Chapter 14: Antiarrhythmic Drugs Flashcards

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

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

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)

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

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

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

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5
Q

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

A

Class 1

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6
Q

Antiarrhythmic Group 1 subtype that prolong the AP duration

A

Group 1A

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7
Q

Antiarrhythmic Group 1 subtype that shorten the AP duration

Best post MI

A

Group 1B

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8
Q

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

Contraindicated for post-MI arrhythmias

A

Group 1C

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9
Q

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

Crosses the breastmilk and may cause lupus-like syndrome

A

Procainamide

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10
Q

Class 1A antiarrhythmic used for atrial and ventricular arrhythmias

May cause antimuscarinic effects, heartfailure; crosses the breastmilk

A

Disopyramide

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11
Q

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

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

A

Quinidine

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12
Q

Treatment of Class 1A antiarrhythmic drug overdose

A
  1. Sodium lactate (for drug-induced arrhythmias)

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

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13
Q

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

A

Lidocaine

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14
Q

Class 1C antiarrhythmic used for refractory arrhythmia

A

Flecainide

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15
Q

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

A
  1. Procainamide

2. Amiodarone

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16
Q

Antiarrhythmic group acting on Phase 4 of the cardiac action potential

A

Class 2

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17
Q

Mechanism of action of Class 2 antiarrhythymics

A
  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
18
Q

Nonselective beta blockers

A
  1. Propranolol

2. Timolol

19
Q

Beta 1 selective

A

(A–>M)

  1. Acebutolol
  2. Betaxolol
  3. Esmolol
  4. Atenolol
  5. Metoprolol
20
Q

Partial agonist beta blockers

A
  1. Pindolol

2. Acebutolol

21
Q

Beta blocker lacking local anesthetic effect

A

Timolol

22
Q

Beta blocker with low lipid solubility

A

Atenolol

23
Q

Shortest acting beta blocker

A

Esmolol

24
Q

Longest acting beta blocker

A

Nadolol

25
Q

Combined alpha and beta blockade

A
  1. Carvedilol

2. Labetalol

26
Q

Antiarrhythmic group acting on Phase 3 of the cardiac action potential

A

Class 3

27
Q

Mechanism of action of Class 3 antiarrhythmics

A
  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
28
Q

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

A

Dofetilide

29
Q

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

A

Sotalol

30
Q

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

A

Amiodarone

31
Q

Why are dihydropyridine calcium channel blockers not useful as antiarrhythmics?

A

Dihydropyridine CCBs evoke compensatory sympathetic

discharge which facilitates arrhythmias rather than terminating them

32
Q

Class 4 antiarrhythmic drug causing gingival hyperplasia

A

Verapamil

33
Q

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

A

Class 1A antiarrhythmic

34
Q

Shortens the AP duration

No effect on normal cells on ECG

A

Class 1B antiarrhythmic

35
Q

No effect on AP duration

Prolongs QRS duration

A

Class 1C antiarrhythmic

36
Q

No effect on AP duration

Prolongs PR interval

A

Class 2 antiarrhythmic

Class 4 antiarrhythmic

37
Q

Prolongs AP duration

Prolongs QT interval

A

Class 3 antiarrhythmic

38
Q

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

A

Adenosine

39
Q

Depresses ectopic pacemakers, including those caused by digitalis toxicity

Decreased levels is associated with an increase incidence of arrhythmias, especially in patients receiving digitalis

A

Potassium ion

40
Q

Similar depressant effects as potassium on digitalis-induced arrhythmias

Effective in some cases of Torsades de Pointes

A

Magnesium ion

41
Q

Digitalis toxicity is increased by:

  1. _____
  2. _____
  3. _____
A
  1. Hypokalemia
  2. Hypomagnesemia
  3. Hypercalcemia