Chapter 14: Antiarrhythmic Drugs

Question 1

Class 1 Antiarrhythmics
aka Group 1 (\_\_\_\_\_)
MOA: \_\_\_\_\_
Prototypes and mnemonic: 
\_\_\_\_\_

Answer 1

Class 1 Antiarrhythmics
Group 1 - Na channel blockers

MOA: slow the upstroke of sodium-dependent action potentials and usually prolong QRS duration

Group 1A (prototype procainamide)

• Prolong the AP
• “Double Quarter Pounder”
• Disopyramide, Quinidine, Procainamide

Group 1B drugs (prototype lidocaine)

• Shorten the AP in some cardiac tissues, especially Purkinje fibers.
• “with Lettuce, Mayo, Tomato”
• Lidocaine, Mexeletine, Tocainide

Group 1C drugs (prototype flecainide)

• Have no effect on AP duration.
• “More Fries Please”
• Moricizine, Flecainide, Profepanone

Question 2

Class 2 Antiarrhythmics
aka Group 2 (\_\_\_\_\_)
MOA: \_\_\_\_\_
Prototypes and mnemonic: 
\_\_\_\_\_

Answer 2

Class 2 Antiarrhythmics
aka Group 2 (Beta blockers)

MOA:

• Primarily cardiac β-adrenoceptor blockade and reduction in cAMP, which results in a modest reduction of both sodium and calcium currents and the suppression of abnormal pacemakers
• PR interval is usually prolonged

Prototype:

• Propranolol
• Esmolol

Mnemonic:
-LOL (Propranolol, Atenolol, Metoprolol)

Question 3

Class 3 Antiarrhythmics
aka Group 3 (\_\_\_\_\_)
MOA: \_\_\_\_\_
Prototypes and mnemonic: 
\_\_\_\_\_

Answer 3

Class 3 Antiarrhythmics
aka Group 3 (Potassium Ik channel blockers)

MOA:

• Antiarrhythmic action through K-channel block
• Markedly prolongs AP duration as well as blocking other channels and β receptors
• AP prolongation is caused by blockade of the IK potassium channels, chiefly IKr, that are responsible for the repolarization of the AP

Prototypes:

• Dofetilide
• Ibutilide

Mnemonic:

• This is “SAD”
• Sotalol, Amiodarone, Dofetilide

Question 4

Class 4 Antiarrhythmics
aka Group 4 (\_\_\_\_\_)
MOA: \_\_\_\_\_
Prototypes and mnemonic: 
\_\_\_\_\_

Answer 4

Class 4 Antiarrhythmics
aka Group 4 (Calcium L-Type channel blockers)

MOA:

• Effective in arrhythmias that must traverse calcium-dependent cardiac tissue such as the AV node
• These agents cause a state- and use-dependent selective depression of calcium current
• AV conduction velocity is decreased, and effective refractory period and PR interval are increased by these drugs

Prototype:
- Verapamil

Mnemonic:
- I and V in Class IV

Question 5

Antiarrhythmic group acting on Phase 0 (zero) of the cardiac action potential

Answer 5

Class 1

Question 6

Antiarrhythmic Group 1 subtype that prolong the AP duration

Answer 6

Group 1A

Question 7

Antiarrhythmic Group 1 subtype that shorten the AP duration

Best post MI

Answer 7

Group 1B

Question 8

Antiarrhythmic Group 1 subtype that have no effect on the AP duration

Contraindicated for post-MI arrhythmias

Answer 8

Group 1C

Question 9

Class 1A antiarrhythmic used for atrial and ventricular arrhythmias, especially after MI

Crosses the breastmilk and may cause lupus-like syndrome

Answer 9

Procainamide

Question 10

Class 1A antiarrhythmic used for atrial and ventricular arrhythmias

May cause antimuscarinic effects, heartfailure; crosses the breastmilk

Answer 10

Disopyramide

Question 11

Class 1A antiarrhythmic used for atrial and ventricular arrhythmias, and malaria

May cause cinchonism (headache, vertigo, tinnitus), cardiac depression, GI upset, and ITP

Answer 11

Quinidine

Question 12

Treatment of Class 1A antiarrhythmic drug overdose

Answer 12

1. Sodium lactate (for drug-induced arrhythmias)

2. Pressor sympathomimetics (to reverse drug-induced hypotention) if indicated

Question 13

Class 1B antiarrhythmic used as drug of choice for ventricular arrhythmias post-MI, and digoxin-induced arrhythmias.

This is the least cardiotoxic among conventional antiarrhythmics

Answer 13

Lidocaine

Question 14

Class 1C antiarrhythmic used for refractory arrhythmia

Answer 14

Flecainide

Question 15

Class 1 antiarrhythmic for Wolff-Parkinson-White Syndrome (WPW)

Answer 15

1. Procainamide

2. Amiodarone

Question 16

Antiarrhythmic group acting on Phase 4 of the cardiac action potential

Answer 16

Class 2

Question 17

Mechanism of action of Class 2 antiarrhythymics

Answer 17

1. Primarily cardiac beta-adrenoceptor blockade and reduction in cAMP
2. Reduction of both sodium and calcium currents
3. Suppression of abnormal pacemakers
4. AV node is particularly sensitive to blockers
5. PR interval is usually prolonged

Question 18

Nonselective beta blockers

Answer 18

1. Propranolol

2. Timolol

Question 19

Beta 1 selective

Answer 19

(A–>M)

1. Acebutolol
2. Betaxolol
3. Esmolol
4. Atenolol
5. Metoprolol

Question 20

Partial agonist beta blockers

Answer 20

1. Pindolol

2. Acebutolol

Question 21

Beta blocker lacking local anesthetic effect

Answer 21

Timolol

Question 22

Beta blocker with low lipid solubility

Answer 22

Atenolol

Question 23

Shortest acting beta blocker

Answer 23

Esmolol

Question 24

Longest acting beta blocker

Answer 24

Nadolol

Question 25

Combined alpha and beta blockade

Answer 25

1. Carvedilol | 2. Labetalol

Question 26

Antiarrhythmic group acting on Phase 3 of the cardiac action potential

Answer 26

Class 3

Question 27

Mechanism of action of Class 3 antiarrhythmics

Answer 27

1. Hallmark is the prolongation of the AP duration 2. Caused by blockade of the Ik potassium channels that are responsible for the repolarization of the AP 3. Results in an increase in the ERP and reduces the ability of the heart to respond to rapid tachycardias 4. ECG: increase in QT interval

Question 28

Class 3 antiarrhythmic with prolonged AP duration and QT interval, used for treatment and prophylaxis of atrial fibrillation

Answer 28

Dofetilide

Question 29

Class 3 antiarrhythmic with beta adrenoceptor blocking property used for ventricular arrhythmias, atrial fibrillationo and supraventricular tachycardia

Answer 29

Sotalol

Question 30

Class 3 antiarrhythmic with strong Ik block produces marked prolongation of action potential and refractory period. It is used for refractory arrhythmias and used as off-label in many arrhythmias. It is the most efficacious of all antiarrhythmic drugs and has the longest half life. Side effects include thyroid dysfunction, microcrystalline deposits in the cornea and skin. Other toxicities include pulmonary fibrosis, paresthesia, tremors, thyroid dysfunction, corneal deposits, skin deposits

Answer 30

Amiodarone

Question 31

Why are dihydropyridine calcium channel blockers not useful as antiarrhythmics?

Answer 31

Dihydropyridine CCBs evoke compensatory sympathetic | discharge which facilitates arrhythmias rather than terminating them

Question 32

Class 4 antiarrhythmic drug causing gingival hyperplasia

Answer 32

Verapamil

Question 33

Prolongs the AP duration Prolongs the PR interval Prolongs QRS duration Prolongs QT

Answer 33

Class 1A antiarrhythmic

Question 34

Shortens the AP duration | No effect on normal cells on ECG

Answer 34

Class 1B antiarrhythmic

Question 35

No effect on AP duration | Prolongs QRS duration

Answer 35

Class 1C antiarrhythmic

Question 36

No effect on AP duration | Prolongs PR interval

Answer 36

Class 2 antiarrhythmic | Class 4 antiarrhythmic

Question 37

Prolongs AP duration | Prolongs QT interval

Answer 37

Class 3 antiarrhythmic

Question 38

Antiarrhythmic drug used in AV nodal arrhythmias, and drug of choice for paroxysmal supraventricular tachycardia, by increasing diastolic Ik of AV node causing marked hyperpolarization and conduction block; reduced ICa

Answer 38

Adenosine

Question 39

Depresses ectopic pacemakers, including those caused by digitalis toxicity Decreased levels is associated with an increase incidence of arrhythmias, especially in patients receiving digitalis

Answer 39

Potassium ion

Question 40

Similar depressant effects as potassium on digitalis-induced arrhythmias Effective in some cases of Torsades de Pointes

Answer 40

Magnesium ion

Question 41

Digitalis toxicity is increased by: 1. _____ 2. _____ 3. _____

Answer 41

1. Hypokalemia 2. Hypomagnesemia 3. Hypercalcemia