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CV Pharmacology- Parker > Anti-arrhythmatics > Flashcards

Anti-arrhythmatics Flashcards

1
Q

The class I sodium channel blockers are

A

PLF: Procaineamide, Lidocaine, Flecanide

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2
Q

The class II beta blockers are

A

PMA: Propranolol, Metaprolol, Acebutolol

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3
Q

The class III potassium channel blockers are

A

ASI: Amiodarone, Sotolol, Ibutilide

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4
Q

The class IV calcium channel blockers are

A

VD: Verapamil, Deltiazem

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5
Q

This class of anti-arrhythmatic drugs suppresses abnormal automaticity in ventricular myocytes

A

Class I sodium channel blockers

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6
Q

What would abnormal automaticity in ventricular myocytes look like on ECG?

A

Pre ventricular beats; QRS complexes are too close together with no P waves separating them

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7
Q

This class I sodium channel blocker drug is class IA. It has a dissociation rate of greater than 1 second so it slows conduction rate even at slow heart rates

A

Procaineamide

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8
Q

This class I sodium channel blocker is class IB. It has a rapid dissociation rate of less than 1 second so conduction is slowed only in places where there is a very fast conduction velocity

A

Lidocaine- probably the best because it is specific for highly tachycardic cells

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9
Q

This class I sodium channel blocker is class IC. It has a very slow dissociation rate of over 10 seconds. It has a very pronounced effect of slowing conduction velocity

A

Flecanide

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10
Q

Prominent side effect of Procaineamide?

A

Drug induced lupus.. also Torsades de Pointes

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11
Q

Whats the classic presentation for a patient in which Procaineamide would be indicated?

A

Ventricular arrhythmia (also can treat atrial arrhythmias.. Lidocaine cannot!)

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12
Q

Broad overall mech of action of Procaineamide?

A

Inhibits ectopic pacemaker activity in places other than SA or AV node

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13
Q

Lidocaine is the classic class IB anti-arrhythmatic. It also blocks sodium channels so how is it different from procaineamide?

A

Lidocaine has faster kinetics so it only blocks the sodium channels that are tachycardic. Also, lidocaine DOES NOT treat atria arrhythmias.. only ventricular ones

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14
Q

Classic presentation for indication of lidocaine?

A

Ventricular tachycardia. For vent tach, lidocaine would be more effective than procaineamide

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15
Q

The classic class IC anti-arrhythmatic is Flecanide. What would be the presentation of a patient in which Flecanide is indicated?

A

Someone with a supraventricular arrhythmia with NO STRUCTURAL HEART DISEASE!!!!

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16
Q

How is Flecainde different kinetically than the other sodium channel blockers?

A

It has a very long dissociation rate of over 10 seconds.. it binds to sodium channels for a long ass time

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17
Q

Do class I antiarrhythmatics work in the SA or AV nodes where depolarization is Ca2+ dependent?

A

No, the sodium channels in these nodes are funny channels and are not responsive to the sodium channel blockers

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18
Q

Big picture.. what do class I antiarrhythmatics do?

A

They suppress abnormal automaticity by blocking sodium channels. They “reduce membrane responsiveness in partially depolarized myocytes”

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19
Q

Class III anti-arrhythmatics block what channel?

A

Potassium

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20
Q

What are the class III potassium channel blockers?

A

KASI: potassium- Amiodaride, Sotolol, Ibutilide

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21
Q

Amiodaride is the prototype class III antiarrhythmatic. But it also can act like other classes.. which ones?

A

All of them. Amiodaride can act as a class 1, 2, 3, or class 4 antiarrhythmatic. That makes it very effective and it is the drug of choice for cardiac resuscitation

22
Q

Explain how the class III potassium channel blockers work

A

They prolong the effective refractory period (phase 3) of the action potential by binding to potassium channels

23
Q

Amiodarone has some pretty serious and common side effects. Name two

A

Pulmonary fibrosis, photosensitivity dermatitis

24
Q

You have to be careful of drug-drug interactions (especially with warfarin) with Amiodaride.. Why?

A

Because amiodaride inhibits CYP3A4

25
Q

This class III antiarrhythmatic is actually a beta blocking drug with class III activity

A

Sotolol.. duh, it ends in “lol”

26
Q

Is sotolol as effective as amiodaride? Is it as toxic?

A

No, and no

27
Q

What are you worried about if you give sotolol and the pts QT interval starts to get too prolonged?

A

Torsade de Pointe

28
Q

This class III antiarrhythmatic is a “pure” class III because?

A

Ibutilide.. It only acts on potassium channels (prolonging the ERP)

29
Q

What exactly is ibutilide indicated to treat?

A

Acute atrial fibrillation/flutter

30
Q

What class of antiarrhythmatics are infamous for causing torsade de pointes?

A

Class III

31
Q

Best drug for treating ventricular tachycardia?

A

Amiodarone > Lidocaine > Procaineamide

32
Q

Best thing to prevent sudden cardiac death in someone who’s ejection fraction is < 30%

A

Implantable cardiac defibrillator

33
Q

Describe whats happening in atrial fibrillation?

A

Too many impulses are coming from SA node so the HR is going to go way up

34
Q

Best way to treat atrial fibrillation? think big picture

A

Stop all those atrial impulses from getting to the ventricles. Do this by managing the AV node with drugs

35
Q

The class IV (Ca2+ channel blockers) antiarrhythmatics are?

A

Verapamil, Deltiazem

36
Q

What do the class IV drugs treat?

A

Atril fibrillation, flutter

37
Q

What are the effects of verapamil?

A

Reduces SA node automaticity and AV node conduction velocity

38
Q

Possible adverse effects of Verapamil?

A

SA or AV block

39
Q

Why would beta blockers work for atrial fibrillation?

A

The SA node is under sympathetic control (epinephrine/norepinepherine) so a Beta blocker will block the binding of those neuroreceptors

40
Q

Digoxin has antiarrhythmatic and arrhythmogenic effects. How are the antiarrhythmatic effects mediated?

A

Digoxin increases vagus nerve activity (parasympathetic) which leads to a decreased HR and slower AV conduction velocity

41
Q

How are Digoxin’s arrhythmogenic effects mediated?

A

Na/K ATPase pump inhibition leads to increased intracellular Ca2+ which increases contractility

42
Q

Digoxin’s arrhythmogenic effects lead to increased contractility. This can be dangerous. List 4 side effects of Digitoxin

A
  1. increased SA (normal) automaticity leading to increased HR
  2. Delayed afterdepolarizations (DADs)
  3. APC’s
  4. VPC’s
43
Q

What is the treatment for DAD from Digoxin toxicity?

A

Digibind: a Digoxin antibody

44
Q

Ppl in atrial fib are at increased risk of?

A

Stroke

45
Q

What is paroxysmal supraventricular tachycardia (PSVT)?

A

Re-entry in the AV node

46
Q

Preferred treatment for PSVT?

A

Adenosine

47
Q

Half life of adenosine?

A

10 seconds

48
Q

Describe how adenosine is diagnostic

A

If you have a suspected PSVT and you give adenosine and the arrhythmia goes away, you have confirmed that it was a PSVT arrhythmia

49
Q

What is Wolf Parkinson White syndrome?

A

means there is an accessory pathway between the atria and ventricle.. Impulses can go from atria to ventricle without having to go through AV node

50
Q

If you have WPW syndrome and get an atrial fibrillation what can it lead to?

A

Well, all the impulses from the atrial fib can go straight to the ventricles and cause vent fib.. can also cause supraventricular tachycardias

CV Pharmacology- Parker (14 decks)

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