Pharmacology Antiarrhythmics 2

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249691
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Pharmacology Antiarrhythmics 2
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2013-11-29 19:53:57
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Pharmacology Antiarrhythmics
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Pharmacology Antiarrhythmics 2
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  1. What are the characteristics of Class II Vaughn-Williams drugs?
    • Beta adrenergic blockers
    • Some have Na channel blockade (Propranolol)
  2. What are the characteristics of Propranolol?
    Causes both Na channel and B blockade, slows SA node and ectopic pacemaking, blocks arrhythmias induced by exercise or apprehension
  3. What drugs are Class II Vaughn-Williams drugs?
    Propranolol, Metoprolol, Atenolol, Sotalol, Esmolol
  4. What are the characteristics of Class III Vaughn-Williams drugs?
    K channel blockers, Delayed repolarization and prolonged refractory period
  5. What are the Class III Vaughn-Williams drugs?
    Amiodarone, Ibutilide, Bretylium, Dofetilide
  6. What are the basic characteristics of Amiodarone?
    Prolongs AP by delaying K efflux (also other effects)
  7. What are the basic characteristics of Ibutilide?
    Slows inward movement of Na in addition to delaying K efflux
  8. What are the basic characteristics of Bretylium?
    Supresses Ventricular fibrillation associated w/ MI, first used to treat hypertension
  9. What are the basic characteristics of Dofetilide?
    Prolongs AP by delaying K efflux
  10. How do Class IV drugs work?
    Slow rate of AV conduction in patients with atrial fibrillation, Ca channel blcokers
  11. What drugs are included in Class IV?
    Verapamil and Diltiazem
  12. What are the basic characteristics of Verapamil?
    Blocks Na channels in addition to Ca, Slows SA node in tachycardia
  13. What are the pharmacological actions of Quinidine?
    Inhibits VGSC (open channel blocker), Inhibits delayed rectifier K+ channels (at slower rates greater block of Na+ than K+ channels), Muscarinic receptor antagonist ( AV nodal conduction), Alpha adrenergic receptor antagonist
  14. What are the actions of Quinidine?
    Antimuscarinic (increase in AV nodal transmission of atrial flutter and fibrillation), ↑ threshold for excitability and ↓ automaticity, ↓ conduction velocity (decreases slope of phase 0),↑ duration of QRS (delays conduction),↑ duration of QT interval (delays repolarization), Vasodilation
  15. What are the adverse actions of Quinidine?
    Cinchonism: dizziness, tinnitus, N/V, diarrhea, Hypotension and syncope, Ventricular arrhythmia (2-8% of patients develop torsades de pointes, Women>Men)
  16. What is Quinidine used for?
    Symptomatic ventricular arrhythmias with impaired ventricular function, Recurrent atrial fibrillation after conversion to sinus rhythm
  17. What has Quinidine use diminished?
    Due to high incidence of proarrhythmias
  18. Does Quinidine compromise ventricular contractility?
    No
  19. Does Lidocaine decreases automaticity?
    Yes, especially in ectopic pacemakers
  20. What type of arrhythmias is Lidocaine not useful in?
    Atrial arrhythmias
  21. Why is Lidocaine not useful for Atrial arrhythmias?
    Atrial action potentials are so short that the Na+ channel is in the inactivated state only briefly
  22. Does Lidocaine block open or inactivated Cardiac Na channels?
    Both
  23. What adverse reactions may Lidocaine cause?
    Tremor, dysarthria, ∆ in consciousness most common, also Large IV doses administered rapidly may produce seizures
  24. What type of Arrhythmias is Lidocaine used to treat?
    Acute IV therapy of ventricular arrhythmias
  25. What drug is Mecilitine a congener of and similar to?
    Lidocaine
  26. Can Mexilitine be given orally?
    Yes
  27. What is Mexilitine used for?
    Ventricular arrhythmias
  28. What are the MOAs of Flecainide?
    Blocks Na+ and delayed rectifier K+ currents with similar potencies, Very long recovery from Na+ channel block, Also blocks Ca2+ channels, ↓Decreases sinus node automaticity
  29. What are the adverse effects of Flecainide?
    Dose-related blurred vision = most common

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