Antiarhythmics Flashcards

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1
Q

What are the 3 catergories of arrhytmias origin?

A

Atrial (Supraventricular)
Nodal (Supraventricular)
Ventricular

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2
Q

What are 3 types of supraventricular tachyarrhythmias?

A

Paroxysmal supraventricular tachycardia (PSVT)
Atrial Fibrillation
Atrial Flutter with variable AV conduction

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3
Q

What are 3 common types of ventricular arrhythmias?

A

Monomorphic ventricular tachycardia
Torsades de pointed
Ventricular fibrillation

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4
Q

What are 2 drug classes that reduce automaticity of cardiac myocytes by decreasing the phase 4 slope?

A

Beta blockers

Calcium channel blockers

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5
Q

What are 2 drug classes that reduce automaticity of cardiac myocytes by increasing the threshold of action potentials?

A

Sodium blockers

Calcium channel blockers

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6
Q

What drug class reduces automaticity of cardiac myocytes by increasing action potential duration?

A

Potassium channel blocker

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7
Q

What drug class reduces automaticity of cardiac myocytes by increasing the maximum diastolic potential?

A

Adenosine

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8
Q

What are 2 mechanism by which reentry can be abolished by cardiac drugs?

A

Slowing depressed conduction

Lengthening refractory period

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9
Q

What are 2 drugs that can be used to lengthen the refractory period?

A

Sodium channel blockers

Potassium channel blockers

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10
Q

Regarding cardiac drugs, what is a “state / use” dependent drug? What is an example of a sodium channel blocker to which this principle applies?

A

A drug that only affects channels in the open state

Lidocaine

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11
Q

What are the 4 classes of antiarrhythmics and what are the component drug classes?

A

I - Sodium channel blockers
II - Beta blockers
III - Potassium channel blockers
IV - Calcium channel blockers

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12
Q

Among the sodium channel blockers, what are the 2 major mechanisms of action?

A

Slow phase 0 depolarization

Slow conduction

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13
Q

Among class 1A, 1B and 1C sodium channel blockers, which bind / unbind with slow, medium and fast kinetics? Which are considered the “smart / use-dependent” drugs?

A

1A - Medium
1B - Fast (Smart drugs)
1C - Slow

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14
Q

Among class 1A, 1B and 1C sodium channel blockers, which will prolong the action potential? Have no effect on the action potential? Shorten the action potential?

A

Prolong - 1A
Shorten - 1B
No Effect - 1C

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15
Q

What are the 3 examples of type 1A sodium channel blockers? Which should be avoided in heart failure? What are they used for (2)?

A
Procainamide
Quinidine
Disopyramide (Avoid in heart failure)
- Ventricular arrhythmia
- Recurrent Atrial arrhythmia
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16
Q

What are the 2 examples of class 1B sodium channel blockers? What is their shared major side effect? How are the used differently?

A

Lidocaine (acute ventricular arrhythmias)
Mexiletine (Chronic ventricular arrhythmias)
- CNS toxicity is shared side effect

17
Q

What are the 2 class 1C sodium channel blockers? What are their major side effect? What are they used for?

A

Flecainide
Propafenone
- Both arrhythmogenics
- Used for recurrent atrial arrhythmias

18
Q

What is a major consideration when using class 1C sodium channel blockers? What patient population should not use these drugs (2)?

A

Can cause life threatening arrhythmias

Don’t use in patients with underlying structural heart disease or after MI

19
Q

What is the major mechanism by which beta blockers work as antiarrhythmics?

A

They reduce automaticity (slow the action potential)

20
Q

What are the 4 beta blockers used in the treatment of arrhythmias? What are their shared side effects?

A
Propranolol
Metoprolol
Atenolol
Esmolol
- Bradycardia
- Negative ionotrope
21
Q

What are the 2 beta 1 selective beta blockers used to treat arrhythmias?

A

Metoprolol

Atenolol

22
Q

Among the beta blockers used to treat arrhythmias, propranolol has a specific side effect not shared by the others. What is it? Why does it have this property?

A

It can cause bronchospasm

It blocks beta 2 receptors

23
Q

What are the 2 therapeutic uses of beta blockers?

A

Atrial arrthythmias

Slow AV node conduction

24
Q

What is a therapeutic use of the beta 1 selective beta blockers not shared by the other agents?

A

Prevent sudden cardiac death post MI

25
Q

What are the 4 examples of potassium channel blockers provided?

A

Amiodarone
Sotalol
Dofetidile
Ibutilide

26
Q

Potassium channel blockers are noted for what major side effect that needs to be monitored? What drug is this class is the exception?

A

Noted for marked QT prolongation - torsade de pointes

Amiodarone

27
Q

The major side effects associated with amiodarone are because of its _ property. It causes toxicity to what 5 areas?

A
Lipid solubility
Lings 
Liver 
Thyroid
Eyes
Skin
28
Q

What 3 potassium channel blockers can be used to treat atrial arrhythmias? Which 2 can be used to treat ventricular arrhythmias? Which potassium channel blockers is used for acute conversion of atrial fibrillation / flutter?

A

Atrial - Amiodarone, sotalol, dofetilide
Ventricular - Amiodarone, sotalol
Acute conversion - Ibutilide

29
Q

What is the potassium channel blocker that is less arrhythmogenic in patients
with heart failure or post-MI?

A

Amiodarone

30
Q

What are the 2 examples of calcium channel blockers used for the treatment of arrhythmias?

A

Verapamil

Diltiazem

31
Q

What are the 3 side effects associated with calcium channel blockers?

A

Bradycardia
Hypotension
Negative Iontrope

32
Q

What are the 2 uses of calcium channel blockers?

A

Re-entry SVT involving AV node

Slow AV node conduction

33
Q

What drug can be used to diagnose atrial fibrilation / flutter?

A

Adenosine

34
Q

What is the mechanism of action of adenosine (i.e. what current is activated, what is inhibited)?

A

Activates Inwardly rectifying potassium and inhibits calcium current

35
Q

What are the 2 main effects of digoxin?

A

Sensitize parasympathetic efferents

Inhibits calcium currents

36
Q

What is the therapeutic use of adenosine? (2)

A

Supraventricular tachycardia

Diagnose atrial fibrilation / flutter

37
Q

What is the therapeutic use of digoxin? Under what conditions in it arrhythmogenic?

A

Slows ventricular response in atrial fibrillation

At toxic levels