This document discusses anti-arrhythmic drugs used to treat cardiac arrhythmias. It defines arrhythmias as irregular, too fast, or too slow heartbeats and describes common types like atrial fibrillation, supraventricular tachycardia, bradycardia, and heart block. The document outlines the Vaughan Williams classification system for anti-arrhythmic drugs, which includes 5 classes based on their mechanisms of action such as blocking sodium, potassium, calcium channels or having other effects. Class I drugs like quinidine, procainamide, and lidocaine are sodium channel blockers. The document provides details on cardiac action potentials, ion channels, and how anti-arrhythmic drugs work to

1. Anti-arrhythmic Drugs:
By – Mr R. B. Darade
(Assistant Professor)
Abasaheb Kakade College of B. Pharmacy,
Bodhegaon Dist - Ahmednagar

2. Anti-arrhythmic Drugs:
Quinidine sulphate, Procainamide hydrochloride, Disopyramide
phosphate, Phenytoin sodium, Lidocaine hydrochloride, Tocainide
hydrochloride, Mexiletine hydrochloride, Lorcainide hydrochloride,
Amiodarone, Sotalol.

3. Introduction:
 Arrhythmia, also known as cardiac arrhythmia or heart
arrhythmia, is a group of conditions in which the
heartbeat is irregular, too fast, or too slow.
 The heart rate that is too fast – above 100 beats per
minute in adults – is called tachycardia, and a heart rate
that is too slow – below 60 beats per minute – is called
bradycardia.
 Symptoms when present may include palpitations or
feeling a pause between heartbeats. In more serious
cases, there may be light headedness, shortness of breath
or chest pain.

4. Types of arrhythmia:
 Atrial fibrillation (AF) – this is the most common type, where
the heart beats irregularly and faster than normal. Upper
heart chambers contract irregularly.
 Supraventricular tachycardia – episodes of abnormally fast
heart rate at rest
 Bradycardia – the heart beats more slowly than normal
 Heart block – the heart beats more slowly than normal and
can cause people to collapse
 Ventricular fibrillation – a rare, rapid and disorganised rhythm
of heartbeats that rapidly leads to loss of consciousness and
sudden death if not treated immediately. Disorganized
contraction of the lower chambers of the heart.

5. Mechanisms of Arrhythmias
 Cardiac arrhythmias is caused by altered impulse formation (i.e., change in
automaticity), altered conduction, or both, acting simultaneously from
different locations of the heart.
 The generation of cardiac impulses in the normal heart is usually confined to
specialized tissues that spontaneously depolarize and initiate the action
potential.
 These cells are located in the right atrium and are referred to as the SA node
or the pacemaker cells.
 Although the spontaneous electrical depolarization of the SA pacemaker cells
is independent of the nervous system, these cells are innervated by both
sympathetic and parasympathetic fibers, which may cause an increase or
decrease of the heart rate, respectively.
 Other special cells in the normal heart that possess the property of
automaticity may influence cardiac rhythm when the normal pacemaker is
suppressed or when pathological changes occur in the myocardium to make
these cells the dominant source of cardiac rhythm (i.e., ectopic pacemakers).

6. Normal ECG
 Normal ECG

7. Cardiac Action Potential
 The cardiac action potential is a result of ions flowing
through different ion channels.
 Ion channels are passages for ions (mainly Na+, K+, Ca2+
and Cl-) that facilitate movement through the cell
membrane.
 Changes in the structure of these channels can open,
inactivate or close these channels and thereby control the
flow of ions into and out of the myocytes.
 Due to differences in the type and structure of ion
channels, the various parts of the heart have slightly
different action potential characteristics.

8. The different shapes of the cardiac action potential in the
heart.

9. The cardiac ventricular action potential and relevant ion
channels.

10. Antiarrhythmic drugs
 Antiarrhythmic drugs act by blocking myocardial Na+, K+
or Ca2+ channels. Some have additional or even primary
autonomic effects.
 Classification of antiarrhythmic drugs has been
unsatisfactory, because many drugs have more than one
action.
 Vaughan Williams and Singh (1969) proposed a 4 class
system which takes into account the most important
property of a drug which is apparently responsible for its
antiarrhythmic action in the clinical setting.
 This system, though arbitrary, is widely accepted.

11. The five main classes in the Vaughan Williams classification of
antiarrhythmic agents are:
Class I Sodium (Na+) channel blockers / membrane stabilising
agent:
Quinidine sulphate, Procainamide hydrochloride, Disopyramide phosphate,
Lidocaine hydrochloride, Phenytoin sodium, Tocainide hydrochloride,
Mexiletine hydrochloride, Lorcainide hydrochloride
Class II Beta blockers.
Propranolol, Esmolol, Sotalol, Atenolol, Timolol
Class III agents affect potassium (K+) efflux.
Amiodarone, Ibutilide, Dofetilide, Bretylium.
Class IV calcium channels Blockers
Verapamil, Diltiazem
Class V agents work by other or unknown mechanisms.
Adenosine Digoxin, Magnesium sulfate (MgSO4)

13. Thank you!