- Clinical science
Antiarrhythmic drugs are classified into 5 classes based on their electrophysiological effect on the myocardium. The original classification system, which was developed by Vaughn Williams in 1970, consisted of four classes. The fifth class was added to accommodate new antiarrhythmic drugs developed since 1970. Antiarrhythmic drugs are used to prevent recurrent arrhythmias and restore sinus rhythm in patients presenting with cardiac arrhythmias. 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 the proarrhythmic effect they exert on the myocardium. Intravenous administration should, therefore, be monitored with ECG. Several drugs classed as antiarrhythmics, including beta blockers, calcium channel blockers, amiodarone, cardiac glycosides, and lidocaine, also have other medical uses. These are discussed separately in the corresponding learning cards.
Classes of antiarrhythmic drugs
|Class||Drug group||Main mechanism of action||Examples||Use||Adverse Effects|
|Class I antiarrhythmic drugs||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 be done with ECG monitoring!
- Mechanism of action: transient AV node block
- Rapid bolus IV (very short half-life: < 10 seconds)
- May be administered repeatedly if previous dose was unsuccessful
- Warn patients of unpleasant feeling that can follow administration. They may be feel a sense of impending doom.
- Drug of choice for narrow QRS tachycardias, such as paroxysmal supraventricular tachycardias: and orthodromic (except pre-excited tachycardias)
- Diagnostic value: exposing underlying AFib in supraventricular tachyarrhythmias
- Adenosine also has strong physiologic effects on the kidney, particularly constricting the afferent arteriole and triggering profound natriuresis
- Pharmacological stress test in myocardial perfusion scintigraphy
- Adverse Effects:
- Mechanism of action: Inhibition of Na+/K+-ATPases → higher intracellular Na+ concentration → reduced efficacy of Na+/Ca2+ exchangers → higher intracellular Ca2+ concentration → increased contractility, decreased heart rate
- Indications: tachyarrhythmias (e.g., AFib)
- See for details.
- Mechanism of action: decreases calcium influx → prevents early afterdepolarizations
- Loss of reflexes
- Respiratory depression
- Mechanism of action: Lowers heart rate by blocking the If channel in the pacemaker cells of the SA node
- Indications: Drug of last resort for symptomatic relief of stable coronary heart disease and congestive heart failure (NYHA II-IV) in sinus rhythm
- Visual changes