediate association/dissociation)
  • Prolong action potential (AP) duration (right shift)
  • Slow conduction velocity
  • Prolong effective refractory period (ERP) in ventricular APs
  • Weak blockade of the K+ channel
  • Quinidine
  • Procainamide
  • Disopyramide
  • Ajmaline
Class IB antiarrhythmics
  • Weak blockade of Na+ channels (fast association/dissociation)
  • Shorten AP duration
  • Slow conduction velocity
  • No effect on or slight prolongation of ERP
  • Strongest effect on ischemic or depolarized cardiac Purkinje cells and ventricular myocardium
Class IC antiarrhythmics
  • Flecainide
  • Propafenone
Class II antiarrhythmic drugs
Class III antiarrhythmic drugs
  • Inhibit delayed rectifier potassium currents
  • Prolong QT interval
  • Prolong AP duration (reverse use dependence) and ERP
  • No effect on conduction velocity
Class IV antiarrhythmic drugs
  • Inhibit slow calcium channels
  • Decrease slope of phase 0 and 4 slower conduction velocity → increased ERP
  • Prolong AV node repolarization
  • Prolong PR interval
Class V antiarrhythmic drugs
  • Variable mechanisms
  • Inhibits Na+/K+-ATPases → higher intracellular Na+ concentration → reduced efficacy of Na+/Ca2+ exchangers higher intracellular Ca2+ concentration → increased contractility and decreased heart rate
  • Nausea, vomiting
  • Abdominal pain
  • Blurry vision with a yellow tint and halos

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.

References:[6][7][8]

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

Magnesium sulfate [1][13]

Ivabradine [14]

IVabradine slows depolarization in phase IV.

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  2. Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary. Circulation. 2003; 108 (15): p.1871-1909. doi: 10.1161/01.CIR.0000091380.04100.84 . | Open in Read by QxMD
  3. Zehra Pinar K, Necati D, Tansel Ansal B, Ilgin K, Ferat K, Tolga C. Adenosine Stress Myocardial Perfusion Scintigraphy and Echocardiography Application with Same Infusion. International Journal of Clinical Cardiology. 2017; 4 (4). doi: 10.23937/2378-2951/1410106 . | Open in Read by QxMD
  4. McDowell M, Mokszycki R, Greenberg A, Hormese M, Lomotan N, Lyons N. Single‐syringe Administration of Diluted Adenosine. Academic Emergency Medicine. 2019; 27 (1): p.61-63. doi: 10.1111/acem.13879 . | Open in Read by QxMD
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  14. UpToDate. Quinidine: Drug information. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/quinidine-drug-information.Last updated: January 1, 2017. Accessed: October 10, 2017.
  15. Le T, Bhushan V. First Aid for the USMLE Step 1 2015. McGraw-Hill Education ; 2014