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2-Pharm Exam 3 > Antidysrhythmic Drug Part II > Flashcards

Antidysrhythmic Drug Part II Flashcards

1
Q

What drug class does Amiodarone belong?

A

(Class III)

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2
Q

What is the characteristics of Amiodarone (Class III)?

A

Potent antiarrhythmic with wide spectrum of activity against refractory supraventricular and ventricular tachyarrhythmias

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3
Q

What is Amiodarone (Class III) effective in treating?

A
  • Effective in tx WPW, decreases risk of Afib after cardiac surgery
  • Tx of VT/VF resistant to defibrillation (in ACLS protocol)
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4
Q

What can Amiodarone (Class III) decrease?

A

Decreases mortality after MI

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5
Q

What is the MOA of Amiodarone (Class III)?

A
  • Prolongs the ERP in all cardiac tissue (SA & AV node, atrium, His-Purkinje system, ventricles & accessory bypass tracts [WPW])
  • Antiadrenergic effects (noncompetitive alpha and beta receptor blockade)
  • Antianginal (dilates coronary arteries/increases coronary blood flow)
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6
Q

What is the cause of pulmonary toxicity associated with Amiodarone (Class III)?

A

poss R/T production of free oxygen radicals in the lungs

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7
Q

What can pulmonary toxicity with Amiodarone (Class III) lead to?

A

Can lead to ARDS, pulmonary edema

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8
Q

What effect can High FiO2 have on pulmonary toxicity of Amiodarone (Class III)?

A

High FiO2 may accelerate free oxygen radical damage to lung tissue

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9
Q

What effect can lower FiO2 have from pulmonary toxicity of Amiodarone (Class III)?

A

Lower FiO2 to lowest level capable of maintaining adequate systemic oxygenation

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10
Q

What is the side effects of Amiodarone-induced pulmonary toxicity?

A

dyspnea, cough, pulmonary infiltrates on CXR, hypoxemia

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11
Q

What are the CV effects of Amiodarone (Class III)?

A
  • Prolong QTc interval on ECG
  • proarrhythmic effect (incr. risk of torsades)
  • slow HR resistant to atropine
  • decreased responsiveness to sympathomimetics since it blocks these receptors
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12
Q

How is hypotension occurs from Amiodarone (Class III)?

A

Hypotension d/t peripheral vasodilating effect: (tx w/vasopressin)

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13
Q

What can enhance the negative inotropic effects of Amiodarone (Class III)?

A

Negative inotropic effects enhanced w/admin of GA, β-blockers, CCBs

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14
Q

What are some other side effevts associated with Amiodarone (Class III)?

A
  • Optic neuropathy
  • photosensitivity
  • rash
  • cyanotic discoloration of face
  • neurologic toxicity (peripheral neuropathy, tremors)
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15
Q

What is the half life of Amiodarone (Class III)?

A

Long elimination half-time (29 days)

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16
Q

What is the volume of Vd of Amiodarone (Class III)?

A

large Vd

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17
Q

What is the protein binding of Amiodarone (Class III)?

A

Extensive tissue protein binding

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18
Q

What is the active metabolite for Amiodarone (Class III)?

A

longer elim half-time than parent drug leads to accumulation of metabolite w/chronic therapy

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19
Q

What medications can effect Amiodarone (Class III) drug levels?

A

Inhibits P450 enzymes so can increase drug levels: digoxin, procainamide, quinidine, warfarin, cyclosporine, quinidine, procainamide, phenytoin

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20
Q

What is true about digoxin and Amiodarone (Class III)?

A

Displaces digoxin from protein binding sites (digoxin dose should be by 50%)

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21
Q

What does Amiodarone (Class III) contain?

A

Amiodarone contains iodine; has effects on thyroid function (hyper or hypothyroidism)

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22
Q

What are the drug classes of Sotalol?

A

(Class III)

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23
Q

What is the properties of Sotalol (Class III)?

A

Nonselective β-adrenergic antagonist at low doses, higher doses prolongs cardiac AP in atria, ventricles and accessory tracts

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24
Q

What effect can be seen with Sotalol (Class III)?

A

β blockade effects: decreased contractility, bradycardia, delayed AV

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25
Q

What is the clinical uses of Sotalol (Class III)?

A

Treatment of sustained VT/VF, a-tachycardia, & afib

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26
Q

When should Sotalol (Class III) be avoided?

A

Avoid in asthmatics, LV dysfunction, conduction abnormalities such as prolonged QTc interval on ECG

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27
Q

When is Sotalol (Class III) used?

A

Proarrhythmic; use saved for life threatening ventricular arrhythmias

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28
Q

What is the excretion of Sotalol (Class III)? When is this a concern?

A

Excreted by kidneys, concerns with renal dysfunction

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29
Q

What is the metabolism of Sotalol (Class III)?

A

not metabolized

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30
Q

What is the most serious effect of Sotalol (Class III)?

A

side effect is Torsades de pointes that is dose related (prolongs the QTc)

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31
Q

What are the drug class of Ibutilide/Dofetilide?

A

(Class III)

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32
Q

What is the use of Ibutilide?

A

recent onset of Afib/Aflutter

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33
Q

What is a property of Ibutilide?

A

Polymorphic VT with +/- QT prolongation that can be problematic with those with predisposing factors

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34
Q

What is the metabolism of Ibutilide?

A

Hepatic metabolism

35
Q

What is MOA of Dofetilide?

A

potent, pure K+ channel blocker (prolongs cardiac AP duration)

36
Q

What can Dofetilide prolong?

A

Prolongs QTc

37
Q

When is Dofetilide used?

A

in tx of recent onset Afib/Aflutter to convert to NSR and for maintenance

38
Q

What is the exertion of Dofetilide?

A

Mostly excreted unchanged in the urine (renal dysfunction concerns)

39
Q

What is the properites of Dofetilide administered with CCB?

A

Proarrhythmic when coadministered with CCB’s

40
Q

What is the FDA mandate with Dofetilide?

A

must be admitted for cardiac monitoring for at least 72 hrs during initiation of treatment due to determine presence of QT prolongation

41
Q

What is the class of Verapamil?

42
Q

What is the clinical use of Verapamil?

A

Verapamil (phenylalkylamine CCB):Tx of paroxysmal SVT, control ventricular rate in Afib/Aflutter

43
Q

What is the MOA of Verapamil?

A

Inhibits flux of calcium ions across the slow channels of vascular smooth muscle & cardiac cells

44
Q

What effect of does Verapamil have on the cardiac AP?

A
  • Decreases rate of Phase 4 spontaneous depolarization
45
Q

What are the properties of Verapamil?

A
  • Depresses AV node
  • negative chronotropic effect on SA node
  • negative inotropic effect
46
Q

What can be seen in moderate degrees of Verapamil?

A

Moderate degree of coronary and systemic artery vasodilation

47
Q

What causes the side effects with Verapamil?

A

Side effects due to effects on calcium ion flux into cardiac cells

48
Q

What are the side effects of Verapamil?

A
  • AV block, cardiac depressant (enhanced in LV dysfunction), hypotension, exaggerate effects of neuromuscular blocking drugs
49
Q

What can occur when Verapamil is delivered with propranolol?

A

Careful with coadministration with propranolol (severe bradycardia)

50
Q

What can increase Verapamil concentrations?

A

Cimetidine may increase verapamil plasma concentrations

51
Q

What can increase digoxin doses?

A

Quinidine, verapamil, amiodarone may increase digoxin levels

52
Q

What are the vasodilating effects of Verapamil?

A

Vasodilating effects (treat vasospastic angina and HTN), negative inotrope

53
Q

What can Verapamil precipitate?

A

Can precipitate ventricular arrhythmias for patients with WPW syndrome

54
Q

What is the drug class of Diltiazem?

A

A benzothiazepine CCB

55
Q

What is the MOA of Diltiazem?

A

Along with L-type Ca++ channel, may also work on the Na+/K+ pump to decrease the intracellular Na+ exchanged for extracellular Ca++ and may inhibit the Ca++ /calmodulin binding

56
Q

What can Diltiazem be used for?

A

Mainly blocks AV node, used with SVT’s, can be used to tx HTN

57
Q

What are the myocardial effects of Diltiazem?

A

Minimal myocardial depressant effects and unlikely to interact with β blockers

58
Q

What is the dose Diltiazem?

A
  • IV dose 0.25-0.35 mg/kg over 2 minutes and repeated in 15 min.
  • Infusion after bolus for 24 hrs (10mg/hr)
59
Q

What is the elimination of Diltiazem? When is the prolonged?

A
  • 4Elimination half time 4-6 hrs, 20 hrs with active metabolites (prolonged with liver disease)
60
Q

What does Diltiazem control?

A

Commonly used to control HR

61
Q

What are the properties of Diltiazem in comparison to Verapamil?

A

Unlike verapamil: minimal cardiac depressant and unlikely to interact with B-blockers

62
Q

What effect does if have on the Na Channels?

A

Like verapamil: has local anesthetic properties (Na+) channels

63
Q

What is MOA of Adenosine?

A

Endogenous nucleoside that slows conduction through AV node

64
Q

What is the use for adenosine?

A

Used in tx of paroxysmal SVT (including accessory pathways with WPW)

65
Q

When is Adenosine not effective?

A

Not effective for Vtach, Afib, Aflutter

66
Q

What is the dose of Adenosine?

A

Usual dose is 6 mg rapid IV injection followed by 6-12 mg IV 3 minutes later

67
Q

What is the elimination half time of Adenosine?

A

Elimination half life 10 sec

68
Q

What are adenosine receptors are indicated in what?

A

Adenosine receptors indicated for treatment of pain

69
Q

What are adenosine receptors?

A

Adenosine receptors comprise a group of G protein-coupled receptors which mediate the physiological actions of adenosine

70
Q

How many adenosine receptors are there?

A

To date, four AR subtypes have identified in different tissues.

71
Q

What is true about adenosine receptors?

A

These receptors have distinct localization, signal transduction pathways and different means of regulation upon exposure to agonists

72
Q

What do adensoine1 receptors increase?

A

Adenosine1 receptors increase K+ currents, hyperpolarize the cell membrane, shorten AP

73
Q

What does activation of G-protein Adenosine receptors cause?

A

Activation of the G-protein also decreases cAMP, which inhibits L-type calcium channels and therefore calcium entry into the cell

74
Q

What effect do adenosine1 receptors have on the AP of cardiac cells?

A

In cardiac pacemaker cells located in the SA node, adenosine acting through adenosine1 receptors inhibits the pacemaker current which decreases the slope of phase 4 of the pacemaker AP

75
Q

What are side effects of Adenosine?

A

With rapid IV injection: facial flushing, headache, dyspnea, chest discomfort and nausea

76
Q

Patients who recieve Adenosine often have a felling of _________

A

impending doom

77
Q

What can Adenosine produce?

A

May produce transient AV block

78
Q

Who should Adenosine be used cautiously in?

A

Bronchospasm for those predisposed (caution with active wheezing)

79
Q

What antagonizes Adenosine?

A

Antagonized by methylxanthines such as theophylline and caffeine

80
Q

What does this EKG strip show?

A

Adenosine “pause” on ECG

81
Q

What is the function of Digoxin?

A

Cardiac antiarrhythmic drug that stabilizes atrial electrical activity

82
Q

What does Digoxin cause?

A

Slows conduction of cardiac impulses through AV node which slows ventricular response in pts w/afib

83
Q

What are the clinical uses of Digoxin?

A

Can also enhance conduction of cardiac impulses through accessory bypass tracts; can enhance conduction of cardiac impulses through accessory tracts & increase ventricular response rate in pts w/WPW

84
Q

What can digoxin toxicity manifest as?

A

Digoxin toxicity can manifest as cardiac arrhythmias, most commonly atrial tachycardia w/block

2-Pharm Exam 3 (14 decks)

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