Block 3: Antiarrhythmic Drugs

Front 1

5 ways/things that antiarrhythmic drugs alter

Back 1

1. Max diastolic potential in pacemaker cells and/or the resting potential in ventricular cells

2. Phase 4 depolarization

3. Threshold potential

4. AP duration

5. Refractory period through state-dependent binding to Na channels.

Front 2

All antiarrythmics are .... except class..., which... but effectively regulates channel activities

Back 2

Direct ion channel blockers
II
Indirectly

Front 3

4 classes of antiarrhythmics

Back 3

Class 1A- Fast Na channel blockers (prefer active state)

Class 1B- Na channel blockers- perfers active and inactive

Class 1C- Na channel blockers

Class 2- beta blockers

Class 3- K channel blockers

Class 4- Ca channel blockers

Front 4

Name 4 class 1A Na channel blockers

Back 4

Quinidine
Pracainamide*
Disopyramide
Flecainide ( FLEK-a-nide)

Front 5

MA of Class 1A drugs

Back 5

preferentially bind to Na channels in active state and prolong repolarization (SA node and ventricular myocytes) and prolong repolarization of the membrane (by blocking outward K current)

Decreased re-entry

block Na channels -> prolong QRS
also block K channels -> prolong repolarization (QT)

Front 6

Name 3 class 1B drugs

Back 6

Lidocaine
Tocainide
mexiletine

Front 7

MA of class 1B drugs

Back 7

preferentially binds to Na channels in active and inactive state, shortens repolarization

weakly block Na channels -> little to no effect on QRS
actually shorten repolarization -> QT

Front 8

What happens to 1B drugs bound to na channels

Back 8

Dissociate very fast

Front 9

3 1C Na channel blockers

Back 9

Flecainide
Encainide ( en-KAY-nide)
Propafenone

strongest Na channel blockers -> prolong QRS
have no effect on repolarization -> no change to QT

Front 10

Name a non-selective beta blocker

Back 10

Propanolol

Front 11

name 4 Beta 1 selective beta blockers

Back 11

Bisoprolol
Atenolol
Metoprolol
Acebutolol

Front 12

name 3 B1 selective beta blockers that also vasodilate.

Back 12

Labetalol and carvedilol (also block alpha adenergic)

Pindolol (also beta 2 partial agonist)

Front 13

What do lg. hyperpolarizing K currents do?

Back 13

Shorten plateau phase and return membrane potential to resting more quickly
English: can start a new AP more quickly

Front 14

So then what do K channel blockers do?

Back 14

Prolong repolarization, increase refractory, decrease re-entry
*For some reason this facilitates EAD.

prolong repolarization -> long QT
don't effect depolarization -> nl QRS

Front 15

What can too much prolongation of the plateau cause?

Back 15

EAD

Front 16

Name 4 class 3 drugs

Back 16

Bretylium
Ibutilide
Amioderone
Sotalol

Front 17

What's special about Amioderone?

Back 17

Class I, II, III, and IV drug b.c. it alters lipid membranes in which ion channels sit

Front 18

What's special about Sotalol?

Back 18

Class II and III drug

Front 19

Name 2 class IV drugs

Back 19

Diltiazem and verapamil

Front 20

How does adenosine work as an antiarrythmic?

Back 20

Activated Ach sensitive K+ current in the atrium and sinus and AV node

Front 21

What are the consequences of adenosis

Back 21

Shortend AP, hyperpolarization, and slowing of normal automaticity

Front 22

Which kind of current does adenosine reduce

Back 22

Ca currents

Front 23

What is the consequence of adenosine slowing Ca currents

Back 23

Increases AV nodal refractoriness

Inhibits DAD

Front 24

How is adenosis often administered?

Back 24

Bolus i.v. injection to terminate PSVT

Front 25

How does digoxin work? What do you use if for?

Back 25

1. Inhibits Na-K ATPase activity

2. Used for HF pts. w/reetrant tachycardia

Front 26

Is it hypo or hyperkalemia that causes arrhthymias?

Back 26

Both

Front 27

Hypokalemia can cause what kind of arrhythmia?

Back 27

EAD
DAD
Ectopic beats in non pacemaker cells

Front 28

Hyperkalemia causes arrhthymias by...

Back 28

Depolarizing the membrane and slowing conduction velocity

Front 29

Explain EAD

Back 29

Prolongation of the repolarization delays the inactivation of the ion channels responsible for the inward flow of positive depolarizing currents. This leads to a further delay in repolarization and causes early after depolarization (EAD), the triggering event for torsade