Antiarrhythmic drugs satya
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This ppt is on the pharmacology of antiarrhythmic drugs,including description of mechanism of actions with diagrams showing different phases of action potentials...for easy grasping of principles...for medical students...
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Antiarrhythmic drugs satya
- 4. ARRHYTHMIAS • 75% of patients of acute M.I Develop→ • 50% of patients under General Anaesthesia → Develop • CAUSE OF SUDDEN CARDIAC DEATH
- 8. ANTIARRHYTHMIC DRUGS DR. V. SATHYA NARAYANAN M.D PROFESSOR OF PHARMACOLOGY SRM MCH & RC, CHENNAI, INDIA
- 9. ANTIARRHYTHMIC DRUGS • Drugs used to prevent or treat irregularities of cardiac rhythm
- 11. MECHANISMS • Enhanced ectopic pacemaker activity • After – depolarisations • Reentry • Fractionisation of impulse
- 14. TYPES OF ARRHYTHMIAS • Broadly divided into • bradyarrhythmias • tachyarrhythmias
- 15. TACHYARRHYTHMIAS • Extrasystoles • Paroxysmal Supraventricular Tachycardia – (PSVT) • Atrial Fibrillation, AF- Atrial flutter • Ventricular tachycardia, VF – ventricular fibrillation • T.D.P- Torsades de pointes •
- 16. BRADYARRHYTHMIAS • Sinus bradycardia, • A.V Block
- 17. Normal heartbeat and atrial arrhythmia Normal rhythm Atrial arrhythmia AV septum
- 19. Ventricular Arrhythmia • Ventricular arrhythmias are common in most people and are usually not a problem but… • VA’s are most common cause of sudden death • Majority of sudden death occurs in people with neither a previously known heart disease nor history of VA’s • Medications which decrease incidence of VA’s do not decrease (and may increase) the risk of sudden death treatment may be worse then the disease!
- 26. The Action Potential Phase 0 Phase 4 Phase 3 Phase 2 Phase 1 - 90 mV 0 mV 30 mV
- 27. ACTION POTENTIAL & SITE OF ACTION • Phase 0 –rapid depolarisation –inflow of Na • Phase 1-rapid repolarisation –out flow of k • Phase 2 –delay in repolarisation –slow inflow ofCa • Phase 3-rapid repolarisation –outflow k • Phase 4 –fully repolarised - Phase 0 Phase 4 Phase 3 Phase 2 Phase 1 - 90 mV 0 mV 30 mV
- 28. ACTION POTENTIAL & SITE OF ACTION Phase 1 ←IV→ Phase 2 Phase 0 ← III → phase 3 Phase 4 ← I →
- 29. CLASSIFICATION • Class I –Na channel blockers • IA -quinidine, disopyramide, procainamide • IB – lignocaine , mexiletine, phenytoin • IC - flecainide , propafenone, encainide • Class II : β – adrenergic blockers - sotalol (with class IIIactivity) Esmolol propranolol
- 30. CLASSIFICATION • Class III K+ channel blockers Amiodarone, Bretylium, dofetilide • Class IV :Calcium channel blockers Verapamil , diltiazem
- 31. ACTION POTENTIAL & SITE OF ACTION • Phase 1 ←IV→ phase2 Phase 0 ← III → phase 3 Phase 4 ← I →
- 32. Class I Na+ Channel Blockers • IA - Quinidine/Procainamide/Disopyramide • IB - Lidocaine/Mexiletine/Phenytoin • IC - Flecainide/Propafenone/Ethmozine 1 0 2 3 4 ERP RRP Affects Phase 0
- 33. CLASS IA • Lengthen action potential duration &refractoriness • QUINIDINE : prototype, • Rarely used Depress myocardial contraction ADR : cinchonism , Torsades De Pointes, hypotension, Ventricular Fibrillation USE : malaria
- 34. PROCAINAMIDE • Slow 0 phase, impulse conduction,prolongation of APD, ERP • acetylated • ADR: CNS effects ( mental confusion, hallucinations), hypersensitivity reactions,T.D.P. ,S.L.E • USE :to prevent recurrence of VF • not suitable for prolonged therapy
- 37. DISOPYRAMIDE • cardiac depressant • with anti muscarinic effects • Second line drug for prevention of VF, VFib
- 42. CLASSIFICATION IB (LIGNOCAINE) • block Na channels more in inactivated state • Do not alter APD, ERP • suppress automaticity in ectopic foci , • decrease APD in PF, ventricles • used only in VF,Vfib following MI, • Cardiac surgery etc, • prophylaxis • given I.V
- 48. ADR • dose related neurological effects – • drowsiness, • paraesthesia, • convulsions
- 52. MEXILETINE • effective orally • similar to lignocaine • poorly tolerated
- 54. CLASSIFICATION I C • Most potent Na channel blockers in open state • Minimal effects on refractoriness • Highly proarrhythmic • Risk of cardiac arrest, sudden death • PROPOFENONE – reserve drug for ventricular arrhythmias, reentrant tachycardias • FLECAINIDE :reserved for resistant AF, WPW syndrome
- 56. CLASS II BETA BLOCKERS • ↓ Automaticity, conduction velocity, myocardial contractility • Prolong the ERP of AV node • USE : supraventricular arrhythmias associated with exercise , • emotion , • hyperthyroid
- 61. BETA BLOCKERS • Propranolol – used in sinus tachycardia, Extrasystoles, digitalis induced arrhythmias • Sotalol :Has prominent classIII effect, • prolong repolarisation, • effective in polymorphic VT, has risk of TDP • Esmolol : short acting , • β1 selective, • preferred when others are Contraindicated, • t1/2 -- 9 min, • USES : During surgeries, following MI
- 63. CLASS II BETA BLOCKERS • Infusion of i.v esmolol in emergencies • emergency control of ventricular rate in AF/AFl • ADR : heart block , cardiac arrest • D/I : verapamil , diltiazem if concomitantly given increase AV block ,cardiac failure
- 69. CLASS III AMIODARONE • Most powerful antiarrhythmic, commonly used • Blocks Na, K, Ca channels • Prolongs APD, refractoriness • used in both atrial, ventricular arrhythmias • Slow onset of action • Has serious toxicity • Used orally for long term prophylactic therapy • USES : chronic VA, SVA, WPW • after cardioversion for AF , AFl
- 73. CLASS III AMIODARONE ADR : • arrhythmias • corneal microdeposits • Thyroid problems • Photosensitivity • Peripheral neuropathy • Bluish discoloration of skin • Pulmonary alveolitis • D/I : ↑ effects of digoxin, warfarin
- 80. CLASS IV CALCIUM CHANNEL BLOCKADE • Inhibit calcium passage • suppress automaticity, contractility, AV nodal conduction VERAPAMIL : • depress SA node rate, • prolongs conduction in AV node • Uses : to terminate attacks of PSVT, • to control ventricular rate in AF,AFl • ADR: constipation , • hypotension , • bradycardia , • heart block
- 81. PSVT
- 85. DILTIAZEM • alternative to verapamil, • Milder than verapamil • preferred in AF, AFl
- 87. ADENOSINE • suppress automaticity, slow AV conduction, • dilate coronary arteries • given rapid i.v bolus • action lasts for 15 seconds • • USE : drug of choice for acute termination of PSVT WPW syndrome alternative to verapamil in SVT
- 92. ADENOSINE ADR •transient dyspnoea , •flushing , •fall in BP, •Bradycardia CONTRAINDICATIONS •asthma , •AV block , •sick sinus syndrome •Expensive
- 96. OTHERS DIGOXIN : •→slow conduction through AV node •used in Atrial Fibrillation , Atrial flutter • to control the ventricular rate
- 98. DRUGS FOR BRADYARRHYTHMIAS • ISOPRENALINE : • β agonist used in heart block • ADR • tremor , • flushing , • palpitation , • sweating • ATROPINE : sinus bradycardia after MI
- 101. Vaughan-Williams Classification Class Mechanism Example I Na channel blockers Membrane Stabilizers Lignocaine II Beta Blockers Metoprolol III K channel blockers Amiodarone IV Ca channel blockers Verapamil Other Digoxin. Adenosine. MgSO4. Atropine
- 102. Phases of action potential of cardiac cells • Phase 0 rapid depolarisation (inflow of Na+) • Phase 1 partial repolarisation (inward Na+ current deactivated, outflow of K+ ) • Phase 2 plateau (slow inward calcium current) • Phase 3 repolarisation (calcium current inactivates, K+ outflow) • Phase 4 pacemaker potential (Slow Na+ inflow, slowing of K+ outflow) ‘autorhythmicity’ • Refractory period (phases 1-3) Phase 4 Phase 0 Phase 1 Phase 2 Phase 3 0 mV -80mV II I III IV
- 107. SUMMARY • Tt of arrhythmias can be • Physical, electrical, pharmacological, surgical • Drugs are adjunctive • Choice by observations of efficacy ,safety • All drugs can be dangerous • Should be used if condition is compromised • Mostly needed for short periods
- 112. SUMMARY • Adenosine – choice For supraventricular Arrhythmias • Verapamil – Alternative to adenosine • Amiodarone –Most effective for AFl, Preventing VA –But HAS ADR • Digoxin – used in slowing AV conduction in AF
- 114. Take-Home Message • Anti-arrhythmics are also pro-arrhythmics • Dangerous side effects • If patient is unstable rather cardiovert • Enlist expert help • Stick to drugs you know • Limited choice anyway
- 115. THANK U
Editor's Notes
- To be familiar with these properties, we must return to our basic physiology-and review the action potential of the cardiac cell. Remember that the environment inside the cell is negative and the outside of the cell is positive because of the cellular polarization. This sets the resting membrane potential at approximately minus 90 millivolts with respect to the outside of the cell. During Phase 0, the cell depolarizes as the sodium channels are opened and positive sodium ions rapidly move into the heart. During Phase I, there is early rapid repolarization. During Phase II, this repolarization plateaus and at Phase III there is a later phase of repolarization (primarily secondary to potassium and calcium ions). In Phase IV, the cell has again reached the resting membrane potential and it is during this time that the diastolic depolarization can occur in spontaneously excitable cells.
- The sodium channel blockers affect Phase 0 of depolarization-the rapid inflow of sodium through the sodium channels. They are divided into 3 subclasses. 1A includes quinidine, procainamide, and disopyramide. Class 1B includes lidocaine, mexiletine, and phenytoin. Finally, Class IC would include flecainide as well as the others listed on the slide.
- Links AA drugs to a MOA Not all drugs are included – Some commonly used Some drugs overlap classes - Sotalol