Pharm. of Drugs Affecting Arrhythmias Flashcards Preview

Cardiology > Pharm. of Drugs Affecting Arrhythmias > Flashcards

Flashcards in Pharm. of Drugs Affecting Arrhythmias Deck (44)
Loading flashcards...
0

In the Singh-Vaughan Williams classification scheme, what do class I drugs do?

Block Na+ channels (local anesthetics) - slow conduction velocity and reduce excitability.

1

In the Singh-Vaughan Williams classification scheme, what do class II drugs do?

Class II are beta-blockers

2

In the Singh-Vaughan Williams classification scheme, what do class III drugs do?

Class III drug are K+ channel blockers: prolong refractoriness, but don't reduce excitability.

3

In the Singh-Vaughan Williams classification scheme, what do class IV drugs do?

Class IV drugs are Ca++ channel blockers (L-type Ca++ channels)

4

In the Singh-Vaughan Williams classification scheme, what do class IA drugs do?

block both Na+ and K+ channels

5

Name 1 class IA drug to remember?

Procainamide

6

Name 1 class IB drug to remember?

Lidocaine

7

Name 1 class IC drug to remember?

Flecainide

8

How do class IA, IB, and IC vary in their effects on the Na+ channel?

IB are weakest
IC are intermediate
IA are most potent

9

What's one class II drug (aka beta blocker) used for arrhythmias?

Atenolol

10

What's one class III drug to remember?

Dofetilide (specific K+ channel inhibitor)

11

What's one class IV drug (aka. Ca++ blocker) to remember?

Verapamil

12

Aside from it's effects on the Na/K pump, how can digoxin affect arrhythmias?

It's a muscarinic agonist as well.

13

What Singh-Vaughan Williams classes of drugs can be used to treat V Tach?

Class I - Na+ blockers
Class III - K+ blockers
(both slowing conduction/decreasing excitability AND prolonging refractoriness counteract V Tach)

14

What Singh-Vaughan Williams classes of drugs can be used to treat A Fib?

Class I - Na+ blockers
Class III - K+ blockers
(both slowing conduction/decreasing excitability AND prolonging refractoriness counteract A Fib)

15

What Singh-Vaughan Williams classes of drugs can be used to treat AV reentry?

Class I - Na+ blockers
Class II - beta blockers
Class III - K+ blockers

16

What Singh-Vaughan Williams classes of drugs can be used to treat AV nodal reentry?

Class II - beta blockers
Class IV - Ca++ blockers
Others: digoxin and adenosine

17

What 3 parameters can you modify with drugs to affect reentrant tachycardias?

Excitability (class I), conduction velocity (class I), and effective refractory period (class III)

18

What parameter can you modify with drugs to affect automaticity?

Phase 4 depolarization

19

Which parameter is modified by drugs that predispose to tachycardias due to early afterdepolarizations?

Prolonged action potential duration.
(Class III drugs, i.e. K+ blockers, do this... and thus predispose to Torsade des pointes)

20

How does HR modify the effect of Na+ channel blockade?

Faster HR -> the drugs block the channels more.

21

How does membrane potential affect the ability of Class I drugs to block Na+ channels? How is this relevant to choosing a drug in ischemia-related arrhythmia?

More depolarized -> easier to block.
In ischemia, myocytes are more depolarized.
Lidocaine, being class IB and less potent, will thus selectively block Na+ channels in ischemic myocytes.

22

3 parameters that increase the potency of K+ blockers in prolonging action potential duration (APD)?

Slow HR
Low extracellular K+ (makes sense. If there's less K+, blocking it's movement will have greater relative effect)
Low extracellular Mg++

23

What 2 ions do you want to target when dealing with arrhythmia caused by "fast response" tissue i.e. myocytes & His-Purkinje system?

Na+ and K+
Thus, Class I and Class III drugs.

24

What 4 surface molecules can you target when trying to deal with arrhythmias generated by "slow response" tissue i.e. SA and AV nodes?

Beta receptors (causes decreased Ca++ current - I(Ca) )
Ca++ channels
Muscarinic receptors (decreased I(Ca), increased I(KAch) )
Adenosine receptors (decreased I(Ca), increased I(KAch) )

25

Class II, Class IV, digoxin, and adenosine all have what effect on SA rate, AV node ERP, and AV node excitability?

All decrease SA rate
Increase AV node effective refractory period
Decrease AV node excitability

26

If you want to prolong ERP in fast response tissue, what do you use?
In slow response tissue?

Fast response: block K+
Slow response: block Ca++ (or other drugs that indirectly lower Ca++)

27

Do drugs distinguish between cardiac and vascular smooth muscle Ca++ channels?

Yep.

28

What's a Ca++ blocker specific for cardiac Ca++ channels?

Verapamil

29

What's a Ca++ channel blocker specific to vascular smooth muscle Ca++ channels? (what would this do?)

Nifedipine (this drug dilates blood vessels -> rapid and dramatic drops in SVR and BP)