In this essay we will discuss about the various drugs used for the treatment of arrhythmia.

Essay # 1. Drugs Used for the Treatment of Cardiac Arrhythmia:

Disorders of cardiac rhythm can be divided into those due to over excitability of the heart (ectopic beats or circus movement) which are by far the most common and those due to conduction defects in the bundle of His (heart block). Antiarrhythmic drugs act either by decreasing the excitability or contractility or by slowing conduction in the AV node or by increasing the effective refractory period.

Antiarrhythmic drugs can be classified clinically according to their anatomical site of action and clinical range of activity. They are also classified according to their electrophysiological action on isolated cardiac muscle fibers into 4 classes of drugs.

Class I. Sodium Channel Blockers:

These drugs cause slowing of conduction or an increase in the refractory period or both. They usually have local anesthetic properties and membrane stabilizing activity. The electro­physiological effects tend to reduce spontaneous automaticity.

These drugs may be further subdivided according to the influence on duration of action potential, which may lengthen (group 1A, e.g. quinidine, procainamide and disopyramide), shorten (group 1B, e.g. lidocaine), or be unaffected (group 1C, e.g. flecainide).

Class II. β Blockers:

They reduce the potential for arrhythmias to develop in response to catecholamines. Bretylium blocks the release of sympathetic transmitters. β blockers also block the possible arrhythmogenic effect of cyclic adenosine-5-monophosphate.

Class III:

These drugs prolong the duration of action potential, with resultant prolongation of the effective refractory period, without blocking sodium channels (e.g. amiodarone). They also include β adreno-receptor blocking drugs.

Class IV. Calcium Channel Blockers:

Verapamil and diltiazem slow conduction in AV node. Quinidine and procainamide are rarely used as antiarrhythmics because of their low therapeutic margin of safety and tendency to induce arrhythmias (proarrhythmias).

Essay # 2. Drugs Used for the Treatment of Ventricular Arrhythmias:

i. Lignocaine (Lidocaine):

Lignocaine, a local anesthetic, has typical class I electro­physiological effects. It suppresses the excitability of the ventricular muscle with only moderate depression of the heart’s action. In therapeutic doses it is not likely to cause cardiac arrest or a fall of blood pressure. Lignocaine remains the first line drug for treating ventricular arrhythmia after acute myocardial infarction, cardiac operations and digitalis intoxication. It is given by slow intravenous injection.

Adverse effects:

Nausea, vomiting, par-aesthesia or drowsiness may occur. High doses may cause CNS effects such as respiratory depression and convulsions and CVS effects such as hypotension and bradycardia which may lead to cardiac arrest.

Drug interactions:

β blockers, other antiarrhythmic drugs and cimetidine increase the risk of lignocaine toxicity. Diuretics (hypokalemia) antagonize the effects of lignocaine.

ii. Mexiletine:

Mexiletine has electrophysiological actions similar to those of lignocaine. It is used to treat ventricular arrhythmias by intravenous or oral route. Peak plasma concentrations are obtained 2-4 hours after oral administration with a half-life of 9-12 hours. Opioid analgesics reduce oral absorption.

Adverse effects:

Neurological side effects are common and include drowsiness, confusion, convulsions, paresthesia, tremors and nystagmus. Cardiac side effects include hypotension, bradycardia and transient AV block.

iii. Bretylium:

Bretylium, an adrenergic neurone blocking drug, possesses class II and class III electrophysiological effects. It is used only in ventricular fibrillation that is refractory to lignocaine or to repeated electrical defibrillation. It is given both intramuscularly and intravenously but can cause severe hypotension.

Essay # 3. Drugs Used for the Treatment of Supraventricular Arrhythmias:

i. Cardiac Glycosides:

Digoxin is not an antiarrhythmic drug but is of great therapeutic value in slowing the ventricular rate, particularly in atrial fibrillation and flutter where the slower and more regular contractions allow the heart to function more efficiently and to raise cardiac output.

ii. Adenosine:

Adenosine is an endogenous purine nucleoside, which has class IV electrophysiological effects including potassium channel opening, and has an inhibitory effect on the sinus and AV conduction. It is the drug of choice for terminating paroxysmal tachycardia (chemical cardio version). Given intravenously, it has a very short duration of action, lasting for 20-30 seconds. Dyspnoea, flushing and chest pain are common side effects, but are short lived. Bronchoconstriction may occur, which contraindicates the use of adenosine in asthma.

iii. Verapamil:

Verapamil has class IV electrophysiological effects. Its main action is on AV conduction. Ventricular rate in atrial fibrillation and flutter is controlled, and cardio version of paroxysmal supraventricular tachycardia is often achieved. It can be given intravenously or by mouth. Myocardial depression may occur in patients with heart failure. Drug interaction may occur with digoxin and beta blockers, which may result in increased digitalis intoxication and hypotension. Verapamil is contraindicated in sick sinus syndrome, AV node disease and history of heart failure.

Essay # 4. Drugs Used for the Treatment of Supraventricular and Ventricular Arrhythmias: 

i. Amiodarone:

Amiodarone belongs to group of class III antiarrhythmic drugs. It prolongs the refractory period in all cardiac tissue. It is also a noncompetitive α and β adreno receptor antagonist, and may have some additional class I activity.

It is effective in a wide range of supraventricular and ventricular arrhythmias particularly when other drugs are ineffective or contraindicated. It can be given by intravenous infusion as well as by mouth and has the advantage of causing little or no myocardial depression.

Non-cardiac side effects are common and are potentially serious. Cutaneous manifestations of photosensitivity are extremely common. Amiodarone contains a high concentration of iodine and may cause both hypothyroidism and thyrotoxicosis. More potential serious effects are hepatitis, pulmonary infiltration, neuropathy and corneal deposits of yellow brown granules. Amiodarone potentiates the action of warfarin and digitalis.

ii. β Blockers:

These are class III antiarrhythmic drugs. They act by preventing the effects of catecholamine on automaticity and conductivity within the heart. Sotalol is a nonselective β blocker without intrinsic sym­pathomimetic activity, but possesses class III activity that prolongs the AV action potential duration and the refractory period.

Sotalol is used for prophylaxis in paroxysmal supraventricular arrhythmias. It also suppresses ventricular ectopic beats and non-sustained ventricular tachycardia. It has been shown to be more effective than lignocaine in the termination of spontaneous sustained ventricular tachycardia due to coronary disease or cardiomyopathy.

Esmolol, a relatively cardio selective β blockers with a very short duration of action, is used intravenously for short-term treatment of supraventricular arrhythmias, sinus tachycardia or hypertension when induced during anesthesia.

Atenolol and metoprolol may be used as adjunctive treatment to digoxin to control the ventricular rate in atrial fibrillation, especially in patients with thyrotoxicosis.

β blockers may cause myocardial depression and hypotension or cardiac failure in patients with little cardiac reserve. They are contraindicated in asthma or history of obstructive airway disease, uncontrolled heart failure, cardiogenic shock and severe peripheral artery disease.

iii. Disopyramide:

Disopyramide has class I electrophysiological effects. It decreases excitability, slows conduction and has a potentially negative inotropic effect. It can be given either orally or intravenously in atrial or ventricular arrhythmias, including supraventricular tachycardia and ventricular extra-systoles. Myocardial depression may be clinically important and the use of disopyramide is therefore contraindicated in heart failure and cardiogenic shock. It has anticholinergic activity, and urinary retention, dry mouth, and blurred vision often occur. Glaucoma may be precipitated.

iv. Flecainide:

Flecainide belongs to the same general class as lignocaine (class I drug). It reduces excitability and slows conduction in the AV node and bundle of His. Flecainide is useful for a wide range of arrhythmias including recurrent ventricular arrhythmias. It is as successful as amiodarone in converting atrial fibrillation to sinus rhythm. As with quinidine, it may induce dangerous arrhythmias, particularly following myocardial infarction.

Myocardial depression, exacerbation of preexisting conduction disorders and arrhythmogenic (proarrhythmic) effects are the serious side effects of flecainide. Its use is contraindicated in heart failure, history of myocardial infarction and asymptomatic ventricular extra-systole or tachycardia.

v. Propafenone:

Electrophysiological effects are similar to those of other class IC drugs, but propafenone has beta blocking effects and minor calcium channel blocking activity. It also possesses anticholinergic activity. Propafenone has been shown to be effective in treating ventricular arrhythmias and atrial fibrillation.

Propafenone may induce conduction defects and may have arrhythmogenic (proarrhythmic) effects. It may cause atropine like side effects and rarely hypersensitivity reactions. Its use is contraindicated in conduction defects, uncontrolled congestive heart failure, marked hypotension and severe pulmonary obstructive disease.

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