1. Class 1 Antiarrhythmic: Na+ channel blockers
    • Decrease automaticity in SA node by
    • -shifting the threshold to more positive potentials
    • -decreasing the slope of phase 4

    • Decrease the likelihood of re-entry by
    • -decreasing the conduction velocity
    • -increasing the refractory period (class 1A)
  2. Class IA Antiarrhythmic Drugs
    • Quinidine
    • Procainamide
    • Disopyramide
  3. Class IA Drugs Mechanism of Action
    • -A moderate block on Na+ channels
    • -Also block K+ channels (increase refractory period)
    • -Decrease the phase 0 upstroke velocity, which decreases conduction velocity through the myocardium
    • -Have some degree of anticholinergic effects *significant clinically b/c it can increase conduction velocity through the AV node
  4. Quinidine
    Class IA Antiarrhythmic

    • Adverse Effects:  diarrhea, torsade de pointes (prolonged QT), syncope (fainting) secondary to reduction in CO and BP, cinchonism, tinnitus, blurred vision
    • *Quinidine-induced digoxin toxicity - increases serum levels of digoxin by inhibiting Pgp
  5. Quinidine Uses
    Occasionally to suppress atrial flutter, atrial fibrillation, supraventricular and ventricular arrhythmias

    -If patient has atrial fibrillation - first treat with drug that decreases AV node conduction (digoxin) and then give quinidine
  6. Class IA:  Procainamide
    • -Long term uses causes lupus erythematosus (is reversible)
    • -Indications: atrial flutter, Afib, ventricular tachycardia, paroxysmal atrial tachycardia
  7. Class IA:  Disopyramide
    • -Orally to prevent life-threatening sustained ventricular tachycardia
    • -Has greater negative inotropic and anticholinergic effects than other class IAs and therefore should be used with caution in patiens with heart failure and in the elderly
  8. Antiarrhythmic Drugs: Class IB
    • Lidocaine
    • Mexiletine
    • Phenytoin
  9. Antiarrhythmic Drugs: Class 1B MOA
    • -Preferentially bind to both open and inactivated Na+ channels (I>O)
    • -Fast dissociation from Na+ channels
    • -Exhibit use-dependent block
    • -Increases ventricular fibrillation threshold
  10. Lidocaine
    Used most commonly to treat ventricular arrhythmias (ventricular fibrillation & ventricular tachycardia) in emergency situations associated with myocardial ischemia

    High concentrations can cause confusion, dizziness, seizure

    Cimetidine (or other drugs that inhibits P450 enzymes) can precipitate lidocaine toxicity
  11. Mexiletine
    • -Analog of lidocaine
    • -Primary indication: life-threatening ventricular tachycardia
    • -dose related nausea and tremo
  12. Phenytoin
    • -Considered an antiepileptic med
    • -Supresses digoxin-induced delayed after depolatization
    • -ventricular tachycardia
    • -Induces hepatic enzymes (P450 3A4)
  13. Antiarrhythmic Drugs:  Class 1C
    • Flecainide
    • Propafenone
  14. Class 1C drugs MOA
    • -Preferentially bind to both open and inactivated Na+ channels (I=O)
    • -Most potent Na+ channel blockers
    • Little/no effect on AP duration
    • -Prevent paroxysmal supraventricular tachycardia and atrial fibrillation
    • -Depressive effects on cardiac function
  15. Flecainide
    • -Various Atrial and ventricular arrhythmias, except those associated with MI (increased mortalitiy rate)
    • Adverse effects:  bronchospasm, leukopenia, thrombocytopenia, seizures
  16. Propafenone
    • -Treat various atrial and ventricular arrhythmia
    • -Potential ventricular arrhythmias and several hemotologic abnormalities, including agranulocytosis, anemia, and thrombocytopenia
  17. Antiarrhythmic Drugs:  Class II drugs
    • Esmolol
    • Metoprolol
    • Propranolol
  18. Antiarrhythmic Drugs:  Class II drugs MOA
    • -Decrease automaticity by decreasing the slope of phase 4
    • -Decreases the incidence of re-entry by slowing electrical conduction at the AV node
    • -The AV node is more sensitive than the SA node to the effects of B-blockers
    • -The most frequently used agents in the treatment of supraventricular and ventricular arrhythmias precipitate by sympathetic stimulation
  19. Antiarrhythmias: Class III Drugs
    • Amiodarone
    • Dofetilide
    • Ibutilide
    • Sotalol
  20. Class III Drugs MOA
    • -Block K+ channels
    • -Prolongs AP
    • +Decreases the incidence of re-entry by increasing the effective refractory period
    • -Increase the likelihood of developing early afterdepolarization and torsade de pointes
  21. Amiodarone
    • -Mainly class III
    • -Also Class I, II, IV
    • -Alters lipid membrane in which ion channels and receptors are located
    • -decreases re-entry by prolonging AP duration
    • -decreases the rate of firing in pacemarke cells as class I
    • -Class II activity by noncomp. antatgonizing B-receptors
    • -Cna cause significant AV block and bradycardia
  22. Amiodarone continued
    Adverse effects:  hypotension, AV block, various arrhythmias, blue-gray skin discoloration, thyroid abnormalities, fatal pulmonary fibrosis

    Also corneal deposits, blurred vision, photosensitivity, and GI disturbances

    Inhibits metabolism of digoxin, flecainide, phenytoin, procainamide, warfarin
  23. Ibutilide and Dofetilide
    • Used to terminate AFib and atrial flutter
    • -Adverse effects:  torsades de points, may requrie electrical cardioversion
  24. Sotalol
    • Mixed Class II and III
    • -Used for patients that cannot tolerate amiodarone
    • -Prevents recurrent atrial flutter/fib
    • -Causes fatigue, bradycardia, and can induce torsades de pointes
  25. Antiarrhythmic Drugs:  Class IV Drugs
    • Diltiazem
    • Verapamil
  26. Class IV MOA
    • -Block cardiac Ca channels
    • -Act preferentially on SA and AV nodal tissues
    • -Slows AP upstroke in AV node, leading to slowed conduction velocity through the AV node
    • -Use to treat re-entrant paroxysmal sypraventricular tachycardia that involves AV node
  27. Misc:  Adenosine
    • -opens a G protein-coupled K+ channel
    • -inhibits SA nodal, atrial, and
    • AV nodal conduction
    • -also inhibits the potentiation of Ca2+ channel
    • activity by cAMP
    • -has a plasma half-life of less than 10 sec
    • -often used as the first-line agent for
    • converting narrow-complex paroxysmal supraventricular tachycardia
    • -adverse effects include headache,
    • flushing, chest pain, and excessive AV or SA nodal inhibition
  28. Misc: Digoxin
    • -Indirectly increase vagal tone and slows AV node conduction and increases AV node refractory period
    • -Use to slow the ventricular rate in patients with AFib (b-blockers and CCB are usually preferred b/c of their more rapid onset of action and greater degree of AV node blockade)
  29. Misc:  Magnesium sulfate
    • -Mg is second most common intracellular cation
    • -deficiency can cause arrhythmias, CHF, and GI/renal disorders
    • -Mag sulfate IV suppresses drug-induced torsades de pointes to treat digitalis-induced ventricular arrhythmias
    • -Also treats supraventricular arrhythmias associated with Mag deficiency
Card Set
Drugs, etc