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Pharmacology > Anti-Arrhythmia Agents > Flashcards

Anti-Arrhythmia Agents Flashcards

1
Q

What are the 5 phases of the cardiac action potential?

A

0: Upstroke
1: Early-fast repolarization
2: Plateau
3: Repolarization
4: Diastole

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2
Q

Ion Movements Phase 0

A

Na influx

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3
Q

Ion Movements Phase 1

A

K efflux (Transient Outward)

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4
Q

Ion Movements Phase 2

A

Ca influx - counterbalances the K efflux to maintain a plateau period

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5
Q

Ion Movements Phase 3

A

K efflux (Delayed Rectifier)

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6
Q

Ion Movements Phase 4

A

Na/K ATPase Pump

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7
Q

What is the refractory period in atrial and ventricular myocytes determined by?

A

Voltage

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8
Q

What is the refractory period in pacemaker cells determined by?

A

Time

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9
Q

What are the general types of arrhythmias?

A
  • Too fast
  • Too slow
  • Asynchronous
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10
Q

What are the causes of arrhythmias?

A
  1. disturbed impulse formation
  2. disturbed impulse conduction
  3. combination of 1 and 2
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11
Q

What are some examples of disturbed impulse formation?

A 
Early afterdepolarization (EAD)
Delayed afterdepolarization (DAD)
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12
Q

What are some examples of disturbed impulse conduction?

A

SA-block
AV-block
Re-entry

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13
Q

What are the requirements for re-entry?

A
  • Slowed conduction
  • Conduction block
  • Unidirectional block
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14
Q

What are the aims of anti-arrhythmic therapy?

A

Aimed to reduce ectopic pacemaker activity and/or

modify conduction characteristics to disable re-entry circuits

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15
Q

Use-dependent or state-dependent drug action

A

Drug has highest binding affinities to the activated and inactivated channels with low to no affinity for the resting state.

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16
Q

What should be done for the treatment of asymptomatic or minimally symptomatic arrhythmias?

A

Treatment should be AVOIDED

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17
Q

Class I

A

Na+ Channel Blockers

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18
Q

Class II

A

ß-adrenoceptor blockers

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19
Q

Class III

A

Prolong AP Duration

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20
Q

Class IV

A

Ca2+ Channel Blockers

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21
Q

What is a secondary effect of Na+ Channel Blockers?

A

Local anesthesia

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22
Q

What is the general action of the Class I agents?

A

Reduction of conduction velocity by reducing rate and magnitude of depolarization via Na+ channel blockade.

May influence repolarization through effects on K+ channels which will prolong the AP duration.

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23
Q

Class I A

A

Intermediate kinetics, APD is increased

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24
Q

Class I B

A

Fast kinetics, APD is decreased

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25
Q

Class I C

A

Slow kinetics, APD remains the same

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26
Q

Examples of Class I A

A

Procainamide, Quinidine, Disopyramide

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27
Q

Examples of Class I B

A

Lidocaine, Mexiletine

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28
Q

Examples of Class I C

A

Flecainide, Propafenone

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29
Q

Procainamide Actions

A
  • Slows upstroke of AP, conduction, prolongs QRS complex
  • Direct depressant actions on SA and AV nodes
  • More effective in depolarized cells (use/state dependent action)
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30
Q

Procainamide Indications

A

Atrial and ventricular arrhythmias - Drug of second or third choice though

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31
Q

Procainamide SE

A

Ganglion blocking properties,
Risk of hypotension
Anti-cholinergic effects
Induction of torsade de pointes arrhythmia

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32
Q

Quinidine Actions

A

Same as procainamide

  • Slows upstroke of AP, conduction, prolongs QRS complex
  • Direct depressant actions on SA and AV nodes
  • More effective in depolarized cells (use/state dependent action)
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33
Q

Quinidine Indications

A

Same as procainamide

Atrial and ventricular arrhythmias - Rarely used though

34
Q

Quinidine SE

A

Ganglion blocking properties, risk of hypotension
Anti-cholinergic effects, increases sinus rate and AV conduction
Induction of ventricular fibrillation and torsade de pointes Cinchonism: headache, dizziness, tinnitus

35
Q

Lidocaine Actions

A

No effect on conduction, recovery from block between action potential selective depression of conduction in depolarized (ischemic) cells

36
Q

Lidocaine Indications

A

Drug of 1st choice for treatment of ventricular tachycardia and fibrillation after cardioversion in the setting of ischemia/infarction

37
Q

Lidocaine ROA

38
Q

Lidocaine SE

A

Least cardiotoxic among Class I drugs

Large doses may induce hypotension probably through effects on myocardial contractility

39
Q

Mexiletine Actions

A

Orally active lidocaine analogue

Actions/adverse effects similar to lidocain

40
Q

Mexiletine Indications

A

Off label use for chronic pain

41
Q

Flecainide Actions

A

Potent blocker of Na+ and K+ channels with slow kinetics No anti-cholinergic effects

42
Q

Flecainide Indications

A

Supraventricular arrhythmias in patients with otherwise normal hearts

43
Q

Flecainide SE

A

Increases mortality in patients with ventricular tachyarrhythmias, myocardial infarction and ventricular ectopy

44
Q

Propafenone Actions

A

Potent blocker of Na+ channels with slow kinetics, may also block K+ channels
Structural similarity to propranolol with weak -blocking activit

45
Q

Propafenone Indications

A

Supraventricular arrhythmias in patients with otherwise normal hearts

46
Q

Propafenone SE

A

Probably same as flecainide (arrhythmogenic)
Sinus bradycardia/bronchospasm (ß-blockade)
Metallic taste and constipation

47
Q

What are the non-selective Class II agents?

A

Propranolol (other: Sotalol, Timolol)

48
Q

What are the selective Class II agents?

A

Esmolol (other: Acebutolol)

49
Q

What are the actions of the Class II agents?

A

Inhibit sympathetic influences on cardiac electrical activity Reduce heart rate
Decrease intracellular Ca++ overload
Decrease pacemaker currents

50
Q

Class II Agent Indications

A

Prevention of recurrent infarction and sudden death
after myocardial infarction
Exercise-induced arrhythmias
Also used for atrial fibrillation, atrial flutter and AV nodal reentry

51
Q

Class II Agent SE

A

Bradycardia
Bronchospasm
Hypoglycemia (masked in diabetics)

52
Q

Class III Agent Actions

A

Class III drugs typically block K+ currents (Ikr) responsible for Phase 3 repolarization and the delayed repolarization causes prolongation of action potential duration and prolongation of refractory period.

53
Q

What is the EKG finding with Class III agents?

A

QT Prolongation

54
Q

Amiodarone Actions

A
  • Dominant effect is prolongation of action potential duration
  • Blocks K+ and Na+ channels, weakly blocks Ca++ channels and inhibits ß-receptors
  • Prolongs refractoriness and slows conduction, suppresses abnormal automaticity and can slow normal sinus automaticity
  • Prolongs QT interval and QRS complex
55
Q

Amiodarone Indications

A

1st choice drug for recurrent ventricular tachycardia or fibrillation resistant to other drugs, also used for atrial fibrillation

56
Q

What is amiodarone an analog of?

A

Thyroid Hormone

57
Q

Amiodarone SE

A

Pulmonary toxicity (pulmonary fibrosis in 1%)
Cornea microdeposits in almost all patients
Blocks conversion of T4 to T3, source of inorganic iodine:

58
Q

Dronedarone Actions

A
  • Structural analogue of amiodarone without iodine atoms

- Amiodarone like effects

59
Q

What are the advantages of dronedarone over amiodarone?

A
  • As yet, no thyroid or pulmonary toxicity noted
60
Q

Dronedarone Indications

A

Atrial fibrillation/flutter

61
Q

Dronedarone Contraindications

A

Contraindicated in severe or recently decompensated symptomatic heart failure

62
Q

What are the types of Class IV agents?

A

Dihydropyridines
Benzothiazepine
Phenylalkylamine

63
Q

Nifedipine and Nitrendipine Indications

A

High vascular selectivity

Used for hypertension

64
Q

Diltiazem Indications

A

Used for hypertension, angina pectoris and arrhythmia

65
Q

Verapamil Actions

A

Blocks activated and inactivated Ca++ channels primarily in the heart, exhibits use/state-dependent action.

Directly slows AV nodal conduction and increases AV node refractoriness slows SA node automaticity

Lowers heart rate and increases PR-interval

66
Q

Verapamil Indications

A 
Supraventricular arrhythmias (drug of 1st choice) 
Re-entry arrhythmias/tachycardias involving the AV node Slows ventricular rate in atrial flutter/fibrillation
67
Q

Verapamil SE

A

Vasodilation (particularly after bolus injection) and negative inotropic effects
AV block in patients with AV nodal disease or in high doses

68
Q

Verapamil Contraindications

A

ß-blockers

Patients with ventricular tachycardia

69
Q

Adenosine Actions

A
  • Acts via purinergic receptors (GPCR), increases K+ conductance (hyperpolarization) and inhibits cAMP-mediated Ca++ currents
  • Primarily acts on atrial tissues
  • Slows AV node conduction and increases AV node refractoriness
  • Produces transient cardiac arrest
70
Q

Adenosine Indications

A

Drug of choice for conversion of paroxysmal supraventricular tachycardia to sinus rhythm

71
Q

Adenosine SE

A

Flushing and shortness of breath, sinus bradycardia, sinus pauses, AV block, decrease in blood pressure

72
Q

Adenosine PK

A

VERY short half life on the order of seconds - administered via bolus

73
Q

What drugs should be used for the conversion to sins rhythm?

A

Adenosine / Amiodarone Flecainide

74
Q

What drugs should be used for the maintenance of sinus rhythm?

A

Amiodarone / Dronedarone Flecainide / Propafenone

75
Q

What drugs should be used for ventricular rate control?

A

Diltiazem / Verapamil / Propranolol / Esmolol

76
Q

Ventricular tachycardia treatment

A

Amiodarone

Lidocaine

77
Q

Ventricular fibrillation treatment

A

Defibrillation w/wo Amiodarone or Lidocaine

78
Q

Atrial fibrillation treatment

A

Diltiazem/Verapamil Propranolol

79
Q

Paroxysmal supraventricular tachycardia treatment

A

Adenosine/Amiodarone Verapamil/Diltiazem/ Propranolol

80
Q

AV block (Io)/IIo/IIIo treatment

A

Atropine/Pacemaker

Pharmacology (74 decks)

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