This document discusses various types of antiarrhythmic drugs. It begins by describing the different types of cardiac tissue and the cardiac action potential. It then categorizes antiarrhythmic drugs into five classes based on their mechanisms of action. For each drug discussed, it provides information on pharmacological properties, metabolism, side effects, indications, and status of current use. The document focuses on quinidine, procainamide, disopyramide, lidocaine, mexiletine, propafenone, and flecainide, describing their electrophysiological effects, pharmacokinetics, adverse effects, and clinical applications.

2. ANTIARRHYTHMICS
Dr. R. Sudar Codi
(Asst. Professor)
Dept. of Pharmacology

3. Types of cardiac tissue
(on the basis of impulse generation)
• AUTOMATIC/ PACEMAKER/ CONDUCTING
FIBRES
(Ca++ driven tissues)
Includes SA node, AV node, bundle of His,
Purkinje fibres
Capable of generating their own impulse
Normally SA node acts as Pacemaker of heart
• NON-AUTOMATIC MYOCARDIAL CONTRACTILE
FIBRES (Na+ driven tissues)
Cannot generate own impulse
Includes atria and ventricles

4. Cardiac Action Potential - WMCs

9. Class I: Na+ channel Blockers
1a: Quinidine, Procainamide, Disopyramide
1b: Lidocaine, Mexiletine
1c: Propafenone, Flecainide
Class II: Beta Blockers
Propanolol, Esmolol, Sotalol
Class III: Potassium Channel Blockers
Amiodarone, Ibutilide, Dofetilide
Vaughan William & Singh

10. Class IV: Calcium Channel Blockers
Verapamil, diltiazem
Class V: Miscellaneous
Adenosine, Amrinone, Milrinone
Vaughan William & Singh

11.  Derived from Cinchona bark used to treat
palpitations
 Blocks myocardial Na+ Channels in the open state
thereby reduces excitability & automaticity
 Lengthening of APD due to K+ channel blockade
 Other Action:
 Weak α adrenergic blockade and cardiac depressant
 Antivagal action causing paroxysmal tachycardia
QUINIDINE

12.  Cinchonism - Ringing of ear, Vertigo, Visual
Disturbances and Mental Changes
 Most common: Diahorrea due to irritant effect &
vomiting due to bitter nature
 Hypotension & tachycardia due to alpha blockade
 Paradoxical tachycardia – antivagal action at AV node
 Long QT due to increased APD
 Abortifacient due to oxytoxic action
 Thrombocytopenia & bone marrow depression
QUINIDINE

14.  Rise in Blood level and toxicity of Digoxin – due to
displacement interaction & inhibition of P glycoprotein
mediated biliary & renal clearance
 Fall in BP: patients receiving vasodilators.
 Risk of TDP: patients receiving Diuretics.
 Synergistic Cardiac Depression with Beta Blockers
 Inhibition of cyp2D6 – reduced analgesic effect of
codeine & long half life of propafenone
QUINIDINE

15.  Atrial
 Ventricular arrhythmias.
 Present Status: rarely used due to side effects.
 ANTIMALARIAL
 ANTIPYRETIC
 OXYTOXIC
 NOCTURNAL LEG CRAMPS
QUINIDINE

16.  Orally Active Amide Derivative of the Local
Anesthetic Procainamide.
 Electrophysiological actions Identical to those of
Quinidine.
 Significant Differences
 Less effective in suppressing Automaticity
 Less Marked Depression of Contractibility
 Not a alpha Blocker
 Orally active
 Inhibit cyp2d6
 Ganglionic blocker - hypotension
PROCAINAMIDE

17.  Oral Bioavailability: 75%
 Half life 3-4 hrs, metabolite – 8 hrs
 Metabolized in Liver
 N-acetyl Procainamide: Blocks potassium
Channels so class III antiarrhthymic
property
PROCAINAMIDE

18.  GI Intolerance: better than Quinidine
 CNS: Weakness, mental Confusion,
Hallucinations
 Hypotension, nausea
 Ability to cause TDP similar to Quinidine.
 1/5th SLE in slow acetylators but not to its
metabolite.
PROCAINAMIDE

19.  Monomorphic VT
 Used to prevent recurrence of VF.
Present Status:
Not Suitable for Prolonged Therapy because of
SLE.
PROCAINAMIDE

20.  Quinidine like Class 1a drug
 Has prominent Cardiac Depressant and
Anticholinergic actions.
 No alpha adrenergic blocking action.
DISOPYRAMIDE

21.  GI Intolerance: better than Quinidine
 Anticholinergic side effects are more
prominent.
 Cause greater depression of Cardiac
Contractibility.
 Contraindications: Sick Sinus, Cardiac Failure
and glaucoma, prostrate hypertrophy.
DISOPYRAMIDE

22.  Second line drug for recurrences of VT.
 Also used in the cardioversion of AF or AFl
DISOPYRAMIDE

23.  Most commonly Used Local anesthetic.
 Popular antiarrhythmic in ICU.
LIDOCAINE

24.  Suppression of Automaticity of ectopic Foci.
 Enhanced Phase 4 Depolarization in partially
depolarize or stretched PFs.
 Lidocaine is blocker of inactivated Na+
channels.
 Minimal effect on normal ECG.
 More pronounced action on ischemic
Myocardium.
LIDOCAINE

25.  Inactive orally
 Hepatic blood flow dependent metabolism
 Rapid redistribution
 Side effects - Neurological
 Drowsiness, nausea, parenthesis, blurred vision,
disorientation, nystagmus, twitching.
 Metabolite – GX & MEGXmonoethyl glycine xylidide
less effective sodium blockade but compete for it and
hepatic lidocaine metabolisimg enzyme so reduced
efficacy and clearance on continuous infusion
LIDOCAINE

26.  Used Only in Ventricular arrhythmias
 Ineffective in the atrial arrhythmias.
 Because of rapidly developing and titrable
action it is a good drug for emergency setting
– arrhthymias following acute MI
 Least cardiotoxic anti arrhythmic.
LIDOCAINE

27.  Local Anesthetic
 An active antiarrhythmic by oral route due to
reduced hepatic first pass metaolism.
 Chemically and pharmacologically similar to
lidocaine.
 Oral substitute to Lidocaine
MEXILETINE

28.  Most potent sodium Channel Blockers with
prominent action on open state longest
recovery time.
 Has β adrenergic blocking property: can
precipitate CHF and Bronchospasm.
 Inhibit cyp2d6
 Is Reserve Drug for Ventricular Arrhythmias,
Reentrant Tachycardia involving AV node.
PROPAFENONE

29.  Not Used Routinely as in CAST study it was
found to increase mortality in patients
recovering from MI.
FLECAINIDE