Antiarrhythmic drugs

Antiarrhythmic drugs class ppt

1. Antiarrhythmic Drugs Suresh Kumar Ghritlahare Assist. Professor SRU, Raipur, (C.G.)

2. Antiarrhythmic Drugs A r rhythmia: The cardiac arrhythmias are cause by disturbance conduction of impulse through myocardial cell. Arrhythmia is irregularities in cardiac rhythm due to disorder of impulse formation & impulse conduction. Disturbed impulse formation, irregular discharge of impulse from pace maker, tachy arrhythmia. Antiarrhythmic Drugs: These are drugs used to prevent or treat irregularities of cardiac rhythm. The important cardiac arrhythmias are : Atrial flutter (AFI ) Atrial fibrillation (AF ) Ventricular tachycardia (VT ) Ventricular fibrillation (VF ) Atrio -ventricular (A-V) block

3. Antiarrhythmic drugs Class Actions Drugs I Membrane stabilizing agents (Na+ channel blockers) Quinidine , Procainamide , Disopyramide , Lidocaine , Mexiletine , Propafenone , Flecainide etc. II Antiadrenergic agents ( β blockers) Propranolol, Esmolol , Sotalol (also class III) III Agents widening AP ( prolong repolarization and ERP) Amiodarone , Dronedarone , Dofetilide , Ibutilide IV Calcium channel blockers Verapamil , Diltiazem

4. Mechanism of action Membrane stabilizing agents: Quinidine Quinidine block myocardial Na + channel & prevent Na+ enflux . Reduce the maximal rate of 0 phase depolarization & also decrease slope of phase-4 quinidine decrease the availability of Na+ channel as well as deals their reactivation Inhibit action potentials

5. 2. Beta Blocker: Propranolol Propranolol is beta-adrenergic antagonist by nature they are sympathetic antagonist inhibit sympathetic tone & decrease heart rate Prolong the AV conduction inhibit phase- 4 Delayed action potentials

6. 3 . Ca++ channel blocker: verapamil Ca++ channel blocker are block the Ca++ channel in myocardium Verapamil it show the negative inotropic action interfere with Ca++ ion The most action of verapamil is prolongation of AV- noded ERP

7. 4. Agent widening A.P.: Amiodorone Amiodorone block K+ ion channel in myocardial cell Diminish the outward K+ ion currect during repoarization of cardiac muscle cell Prolong the duration of action potential Prolong the ERP

8. Pharmacokinetics ( lidocaine ) Absorption: Lidocaine is inactive orally due to high first pass metabolism in liver . Distribution: Action of an i.v . bolus lasts only 10–20 min because of rapid redistribution . Metabolism: Metabolism of lidocaine is hepatic blood flow dependent . Excreation : It is hydrolysed , deethylated and conjugated; metabolites are excreted in urine

9. use A rrhythmia Atrial flutter (AFI) Atrial fibrillation (AF) Ventricular tachycardia (VT) Ventricular fibrillation (VF) Atrio -ventricular (A-V) block Adverse effects: Fall in BP, bradycardia and myocardial depression Nausea , gastrointestinal upset

10. References Tripathi KD, “Essentials of Medical Pharmacology” published by Jaypee Brothers Medical Publishers (P) Ltd, Seventh Edition: 2013, New Delhi, p.p. no-526-538.

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