Anti-arrhythmic Drugs Flashcards

(65 cards)

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
What are class IV drugs?
Calcium channel blockers
26
What are 2 examples of Class IV drugs?
Diltiazem and Verapamil (CCB)
27
What is the MOA of class IA/Na+ channel blocking drugs?
Slows phase 0 depolarization in ventricular muscle fibers (prolong AP)
28
What is the MOA of class IB/Na+ channel blocking drugs?
Shortens phase 3 repolarization in ventricular muscle fibers (decrease duration of AP)
29
What is the MOA of class IC/Na+ channel blocking drugs?
Markedly slows phase 0 depolarization in ventricular muscle fibers
30
What is the MOA of class II drugs/BB?
Inhibits phase 4 depolarization in SA and AV nodes
31
What is the MOA of class III/K+ channel blocking drugs?
prolongs phase 3 repolarization in ventricular muscle fibers (phase 0 is not altered)
32
What is the MOA of class IV/Ca+ channel blocking drugs?
inhibits action potential in SA and AV nodes
33
The QT interval is ____ with Class IA drugs
prolonged
34
Do Class IA drugs affect atrial arrhythmias, ventricular arrhythmias or both?
Both
35
What are S/S of Quinidine toxicity?
Cinchonism -- HA, tinitus, thrombocytopenia, Torasades
36
What are S/S of procainamide toxicity?
lupus like syndrome
37
Class II antiarrhythmics ___ cAMP
decrease
38
Class II antiarrhythmics ___ Ca+ current
decrease
39
Class II antiarrhythmics ___ slope of phase 4
decrease
40
Class II antiarrhythmics ___ PR interval
increase
41
Class II antiarrhythmics ___ myocardial O2 consumption
decrease
42
What are uses for class II antiarryhtmics?
V-tach, SVT, A Fib, A flutter
43
What are toxicity effects of BB?
impotence, bronchospasm, bradycardia, AV block, mask hypoglycemia
44
Class III antiarrythmic drugs ____ AP duration
increase
45
Class III antiarrythmic drugs ____ effective refractory period
increase
46
When do you use Class III antiarrhytmic drugs?
when other antiarrhythmics fail
47
What is Amiodarone toxicity S/S?
Pulmonary fibrosis Hepatotoxicity Hypo or hyperthyroidsm Corneal Deposits Skin deposits
48
Class IV antiarrhythmics ___ conduction velocity
decrease
49
Class IV antiarrhythmics ___ ERP
increase
50
Class IV antiarrhythmics ___ PR interval
incrase
51
What is the use of class IV (CCB) drugs?
prevents nodal arrhythmias
52
In the heart, adenosine binds with _____
A1 receptor (Gi protein)
53
When adenosine binds to the A1 receptor, it leads to opening of what channels?
K+ channels (which in turn leads to hyperpolarization
54
Adenosine decreases ___ in cardiac cells --> decreased entry of ___
cAMP; Calcium Slows HR and conduction
55
In vascular smooth muscle, adenosine binds to ____
A2 (Gs protein)
56
In vascular smooth, Adenosine causes a ___ of cAMP, which in turn causes ____
increase; vasodilation
57
What is the drug of choice for SVT?
Adenosine
58
What is the DOA of Adenosine?
15 seconds
59
What antagonizes adenosine?
Xanthines (Theophylline and Caffeine)
60
What potentiates adenosines effects?
Dipyridamole "Persantine" (adeonsine uptake inhibitor)
61
Digozin is what type of drug?
Cardiac glycoside
62
Digoxin _____ AV node conduction
decreases
63
Digoxin causes depression of the ___ node
SA
64
What are s/s of digoxin toxicity?
NVD, yellow vision, increased PR, decreased QT, T wave inversion
65
What electrolyte abnormality worsens Digoxin toxicity?
Hypokalemia