1. ARRHYTHMIAS • TACHYCARDIA >100/min • BRADYCARDIA <50/min • CARDIAC ARREST Electrical activity • Chaotic VF • Absent asystole

3. Action potential 0 -60

4. Propagating action potential 0 -60

5. Propagating action potential 0 -60

6. Propagating action potential 0 -60

7. Propagating action potential 0 -60

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

33. 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 • AVJ 98% • AVNRT 97% • AP 93% (L 95%, R 89%) • AFl 95% • Infarct VT 60-90%, long term 50% • Idiopathic VT 90% • Focal AF 60%

38. RFA: treatment of choice • AVJ 98% • AVNRT 97% • AP 93% (L 95%, R 89%) • AFl 95% • Idiopathic VT 90% ______________________________ • Infarct VT 60-90%, long term 50% • Focal AF 60%

41. Atrial flutter

42. Atrial Flutter: RFA vs AA drugsJACC2000;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