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Block C - Circulation > Pharmacology Lecture 1 -- Antiarrhythmic Drugs > Flashcards

Pharmacology Lecture 1 -- Antiarrhythmic Drugs Flashcards

1
Q

Class I antiarrhythmic drugs

A

Sodium channel blockers

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2
Q

Effect of Class I antiarrhythmic drugs

A

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

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3
Q

Class II antiarrhythmic drugs

A

Beta blockers

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4
Q

Targetted tissue of Class II antiarrhythmic drugs

A

Slow channel tissue (sinus and AV nodes)

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5
Q

Class III antiarrhythmic drugs

A

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

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6
Q

Class IV antiarrhythmic drugs

A

Calcium channel blockers (“calcium antagonists”)

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7
Q

Targeted tissue of Class IV antiarrhythmic drugs

A

Slow channel tissue

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8
Q

2 examples of multiaction antiarrhythmic drugs

A 
Sotalol (class II and III action)
Amiodarone (I, II, III, IV action)
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9
Q

4 mechanisms by which drugs depress slow response action potenttials

A

Sympathetic antagonism
Vagal enhancement
Calcium channel blockers
Purigenic antagonists

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10
Q

Define how sympathetic antagonism affects the heart

A

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

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11
Q

Define how vagal enhancement affects the heart

A

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

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12
Q

Define how calcium channel blockers affect the heart

A

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

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13
Q

Define how purigenic agonists affect the heart

A

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

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14
Q

How to treat tachycardia due to slow tissue reentrant circuit

A

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

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15
Q

How to control ventricular response in the event of atrial fibrillation

A

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

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16
Q

Ways to terminate AVN reentry

A

Vagal maneuvers
IV Ca++ channel blockers
IV adenosine

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17
Q

Ways to prevent AVN reentry

A

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

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18
Q

How to control rate in atrial fibrillation

A

Ca++ channel blockers
Digitalis
Beta blockers

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19
Q

2 ways to prevent or terminate sustained tachyarrhythmias

A

Decrease automaticity

Increase refractory period

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20
Q

Effect of decreasing automaticity for VT

A

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

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21
Q

The most important determinant of refractory period in fast channel tissue

A

Action potential duration (APD)

22
Q

Effect of decreasing Na+

A

Can suppress arrhythmias caused by DAD’s

23
Q

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

A

Reetrant mechanisms

24
Q

What are the most important ventricular arrhythmias clinically?

A

VT associated with chronic coronary artery disease

Ventricular fibrillation

25
Q

2 classes of drugs that act predominantly on fast channel tissue

A

Class I and III

26
Q

General function of class I drugs

A

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

27
Q

Subcategories of Class I drugs

A

Class IA
Class IB
Class IC

28
Q

3 drugs that belong to class IA

A

Quinidine**
Disopyramide
Procainamide

29
Q

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

A

Class IA

30
Q

Define Class IB

A

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

31
Q

Effect of Class IB drugs

A

Little effect in normal tissues

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

32
Q

When is Class IB used?

A

Mainly used in IV for emergency

Effective for automatic, DAD, and EAD arrhythmias (NOT reentrant)

33
Q

Define Class IC

A

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

34
Q

Function of Class IC

A

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

35
Q

General function of class III drugs

A

Increase APD in fast channel tissue

36
Q

When are Class III drugs useful?

A

Reentrant arrhythmias (AF, AFL, some VTs)

37
Q

Main risk of using Class III drugs

A

Acquiring LQTS

38
Q

Define ablation

A

Targeted destruction of arrhythmia-generating tissue

39
Q

How is ablation performed?

A

Under light anesthesia or sedation with transvenous electrode catheters

40
Q

What does the effectiveness of ablation depend on?

A

The ability to identify discrete critical tissue zone

41
Q

When is ablation useful?

A

AV reentry, Atrial flutter > VT >= AF

42
Q

What is an implantable defibrillator useful for?

A

Highly effective in rapid termination of VT/VF

43
Q

Most changes in PR interval are due to…

A

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

44
Q

What do longer PR intervals signify?

A

Slowed AV nodal conduction

45
Q

What does longer QRS duration signify?

A

Slowed ventricular conduction (takes longer to activate ventricles)

46
Q

What does a longer QT interval signify?

A

Longer APD

47
Q

What is an indication of effect on SA node?

A

Degree of heart rate slowing

NOTE: Pause or arrest = toxic effect

48
Q

What indicates an effect on AV node

A

PR interval increase

NOTE: block = toxic effect

49
Q

What indicates an effect on ventricular conduction?

A

Degree of QRS prolongation

NOTE: Excessive (>25%) = toxic

50
Q

What is an indicator of ventricular APD?

A

Degree of QT prolongation

NOTE: Excessive (>15 - 20%) = toxic

Block C - Circulation (26 decks)

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