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
This class III antiarrhythmatic is actually a beta blocking drug with class III activity
Sotolol.. duh, it ends in "lol"
26
Is sotolol as effective as amiodaride? Is it as toxic?
No, and no
27
What are you worried about if you give sotolol and the pts QT interval starts to get too prolonged?
Torsade de Pointe
28
This class III antiarrhythmatic is a "pure" class III because?
Ibutilide.. It only acts on potassium channels (prolonging the ERP)
29
What exactly is ibutilide indicated to treat?
Acute atrial fibrillation/flutter
30
What class of antiarrhythmatics are infamous for causing torsade de pointes?
Class III
31
Best drug for treating ventricular tachycardia?
Amiodarone > Lidocaine > Procaineamide
32
Best thing to prevent sudden cardiac death in someone who's ejection fraction is < 30%
Implantable cardiac defibrillator
33
Describe whats happening in atrial fibrillation?
Too many impulses are coming from SA node so the HR is going to go way up
34
Best way to treat atrial fibrillation? think big picture
Stop all those atrial impulses from getting to the ventricles. Do this by managing the AV node with drugs
35
The class IV (Ca2+ channel blockers) antiarrhythmatics are?
Verapamil, Deltiazem
36
What do the class IV drugs treat?
Atril fibrillation, flutter
37
What are the effects of verapamil?
Reduces SA node automaticity and AV node conduction velocity
38
Possible adverse effects of Verapamil?
SA or AV block
39
Why would beta blockers work for atrial fibrillation?
The SA node is under sympathetic control (epinephrine/norepinepherine) so a Beta blocker will block the binding of those neuroreceptors
40
Digoxin has antiarrhythmatic and arrhythmogenic effects. How are the antiarrhythmatic effects mediated?
Digoxin increases vagus nerve activity (parasympathetic) which leads to a decreased HR and slower AV conduction velocity
41
How are Digoxin's arrhythmogenic effects mediated?
Na/K ATPase pump inhibition leads to increased intracellular Ca2+ which increases contractility
42
Digoxin's arrhythmogenic effects lead to increased contractility. This can be dangerous. List 4 side effects of Digitoxin
1. increased SA (normal) automaticity leading to increased HR 2. Delayed afterdepolarizations (DADs) 3. APC's 4. VPC's
43
What is the treatment for DAD from Digoxin toxicity?
Digibind: a Digoxin antibody
44
Ppl in atrial fib are at increased risk of?
Stroke
45
What is paroxysmal supraventricular tachycardia (PSVT)?
Re-entry in the AV node
46
Preferred treatment for PSVT?
Adenosine
47
Half life of adenosine?
10 seconds
48
Describe how adenosine is diagnostic
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
What is Wolf Parkinson White syndrome?
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
If you have WPW syndrome and get an atrial fibrillation what can it lead to?
Well, all the impulses from the atrial fib can go straight to the ventricles and cause vent fib.. can also cause supraventricular tachycardias