Pharmacology Lecture 1 -- Antiarrhythmic Drugs Flashcards Preview

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Flashcards in Pharmacology Lecture 1 -- Antiarrhythmic Drugs Deck (50):
1

Class I antiarrhythmic drugs

Sodium channel blockers

2

Effect of Class I antiarrhythmic drugs

Reduce automaticity and/or Vmax in fast channel tissue (working ventricular and atrial muscle, His-Purkinje system)

3

Class II antiarrhythmic drugs

Beta blockers

4

Targetted tissue of Class II antiarrhythmic drugs

Slow channel tissue (sinus and AV nodes)

5

Class III antiarrhythmic drugs

Drugs that act predominantly by increasing APD in fast channel tissue (mainly potassium channel blockers)

6

Class IV antiarrhythmic drugs

Calcium channel blockers ("calcium antagonists")

7

Targeted tissue of Class IV antiarrhythmic drugs

Slow channel tissue

8

2 examples of multiaction antiarrhythmic drugs

Sotalol (class II and III action)
Amiodarone (I, II, III, IV action)

9

4 mechanisms by which drugs depress slow response action potenttials

Sympathetic antagonism
Vagal enhancement
Calcium channel blockers
Purigenic antagonists

10

Define how sympathetic antagonism affects the heart

Beta-adrenergic (sympathetic) stimulation enhances Ca++ curent
Beta-blockers and other sympatholytics remove Ca++ current resulting from adrenergic stimulation

11

Define how vagal enhancement affects the heart

Reduces Ca++ entry by both direct and indirect (antisympathetic) mechanisms
Includes physical maneuvers such as Valsalva, carotid sinus massage. Also, digitalis

12

Define how calcium channel blockers affect the heart

Directly reduce Ca++ entry through voltage-dependent calcium channel (varapamil, diltiazem)

13

Define how purigenic agonists affect the heart

Adenosine or ATP; produce vagal-like effects via purinergic receptor activation

14

How to treat tachycardia due to slow tissue reentrant circuit

Block slow channel (increase refractory period) = may block reentry circuit

15

How to control ventricular response in the event of atrial fibrillation

Suppress slow channel tissue to enhance filtering function of the AV node

16

Ways to terminate AVN reentry

Vagal maneuvers
IV Ca++ channel blockers
IV adenosine

17

Ways to prevent AVN reentry

Ca++ channel blockers, digitalis, beta blockers (non extremely effective)

18

How to control rate in atrial fibrillation

Ca++ channel blockers
Digitalis
Beta blockers

19

2 ways to prevent or terminate sustained tachyarrhythmias

Decrease automaticity
Increase refractory period

20

Effect of decreasing automaticity for VT

Suppress extrasystoles which can act as trigger for reetrnat arrhythmias.
Can slow or stop VT due to enhanced automaticity

21

The most important determinant of refractory period in fast channel tissue

Action potential duration (APD)

22

Effect of decreasing Na+

Can suppress arrhythmias caused by DAD's

23

What is the most common cause of the most important ventricular arrhythmias

Reetrant mechanisms

24

What are the most important ventricular arrhythmias clinically?

VT associated with chronic coronary artery disease
Ventricular fibrillation

25

2 classes of drugs that act predominantly on fast channel tissue

Class I and III

26

General function of class I drugs

Decrease automaticity and phase 0 Na+ current in fast channel tissue

27

Subcategories of Class I drugs

Class IA
Class IB
Class IC

28

3 drugs that belong to class IA

Quinidine**
Disopyramide
Procainamide

29

Which Class I drug is no longer used for arrhythmias due to adverse effects?

Class IA

30

Define Class IB

Lidocaine** -- voltage-dependent Na+-channel blockers

31

Effect of Class IB drugs

Little effect in normal tissues
Depress INa in sick depolarized tissues or automatic cells which depolarize before firing.

32

When is Class IB used?

Mainly used in IV for emergency
Effective for automatic, DAD, and EAD arrhythmias (NOT reentrant)

33

Define Class IC

Very strong Na+ channel blockers (i.e. flecainide***, propafenone)

34

Function of Class IC

Suppress ventricular automaticity, DAD's (suppress APCs, VPCs)
Can terminate or prevent AF

35

General function of class III drugs

Increase APD in fast channel tissue

36

When are Class III drugs useful?

Reentrant arrhythmias (AF, AFL, some VTs)

37

Main risk of using Class III drugs

Acquiring LQTS

38

Define ablation

Targeted destruction of arrhythmia-generating tissue

39

How is ablation performed?

Under light anesthesia or sedation with transvenous electrode catheters

40

What does the effectiveness of ablation depend on?

The ability to identify discrete critical tissue zone

41

When is ablation useful?

AV reentry, Atrial flutter > VT >= AF

42

What is an implantable defibrillator useful for?

Highly effective in rapid termination of VT/VF

43

Most changes in PR interval are due to...

Changes in conduction time through the AV node (largest part of P interval = most subject to change)

44

What do longer PR intervals signify?

Slowed AV nodal conduction

45

What does longer QRS duration signify?

Slowed ventricular conduction (takes longer to activate ventricles)

46

What does a longer QT interval signify?

Longer APD

47

What is an indication of effect on SA node?

Degree of heart rate slowing
NOTE: Pause or arrest = toxic effect

48

What indicates an effect on AV node

PR interval increase
NOTE: block = toxic effect

49

What indicates an effect on ventricular conduction?

Degree of QRS prolongation
NOTE: Excessive (>25%) = toxic

50

What is an indicator of ventricular APD?

Degree of QT prolongation
NOTE: Excessive (>15 - 20%) = toxic