Cv Pharm - Antiarrhythmia Drugs I-Iii

Front 1

Describe normal sinus rhythm (NSR)

Back 1

The cardiac impulse originates in the sinoatrial node and spreads in an orderly manner throughout the atria, atrioventricular (AV) node, His-Purkinje system and ventricles

Front 2

When is an arrhythmia present?

Back 2

1. If the sinus rate is abnormally rapid or slow

2. If the sinus rhythm is occasionally or frequently interrupted by impulses originating from some other site in the heart (atrial or ventricular premature beats)

3. If all the electrical impulses originate at a site other than the sinus node. (atrial tachycardia, atrial flutter, atrial fibrillation, ventricular tachycardia)

Front 3

How are arrhythmias classified?

Back 3

By the basis of their site of origin (prefix) and their rate (suffix)

1. Sinus bradycardia and tachycardia
2. Atrial premature depolarizations, atrial tachycardia, atrial flutter, atrial fibrillation
3. AV junctional (nodal) tachycardia
4. Ventricular premature depolarizations, ventricular tachycardia, ventricular fibrillation

Front 4

How is the type of arrhythmia diagnosed?

Back 4

By reading an ECG

Front 5

What causes arrhythmias?

Back 5

Pathologically induced alterations in electrophysiology of the heart

Front 6

What is the clinical significant of a rapid or slow HR?

Back 6

It decreases cardiac output and coronary artery perfusion

Front 7

What is the clinical significance of a change in the sequence of depolarizaton (ventricles depolarizing before the atria)

Back 7

It decreases cardiac output and coronary artery perfusion

Front 8

What is an important goal of treatment of arrhythmias?

Back 8

, an arrhythmia with no significant cardiac output

Front 9

What are the consequences of untreated rapid HR?

Back 9

It can cause ventricular "remodeling" that diminishes the contractile function of the ventricles.

Front 10

What are the consequences of untreated ventricular premature impulses and tachycardia?

Back 10

It may turn into ventricular fibrillation, an arrhythmia with no significant CO

Front 11

What are antiarrhytmic drugs used to treat?

Back 11

Tachyarrhythmias (rapid rates)

Front 12

What is the goal of using antiarrhytmic drugs? Why is this not always possble?

Back 12

Goal: To abolish the arrhythmia and restore sinus rhythm

Not always possible because:
1) Drug doses high enough to exert this effect also have toxic effects
2) The pathological mechanism causing arrhythmia cannot be sufficiently influenced by the drug to completely stop the arrhythmia

Front 13

What is the goal of treating ventricular arrhythmias with antiarrhythmic drugs?

Back 13

To prevent ventricular fibrillation that may sometimes follow ventricular premature depolarizations or tachycardia

Front 14

Describe the therapy for bradyarrhytmias

Back 14

-Does not involve the use of a drug from the antiarrhythmic group
-A similar goal to improve CO and coronary perfusion but by increasing HR or improving conduction
-Very often electrical pacemakers are used for this purpose

Front 15

Describe antiarrhythmic treatments not directed at the heart

Back 15

-Directed at extracardiac causes of arrhythmia
-Arrhythmias can result from
-Thyrotoxicosis
-Central or autonomic nervous system disorders
-Abnormalities of ventilation (decreased pO2 and increased pCO2) and acid-base balance
-Correction of these abnormalities may abolish the arrhythmia

Front 16

Describe the classification of antiarrhythmic drugs

Back 16

Drugs can be subdivided into groups according to their primary electrophysiologic effect, e.g., according to the primary membrane channel in the cardiac cell with which they interact (Vaughan-Williams Classification)

Front 17

Describe Class I antiarrhythmic drugs

Back 17

-Decrease fast inward current through Na+ channels (INa).
-These drugs have use-dependent blocking effects on Na+ channels

Front 18

Describe Class IA antiarrhythmic drugs

Back 18

-Decreases Na+ current at moderate and rapid heart rates.
-Decrease If and Ik

-A decrease in INa slows or blocks conduction in atrium and/or ventricle
-A decrease in IK slows repolarization and lengthens action potential duration and the refractory period
-Decrease in If slows pacemaker firing rate

Front 19

What are the important Class IA drugs?

Back 19

-Quinidine
-Procainamide
-Disopyramide

Front 20

Describe Class IB drugs

Back 20

-Decrease Na+ current primarily at rapid heart rates
-Decrease If
-Do not decrease Ik

Front 21

What are the important Class IB drugs?

Back 21

Lidocaine

Front 22

Describe Class IC drugs

Back 22

-Decrease Na+ current at slow to rapid heart rates
-Decrease If
-Possible small decrease in Ik

Front 23

What are the important Class IC drugs?

Back 23

-Flecainide
-Propafenone

Front 24

Describe Class II drugs. What are the important Class II drugs?

Back 24

-Block beta-receptors and prevent arrhythmogenic effect of catecholamines
-Propranolol

Front 25

Describe Class III drugs

Back 25

-Prolong action potential duration and refractory period (mostly reduce IK)

Front 26

What are the important Class III drugs?

Back 26

-Amiodarone (also decreases INa, ICaL, decreases sympathetic effects on heart but is not a beta blocker)
-Sotalol (also a beta blocker)
-Ibutilide
-Dofetilide

Front 27

Describe Class IV drugs

Back 27

-Decrease inward current through L-type calcium channels (ICaL)
-Use-dependent blockade of Ca channel
-Primary effect is on AV node to slow conduction and prolong refractory period

Front 28

What are the important Class IV antiarrhythmic drugs?

Back 28

-Verapamil
-Diltiazem

Front 29

What antiarrhythmic drugs are not part of the antiarrhytmic drug group?

Back 29

-Digitalis
-Autonomic drugs
-Adenosine
-Atropine

Front 30

Describe electrical therapy for arrhythmias

Back 30

-Many types of arrhytmias can be terminated or controlled by electrical stimulation of the heart
-Sometimes used in conjunction with antiarrhythmic drugs

1. Pacemakers
2. Cardioversion (defibrillation)
3. Implantable cardiac defibrillator (ICD)

Front 31

Describe ablation therapy for arrhythmias

Back 31

The site of arrhythmia origin can be destroyed by passing RF current through a catheter in contact with abnormal tissue

Front 32

Class IA drugs
I_Na
Conduction of Normal HR:
Use Dependence:
Conduction of Rapid HR:

I_f
Ectopic pacemakers:
Sinus pacemakers:

I_K
Effect

Back 32

I_Na
Conduction of Normal HR: v
Use Dependence: +++
Conduction of Rapid HR: normal myocardium vv, disease myocardium vvv

I_f
Ectopic pacemakers: vvv (slows firing rate)
Sinus pacemakers: (therapeutic) - <>, v, (toxic) - vvv

I_K
Effect: vv, prolongs repolarization and refractory period

Front 33

Class IB drugs
I_Na
Conduction of Normal HR:
Use Dependence:
Conduction of Rapid HR:

I_f
Ectopic pacemakers:
Sinus pacemakers:

I_K
Effect

Back 33

I_Na
Conduction of Normal HR: <>
Use Dependence: +++
Conduction of Rapid HR: normal myocardium- v, diseased - vvv

I_f
Ectopic pacemakers: vvv
Sinus pacemakers: (therapeutic) - <>, (toxic) - v,<>

I_K
Effect: <>

Front 34

Class IC drugs
I_Na
Conduction of Normal HR:
Use Dependence:
Conduction of Rapid HR:

I_f
Ectopic pacemakers:
Sinus pacemakers:

I_K
Effect

Back 34

I_Na
Conduction of Normal HR: vv
Use Dependence: +++
Conduction of Rapid HR: normal - vvv, diseased - vvvv

I_f
Ectopic pacemakers: vvv
Sinus pacemakers: (therapeutic) <>, v, (toxic) vvv

I_K
Effect v, <> (weak), no important effect on refractoriness

Front 35

Sotalol
I_K:
I_CaL:
I_Na:
I_f:
Sympathetics:

Back 35

I_K: v
I_CaL: <>
I_Na: <>
I_f: no direct effect, v beta block
Sympathetics: v

Front 36

Amiodarone
I_K:
I_CaL:
I_Na:
I_f:
Sympathetics:

Back 36

I_K: v
I_CaL: v
I_Na: v
I_f: no direct effect, v antisympathetic
Sympathetics: v

Front 37

Ibutilide
I_K:
I_CaL:
I_Na:
I_f:
Sympathetics:

Back 37

I_K: v
I_CaL: <>
I_Na: <>
I_f: <>
Sympathetics: <>

Front 38

Dofetilide
I_K:
I_CaL:
I_Na:
I_f:
Sympathetics:

Back 38

I_K: v
I_CaL: <>
I_Na: <>
I_f: <>
Sympathetics: <>