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ARRHYTHMIAS

ARRHYTHMIAS. TACHYCARDIA >100/min BRADYCARDIA <50/min CARDIAC ARREST Electrical activity Chaotic VF Absent asystole. Action potential. 0. -60. Propagating action potential. 0. -60. Propagating action potential. 0. -60. Propagating action potential. 0. -60.

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ARRHYTHMIAS

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

  2. Action potential 0 -60

  3. Propagating 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

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

  9. DEPOL Inward  REPOL outward

  10. Propagating action potential

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

  12. DEPOL Inward  REPOL outward

  13. DEPOL Inward  REPOL outward

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

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

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

  17. 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

  18. 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

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

  20. 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

  21. EP study: standard fixed wires

  22. EP study: standard fixed wires

  23. RADIOFREQUENCY ABLATION

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

  25. 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%

  26. 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%

  27. Atrial flutter

  28. 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

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

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

  31. WPW syndrome

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