Antiarrhythmics Flashcards

1
Q

2 etiologies of arrhythmias

A

Abnormal impulse formation and alterations in impulse conduction

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2
Q

Most life threatening arrhythmias

A

Ventricular tachycardia

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3
Q

Class 1 antiarrhythmic drugs

A

Sodium channel blockers

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4
Q

Class 2 antiarrhythmic drugs

A

Beta blockers

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5
Q

Class 3 antiarrhythmic drugs

A

Potassium channel blockers

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6
Q

Class 4 antiarrhythmic drugs

A

Calcium channel blockers

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7
Q

Fast response fibers

A

Located in muscle–ventricle and atria

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8
Q

Phase 0 of AP in fast response fibers

A

Na channels open, rapid depolarization

Class 1 drugs can slow or block phase 0

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9
Q

Phase 1 of AP in fast response fibers

A

Na+ channels are inactivated

No effect of anti arrhythmic drugs

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10
Q

Phase 2 of AP in fast response fibers

A

Plateau phase due to L type Ca channels
Inward Ca balanced by outward K
Class III drugs prolong plateau by blocking K channels
Class IV drugs have little effect on this type of Ca channel

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11
Q

Phase 3 of AP in fast response fibers

A

Repolarization phase due to K leaving and Ca channels inactivated
Class III drugs prolong repolarization

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12
Q

Phase 4 of AP in fast response fibers

A

Return to resting membrane potential
Due to Na/K pump
Digoxin can be pro-arrhythmic through blockade of phase 4

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13
Q

Slow response fibers

A

SA and AV nodes
No participation of Na
Class 1 drug has no effect

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14
Q

What is solely responsible for AP in slow response fibers

A

Ca

Class IV drugs block phase 0

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15
Q

Prolonging action potential duration with antiarrhythmics

A

Prolongs refractoriness to pathologic stimuli and slows down rhythm

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16
Q

Ischemia causes

A

Decreased O2 supply–> decreased electron transport chain–> decreased ATP–>Decreased Na/K ATPase–> Na stays in the cell keeping it depolarized causing a large amount of channels in inactive state
Requires anti-arrhythmic drug

17
Q

Class 1A drugs

A

Blocks open, activated Na channel

18
Q

Class 1B drugs

A

Blocks refractoriness–decreases rate of firing

19
Q

Class 1C drugs

A

Blocks open, activated Na channel

20
Q

Examples of 1A drugs

A
Quinidine 
Procainamide 
Pyramidine 
Moderate Na binding
Increased AP by blocking K+
Used for both ventricular and atrial dysrythmias
21
Q

Example of 1B drug

A

Lidocaine
Phenytoin
Mexiletine

22
Q

Example of 1C drug

A

Flecainide

Propafenone

23
Q

1B drugs are specific to

A

Ischemia
Used for post MI, digoxin toxicity, open heart surgery
Least Na binding; decreased AP

24
Q

1C drugs used for

A

life threatening V Tach, fibrillation and refractory SVTs
(A fib)
Strong Na binding
No effect on AP length due to no effect on K+

25
Q

FDA approved beta blockers for arrhythmias

A

Metoprolol, Propranolol, Esmolol

26
Q

Amiodarone

A

K+ channel blocker
Very long half life of 20-50 days
Main side effects: pulmonary fibrosis, liver toxicity, thyroid dysfunction
Has 1, 2, 3, 4 properties

27
Q

Calcium channel blockers indicated for arrhythmias

A

Verapamil and diltiazem

28
Q

Side effects of calcium channel blockers

A

Decreased BP, decreased CO, lower extremity edema, constipation

29
Q

Adenosine

A

Rapidly acting AV nodal blocker–administered IV
Quick half life of 30 seconds
Drug of choice for paroxysmal supraventricular tachycardia

30
Q

Digoxin

A

Inhibits Na/K ATPase inhibitor

31
Q

Class 2 anti arrhythmic

A

Beta blocker
Prolongs stage 4 slow depolarization by decreasing Ca depolarization
Treatment of supraventricular arrythmias

32
Q

Class 3 anti arrhythmic

A

Blocks K+ channels–delays repolarization and increases AP length
Can treat both atria and ventricular arrhythmias

33
Q

Sotalol

A

Class 3 anti arrythmic

Also used as beta blocker

34
Q

Dofetilide

A

Class 3 anti arrhythmic

35
Q

Ibutilide

A

Class 3 anti arrhythmic

36
Q

Class 4 anti arrhythmic

A

Non-dihydropyridine Ca channel blockers

Used for supraventricular arrhythmias especially A fib