Pharmacology Antiarrhythmics 3

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  1. Does Flecainide cause EADs or torsades de pointes?
  2. What is Flecainide used to treate?
    Maintains sinus rhythm in patients with supraventricular arrhythmias, may increase mortality 2.5 fold in patients with MI
  3. Propranolol has effects similar to what other drug?
  4. What are the MOAs of Propranolol in the treatment of Arrhythmias?
    B-blockade, ↓ automaticity, ↓conduction and automaticity in AV node, Perkinje and ventricles
  5. What are the adverse effects of Propranolol?
    Reduced Myocardial contractility, Bradycardia, Angina and sudden withdrawal, Bronchospasm
  6. What is Propranolol used for?
    Supraventricular tachycardia
  7. Does Propranolol cause increased risk, like Flecainide after MI?
    No, very beneficial
  8. What is the most widely used antiarrhythmic in clinical use?
  9. What are the indications for Amiodarone?
    Unstable Ventricular Tachycardia, Ventricular Fibrillation, Supraventricular tachycardia, atrial fibrillation (off-label)
  10. What are the adverse effects of Amiodarone?
    Systemic toxicity: Pulmonary arrhythmias and Bradyarrhythmias with Loading Dose
  11. What changes in AP duration and ERP would you expect with Amiodarone?
    Both Increase
  12. What effect does Amiodarone have on Automaticity?
  13. What effect does Amiodarone have on Conduction?
  14. What effect does Amiodarone have on blood vessels?
  15. What channel/receptor types does Amiodarone block?
    Na, Ca, K, B-receptors
  16. By what mechanism does Amioadrone delay repolarization and increase refractory period?
    K channel blockade
  17. What characteristics are being sought after in Antiarrhythmic drug development?
    Multiple pharmacological actions on Cardiac tissue (rather than selective)
  18. A battery of testing including Cardiac, Hepatic, Thyroid, Pulmonary, Dermatologic, Neurologic and Ophthalmic are required for what drug?
  19. What is Amiodarone used for?
    Recurrent ventricular tachycardia, fibrillation resistant to other drugs, atrial fibrillation
  20. Intravenous amiodarone more effective than ________ for out-of-hospital Ventricular Fibrillation resistant to shocks and epinephrine.
  21. Does Amiodarone exacerbate CHF?
  22. Is Amiodarone rarely proarrhythmic?
  23. What s Dronedarone?
    Structural derivative of Amiodarone with reduced toxicity for suppression of atrial fibrillation
  24. What is the MOA of Dronedarone?
    Multichannel blocking properties and sympatholytic abilities similar to Amiodarone, reduces ventricular rate and rate of recurrent AF
  25. What group may Dronedarone increase mortality in?
  26. What is the half-life of Dronedarone?
    24-30 hours
  27. What metabolizes Dronedarone?
  28. Which antiarrhythmatic should not be given with any of the following: ketoconazole, cyclosporine, ritonavir, clarithromycin and nefazodone?
    Dronedarone, because they compete for CYP3A4 metabolism
  29. How does Sotalol prolong Cardiac action potentials?
    By inhibiting delayed rectifier and possibly other K currents
  30. What enantiomer of Sotalol is more potent at the B-receptor and which one is less?
    More: l-enantiomer, Less: d-enantiomer
  31. What is the indication for Sotalol?
    Ventricular tachyarrhythmias and atrial fibrillation or flutter
  32. What is the major toxicity associated with Sotalol and at what rate does it occur?
    Torsades de pointes at ~5%
Card Set
Pharmacology Antiarrhythmics 3
Pharmacology Antiarrhythmics 3
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