pharmaco 4 arrhythmias

  1. ability to initiate own activity via spontaneous depolarization
  2. regularity of depolarization rates
  3. ability to transmit impulses from cell to cell at appropriate rates
  4. ability to resist partially or completely to stimulation during repolarization
  5. P wave
    atrial contraction
  6. QRS wave
    ventricular contraction
  7. T wave
    ventricular relaxation
  8. SA node recovery
    occurs at the same time of ventricular contraction (QRS) so the small peak associated with it is masked
  9. cardiac myocyte (working cell) resting potential
  10. nodal cells (signal cells) resting potential
  11. what is responsible for the depolarization in the nodal cells
    Ca, no "fast" Na channels
  12. "daughter impulses" or reentry circuits in the heart cause what
    • atrial/ventricular fibrillation
    • one or few extra beats or sustained tachycardia
  13. first degree heart block
    • SA node depressed can't send signal fast enough
    • 2 P's per QRS
  14. second degree heart block
    • PR interval becomes progressively prolonged
    • wenckebach phenomenon
  15. third degree heart block
    • high atrial rate (107)
    • low ventricular rate (43)
    • no correlation between number of P's and QRS complex
  16. caused by ectopic atrial focus
    P waves are abnormal
    QRST are normal
    atrial arrhythmias
  17. ventricular premature beat followed by comensatory pause
    does not interrupt regular discharge of SA node
    ventricular arrhythmias
  18. accelerated AV conduction
    additional averrant connection between atria and ventricles (AV node is normal)
    short PR interval
    prolonged QRS deflection
    together they have a normal interval between start of P wave and end of QRS complex
    Wolff-Parkinson-White syndrome
  19. class IA ______  action potential duration
  20. class IB ______  action potential duration
  21. class IC ______  action potential duration
    no effect
  22. order of class I interaction with Na channels
    IB < IC < IA
  23. action of IA agent on the conduction velocity
    decrease - QRS widening
  24. action of IA agent on repolarization
    prolong - longer QT
  25. class IC effect of polarization
  26. what is the atropine like toxicity of quinidine
    • increase in sinus rate and a huge increase in AV conduction
    • atrium and ventricles contract with a huge overlap and decrease in CO. atrium isn't completely filled before ventrical contracts causing syncope
  27. ganglionic blocking properties - hypotension
    lupus like syndrome with prolonged use
    increase in immune response through increased antinuclear antibody titer
    oral/ slow infusion only
  28. first choice for sustained ventriicular arrythmias
  29. second choice for sustainded ventricular arrythmias
  30. class IA
    useful for idiopathic hypertrophic subaortic stenosis
    C/I in pt. with left ventricular dysfunction
  31. which class is indicated for ventricular arrhythmias only
  32. agent of choice for ventricular tachycardia and fibrillation after cardioversion
  33. why is lidocaine a potent local anesthetic
    blocks activated and inactivated Na channels
  34. least cardiotoxic of the Na blockers
    problems with CNS toxicities
  35. used for Digoxin induced ventricular arrhythmias
    weak Na blocker
    CNS toxicities
  36. class I group that is the most potent
    profound slow conduction velocity (QRS wideing) - avoid with heart insuficiency
  37. class IC
    potent blocker of Na & K channels
    used for supraventricular arrhythmias
    C/I in pt with heart failure
    unique K channel not involved with repolarization
  38. class IC
    potent Na block
    prodrug - metabolite has beta blocking effect
    AE - metallic taste
  39. class IC
    used to treat ventricular arrhythmias
    does not prolong action potential duraction
  40. class II agents effects on QRS and QT intervals
  41. class II effects of SA and AV conduction
  42. class II slowing of the SA->AV conduction is what on the ECG
    PR interval
  43. which class of drugs prevents the daughter currents - recurrent infarction
    II - beta blockers
  44. what two drugs are used together to improve conversion of atrial fibrillation to sinus rhythm
    propranolol and quinidine
  45. what two drugs are used together to control ventricular rate in a patient with atrial fibrillation or flutter
    propranolol and digitalis
  46. class III effects on effective refractory period
  47. class III effect of action potential (repolarization)
  48. class III effect on QT intervals
  49. class III that is very effective at blocking inactivated Na channels
    long half life - 103d
    toxicity of yellow brown crystals on cornea
    markedly prolongs AP duration
  50. class III
    short duration of effect
    positive inotropic action
    prolongs ventricular (not atrial) AP duration and effective refractory period
    develop postural hypotensio
    increased digoxin toxicity
  51. class III
    used in supraventricular and ventricular arrhythmias
    toxicity of excess beta blockage
  52. class III
    indicated for conversion of atrial fibrillation and flutter
    avoid in ventricular tachycardia
    ibutilide & dofetilide
  53. class IV effects of conduction (SA -> AV nodes)
  54. class IV effects on effective refractory period
  55. verapamil, diltiazem and bepridil effects on QT interval
  56. class IV
    blocks both activated and inactivated Ca channels
    most marked effect in SA & AV nodes
    used for reentrant suprventricular tachycardia (PSVT), atrial fibrillation & flutter
    AE - increase digoxin
Card Set
pharmaco 4 arrhythmias
pharmaco 4 arrhythmias