Antiarrhythmics Flashcards

1
Q

What is phase 1 of the AP?

A

Na influx, rapid depolarization

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2
Q

What is phase 2 of the AP?

A

Plateau maintained by Ca inflow and K outflow

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3
Q

What is phase 3 of the AP?

A

Ca channels close, K outlfow

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4
Q

Describe the fast sodium channel

A

voltage dependent, lets Na in, keeps K from going out, keeps Ca from blocking the channel

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5
Q

Which channels contribute to regulation of AP duration?

A

potassium

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6
Q

Which Ca channels initiate/sustain an AP?

A

T-type initiate AP, L-type sustain AP

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7
Q

What are funny channels?

A

found in cardiac muscle, highly non-selective for ions

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8
Q

What do antiarrhythmic drugs result in?

A

affect conduction and excitability, suppress abnormal automaticity

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9
Q

What are the class I antiarrhythmics?

A

fast sodium channel blockers: lidocaine (IB), quinidine (IA)

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10
Q

What are the class II antiarrhythmics?

A

Beta blockers: metoprolol*, esmolol

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11
Q

How do class II antiarrhythmics work?

A

suppress phase 4 depolarization

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12
Q

What are the class III antiarrhythmics?

A

amiodarone, sotalol, dofetilide

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13
Q

How do class III antiarrhythmics work?

A

repolarization prolongation, prolongs phase 3 repolarization due to K channel blockade

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14
Q

What are the class IV antiarrhythmics?

A

calcium channel blockers: diltiazem, verapamil

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15
Q

How do class IV antiarrhythmics work?

A

inhibit calcium dependent slow AP in the SA and AV nodes

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16
Q

What is the class V antiarrhythmic?

A

digoxin

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17
Q

How do class V antiarrhythmics work?

A

calcium accumulation, vagal effect

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18
Q

Why is quinidine not used anymore?

A

old, side effects, drug interactions (CYP2D6 inhibitor)

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19
Q

ADR of quinidine?

A

diarrhea, hemolytic anemia, HF, liver failure, digoxin interaction, thrombocytopenia

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20
Q

What drug is a relative of quinidine that is no longer used?

A

procainamide

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21
Q

What can quinidine treat?

A

atrial tachyarrhythmias, AV junctional and ventricular arrhythmias

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22
Q

What can lidocaine treat?

A

ventricular arrhythmias

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23
Q

ADR for lidocaine

A

worsen some arrhythmias, seizures, CNS effects, contraindicated in second degree or complete heart block

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24
Q

Why does lidocaine require more than 1 dose

A

short half-life, may require continuous infusion

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25
Q

What is the only vaugh-williams IC drug still in use today?

A

Propafenone (very potent Na channel blocker)

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26
Q

What is propafenone used for?

A

life-threatening Vtach/fib and refractory SVT

27
Q

What are the effects of propafenone?

A

decreased contractility

28
Q

ADR for propafenone

A

might worsen HF, drug-drug interactions (can increase warfarin/digoxin levels)

29
Q

Which antiarrhythmics are metabolized by CYP2D6 and should not be given with drugs that inhibit this CYP?

A

Classes IC and II

30
Q

when should class IC antiarrhythmics be dose adjusted?

A

liver impairment

31
Q

What can metoprolol as an antiarrhythmic treat?

A

AMI unless HR <100, moderate-severe HF

32
Q

When is esmolol used as an antiarrhytmic?

A

for immediate beta receptor blockade (onset 6-10 minutes, action ceases in 20 mins)

33
Q

How is esmolol administered?

A

loading dose and continuous infusion

34
Q

most prescribed and effective antiarrhythmic agent?

A

amiodarone

35
Q

What can class III antiarrhythmics treat?

A

supraventricular arrhythmias, prevent recurrence of Vtach/Fib

36
Q

ADR of amiodarone

A

dose dependent side effects, pulmonary toxicity, photosensitivity, bradycardia, thyroid toxicity, microdeposits in cornea

37
Q

What tests should be ordered before administration of amiodarone?

A

PFT, TSH

38
Q

How is amiodarone thyrotoxic?

A

provides iodine, prevents formation of T4 from T3 causing hypo/hyperthyroidism

39
Q

what channels does dofetilide block?

A

rapid K channels

40
Q

how is dofetilide metabolised and excreted?

A

CYP2D6 metabolism, renal excretion

41
Q

What is the dose availability for dofetilide?

A

500, 250, or 125mcg (<30CrCl) for no shorter than 72 hours

42
Q

ADR of dofetilide

A

QTc prolongation (should be <500ms) could cause Tdp

43
Q

What labs should be ordered to monitor pts taking dofetilide?

A

K, Mg, CrCl

44
Q

Which isomer of sotalol is nonselective for BB ability?

A

L-isomer

45
Q

How is sotalol excreted?

A

renally - get CrCl

46
Q

ADR of sotalol

A

QTc prolongation (should be <500ms) could cause Tdp

47
Q

When is sotalol contraindicated?

A

heart block

48
Q

What is dronedarone?

A

same as amiodarone except no thyrotoxicity, increased mortality (no longer used)

49
Q

Why are CCBs used to treat arrhythmias??

A

slows ventricular response to Afib/flutter, terminates PSVT

50
Q

ADR for CCB as antiarrhytmics

A

bradycardia, HOTN

51
Q

When are CCB as antiarrhymics contraindicated?

A

WPW and Afib, avoid in HOTN or advanced heart disease

52
Q

Why can diltiazem only be given for 24 hours?

A

pts become refractory after 24 hours

53
Q

What does adenosine treat?

A

PSVT associated with WPW

54
Q

ADR of adenosine

A

chest pressure, flushing, tightness in throat

55
Q

Contraindications of adenosine?

A

second/third degree heart block

56
Q

half life of adenosine?

A

8seconds, give in left arm with .9% NaCl (pt might flatline for 8 seconds)

57
Q

What are the 2 major factors in Afib?

A

the initiation of the arrhythmia and the maintenance of it by the muscle

58
Q

What is the highest risk in a pt who has Afib?

A

stroke

59
Q

Acute and long-term therapy for SVT

A

Acute: adenosine, BB or CCB long-term: Propafenone or flecainide

60
Q

effects of class I antiarrhythmics?

A

proarrhythmic effect

61
Q

Effect of class II antiarrhythmics

A

efficacy in reducing morbidity and mortality

62
Q

effects of class III antiarrhytmics

A

efficacy with lower proarrhythmic effect than class IA agents

63
Q

effects of class IV antiarrhythmics

A

no effect on conduction velocity or repolarization and tend to increase sympathetic activation

64
Q

What drugs should/should not be used in HF?

A

amiodarone: yes (no increased risk of sudden death), class IA and IC: no