Pharmacology Lecture 1 -- Antiarrhythmic Drugs

Question 1

Class I antiarrhythmic drugs

Answer 1

Sodium channel blockers

Question 2

Effect of Class I antiarrhythmic drugs

Answer 2

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

Question 3

Class II antiarrhythmic drugs

Answer 3

Beta blockers

Question 4

Targetted tissue of Class II antiarrhythmic drugs

Answer 4

Slow channel tissue (sinus and AV nodes)

Question 5

Class III antiarrhythmic drugs

Answer 5

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

Question 6

Class IV antiarrhythmic drugs

Answer 6

Calcium channel blockers (“calcium antagonists”)

Question 7

Targeted tissue of Class IV antiarrhythmic drugs

Answer 7

Slow channel tissue

Question 8

2 examples of multiaction antiarrhythmic drugs

Answer 8

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

Question 9

4 mechanisms by which drugs depress slow response action potenttials

Answer 9

Sympathetic antagonism
Vagal enhancement
Calcium channel blockers
Purigenic antagonists

Question 10

Define how sympathetic antagonism affects the heart

Answer 10

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

Question 11

Define how vagal enhancement affects the heart

Answer 11

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

Question 12

Define how calcium channel blockers affect the heart

Answer 12

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

Question 13

Define how purigenic agonists affect the heart

Answer 13

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

Question 14

How to treat tachycardia due to slow tissue reentrant circuit

Answer 14

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

Question 15

How to control ventricular response in the event of atrial fibrillation

Answer 15

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

Question 16

Ways to terminate AVN reentry

Answer 16

Vagal maneuvers
IV Ca++ channel blockers
IV adenosine

Question 17

Ways to prevent AVN reentry

Answer 17

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

Question 18

How to control rate in atrial fibrillation

Answer 18

Ca++ channel blockers
Digitalis
Beta blockers

Question 19

2 ways to prevent or terminate sustained tachyarrhythmias

Answer 19

Decrease automaticity

Increase refractory period

Question 20

Effect of decreasing automaticity for VT

Answer 20

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

Question 21

The most important determinant of refractory period in fast channel tissue

Answer 21

Action potential duration (APD)

Question 22

Effect of decreasing Na+

Answer 22

Can suppress arrhythmias caused by DAD’s

Question 23

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

Answer 23

Reetrant mechanisms

Question 24

What are the most important ventricular arrhythmias clinically?

Answer 24

VT associated with chronic coronary artery disease

Ventricular fibrillation

Question 25

2 classes of drugs that act predominantly on fast channel tissue

Answer 25

Class I and III

Question 26

General function of class I drugs

Answer 26

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

Question 27

Subcategories of Class I drugs

Answer 27

Class IA Class IB Class IC

Question 28

3 drugs that belong to class IA

Answer 28

Quinidine** Disopyramide Procainamide

Question 29

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

Answer 29

Class IA

Question 30

Define Class IB

Answer 30

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

Question 31

Effect of Class IB drugs

Answer 31

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

Question 32

When is Class IB used?

Answer 32

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

Question 33

Define Class IC

Answer 33

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

Question 34

Function of Class IC

Answer 34

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

Question 35

General function of class III drugs

Answer 35

Increase APD in fast channel tissue

Question 36

When are Class III drugs useful?

Answer 36

Reentrant arrhythmias (AF, AFL, some VTs)

Question 37

Main risk of using Class III drugs

Answer 37

Acquiring LQTS

Question 38

Define ablation

Answer 38

Targeted destruction of arrhythmia-generating tissue

Question 39

How is ablation performed?

Answer 39

Under light anesthesia or sedation with transvenous electrode catheters

Question 40

What does the effectiveness of ablation depend on?

Answer 40

The ability to identify discrete critical tissue zone

Question 41

When is ablation useful?

Answer 41

AV reentry, Atrial flutter > VT >= AF

Question 42

What is an implantable defibrillator useful for?

Answer 42

Highly effective in rapid termination of VT/VF

Question 43

Most changes in PR interval are due to...

Answer 43

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

Question 44

What do longer PR intervals signify?

Answer 44

Slowed AV nodal conduction

Question 45

What does longer QRS duration signify?

Answer 45

Slowed ventricular conduction (takes longer to activate ventricles)

Question 46

What does a longer QT interval signify?

Answer 46

Longer APD

Question 47

What is an indication of effect on SA node?

Answer 47

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

Question 48

What indicates an effect on AV node

Answer 48

PR interval increase | NOTE: block = toxic effect

Question 49

What indicates an effect on ventricular conduction?

Answer 49

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

Question 50

What is an indicator of ventricular APD?

Answer 50

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