Pharmacology Of Anti-arrhythmia

Question 1

What are the mechanisms of arrhythmogenesis?

Answer 1

1. Abn. Of impulse conduction— recently of all Arrhythmias (90%)
2. Abn. Of impulse generation— abn. Automaticity and triggered activity

Question 2

Why do we use Anti-Arrhythmic agents?

Answer 2

1. Help maintain sinus rhythm after atrial fibrillation is restored to sinus rhythm
2. Reduce the frequency of ventricular tachycardia/ ventricular fibrillation in patients with structural heart disease and implantable cardioverter defibrillators

Question 3

Phase 0 is

Answer 3

Depolarization caused by sodium

Question 4

Phase 3

Answer 4

Repolarization and potassium exits

Question 5

Phase 2

Answer 5

Calcium enters the cell leading to the initiation of contraction

Question 6

triggered activity that results in early afterdepolarization (EAD) we see an

Answer 6

increase in duration of phase 3 and the QT lengthens

Question 7

triggered activity that results in delayed afterdepolarization (DAD) results

Answer 7

occurs in late phase 4 after a full repolarization. It occurs due to increase Ca2+ levels (toxic levels)

Question 8

2 mechanisms of how antiarrhythmic agents work?

Answer 8

1. slow conduction through NA+ channel blocking drugs

2. extend the refractory period by K+ channel blocking drugs

Question 9

Na channel blockers are use dependent or independent?

Answer 9

dependent

Question 10

K+ channel blockers are known as __________ use dependent

Answer 10

reverse

Question 11

Class I

Answer 11

Na+ channel blockers

Question 12

Class IA

Answer 12

Na and K channel blockade, itermediate binding and dissociation properties

Question 13

Class IB

Answer 13

rapid binding and dissociation properties

Question 14

Class IC

Answer 14

slow binding and dissociation

Question 15

which drug do we use for Afib

Answer 15

Class IC

Question 16

effect of sodium channel blockers

Answer 16

slope of phase 0 decreases and thus QRS widens

Question 17

Class II

Answer 17

Beta adrenergic receptors

Question 18

Beta 1 adrenergic receptor blocker

Answer 18

selective- metoprolol

Question 19

Beta 1 and 2 adrenergic receptor blocker

Answer 19

non-selective- propanalol

Question 20

Bet 1 AND 2 AND ALPHA RECEPTOR BLOCKER

Answer 20

non selective- carvedilol

Question 21

Class II work by

Answer 21

reducing conduction through AV node and thus reduce ventricular response (AFib)

• reduces vtachy risk

Question 22

Class III

Answer 22

potassium channel blockers

Question 23

what do Class III do

Answer 23

increase phase 3 of repolarization and thus increase the QT interval

Question 24

examples of Class III

Answer 24

amiodarone and sotalol

Question 25

Class IV

Answer 25

calcium channel blockers

Question 26

there are two types of Class IV

Answer 26

1. non-dihydropyridine that block AV node in supraventricular tachy. thus they are cardio-selective and slow heart rate
2. dihydropyridine - arterial vasodilator, HTN and chronic stable angina. They are more periphery drugs that are used to lower blood pressure

Question 27

digoxin

Answer 27

parasympathetic mimetic that blocks AV node conduction

Question 28

Digoxin used

Answer 28

was useful in control of ventricular response to Afib when BP is low or when the LVEF is significantly reduced because it does not drop BP

• known toxicity be careful

Question 29

adenosine

Answer 29

blocks AV node conduction and has a rapid onset/offset

Question 30

why do we fear using anti-arrhythmic agents?

Answer 30

1. relatively high risk of inducing a life threatening ventricular arrhythmias
2. low efficacy

Question 31

drug induced pro-arrhythmia

Answer 31

torsade de pointe- a plymorphic ventricular tachy. caused by Class III.

• it leads to a prolonged QT interval by blocking the potassium channel leading to an increased repolarization time

Question 32

what drugs should we not give to patients with structural abn.?

Answer 32

Class I drugs especially IC

Question 33

exacerbation of bradycardia

Answer 33

1. Sinus node dysfunction

2. AV conduction abn

Question 34

precipitation of life threatening ventricular arrhythmias

Answer 34

torsade de pointe

Question 35

exacerbation of pre-existing ventricular arrhythmias

Answer 35

ventricular tachy

Question 36

conversion of atrial fibrillation to atrial flutter

Answer 36

type IC anti-arrhythmic agents

Question 37

promotion fo the development of BBB

Answer 37

type IC anti-arrhythmic agents

Question 38

beta blockers

Answer 38

Class II

Question 39

non-dihydropyridine calcium channel blockers

Answer 39

Class IV

Question 40

useful when blood pressure is low

Answer 40

digoxin

Question 41

normal heart structure and need to control rhythm

Answer 41

consider class IC agent

Question 42

abnormal heart structure and need to control rhythm

Answer 42

class III agent due to risk of pro-arrhythmia with a Class I agent

Question 43

anti-coag. therapy to prevent systemic thromboembolism

Answer 43

• warfarin

- novel anti-coag. that are direct thrombin inhibitors or factor xi

Question 44

rate control strategy

Answer 44

reduce ventricular response

• class II. IV and digoxin

Question 45

chronic tx. for SVT

Answer 45

1. medical therapy: AV node blockade by using a beta-blocker or calcium channel blocker
2. ablation

Question 46

acute Tx for SVT

Answer 46

1. Stable –> vagal maneuvers –> adenosine IV –> CA2+ channel blocker IV –> synchronized cardioversion
2. unstable –> synchronized cardioversion

Question 47

ventricular tachy therapy

Answer 47

lead implanted at R ventricular apex via subclavian vein or externally placed over pectoralis muscle

Question 48

recurrent ventricular tachy leading to heart failure:

1. Tx for Class III/IV HF
2. Tx for Class I/II HF

Answer 48

1. Class III-amiodarone

2. Class III- sotalol

Question 49

what is contraindicated for recurrent ventricular tachy

Answer 49

IA or IC agent due to risk of pro-arrhythmia

Question 50

adenosine will affect atrial tachy by

Answer 50

only terminating a few of them