Classifications of Antiarrhythmic Agents
As the number of available drugs with antiarrhythmic properties increased, the need for a conceptual framework for their classification became increasingly important. [1, 2] The classification scheme most commonly in use today is the eponymously titled Vaughan Williams classification. [3] The basis of this classification is the grouping of agents according to their general effect.
In the years since the widespread adoption of the Vaughan Williams classification, there has been an exponential increase in our understanding of cardiac electrophysiology, the mechanisms of cardiac arrhythmia, and the discovery of new ion channels. In light of these more recent advances, there has been some criticism of the Vaughan Williams classification, most notably by the arrhythmia working group of the European Society of Cardiology, who, in 1991, proposed an alternative classification commonly referred to as the Sicilian gambit. [4] While these investigators raised several valid concerns, the Vaughan Williams classification remains in widespread use and is requisite knowledge for those working in the field of cardiac electrophysiology. [5]
The list below contains the classically described members of each drug class but is not comprehensive.
Class I: Fast sodium (Na) channel blockers
See the list below:
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Ia -Quinidine, procainamide, disopyramide (depress phase 0, prolonging repolarization)
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Ib -Lidocaine, phenytoin, mexiletine (depress phase 0 selectively in abnormal/ischemic tissue, shorten repolarization)
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Ic -Flecainide, propafenone, moricizine (markedly depress phase 0, minimal effect on repolarization)
Class II: Beta blockers (partial list)
See the list below:
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Propranolol (decreases slope of phase 4)
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Esmolol (decreases slope of phase 4)
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Timolol (decreases slope of phase 4)
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Metoprolol (decreases slope of phase 4)
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Atenolol (decreases slope of phase 4)
Class III: Potassium (K) channel blockers
See the list below:
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Amiodarone (prolongs phase 3; also acts on phases 1, 2, and 4)
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Sotalol (prolongs phase 3, decreases slope of phase 4)
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Ibutilide (prolongs phase 3)
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Dofetilide (prolongs phase 3)
Class IV: Slow calcium (Ca) channel blockers
See the list below:
Class V: Variable mechanism
See the list below:
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During phase 0, rapid depolarization occurs, primarily due to sodium influx. In phase 1, there is an outward migration of potassium and chloride, beginning the repolarization process. In phase 2, the plateau phase, potassium efflux is balanced by calcium influx, keeping the membrane potential stable. Phase 3 is characterized by further potassium efflux and a return to a hyperpolarized state. In phase 4, there is relatively little ionic current in healthy ventricular cells.
