1. ARRHYTHMIAS TACHYCARDIA>100/min BRADYCARDIA<50/min CARDIAC ARREST Electrical activity –ChaoticVF –Absentasystole

3. Action potential -60 0

4. Propagating action potential -60 0

5. Propagating action potential -60 0

6. Propagating action potential -60 0

7. Propagating action potential -60 0

8. Propagating action potential

9. TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

10. DEPOL Inward  REPOL outward 

13. Propagating action potential

14. TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

15. DEPOL Inward  REPOL outward 

17. DEPOL Inward  REPOL outward 

18. AUTOMATICITY Physiological: Sinus node Pathological: Reduction/depolarisation of resting membrane potential (e.g. Ischaemia)

19. TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

20. Tachyarrhythmias Antiarrhythmic drugs –Vaughan-Williams Classification –Drugs divided according to EP effects on cells –All are negatively inotropic –Can also be pro-arrhythmic

21. Tachyarrhythmias Class I –Impede Na transport across cell membrane –Ia increase AP duration eg quinidine, disopyramide, procainamide –Ib shorten AP duration eg lignocaine, mexilitene, propafenone –Ic little effect on AP eg flecainide

22. Tachyarrhythmias Class II –Interfere with effects of SNS on the heart eg beta blockers Class III –Prolong AP duration but do not effect initial Na dependent phase eg sotalol, amiodarone Class IV –Antagonise Ca transport across cell membrane –SA and AV node particularly susceptible eg verapamil, diltiazem

25. TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

26. AV Nodal block [Class II –Interfere with effects of SNS on the heart eg beta blockers] Class III –Prolong AP duration but do not effect initial Na dependent phase eg sotalol, amiodarone Class IV –Antagonise Ca transport across cell membrane –SA and AV node particularly susceptible eg verapamil, diltiazem Adenosine –Specific AV nodal block

29. EP study: standard fixed wires

34. RADIOFREQUENCY ABLATION

35. TREATMENT STRATEGY STABILISE AUTOMATICITY PROLONG ACTION POTENTIAL SLOW CONDUCTION INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

37. RFA: success rates AVJ98% AVNRT97% AP93% (L 95%, R 89%) AFl95% Infarct VT60-90%, long term 50% Idiopathic VT90% Focal AF60%

38. RFA: treatment of choice AVJ98% AVNRT97% AP93% (L 95%, R 89%) AFl95% Idiopathic VT90% ______________________________ ?Infarct VT60-90%, long term 50% ?Focal AF60%

41. Atrial flutter

42. Atrial Flutter: RFA vs AA drugs JACC2000;35:1898 prospective, randomised – 61 pts SR at 21 months:36%AAD vs 80% RFA Rehospitalised:63% AAD vs 22% RFA AF:53% AAD vs 29% RFA QOL:no change AAD improvement RFA

45. TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

46. Concepts of AF: 1900-2000 MULTIPLE WAVELETS Ines, Garrey MOTHER WAVE Lewis HYPEREXCITABILITY Engelmann, Winterberg

49. WPW syndrome

51. AV re-entry tachycardia

57. TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

59. Ventricular tachycardia

61. TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

65. Rhythm Strip During Episode of Sudden Death

66. TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

67. Implanatable defibrillators

68. Implanatable defibrillator in-situ

72. Sinus node disease

73. AV node disease 1st degree heart block 2nd degree heart block (2:1)

74. AV node disease Complete (3rd degree) heart block

75. Bradyarrhythmias AV node disease –1st degree; prolonged PR interval –2nd degree; Mobitz type I (Wenckebach); increasing PR interval then non-conducted P wave –2nd degree; Mobitz type II; non-conducted P waves –2nd degree; 2:1 or 3:1 AV node block –3rd degree; complete heart block AV block usually caused by idiopathic fibrosis; other causes include MI, drugs and congenital block

76. TREATMENT STRATEGY PROLONG ACTION POTENTIAL MODIFY CONDUCTION STABILISE AUTOMATICITY INTERRUPT REENTRY –PHARMACOLOGICAL –PHYSICAL ELECTRICAL STIMULATION –ATP/SHOCK TACHY –PACE BRADY

77. Bradyarrhythmias Treatment of symptomatic bradyarrhythmias often consists of pacing In the short-term drugs may be used to augment conduction eg atropine, isoprenaline