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Pharmacology > Anti-Arrhythmic Drugs > Flashcards

Anti-Arrhythmic Drugs Flashcards

1
Q

What is normally the primary determinant of the refractory period in cardiac myocytes?

A

AP duration

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2
Q

In pacemaker cells (SA node/AV node), what causes the initial upstroke (depolarization)?

A

Ca2+ influx through T and L-type Ca2+ channels

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3
Q

In pacemaker cells (SA node/AV node), what causes diastolic depolarization?

A

If (funny) current

Inward Na+ current activated at repolarization

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4
Q

What is normally the primary determinant of the refractory period in pacemaker cells?

A

Time

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5
Q

In general, what are the two problems that can lead to arrhythmias?

A

Disturbed impulse formation (EADs, DADs)

Disturbed impulse conduction (blocks, reentry)

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6
Q

When do drugs that inhibit Na+ channels bind best to the receptor?

A

When the M gate is open (during activation of inactivation)

Binds poorly during resting state (M gate closed)

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7
Q

What drug should you give as prophylaxis for the formation of arrhythmias?

A

No drug!
Anti-arrhythmic drugs do not act specifically and can depress conduction in normal cells, leading to drug-induced arrhythmias. You only use anti-arrhythmics when there is an arrhythmia already present.

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8
Q

List the 4 Vaughan Williams classes of anti-arrhythmic drugs

A

Class I: Na+ channel blockers

Class II: Beta-adrenoceptor blockers

Class III: Prolongation of AP duration

Class IV: Ca2+ channel blockers

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9
Q

What is the general mechanism of Class I anti arrhythmics?

A

Na+ channel blockers, slowing the phase 0 upstroke of the AP

Local anesthetic action

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10
Q

What drugs are in the Class IA anti arrhythmics?

A

Procainamide
Quinidine
Disopyramide

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11
Q

What drugs are in the Class IB anti arrhythmics?

A

Lidocaine

Mexiletine

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12
Q

What drugs are in the Class IC anti arrhythmics?

A

Flecainide

Propafenone

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13
Q

What is the effect of Class IA, IB, and IC on the AP duration?

A

Class IA: Prolongs AP duration

Class IB: Shortens AP duration

Class IC: variable

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14
Q

Procainamide

MOA

A

Class IA Na+ channel blocker
Blocks the Na+ channel and slows upstroke of the AP
Lengthens APD

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15
Q

Procainamide

Indications

A

Atrial and Ventricular arrhythmias

Drug of 3rd choice for ventricular arrhythmias after acute MI

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16
Q

Procainamide

Adverse Effects

A

Ganglion blocking properties
Hypotension
Torsades de Pointes induction through its metabolite (NAPA)

Long term - Lupus syndrome (arthritis, pleuritis…)

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17
Q

Quinidine

MOA

A

Class IA Na+ channel blocker

Lengthens APD

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18
Q

Quinidine

Indications

A

Atrial and ventricular arrhythmias

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19
Q

Quinidine

Adverse Effects

A

Hypotension
Anticholinergic effects - increase sinus rate and AV conduction
Ventricular fibrillation
Torsades de Pointes

Long term - Cinchonism: headache, dizziness, tinnitus

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20
Q

Lidocaine

MOA

A

Class IB Na+ channel blocker

Shortens APD

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21
Q

Lidocaine

Indications

A

DOC for ventricular tachycardia or fibrillation

Arrhythmias after MI

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22
Q

Lidocaine

Adverse Effects

A

Least cardiotoxic among Class I

Hypotension
Neurologic effects due to anesthesia

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23
Q

Mexiletine

MOA

A

Class IB Na+ channel blocker

Shortens the APD

24
Q

Mexiletine

Adverse Effects

A

Similar to lidocaine
Hypotension
Neurologic effects

25
Q

Flecainide

MOA

A

Class IC Na+ channel blocker
Also blocks K+ channels

No anti-cholinergic effects

26
Q

Flecainide

Indications

A

Supraventricular arrhythmias in patients with otherwise normal hearts

27
Q

Propafenone

MOA

A

Class IC Na+ channel blocker that also blocks K+ channels

Some weak Beta-blocking activity

28
Q

Propafenone

Indications

A

Supraventricular arrhythmias in patients with otherwise normal hearts

29
Q

Flecainide

Adverse Effects

A

Increase mortality in ventricular tachyarrhtyhmias, MI, and ventricular ectopy

30
Q

Propafenone

Adverse Effects

A

Do NOT use in ventricular tachyarrhythmias
Sinus bradycardia (B-blockage)
Bronchospasm (B-blockage)

31
Q

What are the class II anti arrhythmics known as?

A

Beta blockers

32
Q

List some nonselective Beta Blockers

A

Propranalol
Nadolol
Timolol
Sotalol

33
Q

List some cardioselective Beta Blockers

A

Metoprolol
Atenolol
Esmolol

34
Q

Which beta blocker also has some Class III action?

A

Sotalol

35
Q

Class II Anti Arrhythmics

MOA

A 
Inhibit sympathetic influences on cardiac conduction
Reduce HR
Lower contractility
Decrease pacemaker currents
Reduce conduction velocity
36
Q

Class II Anti Arrhythmics

Indications

A 
Prevention of recurrent infarction and sudden death
Exercise-induced arrhythmias
Atrial fibrillation
Atrial flutter
AV nodal reentry
37
Q

Class II Anti Arrhythmics

Adverse Effects

A

Bradycardia
Bronchospasm

May mask tachycardia associated with hypoglycemia in diabetics

38
Q

Class II Anti Arrhythmics

Contraindications

A

AV block
Sinus bradycardia
Asthma

39
Q

What is the general mechanism of Class III anti arrhythmics?

A

Prolong the action potential duration by blocking K+ channels responsible for repolarization

40
Q

Amiodarone

MOA

A

Class III
Prolongs the APD

Blocks K+ and Na+ channels
May inhibit Beta receptors
Weakly blocks Ca2+ channels
Suppresses abnormal automaticity

41
Q

Amiodarone

Indications

A

Oral
Recurrent V tachycardia
V fibrillation
Atrial fibrillation

IV
1st DOC for cardiac arrest outside of hospital
Termination of ventricular tachycardia or fibrillation

42
Q

Amiodarone

Adverse Effects

A
  • Bradycardia and heart block in patients with AV/SA node disease
  • Pulmonary toxicity (fibrosis)
  • Hypothyroid symptoms (block T4 -> T3 conversion)
  • Photodermatitis
  • Corneal microdeposits
43
Q

Dronedarone

MOA

A

Class III

Prolongs the AP duration by blocking K+ channels

44
Q

Why would dronedarone be used instead of amiodarone?

A

Dronedarone does not have iodine atoms, so it does not block T4 -> T3 conversion

45
Q

What is the general mechanism of action for Class IV anti arrhythmics?

A

Block Ca2+ channels on vascular smooth muscle, cardiac myocytes, SA/AV nodes

46
Q

What is the only dihydropyridine Class IV drug we discussed? What was its only indication?

A

Nifedipine

Only used for HTN due to high vascular smooth muscle selectivity

47
Q

Verapamil

MOA

A

Class IV
Blocks activated and inactivated Ca2+ channels in the heart

Slows AV node conduction
Slows SA node automaticity
Lowers HR and prolongs PR interval

48
Q

Verapamil

Indications

A
  • Supraventricular arrhythmias
  • Reentry arrythmias/tachycardias involving the AV node
  • Slows ventricular rate in atrial flutter/fibrillation
49
Q

Verapamil

Adverse Effects

A

Vasodilation

Negative inotropic effects

50
Q

Verapamil

Contraindications

A

Could cause heart block in patients on beta blockers

Should NOT be used in patients with a diseased heart and ventricular tachycardia

51
Q

Diltiazem

MOA

A

Class IV
Blocks Ca2+ channels to lower HR and prolong PR interval

Increase AV refractoriness and slow SA automaticity

52
Q

Adenosine

MOA

A

Produces transient cardia arrest

Slows AV node conduction and increases AV refractoriness

53
Q

Adenosine

Indications

A

Used to convert paraoxysal supraventricular tachycardia to sinus rhythm

54
Q

Adenosine

Half life

A

Short (5-6 seconds)

55
Q

Adenosine

Administration

A

Always administered as a rapid IV bolus

56
Q

Adenosine

Adverse Effects

A 
Flushing
SOB
Sinus Bradycardia
Sinus pauses
AV Block
57
Q

What are some non-pharmacological anti-arrhythmic therapies?

A

Vagal maneuvers

  • Carotid sinus massage
  • Diving reflex
  • Valsalva

Radiofrequency ablation of the aberrant cells

Electrical cardioversion

Implantable Cardioverter Defibrillator (ICD)

Pharmacology (67 decks)

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