Anti arrhythmic drugs Dr. S. Parthasarathy - PowerPoint Presentation

1. Anti arrhythmic drugs Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab.DCA, Dip. Software statistics, Phd (physio)Mahatma Gandhi Medical college and research institute , puducherry , India

2. What is normal ??

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4. Electrophysiology - resting potentialA transmembrane electrical gradient (potential) is maintained, with the interior of the cell negative with respect to outside the cellCaused by unequal distribution of ions inside vs. outside cell Na+ Ca +Na+ higher outsideCa+ much higherK+ higher insideMaintenance by ion selective channels, active pumps and exchangersK +

5. Diastole

6. Na

7. Phase 2 - plateau phasesustained by the balance between the inward movement of Ca+ and outward movement of K + Has a long duration compared to other nerve and muscle tissueNormally blocks any premature stimulator signals (other muscle tissue can accept additional stimulation and increase contractility in a summation effect)Corresponds to ST segment of the ECG.

8. Phase 3 – repolarization K+ channels remain open, Allows K+ to build up outside the cell, causing the cell to repolarizeK + channels finally close when membrane potential reaches certain levelCorresponds to T wave on the ECG

9. Reminder

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11. Vaughan Williams classification of drugs Class I --- A – quinidine ,morizicine, procainamide,disopyramide B- lignocaine,mexilitine tocainide, phenytoin C-flecainide , propofenone Class II – beta blockers Class III – sotalol, Bretylium, Amiodarone, Acecainide Dofetilide, Ibutilide, AzimilideClass IV – Verapamil, Diltiazem,BepridilMiscellaneous :digoxin, adenosine

12. Four classes of drugs Some Block Potassium Channels

13. Go into each

14. BAC

15. ON PACEMAKER POTENTIAL

16. Class I A Phase 0- decrease velocity and amplitude APD and ERP increased Quinidine decreases automaticity in atrial and ventricular tissue and in the His-Purkinje and pacemaker fibersSA node - ? Action due to anticholinergic effects

17. Class I A

18. Quinidine 200 mg six hourly tablets Digoxin or verapamil – add to decrease ventricular response But digoxin toxicity ??Diarhoea, thrombocytopenia ,hypotension, arrythmias !!

19. Indications of quinidine conversion of atrial fibrillation, atrial flutter,PSVT, maintenance of sinus rhythm after conversion.In addition, it suppresses ventricular ectopy,tachycardia, and fibrillation.

20. Procainamide 1 gm iv bolus – 1 mg /min.Atrial and ventricular arrhythmias Neg.inotropy, CHF?? Puts a hold NAPA (N acetyl procainamide)– class III actions

21. Difficult private question Disopyramide,procainamide and quinidine

22. Class I B

23. Lignocaine they shorten APD and ERP and increase the ERP-to-APD ratio in the Purkinje fibers,NO effect on the refractory periods in sinus node, atrium, and AV node1 mg/kg – 1 mg/minute infusion – no tapering Effect on SVT ?? PVC s !!

24. Phenytoin I B effects – centrally mediated sympatholysis Prolonged QT interval + atrial and ventricular arrhythmias1 gm IV bolus + 50 mg/ min. Other side effects ??

25. Difficult private questionMarks ?? Pick low marks Phenytoin, lignocaine and mexilitine

26. Class I C

27. Class I C - flecainide, propofenone slow AV node, His-Purkinje and ventricular conduction--ERP unchanged Used for ventricular arrhythmias and also WPW drugs suppress automaticity of the SA node,Negative inotropy, arrest, more mortality

28. Class I –Na+channel blockers Class I a : Used most frequently for conversion of atrial flutter/fibrillation and maintenance of sinus rhythm.Class I b : Used for ventricular arrhythmias, especially those associated with myocardial infarction/ischemia but not for prophylaxis.Class I c : Used for atrial flutter/fibrillation in patients with structurally normal hearts.

29. Difficult private questionPick low marks Final exam proficiency ??Flecainide , encainide , propofenone

30. Class II β–adrenergic blockersBased on two major actions1) blockade of myocardial β–adrenergic receptors2) Direct membrane-stabilizing effects related to Na+ channel blockadeSinus node !! Rate of spontaneous depolarization decreased

31. Beta blockers β-Adrenergic antagonists are effective for the treatment of cardiac dysrhythmias related to enhanced activity of the sympathetic nervous system (perioperative stress, thyrotoxicosis, pheo)Ischemia Acebutolol, propranolol, and metoprolol are approved for the prevention of sudden death following myocardial infarction.

32. Class III – amiodarone

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34. Amiodarone Blocks potassium channels ,Prolongs repolarization Vasodilator -- Even coronary SVT and VT – both √With intravenous therapy, an initial loading dose of 150 mg is given over 10 minutes. continuous infusion of 1 mg/min for 6 hours followed by 0.5 mg/min 5% dextrose solutionThyroid – lipophilic – eye – heart block-new VF

35. Amiodarone - Pulmonary fibrosis

36. Bretylium Class III action , blocks norad release Chemical sympathectomy Loading dose 5 mg / kg – Unresponsive Ventricular arrhythmias Replaced by amiodarone Direct( Increased action)and indirect( less action) vasopressors Bupi induced arrhythmias

37. sotalolPO: 40–80 mg.( class III + beta blocking)Ventricular arrhythmias Ibutilide has been approved for acute termination of atrial fibrillation or flutterIntravenous dosage is 1 mg over 10 minutesNo action on AV node

38. Class IIIDofetilide is approved for acute conversion of atrial fibrillation and atrial flutter to sinus rhythm, and for prevention of recurrence of atrial fibrillation.It is a very potent K channel blockerProblem -- QT prolongation and torsades de pointes

39. Class III IS BADI butilideS otalolB retyliumA miodaroneD ofetilide

40. CALCIUM CHANNEL BLOCKERS

41. VERAPAMIL NIFIDEPINE DILTIAZEM CALCIUM CHANNEL BLOCKERS VERY NICE DRUGS

42. Verapamil Verapamil inhibit the flux of calcium ions across the slow channels of smooth muscle and cardiac cells. decreased rate of spontaneous phase 4 depolarization. Verapamil has a substantial depressant effect on the atrioventricular node and a negative chronotropic effect on the sinoatrial node.

43. Verapamil Supraventricular tachydysrhythmias (action on atrioventricular node)Vasospastic angina pectoris (mild vasodilating effects)Essential hypertension (mild vasodilating effects)Hypertrophic cardiomyopathy40 – 80 mg tds or 100 mic gm / kg IV SA node depression is not with dilzem Cautious use with digoxin

44. Adenosine Adenosine is an endogenous nucleotide natural to all cells of the bodyIn pharmacologic doses, it slows conduction through the AV node Efficacious as acute IV therapy for patients with paroxysmal supraventricular tachycardia in both reentry and accessory pathway (Wolff-Parkinson-White) dysrhythmias.

45. Adenosine SVT – re entry or accessory tract 6mg IV bolus - --then 12 mg – 92 % conversion AF ?? Use Blocks and sick sinus – dangerous Caffeine – decreases levels Wheezing, brady- even asystole intrathecal adenosine might be effective in the treatment of acute and chronic pain

46. PearlsStart everything but amiodarone in house.Drugs work best when the EF is high.Drugs have most proarrhythmia when EF is low. Only amiodarone, sotalol, and dofetilide are known safe in low EF patients.

47. Pearls Use amiodarone, quinidine, mexiletine, moricizine, ibutilide, or lidocaine in renal failure. Amiodarone’s risk of torsades is poorly related to QT prolongation. Classes Ia, Ic, II, IV are negatively inotropic. Use AV blockers with class Ic drugs for PAF.Monitor QRS duration with class Ic drugs.

48. If you don’t know what arrhythmia is that ?? Better use amiodarone

49. In anaesthesia Adenosine Verapamil Lignocaine Amiodarone Beta blockersDigoxin ACLS specialists Not going into the details of perioperative arrhythmias

50. Beta blockers propofenone Verapamil Digoxin QuinidineVerapamil amiodarone Adenosine Lignocaine

51. Why should we read this topic ??

52. The first recorded death during anesthesia, that of Hannah Greener in 1848, was most likely because of ventricular fibrillation (VF) resulting from the “sensitizing” action of chloroform

53. Thank you all