Anti-arrhythmic Drugs

  1. Lidocaine
    • Class Ib
    • Binds to inactivated Na+ channels (primary MoA)
    • Used for: acute ventricular arrhythmias, digitalis toxicity, (prevention of ventricular arrhythmia - controversial)
    • decreases APD and ERP in normal cells
    • Adverse FX: CNS at therapeutic doses (sleepiness, dizziness, paresthesia); CVS effects and allergic reaction at high doses
    • CI: 2nd or 3rd degree heart block, A-fib, sick sinus syndrome*note: lidocaine is the least cardiotoxic anti-arrhythmic
  2. Which is the only supraventricular arrhythmia that can be treated with Lidocaine?
  3. What makes phenytoin different from all other class I anti-arrhythmic agents?
    It is a weak acid, while all of the others are weak bases.
  4. Quinidine
    • Class Ia
    • Binds to activated Na+ channels (primary MoA)
    • (also has anti-muscarinic and alpha-1 antagonist activity)
    • Used for: Ventricular ectopic beats, A-fib and A-flutter after cardioversion, chronic control of SVT and VT
    • *note: rarely used as a first line treatment
    • Increases APD and ERP; decreases conduction velocity (slope of phase 0)
    • Adverse FX: Cinchonism, arrhythmia or asystole, torsade de pointes, sycope or sudden death
    • CI: torsade de pointes, wide QRS, long QT, heart block, digoxin induced arrythmia
  5. What should be given to treat Quinidine toxicity?
    Sodium lactate
  6. What happens when digoxin and quinidine are given together?
    • Digoxin clearance and volume of distribution become greatly reduced,
    • which leads to an increased steady-state concentration. Essentially,
    • this can lead to digitalis toxicity.
  7. How is procainamide different from quinidine?
    • 1. Less anti-muscarinic activity
    • 2. Less effect on Ca++ channels
    • 3. Less alpha-1 antagonist activity
  8. What is one major potential adverse effect of procainamide?
    SLE-like (lupoid) syndrome.

    • Why: Procainamide
    • gets metabolized by acetylation. In slow metabolizers, more
    • procainamide remains in the system. Procainamide also haptens to be a
    • good hapten. So, if it combines with a protein, it can trigger a
    • hypersensitivity reaction.
  9. Flecainide
    • Blocks activated Na+ channels (primary MoA)
    • (blocks K+ channels)
    • Used for: A-flutter, A-fib
    • *note: has a very limited use because it is proarrhythmogenic; second-choice drug
    • No effect on APD or ERP; large effect on phase 0
    • Adverse FX: arrhythmias, dizziness, sudden death
    • CI: Structural cardiac disease
  10. Phenytoin
    • Class Ib
    • Used for: treatment of digitalis-induced arrhythmia
    • ***: also used as an anti-convulsant
    • weak acid
  11. Metoprolol
    • Class II
    • Beta blockers (MoA)
    • Used For: chronic control of A-fib
    • and A-flutter, supraventicular reentry arrhythmias, arrhythmias caused
    • by increased adrenergic activity (thyroid, adrenal tumor)
    • *note: Esmolol is used in ICU because of its short half-life
    • decrease cardiac contractility, decrease HR (and therefore cardiac output)
  12. What effects will a beta blocker have on an EKG?
    -on PR interval
    -on QT interval
    -on QRS duration
    PR interval will be increased, QT interval and QRS duration will not be affected.
  13. Amiodarone
    • Class III
    • Blocks K+ channels and inactivated Na+ channels
    • Used for: A-fib, A-flutter, SVT, V-fib prophylaxis
    • *note: most effective and most commonly prescribed anti-arrhythmic
    • increases refractoriness (phase 3); decreases automaticity (phase 4)
    • Adverse FX: Affects every organ system - hypothyroidism, corneal deposits, torsade de pointes
    • CI: Long QT syndrome, pregnancy, sick sinus, torsade, cardiogenic shock
  14. What effects will amiodarone have on an EKG?
    PR interval will slightly increase, QRS will increase, and QT interval will markedly increase
  15. Sotalol
    • Class III, also has Class II activity
    • Blocks K+ channels
    • Used for: Supraventricular and ventricular arrhythmias
    • increases refractoriness (phase 3)
    • Adverse FX: caused by beta blocker activity, can lead to torsade de pointes
  16. Ibulitide
    • Class III
    • Blocks K+ channels and activates inward Na+ channels
    • Used for: A-flutter, A-fib
    • increases APD
    • Adverse FX: AV block, BBB, V-tach, torsade
    • CI: Long QT syndrome, V-tach
  17. Verapamil
    • Class IV
    • Block Ca++ channels in pacemaker cells (phase 0)
    • Used for: SVT, chronic A-flutter and A-fib
    • decreased conduction, increased refractoriness, decreased automaticity
    • CI: WPW, long QRS complex
  18. What effects do Class IV agents have on the EKG?
    Only PR interval is increased. QRS and QT are unaffected.
  19. Adenosine
    • activates Ach-sensitive K+ channels => hyperpolarization
    • inhibits cAMP-induced influx of Ca++ (secondary MoA)
    • Used for: acute PSVT
    • decreased automaticity, decreased conduction, increased refractoriness
  20. Where in the heart does adenosine act?
    SA node (decreases automaticity) and AV node (decreases conduction and increases refractoriness).
  21. What are the clinical uses of IV Magnesium sulfate?
    • 1. To prevent recurrent torsade de pointes.
    • 2. To treat digitalis induces arrhythmia.
  22. Digoxin
    • parasympathomimetic activity in the heart
    • Used for: A-fib and A-flutter in patients with cardiac failure

    Eliminates AV nodal reentrant tachycardia
Card Set
Anti-arrhythmic Drugs
Class and use, MoA, Adverse Effects, Contraindications