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Antiarrhythmic agents are a group of pharmaceuticals that are used to suppress abnormal rhythms of the heart (cardiac arrhythmias), such as atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation.
Many attempts have been made to classify antiarrhythmic agents. The problem arises from the fact that many of the antiarrhythmic agents have multiple modes of action, making any classification imprecise.
The Vaughan Williams classification was introduced in 1970.
With regards to management of atrial fibrillation, Class I and III are used in rhythm control as medical cardioversion agents while Class II and IV are used as rate control agents.
There are five main classes in the Vaughan Williams classification of antiarrhythmic agents:
|Class||Known as||Examples||Mechanism||Clinical uses in cardiology |
|Ia||fast-channel blockers-affect QRS complex||(Na+) channel block (intermediate association/dissociation)|
|Ib||Do not affect QRS complex||(Na+) channel block (fast association/dissociation)|
|Ic||(Na+) channel block (slow association/dissociation)|
Propranolol also shows some class I action
|III||K+ channel blocker|
|IV||slow-channel blockers||Ca2+ channel blocker|
|V||Work by other or unknown mechanisms (Direct nodal inhibition).||Used in supraventricular arrhythmias, especially in Heart Failure with Atrial Fibrillation, contraindicated in ventricular arrhythmias. Or in the case of Magnesium Sulfate, used in Torsades de Pointes.|
Class I agents are called Membrane Stabilizing agents. The 'stabilizing' word is used to describe the decrease of excitogenicity of the plasma membrane which is brought about by these agents. (Also noteworthy is that a few class II agents like propranolol also have a membrane stabilizing effect.)
Class II agents are conventional beta blockers. They act by blocking the effects of catecholamines at the β1-adrenergic receptors, thereby decreasing sympathetic activity on the heart. These agents are particularly useful in the treatment of supraventricular tachycardias. They decrease conduction through the AV node.
Class III agents predominantly block the potassium channels, thereby prolonging repolarization. Since these agents do not affect the sodium channel, conduction velocity is not decreased. The prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias. (The re-entrant rhythm is less likely to interact with tissue that has become refractory). Drugs include: bretylium, amiodarone, ibutilide, sotalol, dofetilide, and dronedarone. Inhibiting potassium channels, slowing repolarization, results in slowed atrial-ventricular myocyte repolarization. Class III agents have the potential to prolong the QT interval of the EKG.
Class IV agents are slow calcium channel blockers. They decrease conduction through the AV node, and shorten phase two (the plateau) of the cardiac action potential. They thus reduce the contractility of the heart, so may be inappropriate in heart failure. However, in contrast to beta blockers, they allow the body to retain adrenergic control of heart rate and contractility.
Since the development of the original Vaughan-Williams classification system, additional agents have been used that don't fit cleanly into categories I through IV.
It presents the drugs on two axes, instead of one, and is presented in tabular form. On the Y axis, each drug is listed, in approximately the Vaughan Williams order. On the X axis, the channels, receptors, pumps, and clinical effects are listed for each drug, with the results listed in a grid. It is therefore not a true classification in that it does not aggregate drugs into categories.