antiarrhythmic medication - classes, drugs list in details

antiarrhythmic medication - classes, drugs list in details
antiarrhythmic medication

Arrhythmias mean uncontrolled or disturb cardiac rhythm. Its two types of arrhythmias produce. first one tachycardia & second bradycardia.

Tachycardia means to "increase the heart rate" due to increase automaticity or re-entry of an impulse.
Bradycardia means to "decrease the heart rate" due to decrease automaticity or blockage the impulse conduction. 

Impaired conduction or Abnormal automaticity are both underlie cardiac arrhythmias. Imbalance of cardiac impulse.

Arrhythmias are a very important cause of sudden cardiac death. That’s why only a few patients can be treated with antiarrhythmic medication.

Various types of cardiac arrhythmia are like atrial fibrillation, atrial flutter, ventricular tachycardia, ventricular fibrillation, paroxysmal supraventricular tachycardia, AV block etc.

Those drugs can control or restore cardiac rhythm are known as antiarrhythmic drugs or antiarrhythmic medication.

Most common used arrhythmic medicine in the market, 

·        Amiodarone (pacerone)
·        Propafenone (Rythmol)
·        Tocainide (tonocarid)
·        Flecainide (Tambocor)
·        Diltiazem (Tiazac, cardiazem)
·        Verapamil (Verelan. Calan)
·        Nifedipine (Sular)
·        Bisoprolol (Zebeta)
·        Acebutolol (Sectral)
·        Atenolol (Tenormin)

here, I will discuss details arrhythmic drugs via its class so, stay tuned

let's start

Antiarrhythmic medication

It can be acted by blocking the myocardial K+, Na+, or Ca+ channels. Actually, the classification of antiarrhythmic drugs is difficult because many drugs have more than one mechanism of action.

Singh & Vaughan Williams are proposed 4 class of antiarrhythmic drugs. That can set according to the electrophysiological action of drugs.





antiarrhythmic medication - classes, drugs list in details


⇨ Moderately Depress phase 0 depolarization. quinine, procainamide, disopyramide – disopyramide, quinidine, procainamide.

⇨ Minimal effect on phase 0 depolarization. mexiletine, lignocaine.

⇨ Markedly depress phase 0 depolarization. propafenone, flecainide


in antiarrhythmic medication, quinidine is widely used. Antimalarial alkaloids are obtained from cinchona bark. It is decreasing the myocardial contractility, it’s also an adverse effect to heart damage.

Quinidine has blocked the Na+ channel & decrease the excitability, automaticity & conduction velocity. also, a reduce the 0-phase depolarization.

Quinidine is blocks the K+ channel & increase the duration of the action potential.

It prolongs the effective refractory period as a result of block both channels.

It blocks the re-entry of impulsive.

Its direct depressed AV node.

Quinidine is inhibiting the skeletal muscle contractility.

Quinidine is a fall blood pressure due to a-adrenergic blockers.

Quinidine is also used in malaria, pyretic & oxytocic activities.

Drugs interaction of quinidine

Quinidine + verapamil, potassium salt etc β blockers can produce the cardiac arrest (cardiac depression).

Quinine may potentiate produce the effect of neuromuscular blocking agents.

Quinidine are inhibiting the CYP2D56; it reduces the conversion of codeine to morphine.

Patients receiving a vasodilator may fall in blood pressure.

➠ Adverse effect of quinidine:

The side effect produce is thrombocytopenia, diarrhoea, depress blood pressure, hepatitis & fever. It’s also produced syndrome like “cinchonism”. 

Also, some other adverse effect can produce like tinnitus, deafness, headache, blurring of vision, diplopia, confusion, photophobia, delirium, disorientation & psychosis.

➠ Use of quinidine

Quinidine is effective in many ventricular or atrial arrhythmia.

It's beneficial to maintain the normal sinus rhythm in atrial fibrillation or atrial flutter patients.

Sometimes to treat ventricular tachycardia.


It is an orally active amide derivatives.

in antiarrhythmic medication Procainamide drugs effects similar to quinidine, but it has no a adrenergic blocking agent & anticholinergic drugs.

Antivagal action is also a absent.

The bioavailability of procainamide is about 75% (oral). Its well absorbed by oral administered, also a given through i.v or i.m route. its metabolized in the liver through acetylation.

The major metabolism is N – acetyl procainamide (NAPA). This metabolite is excreted in urine

➠ Adverse effect of procainamide

Procainamide produced flushing and hypotension due to ganglion blockade.

Heart blockage is severe adverse effect.

It produces GI disturbance like, nausea & vomiting.

Its produce some CNS side effect like, weakness, depression, hallucination, confusion etc.

Long term procainamide is producing lupus-like syndrome with arthritis & arthralgia.

It produces a hypersensitive a reaction like rashes, angioedema, fever, agranulocytosis & aplastic anemia.

➠ Use of procainamide

It useful to terminate some supraventricular arrhythmia & monomorphic VT.

It’s not useful for the very long term due to frequent dosing & high probability lupus syndrome.


Its effect is similar to quinine but it has no a adrenergic effect produced.

It is usually no any effect on sinus rate due to its antivagal action & direct depression action.

Disopyramide is orally administered & partly metabolize in the liver & also a partly excreted through urine as an unchanged form.

➠ Uses of disopyramide

Its mainly used for ventricular arrhythmias. It’s also uses for maintain the sinus rhythm in flutter & fibrillation patients.

➠ Adverse effect of disopyramide

Disopyramide produce some side effect like benign prostatic hyperplasia (BPH), dryness of mouth, constipation, blurring of vision, urinary retention, glaucoma, constipation, etc.


Also called a lignocaine.

In in antiarrhythmic medication lignocaine is used as a local anesthetic agent.

It's active or non-active that block the sodium channel.

Its minimal effect on normal cardiac tissue & also a decrease the automaticity of ectopic foci.

It causes a very little depressed of arterial blood pressure or cardiac contractility.

It has no significant autonomic action; all the cardiac action is direct action produced.

Lignocaine is not effective oral (first-pass metabolism). Its administered as an intravenous. It metabolizes in the liver. Its metabolite is excreted in the urine.

➠ Use of lignocaine

It's used in the treatment of ventricular arrhythmias. That associated with digitalis toxicity, MI & cardiac surgery.

It's very useful in ventricular arrhythmia because relatively less toxic, rapid onset & short duration of action, it has no action on AV nodal conduction velocity.

Lignocaine efficacy in chronic ventricular arrhythmia is very poor. 

➠ Adverse effect of lignocaine

Lignocaine produce mainly central nervous related adverse effect like, drowsiness, headache, blurred vision, confusion, convulsion & muscle twitching etc. high dose of lignocaine may cause hypotension because of myocardial depression. 

Also, a produce side effect like hepatic & renal failure.

antiarrhythmic medication - classes, drugs list in details


example of beta-blocker drugs

⇨ Atenolol (Tonormin)
⇨ Esmolol (Brevibloc)
⇨ Metoprolol (Lopressor)
⇨ Sotalol (Betapace AF)
⇨ Propranolol (Inderal)

β blocker is an effect on catecholamine on the heart. 

In antiarrhythmic medication β blocker is a depressed phase – 4 depolarization, also a decrease SA node automaticity & ectopic tissue.

It's also a decrease AV node conduction velocity.

It controls the ventricular rate in atrial fibrillation & flutter.


Β1 blocker has a short duration of action & rapid onset of action. Its administrated in I.V is very useful for control of ventricular rate in atrial fibrillation & flutter.

Its also a terminate the supraventricular tachycardia.    

A side effect of esmolol is dizziness, bronchospasm, hypotension in asthmatics.


Sotalol is non – selective β – adrenergic blocker with its additional K+ channel blocker.

Its decrease the automaticity, AV conduction slow & prolong effective refractory period (ERP).

It maintains the sinus rhythm in atrial fibrillation.

Side effect of sotolol is same as a propranolol.

It can cause torsade’s de points.


example of class 3 drugs

⇨ Dronedarone (Multaq)
⇨ Sotalol (Betapace AF)
⇨ Amiodarone (Pacerone)
⇨ Dovetailed
⇨ Butizide, 
⇨ Beryllium.

The action potential is widely & ERP is increased.

Re-entrant arrhythmias are also terminated.


in antiarrhythmic medication, Amiodarone is iodine-containing drugs that structurally similar to thyroid hormones.

Amiodarone is blocking the potassium channel. And prolonged phase 3 repolarization. Also, an increase in the duration of the action potential.  It suppressed abnormal automaticity.

It's also a block the sodium channel to decrease the conduction mainly. It decreases the conduction mainly in the primary depolarized tissue.

In refractory period prolonged blockage of sodium & potassium channel.

It's also a weak calcium channel blocker & β adrenergic blocker. Its decrease the AV conduction & heart rate.

The oral bioavailability of amiodarone is actually 30%. So, given intravenously for its rapid action. Its metabolized in the liver.

It’s also accumulated in lungs, liver, skin & fat etc. Amiodarone is metabolized in the liver.

➠ Drug interaction of amiodarone

Amiodarone and β blocker are depress the SA node & AV node.

Amiodarone is inhibiting the renal clearance of digoxin. Also, an increase the serum digoxin level.

Amiodarone are increase the concentration of procainamide & quinidine.

➠ Adverse effect of amiodarone

Amiodarone is producing some side effect like hypotension, CHF, peripheral neuropathy, pulmonary fibrosis, corneal deposits & hyperthyroidism etc. also produce some GI effect like nausea & hepatitis. 

➠ Use of amiodarone

In antiarrhythmic medication, amiodarone is effective in the treatment of ventricular & atrial arrhythmias. It maintains a sinus rhythm in fibrillation.


Both are pure potassium channel blockers. Also, a they are useful in maintaining normal sinus rhythm in atrial fibrillation.


Example of calcium channel blocker

⇨ Diltiazem (Cardizem)
⇨ Verapamil (Calan, Isoptin)


Verapamil are decrease the L – type calcium channel. They depress the calcium-mediated depolarization.

It also decreases the conduction velocity & increase the refractory period of the AV node.
It reduces the ventricular rate in fibrillation & flutter.

They suppress the automaticity.

In SA node phase 4 depolarization that reduce resulting in bradycardia.


The mechanism of action of diltiazem is similar to verapamil. It's used as an alternative to verapamil, terminated as well as prophylaxis of PSTV.

Diltiazem is preferred more because it can more easily be titrated to its targeted heart rate.


In antiarrhythmic medication various drugs can be used. All of the drugs are used in arrhythmia with a different condition. If you like this article comment out.

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