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Comp Exam #2 - Pharmacology > Anti-arrhythmic Drugs > Flashcards

Anti-arrhythmic Drugs Flashcards

1
Q

Quinidine protein bindings

A

80-90%

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2
Q

Procainamide protein binding

A

15%

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3
Q

Lidocaine protein binding

A

55%

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4
Q

propranolol protein binding

A

90-95%
(Propranolol is Pro Proteins)

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5
Q

Amiodarone protein binding

A

96%

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6
Q

sotalol protein binding

A

0%

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7
Q

verapamil protein binding

A

90%

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8
Q

What triggers Torsades de pointes?

A

early after depolarization in a setting of delayed repolarization and increased duration of refractoriness

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9
Q

What is EKG characteristic of torsades?

A

QTc interval prolongation

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10
Q

What are exacerbating factors of torsades?

A

hypokalemia
hypomagnesemia
poor LV function
concomitant administration of QT prolonging drugs

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11
Q

Incessant ventricular tachycardia is more likely to occur with high doses of class ___ drugs

A

IC

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12
Q

Wide complex ventricular rhythm easily degenerates to what?

A

V Fib

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13
Q

T/F: Lidocaine increases occurence of fatal bradycarrhythmias and asystole with prophylactic treatment of acute MI

A

True

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14
Q

Is CCB recommended as routine treatment of patients with acute MI?

A

No

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15
Q

In patients with HF, ____ reduces the risk of sudden cardiac death by 29%

A

amiodarone

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16
Q

Amiodarone is associated with a 2 and 5 fold increased risk of ____ and ___ toxicity, respectively.

A

pulmonary; thyroid

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17
Q

What is the only drug that plays a role for prophylactic antiarrhythmic medication for the primary prevention of sudden cardiac death in patietns with HF?

A

Amiodarone

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18
Q

Class I drugs are ___ channel blockers

A

sodium

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19
Q

What are 3 examples of class IA drugs?

A

Quinidine
Procainamide
DIsopyramide

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20
Q

What are 3 examples of class IB drugs?

A

Lidocaine
Mexiletine
Tocainide

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21
Q

What are 2 examples of class IC drugs?

A

Flecainide
Propafenone

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22
Q

What are class II drugs?

A

Beat blockers

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23
Q

What are class III drugs?

A

K+ channel blockers

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24
Q

Name 3 class III drugs?

A

Amiodarone
Bretylium
Sotalol

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25
Q

What are class IV drugs?

A

Calcium channel blockers

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26
Q

What are 2 examples of Class IV drugs?

A

Diltiazem and Verapamil (CCB)

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27
Q

What is the MOA of class IA/Na+ channel blocking drugs?

A

Slows phase 0 depolarization in ventricular muscle fibers
(prolong AP)

28
Q

What is the MOA of class IB/Na+ channel blocking drugs?

A

Shortens phase 3 repolarization in ventricular muscle fibers
(decrease duration of AP)

29
Q

What is the MOA of class IC/Na+ channel blocking drugs?

A

Markedly slows phase 0 depolarization in ventricular muscle fibers

30
Q

What is the MOA of class II drugs/BB?

A

Inhibits phase 4 depolarization in SA and AV nodes

31
Q

What is the MOA of class III/K+ channel blocking drugs?

A

prolongs phase 3 repolarization in ventricular muscle fibers
(phase 0 is not altered)

32
Q

What is the MOA of class IV/Ca+ channel blocking drugs?

A

inhibits action potential in SA and AV nodes

33
Q

The QT interval is ____ with Class IA drugs

A

prolonged

34
Q

Do Class IA drugs affect atrial arrhythmias, ventricular arrhythmias or both?

A

Both

35
Q

What are S/S of Quinidine toxicity?

A

Cinchonism – HA, tinitus, thrombocytopenia, Torasades

36
Q

What are S/S of procainamide toxicity?

A

lupus like syndrome

37
Q

Class II antiarrhythmics ___ cAMP

A

decrease

38
Q

Class II antiarrhythmics ___ Ca+ current

A

decrease

39
Q

Class II antiarrhythmics ___ slope of phase 4

A

decrease

40
Q

Class II antiarrhythmics ___ PR interval

A

increase

41
Q

Class II antiarrhythmics ___ myocardial O2 consumption

A

decrease

42
Q

What are uses for class II antiarryhtmics?

A

V-tach, SVT, A Fib, A flutter

43
Q

What are toxicity effects of BB?

A

impotence, bronchospasm, bradycardia, AV block, mask hypoglycemia

44
Q

Class III antiarrythmic drugs ____ AP duration

A

increase

45
Q

Class III antiarrythmic drugs ____ effective refractory period

A

increase

46
Q

When do you use Class III antiarrhytmic drugs?

A

when other antiarrhythmics fail

47
Q

What is Amiodarone toxicity S/S?

A

Pulmonary fibrosis
Hepatotoxicity
Hypo or hyperthyroidsm
Corneal Deposits
Skin deposits

48
Q

Class IV antiarrhythmics ___ conduction velocity

A

decrease

49
Q

Class IV antiarrhythmics ___ ERP

A

increase

50
Q

Class IV antiarrhythmics ___ PR interval

A

incrase

51
Q

What is the use of class IV (CCB) drugs?

A

prevents nodal arrhythmias

52
Q

In the heart, adenosine binds with _____

A

A1 receptor (Gi protein)

53
Q

When adenosine binds to the A1 receptor, it leads to opening of what channels?

A

K+ channels (which in turn leads to hyperpolarization

54
Q

Adenosine decreases ___ in cardiac cells –> decreased entry of ___

A

cAMP; Calcium
Slows HR and conduction

55
Q

In vascular smooth muscle, adenosine binds to ____

A

A2 (Gs protein)

56
Q

In vascular smooth, Adenosine causes a ___ of cAMP, which in turn causes ____

A

increase; vasodilation

57
Q

What is the drug of choice for SVT?

A

Adenosine

58
Q

What is the DOA of Adenosine?

A

15 seconds

59
Q

What antagonizes adenosine?

A

Xanthines (Theophylline and Caffeine)

60
Q

What potentiates adenosines effects?

A

Dipyridamole “Persantine” (adeonsine uptake inhibitor)

61
Q

Digozin is what type of drug?

A

Cardiac glycoside

62
Q

Digoxin _____ AV node conduction

A

decreases

63
Q

Digoxin causes depression of the ___ node

A

SA

64
Q

What are s/s of digoxin toxicity?

A

NVD, yellow vision, increased PR, decreased QT, T wave inversion

65
Q

What electrolyte abnormality worsens Digoxin toxicity?

A

Hypokalemia

Comp Exam #2 - Pharmacology (3 decks)

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