BMS 204 Pharmacology: Drug Therapy of Dysrhythmia (Fall 2024) PDF

BMS 204 Pharmacology Drug Therapy of Dyrrhythmia Ahmed Nour Eldin Hassan Professor of Clinical Pharmacology Faculty of Medicine Fall 2024 By the end of this lecture, you should be able to: Classify antiarrhythmic drugs according to their electrophysiolo...

BMS 204 Pharmacology Drug Therapy of Dyrrhythmia Ahmed Nour Eldin Hassan Professor of Clinical Pharmacology Faculty of Medicine Fall 2024 By the end of this lecture, you should be able to: Classify antiarrhythmic drugs according to their electrophysiological effects. Discuss the choices of different antiarrhythmic drugs in various types of arrhythmias. Discuss the different lines of treatment of atrial fibrillation Explain why digoxin can be used in treatment of atrial fibrillation Explain why lidocaine is used only in ventricular arrythmia List the adverse effects of common antiarrhythmic drugs  Dysrrhythmia Definition: Abnormalities in heart rhythm and in severe case can impair pumping ability of heart Risk Factors: 1- Coronary Artery Diseases (CAD) 2- Myocardial Infarction (MI) 3- Hypoxia 4- Electrolyte imbalance: potassium 5-Drugs induced: theophylline, tricyclic antidepressants, overdose of antiarrhythmic drugs Bradyarrhythmia: < 60 beats/minute: Treatment: Conservative OR 1. Sinus bradycardia 1. Atropine 2-AV Block: with variable degrees 2. Cardiac pacing Normal Heart rate: 60-90 Regular Tachyarrhythmia: 1. Extra beat: atrial or ventricular 2. Supraventricular: Paroxysmal supraventricular tachycardia (PSVT), Atrial Flutter and Atrial Fibrillation (AF) 3. Ventricular: tachycardia/Fibrillation & Prolonged Q-T 4. Accessory bundle  Anti-arrhythmic Drugs: Vaughan Williams classification (1970) Class I: Na+-channel blockers. Class Ia: Procainamide, quinidine & disopyramide Class Ib: Lidocaine (I.V.), phenytoin, mexiletine, tocainide, Class Ic: Propafenone, flecainide, encainide Class II: β-blockers. Class III: K+-channel blockers: Amiodarone, sotalol, ibutilide, Dronedarone. Class IV: Ca++ Channel Blockers (CCB): Verapamil &Diltiazem Others (Non-classified): Adenosine, digoxin and Ivabradine.  MODERNIZED SCHEME BASED ON THE VAUGHAN WILLIAMS APPROACH (2018) (Nice To Know) https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA. 118.035455 Action Potential in Calcium-dependent Cells SAN and AVN K + β1 If funny current  Action Potential in Accessory Bundles, Abnormal Focus and Cardiac Muscles Na + Influx *Rate of Maximum Depolarization (Ѷ Max) or Conduction Velocity K + *Depends on number of β1 Na+ channels available Na+ APD and ERP Correlation between action potential and ECG AVN Ventricle PR Interval QRS Interval ----------QT Interval------------  Class I: Electrophysiology: 1. Na+ channel Blockade (fast fibers):  rate of maximum depolarization (Phase 0)  Vmax & delay conduction.  Slope of Phase 4 →↓automaticity genetrating electric current on their own Class Ia Class Ib Class Ic Procainamide Lidocaine Propafenone Effect on Conduction Moderate Minimal Marked 2- Effect on K+ Channels and ERP/ ~APD Block K+ channel → No effect on K+ But AVN Block beta receptor  APD/ERP → APD /ERP Fast Fibers in Block K+ channel →  K+efflux → No effect on K+ Ventricles  APD/ERP  APD>↓ ERP → ~ APD /ERP  Class Ia Agents: Electrophysiology: Other Cardiovascular Effects: Effect Adverse Effects and Clinical implication Antimuscarinic: Paradoxical ↑ AVN conduction →ventricular tachycardia in AF. Autonomic (blocked by adding digoxin, β Bs or verapamil before) Effects: (Verapamil and β Bs (C.I. with Heart Failure) Prolonged Q-T: "Torsade de Pointes" arrhythmia (↑ QT) → Procainamide Procainamide >Amiodarone Rational Professional Prescription Thank You