Antiarrhythmic Drugs

  1. What is the mechanism of action for Vaughan Williams classification Class 1 antiarrhythmic drugs?
    Inhibits voltage-gated sodium channels
  2. What is the mechanism of action for Vaughan Williams classification class 2 antiarrhthmic drugs?
    Beta blockers
  3. What is the mechanism of action for Vaughan Williams classification class 3 antiarrhythmic drugs?
    Inhibits voltage gated potassium channels- prolonging action potential by prolonging repolarization
  4. What is the mechanism of action for Vaughan Williams classification class 4 antiarrhthmic drugs?
    Calcium channel blockers (L-type)
  5. True/False: ablations and implantable devises are more effective and less harmful in some ways than drug therapy.
    True, they have largely relegated drug therapy to a secondary role
  6. What are the three ways that antiarrhythmic drugs work?
    • By reducing automaticity of abnormal tissues
    • Prolonging refractoriness
    • Slowing conduction
  7. According to the ACLS guideline, what is the main antiarrhythmic drug for cardiac arrest algorithm?
    Amiodarone- indicated for v fib or pulseless v tach
  8. What is an alternative drug to amiodarone in the cardiac arrest algorithm?
  9. Wha class does amiodarone fall in?
    Class 3
  10. Which channels do amiodarone have an effect in?
    • Moderate calcium, alpha and beta receptor blockage
    • Mild fast Na+ channel
    • Strong voltage-gated K+ channel
  11. What is the major effect of amiodarone?
    Block K+ voltage gated channel and phase 3 (repolarization) of cardiac cells
  12. What is the drug half life of amiodarone?
    25-60 days half life
  13. How is amiodarone eliminated?
    Hepatic metabolism and elimination
  14. What are major adverse effects seen in amiodarone?
    • Pulmonary- pneumonia is leading to pulmonary fibrosis – often fatal
    • Thyroid issues
    • Elevated liver enzymes
    • Skin discoloration (irreversible)
  15. What are some drug interaction with amiodarone?
    Inhibits o-glycoprotein and certain CYP450 enzymes causing high plasma levels of other drugs which are metabolized by those CYP450 enzymes or substrates of p-glycoprotein
  16. What is the second line of drug in cardiac arrest algorithm?
  17. What does the stem -Caine tell you about the drugs mechanism of action?
    Blocks Na+ channel
  18. True/False: lidocaine can be given orally, IV and topically for cardiac arrhythmia
    False; only IV bolus for cardiac arrhythmia
  19. What class of Vaughan Williams classification does lidocaine belong to?
    Class I
  20. What is the preferred drug for bradycardia with a pulse?
  21. What is the mechanism of action for atropine?
    Anticholinergic- blocks muscarinic receptors (M2)
  22. How does atropine affect the heart?
    Increase HR and AV nodal conduction
  23. What is the first line drug for tachycardia with a pulse and no wide QRS?
    • Adenosine
    • Beta blockers
    • Calcium channel blockers
  24. What is the half life for adenosine?
    10 second half life
  25. How does adenosine affect the heart?
    • Decrease HR
    • Decrease AV nodal conduction
  26. Which ion channel does adenosine block?
    L type calcium channels
  27. What are alternative drug to adenosine?
    • Verapamil (L type calcium channel blocker)
    • Diltiazem (L type calcium channel blocker)
  28. How does calcium channel blockers affect the heart?
    • Decrease contractility
    • Decrease heart rate
    • Decrease conduction velocity
  29. How does calcium channel blocker affect vasculature?
    Smooth muscle relaxation (vasodilation)
  30. What does the stem -dipines have in common?
    • They are calcium channel blockers
    • Arterial vasodilator
  31. Are versatile and diltiazem a dihydropyridine?
  32. What are some dihydropyridines?
    • Nicardipine
    • Nifedipine
    • Amlodipine
  33. What are the preferred drugs when there is a widen QRS in tachycardia with a pulse?
    • Procainamide
    • Amiodarone
    • Sotalol
  34. What is the drug of choice for ventricular tachycardia?
  35. What are alternatives of amiodarone for treatment of ventricular tachycardia?
    • Class 1A agent: procainamide
    • Class 3 agent: sotalol
  36. What are amiodarone good for?
    • Cardiac arrest (v fib)
    • Ventricular tachycardia
  37. How is procainamide given?
    IV and IM
  38. Why isn’t oral procainamide available?
    Had potential to cause drug induced lupus syndrome
  39. What is the classification for sotalol?
    Class III - voltage gated potassium channel blocker
  40. What is an adverse effect of sotalol?
    Proarrhythmia – induce v tach and v fib
  41. True/False: sotalol has beta blocking ability
  42. How does Torsades de Pointes rhythm occur?
    Can be induced by drugs – prolonged QT intervals
  43. What are the two class 3 antiarrhythmic drugs we learned?
    • Amiodarone
    • Sotalol
  44. If QT interval becomes too prolonged with Class 3 K+ blockers, what could result?
    Torsade de pointes – V tach and turn into V fib
  45. If patient already has QT, should you give Class 3 drugs?
  46. Patients who have hypokalemia and hypomagnesia, what could result if given class 3 drugs?
    Torsade de pointes
  47. How to treat torsade de pointes?
  48. Which drug to treat atrial tachycardia/SVT?
    • Adenosine
    • Verapamil
    • Diltiazem for a-fib
  49. Which drugs to treat bradycardia?
    • Atropine
    • Dopamine
    • Epinephrine
  50. Which drugs to treat V-tach/V-fib?
    • Amiodarone
    • Lidocaine
    • Procainamide
    • Sotalol
    • Magensium sulfate
  51. List two class 1 drugs:
    • Procainamide
    • Lidocaine
  52. List two class 3 drugs:
    • Amiodarone
    • Sotalol
  53. List two class 4 drugs:
    • Verapamil
    • Diltiazem
    • Which class of drug are the beta blockers?
    • Class II
  54. What class does atropine belong to?
    None, they are not classified as they are anticholinergic drug
  55. What is an antiarrhythmic effect of atropine?
    It is used to treat bradycardia via anticholinergic effect thereby raising HR
Card Set
Antiarrhythmic Drugs
Cardiovascular final