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CRP > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

What are the class Ia antiarrhythmics?

A

Quinidine, Procainamide, Disopyramide

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2
Q

What is the MOA of Quinidine?

A

Blocks cardiac Na channels to increase excitation threshold

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3
Q

What are the EKG manifestations of Quinidine?

A

Increase in QRS and QT; PR changes can be variable

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4
Q

When would you use Quinidine?

A

Supraventricular (AV node and above) and Ventricular Arrhythmias; PO, can block alpha receptors, decreases digoxin clearance and increases Digoxin toxicity;

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5
Q

What are the side effects of Quinidine?

A

NVD, Cinchonism, Torsade de Pointes, Prolongs RP; hyperkalemia may increase toxicity

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6
Q

What is the MOA of Procainamide?

A

Blocks cardiac Na channels to increase excitation threshold

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7
Q

What are the EKG manifestations of Procainamide?

A

Increase in QRS and QT, PR changes can be variable

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8
Q

When would you use Procainamide?

A

Ventricular Arrhythmias; Good PO and available IV; No alpha receptor interference; Half excreted, half converted to class 3 arrhythmic metabolite (NAPA); short (3-4hr) half life; sustained release preparations

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9
Q

What are the side effects of Procainamide?

A

Formation of ANA, Lupus-like syndrome; Prolongs RP; hyperkalemia may increase toxicity

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10
Q

What is the MOA of Disopyramide?

A

Blocks cardiac Na channels to increase excitation threshold

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11
Q

What are the EKG manifestations of Disopyramide?

A

Increase in QRS and QT; PR changes can be variable

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12
Q

When would you use Disopyramide?

A

Ventricular arrhythmias when other drugs dont work; use cautiously

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13
Q

What are the side effects of Disopyramide?

A

High anticholinergic effects; Prolongs RP; hyperkalemia may increase toxicity

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14
Q

What are the class Ib antiarrhythmics?

A

Lidocaine, Mexiletine, Tocainide

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15
Q

What is the MOA of Lidocaine?

A

Acts on inactivated Na Channels, esp those that are ischemic or rapidly-driven; minimal K channel blockade; phase 4 automaticity and afterpotentials decreased

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16
Q

What are the EKG manifestations of Lidocaine?

A

Decrease in QT; Decreased APD; ERP/ADP increased

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17
Q

When would you use Lidocaine?

A

Ventricular arrhythmias; IM via LidoPen

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18
Q

What are the side effects of Lidocaine?

A

Lidocaine toxicity (cardiac depression, bradycardia, asystole)

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19
Q

What is the MOA of Mexiletine?

A

Acts on inactivated Na channels, esp those that are ischemic or rapidly-driven; minimal K channel blockade; phase 4 automaticity and afterpotentials decreased

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20
Q

What are the EKG manifestations of Mexiletine?

A

Decrease in QT; Decreased APD; ERP/ADP increased

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21
Q

When would you use Mexiletine?

A

Ventricular arrhythmias

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22
Q

What are the side effects of Mexiletine?

A

GI/CNS disturbances

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23
Q

What is the MOA of Tocainide?

A

Acts on inactivated Na channels, esp those that are ischemic or rapidly-driven; minimal K channel blockade; phase 4 automaticity and afterpotentials decreased

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24
Q

What are the EKG manifestations of Tocainide?

A

Decrease in QT; Decreased APD; ERP/ADP increased

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25
Q

When would you use Tocainide?

A

Ventricular Arrhythmias; need periodic blood cell counts

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26
Q

What are the side effects of Tocainide?

A

GI/CNS disturbances, agranulocytosis and blood dyscrasias

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27
Q

What are the class Ic antiarrhythmics?

A

Flecainide, Propafenone, Moricizine

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28
Q

What is the MOA of Flecainide?

A

Decreases depolarization/conduction, especially in BoH-PF system

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29
Q

What are the EGK manifestations of Flecainide?

A

Increase PR and QRS; unchanged QT

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30
Q

When would you use Flecainide?

A

Serious supraventricular arrhythmias

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31
Q

What are the side effects of Flecainide?

A

Potential for lethal arrhythmias; > increased morbidity post-MI

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32
Q

What is the MOA of Propafenone?

A

Decreases depolarization/conduction esp in BoH-PF system; weak beta-blocking activity

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33
Q

What are the EKG manifestations of Propafenone?

A

Increase in PR and QRS; QT unchanged

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34
Q

When would you use Propafenone?

A

Serious supraventricular arrhythmias

35
Q

What are the side effects of Propafenone?

A

Potential lethal arrhythmias

36
Q

What is the MOA of Moricizine?

A

Decreases depolarization/conduction, esp in BoH-PF system

37
Q

What are the EKG manifestations of Moricizine?

A

Increase in PR and QRS; QT unchanged

38
Q

When would you use Moricizine?

A

Serious ventricular arrhythmias

39
Q

What are the side effects of Moricizine?

A

Potential lethal arrhythmias; increased morbidity post-MI

40
Q

What are the class II antiarrhythmics?

A

Propranolol, Metoprolol, Atenolol, Esmolol

41
Q

What is the MOA of Propranolol?

A

Decrease SNS stimulation of SA node, AV node, PFs, and ventricles; beta blocker

42
Q

What are the EKG manifestations of Propranolol?

A

Increased PR; QRS and QT unchanged

43
Q

When would you use propranolol?

A

Supraventricular and ventricular tachyarrhythmias, PVCs

44
Q

What is the MOA of Metoprolol?

A

Decrease SNS stimulation of SA node, PFs, and ventricles; Beta blocker

45
Q

What are the EKG effects of Metoprolol?

A

Increased PR; QRS and QT unchanged

46
Q

When would you use Metoprolol?

A

Supraventricular and ventricular tachyarrhythmias PVCs

47
Q

What is the MOA of Atenolol?

A

Decrease SNS stimulation of SA node, AV node, PFs and ventricles; beta blocker

48
Q

What are the EKG manifestations of Atenolol?

A

Increased PR; QRS and QT unchanged

49
Q

When would you use Atenolol?

A

Supraventricular and ventricular tachyarrhythmias, PVCs

50
Q

What is the MOA of Esmolol?

A

Decrease SNS stimulation of SA node, AV node, PFs and ventricles; beta blocker; metabolized by RBC esterases

51
Q

What are the EKG manifestations of Esmolol?

A

Increased PR; QRS and QT unchanged

52
Q

When would you use Esmolol?

A

Supraventricular and ventricular tachyarrhythmias; PVCs; emergency IV treatment for A Flutter/AFib and sinus tachycardia; 9min half life

53
Q

What are the class III antiarrhythmics?

A

Sotalol, Bretylium, Ibutilide, Dofetilide, Amiodarone

54
Q

What is the MOA of Sotalol?

A

Non-selective beta-blocker that also has class III action; K channel blocker

55
Q

When would you use Sotalol?

A

Ventricular arrhythmias

56
Q

What are the side effects of Sotalol?

A

Proarrhythmias possible

57
Q

What is the MOA of Bretylium?

A

Blocks K channels and depletes neuronal release of catecholamines

58
Q

When would you use Bretylium?

A

Serious ventricular fibrillation; as emergency IV

59
Q

What is the MOA of Ibutilide?

A

Blocks K channels

60
Q

When would you use Ibutilide?

A

Rapid conversion of AFib/AFlutter to NSR; IV

61
Q

What is the MOA of Dofetilide?

A

Blocks K Channels

62
Q

When would you use Dofetilide?

A

Maintains NSR in AFib patients; inpatient due to ADR potential

63
Q

What are the side effects of Dofetilide?

A

Proarrhythmias possible

64
Q

What is the MOA of Amiodarone?

A

Has Class 1-4 effects; structural analog of thyroxine; K channel blocker

65
Q

What are the EKG manifestations of Amiodarone?

A

Increased PR, QRS, and QT; increased RP, ERP, APD

66
Q

When would you use Amiodarone?

A

Supraventricular and ventricular arrhythmias; >50day half life

67
Q

What are the side effects of Amiodarone?

A

Blue deposits in eyes/skin; pulmonary fibrosis, GI disturbances, thyroid issues, cardiac issues; increases toxicity of digoxin and warfarin

68
Q

What are the class IV antiarrhythmics?

A

Verapamil, Diltiazem

69
Q

What is the MOA of Verapamil?

A

Blocks Ca channels to slow SA rate and AV conduction

70
Q

What are the EKG manifestations of Verapamil?

A

Increased PR

71
Q

When would you use Verapamil?

A

Suppress ventricular rate in AFlutter/AFib

72
Q

What are the side effects of Verapamil?

A

Constipation, hypotension, bradycardia, AV block; Increased dose decrease myocardial contractility

73
Q

What is the MOA of Diltiazem?

A

Blocks Ca channels to slow SA rate and AV conduction

74
Q

What are the EKG manifestations of Diltiazem?

A

Increased PR

75
Q

When would you use Diltiazem?

A

Suppress Ventricular rate in AFlutter/AFib

76
Q

What are the side effects of Diltiazem?

A

Hypotension, bradycardia, AV block; increased doses decrease myocardial contractility

77
Q

What is the MOA of Adenosine?

A

Stimulates P-1 purinergic receptor to open K channels; decreases Ca2 influx; decreases automaticity of and conduction through AV node

78
Q

What are the EKG manifestations of Adenosine?

A

Short “flatline” prior to NSR

79
Q

When would you use adenosine?

A

Emergency IV bolus to halt SVT

80
Q

What are the side effects of Adenosine?

A

Vasodilation > hypotension; maybe brief bronchospasm

81
Q

What is the MOA of Magnesium Sulfate?

A

Adds Mg2+ ions to counteract arrhythmias

82
Q

When would you use Magnesium Sulfate?

A

Torsade de Pointes, digitalis-induced ventricular Arrhythmias, Mg-Deficient Arrhythmias

83
Q

What are the side effects of Magnesium Sulfate?

A

Can cause other arrhythmias

CRP (10 decks)

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