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2-Pharm Exam 3 > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

What drug class does Quinidine belong to?

A

Class IA

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2
Q

Quinidine: ______ used any more

A

Rarely

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3
Q

What is the clinical use of Quinidine?

A

Effective in supraventricular tachycardias WPW, and suppress premature ventricular contractions

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4
Q

What is the effect of Quinidine administered with afib and flutter?

A

Increases threshold for atrial fibrillation/flutter (can convert or slow the ventricular response)

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5
Q

What is Quinidine derived from?

A

Derived from quinine

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6
Q

What is the metabolism of Quinidine?

A

Hydroxylated in the liver/excreted in urine

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7
Q

When does Quinidine accumulate?

A

Accumulates with liver/renal insufficiency, sensitive to hepatic enzyme activity

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8
Q

What is the side effect of Quinidine?

A

Low therapeutic threshold: heart block, hypotension, pro-arrhythmic as plasma levels increase d/t prolongation of P-R, QRS complex, & QTc interval on ECG

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9
Q

Who is Quinidine contraindicated with?

A

Patients w/preexisting prolongation of the QTc interval or AV heart blocks should not be tx w/ quinidine

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10
Q

What are other properties of Quinidine?

A

Has anticholinergic/sympathomimetic effects (pts exhibit increased HR – digoxin often given before quinidine tx started)

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11
Q

What are the adverse effects of Quinidine?

A

Prone to allergic reactions and thrombocytopenia

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12
Q

What can Quinidine be added with? What does it cause?

A

Possess alpha-adrenergic blocking effects therefore additive with other vasodilating agents (hypotension d/t vasodilation)

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13
Q

What does Quinidine accentuate?

A

Accentuates the effects of neuromuscular blocking agents

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14
Q

What is chinchonisms?

A

Quinidine

  • Unique side effect symptomology called cinchonism: tinnitus, visual-hearing-GI issues
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15
Q

What class does procrainamide belong to?

A

Class IA

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16
Q

What is the clinical use of Procainamide?

A
  • Used for tx of ventricular tachyarrhythmias (less effective w/atrial)
  • Not used as much any more
  • Used in Afib to reduce ventricular irritability
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17
Q

What is Procainamide an anaglogue to?

A

Analogue of procaine

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18
Q

What are the effects of Procainamide?

A

Prolongs QRS duration, less QTc prolongation than quinidine

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19
Q

What can Procainamide precipitate?

A

May precipitate ventricular arrhythmias w/excessive plasma concentrations

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20
Q

What can be a side effect of Procainamide?

A
  • Causes hypotension
  • Due to direct myocardial depressant effects - exaggerated with hyperkalemia
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21
Q

When can asytole or VF occur with Procainamide?

A

Asystole or VF when given with heart block

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22
Q

What is the metabolism of Procainamide?

A
  • Undergoes hepatic metabolism & renal excretion
  • hepatic acetylation metabolite NAPA (N-acetyl procainamide) which is renally excreted
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23
Q

Define NAPA.

A

cardioactive, contributes to antiarrhythmic effect

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24
Q

What dose is needed in renal dysfunction?

A

Procainamide

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25
Q

What is N-acetyltransferase enzyme important in?

A

acetylation of procainamide (slow v fast acetylators)

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26
Q

What syndrome can occur with chronic administration of Procainamide?

A

Lupus-like syndrome with chronic administration (serositis, arthritis, pleurisy, pericarditis

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27
Q

What are other medications in the Class IA?

A

Disopyramide/Moricizine

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28
Q

What is the use of Disopyramide?

A

Used for atrial and ventricular tachyarrhythmias

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29
Q

What is the form of Disopyramide?

A

Oral form only

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30
Q

What are side effects of Disopyramide?

A
  • Significant myocardial depressant and precipitate CHF
  • Prolongation of QT and risk of paroxysmal ventricular arrhythmias
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31
Q

What is the clinical use of Moricizine?

A

Reserved for life threatening ventricular arrhythmias when cannot use others

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32
Q

When is Moricizine not effective?

A

Not effective in atrial arrhythmias

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33
Q

What are the effects of Moricizine?

A

Proarrhythmic and may increase BP and HR

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34
Q

What is the clinical use of Lidocaine?

A
  • Primarily used for suppression of ventricular arrhythmias especially re-entry ventricular arrhythmias (PVCs & V-tach)
35
Q

What class does Lidocaine belong to?

A

(Class IB)

36
Q

Why is Lidocaine (Class IB) recommended drug of choice?

A

More rapid acting than quinidine or procainamide, greater therapeutic index, reduced side effect profile

37
Q

When is Lidocaine (Class IA) not effective?

A

Not effective in atrial tachyarrhythmias

38
Q

What is the metabolism of Lidocaine (Class IA)?

A

Metabolized in liver

39
Q

Lidocaine (Class IA): Decreased CO or hepatic blood flow requires ________

A

decrease dose

40
Q

What can effect metabolism of Lidocaine (Class IA)?

A
  • Affected by P450 enzyme inhibition as caused by propranolol or cimetidine
  • Concomitant administration with cimetidine & propranolol can lead to decreased hepatic clearance of lidocaine
41
Q

What is the inital dose of Lidocaine (Class IA)?

A

Initial dose: 2mg/kg followed by infusion 1-4 mg/min achieves therapeutic plasma concentration 1-5 mcg/ml

42
Q

What effect does lidocaine have at the AP?

A
  • Decreases the rate of spontaneous Phase 4 depolarization in ventricular cells
  • Affects K+ permeability during phase 4 of ventricular AP and prevents spontaneous depolarization
43
Q

What are the effects of Lidocaine (Class IA) toxicity?

A

peripheral dilation and cardiac depression with bradycardia, prolonged PR and widened QRS

44
Q

What is the plasma concetration with Lidocaine (Class IA) toxicity?

A

Lidocaine toxicity (plasma concentration 5-10 mcg/ml)

45
Q

When are effects of Lidocaine (Class IA) toxicity seen?

A

CNS symptoms start appearing at plasma 5 mcg/ml; Seizure threshold decreases with hyperkalemia, acidosis, hypoxemia (review LAST s/s)

46
Q

What is the clinical indications of Phenytoin?

A
  • Effective in suppression of ventricular arrhythmias asso/w digitalis toxicity
  • Can be useful in tx of VT or Torsades asso w/ prolonged QTc interval on ECG
47
Q

What is the MOA of Phenytoin?

A
  • affects automaticity and velocity of conduction of cardiac impulses (similar to lidocaine)
  • may depress SA node
48
Q

Why should caution be taken when administering volatile anesthetics and Phenytoin?

A

may depress SA node (caution if coadministering with volatile anesthetics)

49
Q

What is the dose of Phenytoin?

A

Dose 100 mg q 5 min until arrythmia controlled (max 1000 mg)

50
Q

What can Phenytoin be non effective in?

A

Not effective for atrial tachyarrhythmias

51
Q

What is the IV administration of Phenytoin?

A

Given slow IV in large peripheral vein diluted in normal saline

52
Q

What is the metabolism of Phenytoin?

A

Hepatic metabolism- impaired hepatic function can lead to higher than normal blood levels

53
Q

What id the elimination half time of Phenytoin?

A

24 hrs

54
Q

What lowers blood levels of Phenytoin?

A
  • Blood levels lowered by barbiturates
55
Q

What raises Phenytoin levels?

A

warfarin, phenylbutazone, isoniazid inhibit metabolism of phenytoin & increase blood levels

56
Q

What are the side effects of phenytoin toxicity?

A

CNS disturbances (cerebellar): ataxia, nystagmus, vertigo, slurred speech, sedation, mental confusion

57
Q

What is the class of Flecainide?

A

(Class IC)

58
Q

What is the analogue of Flecainide (Class IC)?

A

Fluorinated local anesthetic analogue of procainamide

59
Q

What is the indication of Flecainide (Class IC)?

A

Increased incidence of sudden death (pro-arrhythmic); use reserved for tx of life-threatening arrhythmias

60
Q

What is Flecainide (Class IC) effective in supressing?

A

Effective in suppressing PVCs, Vtach, atrial tachyarrhythmias, & re-entry arrhythmias (i.e.,WPW)

61
Q

What are the properties of Flecainide (Class IC)?

A

Negative inotropic effect and proarrhythmic (esp in presence of decreased LV function)

62
Q

What can Flecainide (Class IC) increase? Why?

A

Competes w/metabolic pathways used by other drugs – may increase plasma concentration of digoxin & propranolol

63
Q

Coadministration with amiodarone will ______ flecainide concentration

A

double

64
Q

What are side effects of Flecainide (Class IC)?

A

prolongs QRS complex and PR interval; not administered w/ 2nd or 3rd AVBs

65
Q

What is the most common non cardiac effect?

A

blurred vision

66
Q

What is the drug class of Propafenone?

A

Propafenone (Class IC)

67
Q

What are the clinical uses of Propafenone (Class IC)?

A

Possesses weak β-adrenergic blocking & calcium blocking effects

68
Q

What are the proarrhythmic properties of Propafenone (Class IC)?

A

Proarrhythmic esp in pts w/poor LV function & sustained v-tach

69
Q

What properies are seen with Propafenone (Class IC)?

A

Depresses myocardium & may cause SA node slowing, AVB, & BBB

70
Q

What can increase plasma concentration to Propafenone (Class IC)?

A

Increases plasma concentration of warfarin

71
Q

What are the indications for β-adrenergic Antagonists (Class II)?

A

Effective for tx of cardiac arrhythmias r/t enhanced SNS (periop stress, thyrotoxicosis, pheochromocytoma)

72
Q

What are propranolol and esmolol effective in treating?

A

controlling ventricular rate with Afib and Aflutter

73
Q

What can effectively treat multifocal atrial tach?

A

Esmolol & metoprolol effective for multifocal atrial tach (amiodarone better)

74
Q

Which β-adrenergic Antagonists (Class II) are associated with sudden death post MI?

A

Acebutolol, propranolol and metoprolol approved to prevent sudden death post MI

75
Q

What is a specific indication of Propranolol?

A
  • Propranolol to emergently suppress ventricular arrhythmias: 1 mg/min (3-6 mg)
  • Effective blockade is reflected in HR 55-60
76
Q

What is the MOA of β-adrenergic Antagonists (Class II)?

A

Block the cardiac β-receptors to affects of SNS stimulation & circulating catecholamines

77
Q

What affect does β-adrenergic Antagonists (Class II) have on the heart?

A
  • Decreasing rate of spontaneous phase 4 depolarization and SA node discharge
  • Slow impulses through AV node (prolonged PR interval)
  • Direct cardiac depressant effects as well as through beta blockade
78
Q

What does β-adrenergic Antagonists (Class II) cause?

A

**Membrane stabilization by altering the membrane electrical activity

79
Q

What are side effects of β-adrenergic Antagonists (Class II)?

A

bradycardia, hypotension, myocardial depression, bronchospasm, drug fever, mental depression, fatigue

80
Q

What can β-adrenergic Antagonists (Class II) accentuate?

A

Can accentuate CHF

81
Q

What is a contraindication of β-adrenergic Antagonists (Class II)?

A

Contraindicated in preexisting AV block

82
Q

How does upregulation of β-adrenergic Antagonists (Class II) occurs

A

Upregulation of β-receptors occurs w/chronic administration of β-antagonists

83
Q

What does abrupt d/c of β-adrenergic Antagonists (Class II) lead to?

A

May lead to SVT

2-Pharm Exam 3 (14 decks)

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