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Pharm Exam 2 > 21-31 - Antiarrhythmic Drugs > Flashcards

21-31 - Antiarrhythmic Drugs Flashcards

1
Q

four ways of decreasing spontaneous activity

A
  • decrease slope of phase 4
  • increase threshold
  • increase maximum diastolic potential
  • increase action potential duration
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2
Q

two ways of increasing refractoriness

A
  • sodium channel blocker

- action potential prolonging durg

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3
Q

sicilian gambit: class 1 MOA

A

block fast inward sodium channels to varying degrees in conductive tissues of the heart

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4
Q

how do class I drugs effect maximum depolarization rate (vmax of phase 0)?

A

decrease

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5
Q

class I drugs _________ automaticity and _____ conduction

A

reduce

delay

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6
Q

how do class I drugs effect the ERP?

A

prolonged

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7
Q

do class I drugs completely block the sodium channel?

A

no - moderate binding to Na channel also block the potassium channel

–> prolonged QRS and QT

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8
Q

do class I drugs block the calcium channel?

A

only at high doses

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9
Q

review the sicilian gambit table

A

page 10 of handout –> look for patterns

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10
Q

quinidine MOA

A

block rapid inward sodium channel –> slows conduction

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11
Q

is quinidine used clinically?

A

no

only in refractory pts to convert afib or aflutter, prevent reoccurrance of afib and to treat ventricular arrhythmias

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12
Q

adverse effects quinidine

A
  • diarrhea
  • cinchonism
  • hypotension
  • torsades de pointes (proarrhythmic)
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13
Q

cinchonism is what? it is an adverse effect of what drug?

A

= tinnitus, hearing loss, blurred vision

quinidine intoxication

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14
Q

MOA procainamide

A

block rapid inward Na channel –> slows stuff down

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15
Q

what is the effect of procainamide on APD and refractoriness?

A

blocks K channels –> prolongs APD and refractoriness

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16
Q

quinidine v. procainamide

A

procainamide has little vagolytic activity and does not prolong the QT interval to as great an extent

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17
Q

clinical use of procainamide

A

ventricular arrhythmias

acute treatment of reentrant SVT, afib, aflutter with WPW sydnrome

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18
Q

ventricular tachycardia following an Mi presents to your ER: why don’t you treat with procianamide?

A

although this drug can be used to treat ventricular arrhythmias, it takes too long (20 min IV loading)

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19
Q

observe SLE-like syndrome in a pt: what drug are they taking?

A

this is an adverse effect of procainamide

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20
Q

class Ib general MOA

A

weak binding of Na channels

due to rapid on off kinetics

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21
Q

how do class Ib drugs effect action potential

A

accelerated phase 3 repolarization

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22
Q

indications for class Ib drugs

A

digitalis and MI induced arrhythmia

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23
Q

lidocaine MOA

A

blocks open and inactivated sodium channels –> reduces vmac and shortens AP (When unnaturally long)

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24
Q

would you use lidocaine in an infranodal block?

A

no - potentiates infranodal blocks

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25
Q

indications for lidocaine

A

second choice for ventricular arrhythmias

26
Q

can lidocaine be used for atrial issues?

A

no - ineffective in atrial tissue

27
Q

first choice drug for immediately life threatening/symptomatic arrhythmias

A

amiodarone

28
Q

storngest binding class to sodium channels

A

class Ic

because slow on/off kinetics

29
Q

MOA propafenone

A

strong inhibitor of Na channel

30
Q

indications for propafenone

A

treat atrial arrhythmias, PSVT, and ventricular arrhythmias **in pt with no or minimal heart disease and preserved ventricular function

31
Q

MOA flecainide

A

potent NA channel blocker –> slows intraventricular conduction

32
Q

clinical use of flecainide

A

only refractory ectopic ventricular arrhythmia

**not first line because can cause fatal proarrhythmic effects

33
Q

beta-adrenergic antagonists =

A

class II agents

34
Q

indications for beta-adrenergic antagonists

A

supraventricular arrhythmias due to excessive sympathetic activity

35
Q

only antiarrhythmic drus found to be clearly effective in preventing sudden cardiac death in pt wit hprior MI

A

b adrenergic antagonist

36
Q

main MOA of class III agents

A

potassium blockers

but really block all the channels to some extent

37
Q

main effect of class III agents

A

prolong phase 3 repolarization , increase QT interval

38
Q

amiodarone half life

A

after IV: 5-68 hrs

after saturation in tissue (lipophilic) = 13-103 days

39
Q

most dangerous complication of amiodarone

A

lethal interstitial pneumonitis

could also see hypotension and hypothyroidism

40
Q

MOA class IV agents

A

calcium channel blockers

–> depressed SA nodal automaticity, AV nodal conduction, decreased ventricular contractility

41
Q

major cardiovascular site of action for calcium channel blockers

A
  • vascular smooth muscle cells
  • cardiac myocytes
  • SA and AV nodal cells
42
Q

do calcium channel blockers completely block the pore?

A

no - blockade is incomplete

no CCB binds to all pores

43
Q

calcium channel blocker which effects mainly the vasculature

A

dihydropyridines

ex: nifedipine

44
Q

calcium channel blockers with effects mainly in the heart

A

non-dihydopyridines

ex: verapamil and diltiazem

45
Q

do calcium channel blockers effect smooth muscle? uterine muscle? skeletal muscle?

A

NO
YES - relaxes, can be used for preterm contractions
NO

46
Q

4 main clinical applications for calcium channel blockers

A
  • HTN
  • angina pectoris
  • SVT supraventricular tachycardia
  • post-infarct protection
47
Q

MOA verapamil

A

blocks slow Ca channels in nodal tissue –> decreased HR and increased PR interval, cardiac depression

48
Q

is verapamil a good drug for ventricular arrhythmias?

A

no - ineffective on ventricular arrhythmia

49
Q

indications for verampamil

A
  • SVT
  • rate control in afib
  • angina pectoris
  • HTN
50
Q

adverse effects of verapamil

A

constipation and exacerbate CHF

51
Q

contraindications for verapamil

A
  • WPW with afib

- ventricular tachycardia

52
Q

what type of drug is diltiazem?

A

type IV calcium channel blocker like verapamil

53
Q

MOA adenosine

A

A1 receptor in SA and A nodes –> decrease firing rate

also does vasodilation and stimulates pulmonary stretch receptors

54
Q

treatment for paroxysmal supraventricular tachycardia caused by reentry involving accessory bypass pathways

A

adenosine - rapid acting

55
Q

half life adenosine

A

10-15 sec

56
Q

adverse effects of adneosine

A

hypotension
flusing
complete heart block

57
Q

management for bradycardia (3 things)

A
  • atropine
  • isoproterenol
  • pacemaker
58
Q

non-pharmacological management for sinus tachycardia, PSVT

A

vagal stimulation through caroid sinus massage or valsalva maneuver

59
Q

AV nodal reentry tachycardia: drug of choice to treat

A

adenosine - rapidly reduces HR

60
Q

ventricular tachycardia - drug of choice to treat?

A

amiodarone or lidocaine

Pharm Exam 2 (12 decks)

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