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CVS πŸ«€ > W2, 6 Antiarrhythmic Drugs > Flashcards

W2, 6 Antiarrhythmic Drugs Flashcards

1
Q

What is cardiac arrhythmia or dysrhythmia?

A
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2
Q

Classification of Cardiac arrhythmias

A
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3
Q

Action potential of cardiomyocytes (what happens in each phase?)

A
  • Phase 0: Depolarization of the cardiomyocytes (Starts with influx of Na and Ca through there channels)
  • Phase 1: Partial Repolarization due to the closure of Na channels
  • Phase 2: The Plateau Phase (there is maintained depolarization due to continuous influx of Ca channels. By the END of this phase, Ca channels CLOSE and K ions begin to exit the cell)
  • Phase 3: Repolarization of the heart muscle due to K efflux until the potential returns back to RMP
  • Phase 4: Resting stage of the heart (It’s where the heart is fully relaxed)
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4
Q

Classification of antiarrhythmic drugs

A
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5
Q

What drugs are under the class IA?

A

Quinidine, Procainamide, Disopyramide

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6
Q

Quinidine pharmacodynamics

A
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7
Q

Route of administration of Quinidine?

A

Well absorbed after oral administration, peak plasma levels in 60-90min

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8
Q

Quinidine: Bound or free? And half life?

A

~90% bound to plasma proteins, which prolongs the drug half life (5-12hr)

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9
Q

How is Quinidine metabolized & excreted?

A

Metabolized in the liver (by P450 enzymes) and excreted in urine.

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10
Q

Quinidine Indications

A
  • Ventricular and supraventricular tachyarrhythmia
  • Antimalarial
    (Note: Quinidine use in arrhythmia is much less now because of its severe cardiac and systemic toxicity)
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11
Q

Quinidine Adverse Effects?

A
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12
Q

MOA of Procainamide?

A

Same as quinidine

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13
Q

How does Procainamide differ from Quinidine?

A
  • It is Minimally bound to plasma proteins (~ 20%)
    -Compared with quinidine, it has less anticholinergic activity
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14
Q

What’s the half life of procainamide

A

half-life 3-4 hr

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15
Q

Metabolism of procainamide

A
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16
Q

Indications of procainamide

A

Used for ventricular and supraventricular arrhythmias

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17
Q

What’s the effect of prolonged therapy with procainamide?

A

Prolonged therapy leads to lupus-like syndrome (disappears upon drug withdrawal)

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18
Q

MOA of Disopyramide?

A

Same as Quinidine

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19
Q

Disopyramide is mainly used for … ?

A

Used mainly for ventricular tachyarrhythmias

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20
Q

When to prescribe Disopyramide?

A

Reserved for patients who are intolerant or unresponsive to quinidine or procainamide

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21
Q

side effects of disopyramide?

A
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22
Q

What drugs are under the Class IB ?

A

Lidocaine, Mexiletine, Phenytoin

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23
Q

Class IB drugs are used in … ?

A

Used in ventricular, not supraventricular, arrhythmia
(like disopyramide)

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24
Q

MOA of class IB?

A
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25
Q

Route of administration of Lidocaine (Lignocaine)?

A

Lidocaine is given through i.v.or i.m

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26
Q

Why Lidocaine is not given orally ?

A
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27
Q

What is the half life of Lidocaine?

A

Short half-life (1.5-2hr)

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28
Q

How is Lidocaine metabolized & excreted?

A

Metabolized in liver
excreted in urine

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29
Q

Lidocaine-Indications

A
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30
Q

Lidocaine adverse effects

A

Rare but serious side effects such as:
β€’ Nausea, vomiting and anorexia
β€’ CNS effects: drowsiness, disorientation, ataxia, muscle twitching, convulsions
β€’ Impaired hearing
β€’ Respiratory arrest
β€’ Bone marrow depression, agranulocytosis

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31
Q

Mexiletine side effects

A

Side effects: tremors and nausea

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32
Q

What drug is analog of lidocaine, but it is effective orally?

A

Mexiletine (Used in ventricular arrhythmias, mostly used as an adjunct to other drugs)

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33
Q

Anticonvulsant agent with limited use in the treatment of arrhythmias

A

Phenytoin

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34
Q

Phenytoin (slide)

A
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35
Q

What drugs are classified under IC?

A

Flecainide, Propafenone

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36
Q

MOA of class IC?

A
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37
Q

Route of administration of class IC?

A

Given i.v. or orally

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38
Q

How is Flecainide eliminated?

A

Flecainide is mostly eliminated via kidneys, the rest metabolized by hepatic CYP2D6

39
Q

What anti arrhythmic drug can increase flecanide levels & how?

A

Quinidine strongly inhibits CYP2D6 and may increase flecainide levels

40
Q

Half life of flecanide

A

Highly bound to plasma proteins(>75%).
Plasma half-life is around 20hr

41
Q

Flecainide Adverse effects

A

Cardiac arrest, dizziness, visual disturbances, granulocytopenia

42
Q

Flecainide Indications

43
Q

What are Class II antiarrhythmic drugs?

A

Propranolol, Atenolol, Esmolol, Metoprolol, Sotalol

44
Q

Class II anti arrhythmic drugs are …. blockers

A

Ξ²-adrenoceptor blockers

45
Q

MOA of class II

46
Q

Ξ²-adrenoceptor blockers: Indications

A

The f irst line of medications used in treatment of ventricular and supraventricular tachyarrhythmias

47
Q

Ξ²-adrenoceptor blockers: Adverse Effects

A

β€’ Bradycardia,fatigue,dizziness
β€’ AV block
β€’ Bronchospasm(especially with nonselective blockers)
β€’ Hypoglycemia (inhibition of Ξ²-receptor-mediated hepatic glycogenolysis)
β€’ Withdrawal symptoms (severe hypertension,chestpain,heart attacks)

48
Q

What are Class III antiarrhythmic drugs

A

Amiodarone, Sotalol

49
Q

What do class III drugs block?

A

K+ Channel Blockers

50
Q

MOA of Class III antiarrhythmic drugs ?

51
Q

Pharmacodynamics Class III antiarrhythmic drugs ?

52
Q

Amiodarone oral absorption

A

Oral absorption is poor/erratic (20-90%).

53
Q

Amiodarone action takes how long to appear?

A

Antiarrhythmic action takes 1-3 weeks to appear

54
Q

How is amiodarone metabolized ? And into what?

A

Metabolized by CPY3A4 into desethylamiodarone

55
Q

Amiodarone has Slow clearance and long half-life of almost 2 months (why?)

A
  1. Both amiodarone and its metabolite are lipid soluble, accumulate in fats and other tissues, delay elimination
  2. Elimination is mainly via biliary excretion (reabsorption via enterohepatic circulation)
56
Q

Amiodarone: Indications

A

Ventricular and supraventricular tachyarrhythmia

57
Q

Amiodarone: Adverse Effects

58
Q

What are Class IV antiarrhythmic drugs ?

A

Verapamil, Diltiazem

59
Q

Class IV antiarrhythmic drugs are ….. blockers

A

Ca2+Channel Blockers

60
Q

Pharmacodynamics of class IV

61
Q

Ca2+ Channel Blockers: Indications

A

Drugs of choice in supraventricular tachycardia caused by AVN
reentry rhythm (decrease AV conduction and↑ AV refractory period)

62
Q

Ca2+ Channel Blockers: Adverse effects

A

Hypotension, bradycardia, constipation, headache, dizziness, nausea, skin reactions

63
Q

What drug has narrow therapeutic index, may cause new or worsened arrhythmias?

A

Class IC – Flecainide

64
Q

What drug activates cytochrome P450 enzymes and interact with co-administered drugs?

A

Class IB – Phenytoin

65
Q

The antiarrhythmic effect of this drug continues for weeks/months after drug discontinuation, which may increase toxicity

A

Amiodarone

66
Q

This drug is mostly eliminated via kidneys

67
Q

analog of lidocaine, but it is effective orally

A

Mexiletine

68
Q

What drug is used in Treatment of digitalis-induced tachyarrhythmias

69
Q

What drug is the strongest among the 1A class in anticholinergic activity

A

disopyramide

70
Q

Prolonged therapy of this drug leads to lupus-like syndrome

A

Procainamide

71
Q

An adverse effect of this drug is torsades de pointes

72
Q

What drug has Local anesthetic effect?

73
Q

Mcq: Which drug has anti-vagal activity resulting in sinus tachycardia?

74
Q

Mcq: Which of the following drugs is highly concentrated in the heart as compared to its plasma concentration?

A

Amiodarone

75
Q

Mcq: Which is a potassium channel blocker?

A

Class III (Amiodarone, Sotalol)

76
Q

Mcq: Why doesn’t flecainide concentration correlate with its therapeutic action?
A. highly bound to plasma proteins and does not dissociate easily
B. excreted unchanged in urine
C. strongly metabolized by oral administrations
D. Highly concentrated in cardiac muscle

A

D. Highly concentrated in cardiac muscle

77
Q

Mcq: Flecainamide is used to treat ventricular arrythmias. It exerts its therapeutic action by affecting which phases of the ventricle AP? (AP graph was given)

A

A. Phase 0 & Phase 4

78
Q

Mcq: Which of the following drugs dissociate slowly from Na channels and have no effect on action potential?

A

A. Flecaidine

79
Q

Mcq: Which drug has no action potential of atrial myocytes?

A

A. Lidocaine

80
Q

Mcq: Whats the mechanism of action of Verapmil?

A

Ca channel blocker

81
Q

Mcq: What drug causes constipation as a side effect?

82
Q

Mcq: What phases are affected when verapamil is administered?

A

Phase 2 & phase 4

83
Q

Mcq: Which drug requires activation and undergoes enterohepatic circulation?

A

Amiodarone

84
Q

Mcq: A patient comes to the clinic suffering from atrial flutter. The dr prescribes him lidocaine to manage his arrythmia. After a few days, he returns to the clinic with no apparent improvement in his condition. What would be the cause?

A

Lidocaine has little or no effect on the action potential duration of atrial myocytes

85
Q

Mcq: Which of the following drugs binds to activated Na channels only?

86
Q

Mcq: A drug that blocks Na channels and reduce the slope of phase 4?

87
Q

Mcq: Which of the following is a class 1B Na blocker?

88
Q

Mcq: Which drug is contradicted in patients with long QT syndrome?

A

Potassium channel blocker

89
Q

Mcq: Which of the following effects is responsible for quinidine’s induced tachycardia?/ Patient taking disopyramide has tachycardia, what is it due to?
A. Hyperpolarization of the AV node
B. Reduces the slope of phase 4 of the action potential
C. It has anti-vagal activity
D. Prolongs the QT interval

A

C. It has anti-vagal activity

90
Q

Mcq: Which drug is contraindicated in asthma?
A. Beta blocker
B. ACEI

A

A. Beta blocker

91
Q

Mcq: All arrhythmia drugs share one thing, which is?

A

A. Decrease phase 4

92
Q

Mcq: Which of the following characteristics of class IB antiarrythmic drugs?
A. Block activated and inactivated Na channel
B. Block Ca channel
C. Used to treat ventricular and suptaventricular tachyarrhythmia

A

A. Block activated and inactivated Na channel

93
Q

Mcq: What is correct regarding lidocaine - Class 1b antiarrhythmic drug?
A. Blocks both activated and inactivated Na channels
B. Blocks Ca Channels
C. Used primarily for supraventricular tachycardia
D. Is most effectively when administered orally

A

A. Blocks both activated and inactivated Na channels

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