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CardioRenal I > Cardio Pharm: Antiarrhythmic Drugs > Flashcards

Cardio Pharm: Antiarrhythmic Drugs Flashcards

1
Q

in what phase to EADs occur

A

Phases 2 and 3 - due to reactivation of voltage gated Ca channels during repolarization

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2
Q

in what pases to DADs occur

A

Phase 4 - due to intracellular calcium overlaoad (Na Ca exchanger cant keep up resulting in depolarization that generates another raction potential)

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3
Q

Discuss the proarrythmic actions of antiarrhytmic drugs

A

1.) profound slowing of conduction velocity 2.) increase AP duration (LQT)

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4
Q

Class I

A

Sodium channel blockers

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5
Q

Class II

A

Beta Blockers

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6
Q

Class III

A

Potassium chanel blockers

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7
Q

Class IV

A

Calcium Channel Blockers

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8
Q

Which class I subset extends the AP duration

A

Class IA

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9
Q

Which subset of class I should be avoided in patients with structural heart damage

A

Class IC

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10
Q

Class IA drugs

A

Quinidine, Proclamamide, Dyspramide

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11
Q

Class IB drugs

A

Lidocaine, Mexiletine, Phenytoin

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12
Q

Class IC drugs

A

Propafenone, Flecanide

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13
Q

unique effects of class IA

A

1.) antimuscarinic action (enhance conduction through ABV node) - results in high ventricular rates in patients with atrial tachycardia (should be administered with calss IV to bring rate back down) 2.) Blocks Ikr channels ( prolongs QT - increased risk of torsades

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14
Q

Quinidine uses

A

rarely used clinically - may be used in pregant women or women who are trying to beocme pregnant. AT and VT

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15
Q

Quidine blocks what CYP

A

CYP2D6

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16
Q

Quidine adverse effects

A

1.) Cinchinism (headache, nausea, tinnitus) 2.) Torsades 3.) thrombocytopenia (rare)

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17
Q

Procainamide uses

A

convert AT or VT to sinus rhythm (short term application)

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18
Q

Procainamide pharmacokinetics

A

IV ONLY: t1/2 = 3-4 hours, hepatic acetylation yeilds an active metabolite = NAPA which blocks Ikr

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19
Q

Procainamide AE

A

1.) Lupus like disorder (arthralgia and arthritis) 2.) Long QT - high risk for torsades de pointes

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20
Q

Disopyramide uses

A

AT and VT

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21
Q

Disopyramide AE

A

1.) Strong antimuscarinic effect ( uniary retention in men, dry mouth, blurred vision, constipation, worsening of preexisting glaucoma) 2.) Negative ionotropic effect (supresses heart contraction)

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22
Q

Disopyramide contraindication

A

heart failure - may induce heart failure in susceptible patients

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23
Q

Class IB general uses

A

Ventricular arrythmias only

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24
Q

Lidocaine uses

A

terminates VT

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25
Q

Lidocaine Pharmacokinetics

A

IV ONLY, hepatic metabolism - dose reduced in patients with liver disease

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26
Q

Lidocaine AE

A

tremor, blurred vision, lethargy - overdose can cause seizures

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27
Q

Mexiletine uses

A

post MI VT - often given with another drug as its not effective on its own

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28
Q

Mexiletine AE

A

tremors, blurred vision, lethargy

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29
Q

Phenytoin

A

antiepileptic drug

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30
Q

Class IC uses

A

1.) SVT 2.) Prevent recurrence of ventricular tachycardua

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31
Q

Flecanide pharmacokinetics

A

metabolized by CYP2D6 ( inhibited by quinidine)

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32
Q

Flecanide AE

A

dizzy, blurred vision, tremor, headache, bradycardia, heartblock, ventricular arrythmia, HF

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33
Q

Propafenone pharmacokinetics

A

metabolized by CYP2D6 ( inhibited by quinidine). Good for renal patients. ALSO acts as B-blocker (nonselective)

34
Q

Propafenone AE

A

dizzy, blurred vision, tremor, headache, bradycardia, heartblock, ventricular arrythmia, HF, ** Metalic taste, bronchospasm (due to non-selective beta block)

35
Q

Rate control

A

control rate of only the ventricles by slowing down AP through AV node ( Class II and IV)

36
Q

Rhythm control

A

controle both atrial and ventricular rate to bring back into rhythm ( Class I and III)

37
Q

Class II agents act on what channel

A

Funny channels

38
Q

Class II drugs

A

Propranolol, esmolol, atenolol, metoprolol

39
Q

Cardiac effects of beta blockers

A

1.) Decrease stimulation by SNS 2.) decrease pacemaker current to decrease HR 3.) Decrease Ca current to decrease conduction velocity

40
Q

which drug calss reduces mortality following acute MI in HF patients

A

Class II (B-Blockers)

41
Q

Propranolol AE

A

nonselective B-Blocker. Nightmares (crosses BBB), fatigue, depression, brocnhospasm

42
Q

Propranolol contraindication

A

asthma and COPD

43
Q

Metoprolol AE

A

cardioselective. Still slightly lipophilic - crosses BBB = nightmares , Bradycardia, heart block, hypotension, heart failure, exercise intolerance

44
Q

Atenolol pharmacokinetics

A

Cardioselective. Excreted by the kidney unchanged (less drug drug interactions) Plasma levels increase in pt who have renal disease

45
Q

Atenolol AE

A

bradycardia, heart block, hypotension, heart failure, exercise intolerance

46
Q

Esmolol use

A

IV ONLY- used for intraoperative arrythmia

47
Q

Esmolol pharmacokinetics

A

very short half life t1/2 = 10 seconds - as soon as it gets in the blood it is destroyed by plasma esterases

48
Q

Esmolol AE

A

cardiac hypotension 20-50% of patients (12% become symptomatic)

49
Q

Class III block which current

A

Ikr during phase 3 (repolarization)

50
Q

Amiodarone blocks

A

Ikr, Ina, Ica, and B-receptors

51
Q

Amiodarone IV uses

A

termination of SVT and VT

52
Q

Amiodarone oral uses

A

SVT (A fib, VT, reduce shock frequency in patients with pacemaker device

53
Q

Amiodarone Drug- Drug interactions

A

inhibits metabolism of warfarin (CYP2C9), statins (CYP3A4 and 2C9) and digoxin (P-glycoproteins)

54
Q

Amiodarone pharmacokinetics

A

T1/2 = 40-45 days - takes seveal weeks to get to full effect

55
Q

You have a patient that experiences ventricular tachycardia. You treat them with a loading dose of 400-1200 mg/ day for 10 days and then taper them to a maintainace dose of 200 mg/day. What drug did you give them for their VT

A

Amiodarone

56
Q

amiodarone adverse effects

A

1.) Hepatic- must monitor liver function 2.) LQT but LOW RISK OF TORSADES (blocks Ina, Ica, and B-receptors) 3.) Pulmonary fibrosis 4.) thyroid dysfunction 5.) tissue deposition 6.) Skin reactions - photosensitivity

57
Q

why does amiodarone have a low risk of Torsades despite the fact that it prolongs QT interval

A

also blocks Ina, Ica, and B-receptors

58
Q

Sotalol

A

also a nonselective B-blocker. Class III

59
Q

Sotalol uses

A

A flutter/Fib,Ventricular arrythmias

60
Q

Sotalol adverse effects

A

1.) Torsades (RECOMMEND initiation while in the hospital) 2.) Bronchospasm

61
Q

Sotalol pharmacokinetics

A

renal excretion unchanged - decreased drug drug interactions

62
Q

Dofetellide pharmacokinetics

A

20% metabolized by CYP3A4 80% metabolzed through renal excretion unchaned

63
Q

Dofetellide drug-drug interactions

A

plasma levels are increased by verapamil, ketoconazole, trimethoprim/sulfamethoxazole, and cimetidine (OTC)

64
Q

Dofetellide adverse effects

A

narrow theraputic window - REQUIRED initiation in hospital setting - Torsades de pointe

65
Q

Ibutillide use

A

convert Atrial flutter or fib to sinus rhythm (IV only)

66
Q

Ibutillide adverse effects

A

torsades de pointes - patients should be monitored for several hours folowng termination

67
Q

Dihyodropyridines

A

selectively inhibit smooth muscle L-ca channels to cause smooth muslce relaxation, antihypertesnive, and antianginal

68
Q

Non-Dihydropyridines

A

Class IV antiarrythmetic drugs that more selectively inhibit cadiac muscle Ica-L current to slow heart rate, antiarrythic, and antanginal

69
Q

action of Class IV on SA node

A

decrease diastolic depolarization and decrease AP rate (decreases HR) Decreases NCX

70
Q

action of Class IV on AV node

A

decrease upstroke, slow conduction velocity and increase refractory period

71
Q

class IV drugs

A

Diltiazem, Verapamil

72
Q

class IV uses

A

SVT, VT, atrial fibrillation/flutter

73
Q

Class IV contraindication

A
  1. ) heart failure with LOW ejection fraction 2.) Slow heart rate 3.) low blood pressure 4.) WPW
74
Q

Adenosine MOA

A

activates G-protein activated inward K rectifier (GIRK) channels to produce a muscarinic affect that slows heart rate. Inhibits Ica

75
Q

Adenosine uses

A

termination of PSVT

76
Q

Adenosine pharmacokinetics

A

IV only T1/2 = 10 seconds

77
Q

Adenosine AE

A

flushing, dyspnea, chest pain, transient heart block, bronchoconstriction

78
Q

Digoxin MOA

A

inhibits Na K ATPase leading to increased levels of Ca in myocites. Slows conduction velocity and increases refractory periord in AV node (due to vagomimetic action)

79
Q

Digoxin drug drug interactions

A

Amiodarone, diltiazem, quinidine, verapamil

80
Q

Digoxin side effects

A

1.) DADs (due to increased intracellular Ca) 2.) AV block 3.) Bradycardia 4.) Anorexia, nausea, headache, halo vision, altered color perception

81
Q

magnesium sulfate

A

corrects hypomagnesimia, may surpress EADs, used to treat torsades de pointes

82
Q

Potassium chloride

A

corrects hypokalemia - may supress ectopic pace makers and prevent or terminate arrhythmias

CardioRenal I (13 decks)

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