Term 1 Pharm - Antiarrhythmic Drugs

Question 1

The only antiarrhythmic that has ever been shown to improve mortality in the post infarct patient:

Answer 1

Beta blocker

Question 2

Areas of concern with Anti-arrhythmic medicines:

Answer 2

• Limited efficacy
• pro-arrhythmia is a concern, particularly chronic therapy
  K+ channel blockers – Torsades de pointes
  Na channel blockers – re-entry arrhythmias
• Genetic polymorphisms and drug-drug interactions can also impact efficacy and safety

Question 3

(3) Mechanisms of Arrhythmia

Answer 3

1. Re-entry
2. Increased / enhanced automaticity
3. Triggered activity

Question 4

Explain Enhanced Automaticity

Answer 4

Intrinsic property of all myocardial cells

Spontaneous generation of an action potential

Slow progressive depolarization of the membrane potential (phase 4) until a threshold potential is reached at which point a regenerative response is initiated

Question 5

Explain Triggered Activity

Answer 5

Impulse initiation caused after depolarization (Early/Late)

Question 6

How to Prevent Re-entry?

Answer 6

2 Options

(1) Prolong conduction velocity of this limb so the retrograde impulse will collide with the next incoming antegrade impulse in the area of block (Na channel blocker, prolong PR)
(2) Prolong refractory period of the area of unidirectional block so that retrograde conduction cannot occur (K channel blocker prolong QT)

Question 7

What are the Four Ways by Which Antiarrhythmic Drugs Reduce Spontaneous Discharge in Autonomic Tissues?

Answer 7

1. Decrease phase 4 slope
2. Increase threshold
3. Increase max depolarization potential (max diastolic potential)
4. Increase duration of action potential

Question 8

How to Prevent Triggered Activity

Answer 8

Typically remove the offending agent

Typically CLASS 3 or 1A agents for EAD’s-early
or Digoxin for DAD’s - delayed

EAD - Early After Depolarizations
DAD - Delayed After Depolarizations
(Treating Bradycardia and Hypokalemia)

Question 9

Antiarrhythmic drugs (AAD’s) have moderate efficacy and _____________ is replacing the use of AAD’s in regular SVT

Answer 9

catheter ablation

Question 10

Antiarrhythmics with K channel blocking properties can significantly prolong 1. ___________ and facilitate 2. ____________ leading to PMVT (Torsade de Pointe) as a form of 3. ____________.

Answer 10

1. repolarization (QT)
2. early after depolarizations
3. Proarrhythmia

Question 11

Sodium channel blockade (1. e.g. _____________) in the presence of structural heart disease (eg. Post myocardial infarction) can be 2. _______________.

Answer 11

1. Flecainide

2. Pro-arrhythmic

Question 12

The only ‘antiarrhythmic ‘that has ever been shown to improve mortality in the post infarct patient is a ________________.

Answer 12

Beta Blocker

Question 13

The use of an 1. ________ is preferable to any 2._____________ in the treatment of high risk arrhythmia patients (low EF

Answer 13

1. ICD

2. antiarrhythmic

Question 14

Are there drug-drug interactions with medications used to anti-arrhythmia?

Answer 14

YES, a lot (particularly regarding CYP 450 enzyme)

Question 15

Ablation for SVT - has replaced traditional antiarrhythmic therapy (except for ______________)

Answer 15

atrial fibrillation

Ablations has:

• High Success (90%+)
• Low complications (3%)
• Low death 0.1-0.3%

Question 16

What are the types of SVT

Answer 16

AV node is a bystander

• Atrial Tachycardia
• Atrial flutter
• Atrial fibrillation

Utilizing AV node:

• AV Nodal Reentrant Tachycardia
• AV Reciprocating Tachycardia

Question 17

What is the approach for drug therapy for arrhythmias?

Answer 17

Anti-arrhythmic medicines are moderately effective, come with risk of side effects and pro-arrhythmia, so they are generally now used as second line agents in ‘regular’ SVT, as supportive agents with VT (eg in addition to ICD)

(Atrial fibrillation is the exception)

Question 18

Class I Antiarrhythmic Drugs

Answer 18

Na Channel Blockers (prolongs conduction), reduces phase 0

Class Ia (moderate): Quinidine, Procainamide, Disopyramide
Class Ib (weak): Lidocaine, Mexilitine (VT ONLY)
Class Ic (strong): Flecainide, Propafenone

Question 19

Class II Antiarrhythmic Drugs

Answer 19

Beta Blocker

Blocks sympathetic activity

Question 20

Class III Antiarrhythmic Drugs

Answer 20

K Channel Blocker
Prolongs repolarization (phase 3),  lengthening AP duration and effective refractory period 

eg: Sotalol, Dofetilide, Amiodarone, Dronedarone

Question 21

Class IV Antiarrhythmic Drugs

Answer 21

Blocks L type Ca channels

Most effective at SA and AV nodes, reducing rate and conduction