Cardio: Class I Antiarrhythmics Flashcards Preview

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Flashcards in Cardio: Class I Antiarrhythmics Deck (24)
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1
Q

What is the name of the cardiac action potential’s initial upslope?

A

Phase 0

2
Q

The class I drugs target the _________. What effect does this have on the cardiac action potential?

A

Open sodium channels (think of the singer clutching the jar of peanut butter that is OPEN) This decreases the slope of the action potential (think of him leaning the microphone over, decreasing the slope of the cord’s wave), this ultimately slows the action potential through the cardiac tissue.

3
Q

The class I anti-arrhythmics have _______ dependence.

A

use (because they only bind to open Na channels)

4
Q

The nodal upstroke relies on __________, and so is not affected by class I anti-arrhythmics.

A

calcium

5
Q

Where do the class I anti-arrhythmics act?

A

On the His-Purkinje system (think of the neon lights on the HP system, not the SA or AV)

6
Q

What ECG finding might you see in someone taking class I anti-arrhythmics?

A

A widened QRS (think of the wide QRS-shaped crack in the neon sign) because the His-Purkinje fibers have been slowed and the ventricles take longer to depolarize

7
Q

The three class IA drugs are ________________.

A

quinidine, procainamide, and disopyramide

8
Q

IA can treat ______________.

A

supraventricular and ventricular arrhythmias

9
Q

Specifically, IA drugs can treat ______________.

A

Wolff-Parkinson-White syndrome

10
Q

What are the side effects of quinidine?

A

Cinchonism (tinnitus – tin plates –headache, and dizziness) and thrombocytopenia (broken plates)

11
Q

The IA drugs also ________________.

A

block potassium channels (just like the prom queen tossing back the banana curtains), thus prolonging the depolarization of the ventricles

12
Q

Long-term use of procainamide can cause ______________.

A

lupus (think of the PROm king’s wolf)

13
Q

Do not give disopyramide to those with heart failure! Why?

A

Because at high doses it has a negative inotropic effect

14
Q

All IA drugs can cause ___________.

A

torsades (think of the banner twisting across the ground floor)

15
Q

Why does prolonged QT interval cause torsades?

A

Because the voltage-sensitive sodium channels can fire again

16
Q

Any drug that blocks __________ can cause torsades.

A

potassium channels (because it prolongs the QT interval)

17
Q

Class IB drugs have what effect?

A

They have the lowest affinity for sodium channels of the class I drugs, so they don’t cause torsades or prolonged QT. Also, they don’t block potassium channels as much (think of Libby closing the potassium curtain), and thus speed up the action potential –shortening its duration. (think of Libby shutting the potassium blinds quickly).

18
Q

What antiseizure medication has antiarrhythmic effects?

A

Phenytoin (it is a class IB drug –think of the friendly towing truck outside Libby’s window)

19
Q

IB drugs target ___________ tissue.

A

ischemic/damaged (B = Broken) As such, they’re great for treating ischemia-induced arrhythmias.

20
Q

Which antiarrhythmics can cause neurologic effects?

A

IB (think of Libby and her boyfriend’s hats –the hat “he got on their first date” that looks like a brain) IB can cause paresthesias or slurred speech.

21
Q

What are the IC drugs?

A

Propafenone (PuRPle PHONE on the 3rd floor) and flecainide (FLaKes cereal)

22
Q

Which antiarrhythmics do not bind to potassium channels?

A

The IC. (Think of the untouched curtain on the 3rd floor.) As such, they do not prolong the action potential.

23
Q

IC drugs are great at treating _____________.

A

atrial fibrillation (at least, the rhythmic aspect of it; other drugs are used to slow the rate) Think of the static, irregularly irregular rhythm on the TV and the guy zapping the channel to a more regular rate.

24
Q

Why should IC drugs not be used in someone with structural defects?

A

Because they tightly bind sodium channels and thus have the strongest effect on the phase 0 upslope