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ALL THE PHARM > Anti-arrhythmics > Flashcards

Anti-arrhythmics Flashcards

1
Q

Which conformation of the fast Na channel does each subtype of Class I block?

A

IA - Blocks the activated form
IB - Blocks the inactivated/refractory form
IC - Blocks the resting form (in reality can block all of them; fairly nonspecific)

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2
Q

Why do we prefer to use Class IB after an MI?

A

Class IB is selective for inactivated/refractory form of Na channel (i.e. tissue that is already depolarized) - this will select for the hypoxic or damaged tissue that we are worried about post-MI

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3
Q

What is the effect of Class IA channel blockers on the action potential?

A

Increases AP duration (decreases the slope of phase 0; slows down the AP) and effective refractory period

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4
Q

What are 3 class IA drugs?

A

Mnemonic: The queen proclaims Diso’s pyramid.

Quinidine, Procainamide, Disopyramide

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5
Q

Why is there a risk of tachycardia with quinidine?

A
  1. Muscarinic antagonist (antagonizes M2)

2. Alpha blocker

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6
Q

What do we really like to use quinidine for?

A

Atrial fibrillation

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7
Q

What do we often give with quinidine and why?

A

Digoxin - to slow AV conduction (mitigate the potential risk of tachycardia)

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8
Q

What is cinchonism and what drug is associated with it?

A

Cinchonism - side effects from the ANS activity

Quinidine

In the case of quinidine we get: GI distress, ocular dysfunction, tinnitus, CNS excitation

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9
Q

Why is there a risk of Torsades de Pointes with quinidine?

A

Anti-muscarinic effect (tachycardia causes prolongation of QRS and increased QT interval)

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10
Q

What enzyme is used to metabolize procainamide?

A

N-acetyltransferase

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11
Q

What 3 drugs are associated with producing SLE like syndrome?

A

Procainamide, hydralazine, isoniazid

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12
Q

What hematologic side effect are you concerned about with procainamide?

A

Thrombocytopenia

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13
Q

Which antibody is more specific for drug-induced SLE vs. general SLE?

A

Antihistone

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14
Q

How does Class IB affect action potential?

A

Decreases action potential duration by blocking the slow Na “window currents (this reduces the K/Ca plateau phase which also have some influence from Na)

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15
Q

What is the one Class IB drug to remember?

A

Lidocaine

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16
Q

When do we use lidocaine?

A

Think: depolarized tissue (has more inactivated/refractory sodium channels)

  1. Post-MI
  2. Open heart surgery
  3. Digoxin toxicity
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17
Q

What is the least cardiotoxic drug of the anti-arrhythmics?

A

Lidocaine

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18
Q

What toxicity do we worry about with lidocaine?

A

CNS (e.g. seizures)

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19
Q

How do we typically give lidocaine?

A

IV use (first pass metabolism)

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20
Q

What is different about mexiletine and tocainide from lidocaine?

A

They can be given orally

21
Q

Give 2 examples of Class IC drugs.

A

Flecainide, propafenone

22
Q

When do we use class IC?

A

Last resort in refractory ventricular tachycardia

23
Q

What is the effect of class IC on AP duration?

A

Minimal effect

24
Q

What do Class II antiarrhythmics act on?

A

Beta blockers that work on NODAL cells (SA, AV nodes)

By decreasing cAMP in the cells, it leads to decreased phosphorylation of all the channels which means closed Na and Ca channels and open K channels (slowed depolarization)

25
Q

What do you see in action potential with Class II?

A

Decreased slope of phase 4

26
Q

Give 3 examples of beta blockers used as class II antiarrhythmics.

A

Nonselective - propanolol

Selective - acebutolol, esmolol

27
Q

Why do we like to give beta blockers after MI?

A

Prophylaxis - negative inotropic effect (decreases oxygen demand)

28
Q

How is esmolol given?

A

IV

29
Q

Which Class II drug is very short acting?

A

Esmolol

30
Q

How does Class III affect action potential?

A

Increased AP and ERP by decreasing slope of phase 3 (prolonged repolarization)

31
Q

Give 4 class III drugs.

A

Amiodarone, ibutilide, dofetilide, sotalol

32
Q

What are the pros/cons of amiodarone?

A

Great because it mimics class I, II, III, IV (basically like a miracle drug)

BUT the really bad thing is that it’s half life is > 80 days and has many potential side effects

33
Q

Why does amiodarone have so many side effects?

A

It has high protein binding capacity (can iodinate proteins which makes it stick) so it has high volume of distribution

34
Q

What are the side effects of amiodarone?

A

Pulmonary fibrosis, blue pigmentation of the skin (“smurf skin”), phototoxicity, corneal deposits, hepatic necrosis, thyroid dysfunction

35
Q

What is significant about sotalol aside from its class III action?

A

Excessive beta blockade - can cause torsades de pointes

36
Q

What is the target of class IV antiarrhythmics?

A

Slow Ca channels (L type) in nodal cells

Will slow SA and AV node activity

37
Q

How does class IV affect action potential?

A

Increase APD and ERP by decreasing the slope of phase 0 depolarization (since we’re blocking calcium)

38
Q

Name 2 class IV drugs.

A

Diltiazem, verapamil

39
Q

What do we use class IV for?

A

Supraventricular tachycardia

40
Q

What are the side effects of class IV?

A

AV block (!!!), constipation (verapamil), dizziness, flushing, hypotension

41
Q

What drug interactions should you be wary of with class IV and why?

A

Beta blockers and digoxin in case of additive AV block

42
Q

What are 2 unclassified antiarrhythmics?

A

Adenosine and Mg

43
Q

Describe how adenosine functions as an antiarrhythmic.

A

Causes Gi-coupled decrease in cAMP (basically like an M2 muscarinic agonist) which decreases SA and AV nodal conduction

44
Q

Is adenosine short or long acting?

A

SHORT (half life of about 10 seconds)

45
Q

What is adenosine used for?

A

Drug of choice in diagnosing/abolishing paroxysmal supraventricular tachycardia

46
Q

What are the adverse effects of adenosine?

A

Flushing, hypotension, chest pain

47
Q

What is adenosine antagonized by?

A

Methylxanthines (theophylline and caffeine)

48
Q

How does Mg work as an antiarrhythmic?

A

Basically competes with calcium

49
Q

What do we use Mg for?

A

Torsades de pointes and digoxin toxicity

ALL THE PHARM (10 decks)

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