What is the main action of Antidysrhythmic medications?

INTRODUCTION

Antidysrhythmic agents, which are also known as antiarrhythmic agents, are a broad category of medications that help ameliorate the spectrum of cardiac arrhythmias to maintain normal rhythm and conduction in the heart. Arrhythmias generally arise as a result of abnormal impulse generation or abnormal conduction, or a combination of the two. Abnormal impulse generation falls into one of two categories: abnormal automaticity or triggered activity. Abnormal automaticity is thought to occur due to reduced resting membrane potential, causing the membrane to be closer to the threshold for generating an action potential. Triggered activity, or after-depolarization, occurs during the early stages after depolarization, such as in phase 2 and 3, or in the later stage during phase 4. With either form, it requires a preceding triggering beat to create the abnormal depolarization. Abnormal conduction is usually due to conduction block or a reentry phenomenon, with the latter being the most common cause of dysrhythmias. Antidysrhythmics exert their effect on specific ion channels on the cardiac cell membrane which then alters the shape of the action potential, and thus have inotropic, chronotropic, and toxic actions as a result.

CLASSIFICATION

The most common classification system for antidysrhythmic agents is the Harrison modification of Vaughan Williams (Table 166-1). This system classifies each agent based upon its unique electrophysiologic and pharmacological properties. Vaughan Williams classification divides these agents in one of four groups, Class I, II, III, and IV. There is a further subdivision of Class I agents, the so-called sodium channel blockers, into IA, IB, and IC.

TABLE 166-1Classification of Antidysrhythmic Agents

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TABLE 166-1 Classification of Antidysrhythmic Agents

Vaughan Williams ClassificationElectrocardiographic EffectMembrane/Ion ChannelExamples of Agents
IA ↑QRS and Q-T intervals Blocks fast Na+ and intermediate K+ Quinidine/procainamide/disopyramide
IB ↓ →Q-T interval Fast sodium channel blocker Lidocaine/tocainide/mexilitine
IC ↓ QRS Interval Sodium channel blocker Flecainide/propafanone
II ↓ HR; ↑P-R interval β adrenergic receptor blockade Propranolol/esmolol/metoprolol
III ↑ Q-T interval K+ channel blocker Amiodarone/sotalol/ibutilide/dronedarone
IV ↓ HR; ↑ P-R interval L-type Ca2+ channel blocker Verapamil/diltiazem
Digoxin ↑ P-R interval; ↓ Q-T interval Na+/K+ ATPase inhibitor
Adenosine ↓ HR; ↑ P-R interval Purinergic A1 receptor agonist

  • Class I agents block the rapid inward sodium channel, slow the rate of rise of phase 0, and so decrease the rate of depolarization. The subgrouping of Class I agents allows for differentiating their electrophysiologic effects. Class IA drugs (quinidine, procainamide, and disopyramide) prolong the repolarization and the refractoriness of isolated myocardial tissue as well as block the inward sodium current. They also have potassium channel blocking properties, and so increase action potential duration and the effective refractory period. Class IB drugs (lidocaine, tocainide, and mexiletine) produce only modest inhibition of the rapid inward sodium current and so shorten the refractory period, and reduce the action potential duration. ...

Therapeutic Use and Rationale

The ultimate goal of antiarrhythmic drug therapy is to restore normal rhythm and conduction. When it is not possible to revert to normal sinus rhythm, drugs may be used to prevent more serious and possibly lethal arrhythmias from occurring. Antiarrhythmic drugs are used to:

  • decrease or increase conduction velocity
  • alter the excitability of cardiac cells by changing the duration of the effective refractory period
  • suppress abnormal automaticity

All antiarrhythmic drugs directly or indirectly alter membrane ion conductances, which in turn alters the physical characteristics of cardiac action potentials. For example, some drugs are used to block fast sodium channels. These channels determine how fast the membrane depolarizes (phase 0) during an action potential. Since conduction velocity is related to how fast the membrane depolarizes, sodium channel blockers reduce conduction velocity. Decreasing conduction velocity can help to abolish tachyarrhythmias caused by reentry circuits. Other types of antiarrhythmic drugs affect the duration of action potentials and the effective refractory period. By prolonging the effective refractory period, reentry tachycardias can often be abolished. These drugs typically block potassium channels and delay repolarization of action potentials (phase 3). Drugs that block slow inward calcium channels are used to reduce pacemaker firing rate by slowing the rate of rise of depolarizing pacemaker potentials (phase 4 depolarization). These drugs also reduce conduction velocity at the AV node, because those cells, like SA nodal cells, depend on the inward movement of calcium ions to depolarize. 

Because sympathetic activity can precipitate arrhythmias, drugs that block beta1-adrenoceptors are used to inhibit sympathetic effects on the heart. Because beta-adrenoceptors are coupled to ion channels through defined signal transduction pathways, beta-blockers indirectly alter membrane ion conductance, particularly calcium and potassium conductance.

In the case of AV block, drugs that block vagal influences (e.g., atropine, a muscarinic receptor antagonist) are sometimes used. AV block can occur during beta-blocker treatment and therefore simply removing a beta-blocker in patients being treated with such drugs may normalize AV conduction.

Sometimes ventricular rate is excessively high because it is being driven by atrial flutter or fibrillation. Because it is very important to reverse ventricular tachycardia, drugs are often used to slow AV nodal conduction to control ventricular rate. Calcium channel blockers and beta-blockers are useful for this indication. Digitalis, because of its ability to activate the vagus nerve (parasympathomimetic effect), can also be used to reduce AV conduction velocity in an attempt to normalize ventricular rate during atrial flutter or fibrillation, particularly in heart failure patients.

Classes of Drugs Used to Treat Arrhythmias

Classes of drugs used in the treatment of arrhythmias are given below.  Clicking on the drug class will link you to the page describing the pharmacology of that drug class and specific drugs. Please note that many of the drugs comprising the first five listed classes have considerable overlap in their pharmacologic properties.

Antiarrhythmic drug classes:

  • Class I - Sodium-channel blockers
  • Class II - Beta-blockers
  • Class III - Potassium-channel blockers
  • Class IV - Calcium-channel blockers
  • Miscellaneous - adenosine
    - electrolyte supplement (magnesium and potassium salts)
    - digitalis compounds (cardiac glycosides)
    - atropine (muscarinic receptor antagonist)

Click here to see a table summarizing the types of drugs that may be used to treat different types of arrhythmias.

Revised 09/06/22

What is the purpose of Antidysrhythmic medications?

Antidysrhythmic medications are widely used to treat or prevent abnormalities in cardiac rhythms.

What is the action of Antidysrhythmic?

Antidysrhythmics, also known as antiarrhythmics, are drugs used to prevent abnormal cardiac rhythms such as atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation. These drugs work by blocking sodium, potassium, and calcium channels in the heart muscles.

What is the action of Group 1 Antidysrhythmic drugs?

What are Group I antiarrhythmics? Group 1 antiarrhythmics: Sodium-channel blockers, which block the fast sodium channels, thereby slowing electrical conduction in the heart.

What is the desired action of antiarrhythmics?

Antiarrhythmics help manage electrical problems in your heart that cause irregular heart rhythms, like atrial fibrillation or tachycardias (fast heartbeats).