Pharmacology - Anti-Arrythmic Drugs

Front 1

List the 4 classes of anti-arrhythmics drugs

Back 1

I - Na Channel Blockers
II - B- Receptor Blockers
III - AP Duration Extenders
IV - Ca Channel Blockers

Front 2

What are the three class I-A anti-arrhythmics?

Back 2

Quinidine
Procainamide
Disomyramide

Front 3

What are the primary indications of Quinidine?

Back 3

A-fib, A-flutter

Front 4

What is the MOA of the class I-A anti-arrhythmic?

Back 4

Use dependent Na channel blocker, it slows phase 0 and depresses phase 4. Overall, it increases AP duration and refractory period length

Front 5

What are the adverse effects of Quinidine?

Back 5

Alpha block (vasodilation)
Muscarinic Block (tachycardia)
Can elicit V-fib or EAD's

Front 6

What is the primary indication for Procainamide?

Back 6

Used as a backup to lidocaine in treatment of ventricular arrhythmias

Front 7

Rank the class I-A drugs in order of muscarinic effect from weakest to strongest.

Back 7

Procainamide, Quinidine, Disopyramide

Front 8

What is the indication of Disopyramide?

Back 8

Treatment of ventricular arrhythmias (backup to the other I-A's)

Front 9

Procainamide can be considered a class III in some ways. Why?

Back 9

Its NAPA metabolite acts to slow AP duration much like class III drugs.

Front 10

What are the side effects of Procainamide?

Back 10

Lupus-like symptoms
EAD's

Front 11

What are the side effects of Disopyramide?

Back 11

Negative ionotropic effects
Atropine-like effects (urinary retention, dry mouth, constipation)
EAD

Front 12

What class of anti-arrhythmic is Lidocaine?

Back 12

I-B

Front 13

What is the indication of Lidocaine?

Back 13

Ventricular arrhythmia after MI. Not good for atrial issues

Front 14

What is the MOA of Lidocaine. Be sure to describe it's state affinity.

Back 14

It blocks Na channels. Particularly, it blocks inactivated channels in a use-dependent manner.

By doing so, it can extend the refractory period.

Front 15

What are the side effects of Lidocaine?

Back 15

Primarily neurological (parastesia, tremors, convulsions)

It is the least cardiotoxic anti-arrhythmic

Front 16

Name the class I-C anti-arrhythmic.

Back 16

Flecainide

Front 17

What is the indication of Flecainide

Back 17

Ventricular arrhythmias (second line) PVT's SVT's

NOT post MI

Front 18

What is the MOA of Flecainide? Be sure to describe it's state affinity.

Back 18

Blocking BOTH Na and K channels. It prefers resting states (even in tissue).

It prolongs the refractory period and slows conduction.

Front 19

List three class I-B anti-arrhythmics.

Back 19

Lidocaine
Mexiletine
Tocainide

Front 20

List three class I-C anti-arrhythmics

Back 20

Flecainide
Propafenone
Moricizine

Front 21

List 4 class II anti-arrhythmics.

Back 21

Propanolol
Metoprolol
Esmolol
Atenolol

Front 22

What are the indications of Propanolol?

Back 22

Exercise induced arrhythmias, Prolonged Q-T syndrome, post MI protection

Front 23

What are electrical effects of Propanolol on the heart?

Back 23

Extend phase 4 (automaticity)
Slow sinus rate
Increase AV conduction
Increase refractoryness

Front 24

What are the side effects of Propanolol?

Back 24

Bradycardia
Bronchospasm
Increased LDL/HDL

Front 25

List 4 Class III Anti-Arrhythmics.

Back 25

Amiodarone
di-Sotalol
Ibutilide
Bretyllium

Front 26

What are the indications of Amiodarone?

Back 26

Refractory SVT, v-Tach, A-fib, a tach

Front 27

What is the MOA of Amiodarone?

Back 27

Blocking Na channels, B-receptors, and weakly Ca channels.

It prolongs AP duration, refractoriness, and delays conduction

Front 28

What are the side effects of Amiodarone.

Back 28

Pulmonary Fibrosis
Thyroid Dysfunction
Weakness
Photo sensitivity

It and it's metabolites are highly lipophilic. Note: It's cousin Dronedarone is newer and has reduced side effects

Front 29

What are the indications of di-Sotalol?

Back 29

SVT and Ventricular Arrythmias

Front 30

What is the MOA of di-Sotalol

Back 30

At low concentrations: B-Blocker
At high concentrations: B-Blocker and Anti-Arrhythmic.

It slows depolarization, increases refractoriness, and increases AP duration.

Front 31

What are the adverse effects of di-Sotalol?

Back 31

B-Blockade (Bradycardia, Bronchospasm, increased LDL)

EAD's (anything that prolongs AP's can cause EAD's)

Front 32

List two class IV anti-arrhythmics used in treating arrhythmias.

Back 32

Diltiazem
Verapamil

Front 33

What are the indications for Ca-channel Blockers in arrhythmias?

Back 33

Superventricular tachycardia, A-fib, A-flutter

Front 34

What are the side effects of Ca-channel blockers when used to treat arrhythmias?

Back 34

Negative ionotropic effects

Do not give with B-blockade (double whammy)

Front 35

What is the treatment for DAD's caused by Digitalis toxicity?

Back 35

Magnesium

Front 36

What drug is used to cardiovert?

Back 36

Adenosine

Front 37

What is the MOA of Adenosine?

Back 37

Increases K conductance, inhibit Ca currents. Blocks AV node

Primarily atrial effects (doesn't work well for ventricular cardioversion)

Front 38

What is the indication of Digitalis in treating arrhythmias?

Back 38

Atrial stuff (fib and flutter)

Front 39

What is the MOA of Digitalis

Back 39

Increases AV node refractoriness and AV node conduction (blocks Na/K transporter) This manages to slow transmission or SVT rates