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Antiarrythmia

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Antiarrythmia

  1. 1. CARDIAC ARRHYTHMIAStacy Arvinna J,Group 3KSMU
  2. 2. TOPICS COVERED• Types of Arrhythmias – Ventricular• Cardiac Action Potential• Ion Channels of Interest• Classification of Anti-arrhythmic drugs• Drugs and Re-entry• Class I Drugs• Class III Drugs• Side Effects• Alternative Treatments and Future Drug Development
  3. 3. MECHANISMS OF CARDIAC ARRHYTHMIAS1. Enhancement or depression of impulse generationa. Enhanced or depressed normal automaticity from the SA node,b. Abnormal automaticity develop in atrial or ventricular myocardium.c. Triggered activity develop from normally quiescent cardiac tissueperi AV nodal or Purkinje system. due toI.early. afterdepolarizationsII.late"afèé1^depolarízations2. Abnormal conduction of the cardiac impulsea. Conduction blockb. Delayed conductionc. Unídirectional block and reentry or reflection
  4. 4. VENTRICULAR RE-ENTRY •Abnormal pattern of depolarization through the heart •Functional •Anatomic
  5. 5. THE CARDIAC ACTION POTENTIAL
  6. 6. ION CHANNELS RELEVENT TO THE CARDIAC ACTION POTENTIAL
  7. 7. Antiarrhythmic Drug Pathways
  8. 8. THE VAUGHAN WILLIAMS CLASSIFICATION SYSTEM OF ANTI- ARRHYTHMIC DRUGSClass Basic MechanismI-Sodium Channel Blockade Reduce phase 0 slope and peak of action potentialIA   Moderate reduction in phase 0 slope; increase APD; increase ERPIB Small reduction in phase 0 slope; reduce APD; decrease ERPIC Pronounced reduction in phase 0 slope; no effect on APD or ERPII-Beta-blockade Delay repolarization (phase 3) and thereby increase action potential duration and effective refractory period.III-potassium-channel blockade Prolongation of APD and increase ERP; no effect on phase 0IV-Calcium channel blockade Block L-type calcium-channels; most effective at SA and AV nodes; reduce rate and conduction.
  9. 9. HOW THESE DRUGS AFFECT RE-ENTRY • Class I: retards conduction enough so that beat still gets through normal cardiac tissue but not through any weakened tissue • Class III: prolongs refractoriness
  10. 10. CLASS I• IA – moderate• IB – weakest• IC – strongest
  11. 11. CLASS IA
  12. 12. CLASS IA-Procainamide Procainamide N-Acetyl Procainamide
  13. 13. CLASS IB
  14. 14. CLASS IB-Lidocaine
  15. 15. CLASS IC
  16. 16. CLASS IC-flecainide
  17. 17. Cardiac Side Effects-Proarrhythmia•Potential re-entrant circuit can • Increased incidence of death inbe turned into an actual re-entrant the case of myocardialcircuit infarction
  18. 18. Class III
  19. 19. CLASS III-Sotalol
  20. 20. Torsades desPointes •Long Q-T syndrome •Polymorhic Ventricular Tachycardia •IA drugs can also cause this •Blocking of potassium channels and prolonging repolarization
  21. 21. ALTERNATIVE TREATMENTS • Ablation • Implanantable Cardioverter Defibrillators (ICDs)
  22. 22. ICD Placement In the Heart
  23. 23. FUTURE OF DRUG DEVELOPMENT• Drugs with defibrillating effects – Sotalol – Tedisamil • Sympathomimetic-modulates cAMP • Protects Gap junctions and enhances Ca2+ uptake by SR• Drugs affecting Ion Channelopathy – hyperphosphorylation• Drugs or Devices?
  24. 24. Antiarrhythmic Drug Pathways
  25. 25. • : www.aavpt.org/symposia/documents/Muir 213-221.pdf

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