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CVS II Pharmacology > Antiarrhythmic drugs > Flashcards

Antiarrhythmic drugs Flashcards

1
Q

list the 5 categories of the vaughn Williams classification of antiarrhythmic drugs

A
  1. Na+ channel blockers
  2. Beta blockers
  3. K+ channel blockers
  4. Calcium channel blockers
  5. Miscellaneous Drugs
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2
Q

what are the 3 miscellaneous drugs in the vaughn Williams classification of antiarrhythmics

A

Adenosine, Digoxin, magnesium sulfate

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3
Q

what is phase 0 of the non-pacemaker action potential curve

A

activated Na+ channels open, Na+ ions inward

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4
Q

what is phase 1 of the non-pacemaker action potential curve

A

Na+ channels are inactivated, K+ outward

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5
Q

what is phase 2 of the non-pacemaker action potential curve

A

Plateau phase; Ca++ ions inward are balanced by K+ ions outward

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6
Q

what is phase 3 of non-pacemaker action potential curve

A

repolarization due to K+ ions outward and inactivation of Ca++ channels

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7
Q

what is phase 4 of non-pacemaker action potential curve

A

RMP by Na+/K+ ATPase pump

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8
Q

what is phase 0 of the pacemaker action potential curve

A

activation of L-type Ca++ channels

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9
Q

what is phase 3 of the pacemaker action potential curve

A

K+ ions outward

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10
Q

what is phase 4 of the pacemaker action potential curve

A

pacemaker current made of inward Na+/Ca++ ions and Outward K+

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11
Q

what is responsible for the depolarization of the action potential of pacemaker cells

A

Ca++

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12
Q

what maintains the RMP of non-pacemaker cells

A

K+

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13
Q

define effective refractory period (ERP)

A

impossible to produce a response regardless of the stimulus

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14
Q

define relative refractory period

A

period during which a strong impulse may elicit a response

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15
Q

define refractoriness

A

ERP/APD (as ERP decreases, you run a greater risk of the formation of premature impulses)

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16
Q

what are the 3 states the sodium channel toggles between

A

resting, active, and refractory (inactivated)

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17
Q

what class do quinidine, procainamide, and disopyramide belong to

A

Class 1a (Na+ channel blockers)

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18
Q

list the class 1a Na+ channel blockers

A

quinidine, procainamide and disopyramide

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19
Q

what is the MOA of class 1a Na+ channel blockers

A

decrease Vmax and prolong APD
(decrease rate of depolarization)

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20
Q

what is the clinical significance of prolonging the action potential duration (extend the refractory period)

A

it reduces the likelihood of arrhythmias

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21
Q

which of the class 1a drugs is most anticholinergic

A

disopyramide

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22
Q

what are the adverse effects of quinidine

A

tinnitus, GI upset, diplopia, increase QT interval (torsades de pointes); displaces digoxin from tissue binding sites

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23
Q

which class 1a drug doesnt have alpha blocking activity

A

procainamide

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24
Q

what are the adverse side effects of procainamide

A

agranulocytosis and SLE like syndrome in slow acetylators

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25
Q

how do class 1b drugs differ from class 1a na+ channel blockers

A

they have no effect on Vmax and they have a preference for ischemic tissue bc they only work on inactivated Na+ channels, and they increase the threshold for V fib

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26
Q

what class of drugs do lidocaine, tocainide, and mexiletine belong to?

A

class 1b Na+ channel blockers

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27
Q

what is lidocaine indicated for?

A

vtac after MI

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28
Q

what is the most notable adverse effect of lidocaine

A

convulsions (be careful with dose)

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29
Q

what two class 1b na+ channel blockers are given orally

A

mexiletine and tocainide

30
Q

what are the three class 1b Na+ channel blockers

A

lidocaine, tocainide, and mexiletine

31
Q

what are the three class 1c Na+ channel blockers

A

flecainide, propafenone, and moricizine

32
Q

what class of drugs do flecainide, propafenone, and moricizine belong to

A

class 1c Na+ channel blockers

33
Q

what is the MOA of class 1c Na+ channel blockers

A

decrease Vmax significantly but no effect on APD

34
Q

what is the main difference between class 1a, 1b and 1c Na+ channel blockers with regard to MOA

A

1a. decrease Vmax and APD
1b. no effect on Vmax and only effective at inactive Na+ channels
1c. no effect on APD

35
Q

What are the clinical uses for flecainide, propafenone and moricizine (Na+ channel blockers)

A

life-threatening Vtac and Vfib

36
Q

what are the adverse effects of the class 1c Na+ channel blockers

A

proarrhythmic effect
risk of sudden death and cardiac arrest
decrease in LV function after MI

37
Q

what are the class 2 beta blockers used to treat arrhythmias

A

metoprolol, propranolol, acebutolol and Esmolol

38
Q

what is the MOA of class 2 beta blockers

A

decrease SA and AV nodal conduction and decrease the slope of phase 4

39
Q

what are the clinical uses of the class 2 beta blockers: metoprolol, propranolol, acebutolol, and esmolol

A

prophylaxis for ventricular arrhythmias post MI

40
Q

what are the adverse effects of class 2 beta blockers

A

proarrhythmic: can cause AV block

41
Q

what is esmolol indicated for

A

emergency rx of SVT

42
Q

what beta blocker is used in an emergency rx of SVT

A

esmolol

43
Q

what are the 5 class 3 K+ channel blocker drugs

A

amiodarone, dofetilide, ibutilide, sotalol, and dronaderone

44
Q

what is the MOA of class 3 K+ channel blockers

A

increase APD, and ERP; prolong repolarization and lengthen phase 2

45
Q

what class of antiarrhythmic drugs do amiodarone, dofetilide, ibutilide, sotalol, and dronaderone belng to?

A

class 3 K+ channel blockers

46
Q

what is the significance of amiodarone

A

is mimics class 1, 2, 3, and 4
binds to Na+ Channel (inactivated)
blocks K+ and Ca++ channels
non-competitive inhibitor of beta receptors
long 1/2 life: 25-60 days

47
Q

what are the clinical uses of class 3 antiarrhythmic K+ channel blockers

A

atrial fibrillation and Vtach

48
Q

what are the adverse effects of amiodarone, dofetilide, ibutilide, sotalol, and dronaderone (K+ channel blockers)

A

pulmonary fibrosis, hepatotoxicity, smurf skin, hypothyroidism, and hyperthyroidism and notably TdP.

49
Q

what are the 2 class 3 K+ channel blocker antiarrhythmics that selectively block outward potassium channel called delayed rectifier potassium channel

A

Ibutilide and deofetilide

50
Q

what is the significance of ibutilide and deofetilide selectively blocking delayed rectifier potassium channels

A

it prolongs the ventricular repolarization and increases the QT interval

51
Q

what are the uses of ibutilide and dofetilide

A

used for pharmacological cardioversion of atrial fibrillation and flutter

52
Q

what makes Sotalol unique as an antiarrhythmic drug?

A

it has properties of both Class 2 and class 3 drugs (beta blocker and a K+ channel blocker)

53
Q

what are the 2 MOAs of sotalol

A

decrease heart rate and AV conduction and prolong APD and ERP

54
Q

what is the clinical use of sotalol

A

A fib, and life-threatening ventricular arrhythmias

55
Q

what are the adverse effects of Sotalol

A

TdP, headache, depression, and impotence
use with caution in asthmatics

56
Q

what are the class 4 CCB antiarrhythmic drugs

A

Diltiazem and verapamil

57
Q

what class of antiarrhythmic drugs wo diltiazem and verapamil belong to

A

class 4: CCB

58
Q

what is the MOA of the class 4 CCB drugs, Diltiazem and verapamil

A

decrease SA and AV conduction and slope of phase 4

59
Q

what is the clinical use of diltiazem and verapamil

A

PSVT due to AV nodal re-entry

60
Q

what are the adverse effects of diltiazem and verapamil

A

orthostatic hypotension, reduce cardiac output, lower extremity edema, constipation
Verapamil displaces digoxin, increasing its toxicity
Proarrhythmic AV block if used with beta blockers
Caution: Atrial tachycardia due to WPW

61
Q

what are the miscellaneous antiarrhythmic drugs

A

Adenosine, Digoxin, and magnesium sulfate

62
Q

what is the MOA of adenosine

A

AV nodal blocker

63
Q

what are the clinical uses of adenosine

A

drug of choice for PSVT

64
Q

what is the prophylaxis drug of choice after administration of adenosine for SVT

A

class 2 (b blocker) or class 4 (ccb)

65
Q

what drugs increase risk of torsade de pointes

A

amiodarone, quinidine, sotalol, thioridazine, and TCAs

66
Q

what is the mechanism behind antiarrhythmics causing torsades de pointes

A

prolongation of QT intervals

67
Q

what is the rescue therapy for torsades de pointes

A

mg sulfate and K+

68
Q

what is the clinical use of digoxin

A

heart failure and to control ventricular rates in afib and afluter

69
Q

what is the antagonist of adenosine

A

theophylline

70
Q

what is the antidote for digitalis toxicity

A

digifab (digibind)

71
Q

what drugs are proven to decrease mortality in hear failure

A

ACEI and MRA (i.e. spirinolactone)

CVS II Pharmacology (9 decks)

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