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
What is the only vaugh-williams IC drug still in use today?
Propafenone (very potent Na channel blocker)
26
What is propafenone used for?
life-threatening Vtach/fib and refractory SVT
27
What are the effects of propafenone?
decreased contractility
28
ADR for propafenone
might worsen HF, drug-drug interactions (can increase warfarin/digoxin levels)
29
Which antiarrhythmics are metabolized by CYP2D6 and should not be given with drugs that inhibit this CYP?
Classes IC and II
30
when should class IC antiarrhythmics be dose adjusted?
liver impairment
31
What can metoprolol as an antiarrhythmic treat?
AMI unless HR \<100, moderate-severe HF
32
When is esmolol used as an antiarrhytmic?
for immediate beta receptor blockade (onset 6-10 minutes, action ceases in 20 mins)
33
How is esmolol administered?
loading dose and continuous infusion
34
most prescribed and effective antiarrhythmic agent?
amiodarone
35
What can class III antiarrhythmics treat?
supraventricular arrhythmias, prevent recurrence of Vtach/Fib
36
ADR of amiodarone
dose dependent side effects, pulmonary toxicity, photosensitivity, bradycardia, thyroid toxicity, microdeposits in cornea
37
What tests should be ordered before administration of amiodarone?
PFT, TSH
38
How is amiodarone thyrotoxic?
provides iodine, prevents formation of T4 from T3 causing hypo/hyperthyroidism
39
what channels does dofetilide block?
rapid K channels
40
how is dofetilide metabolised and excreted?
CYP2D6 metabolism, renal excretion
41
What is the dose availability for dofetilide?
500, 250, or 125mcg (\<30CrCl) for no shorter than 72 hours
42
ADR of dofetilide
QTc prolongation (should be \<500ms) could cause Tdp
43
What labs should be ordered to monitor pts taking dofetilide?
K, Mg, CrCl
44
Which isomer of sotalol is nonselective for BB ability?
L-isomer
45
How is sotalol excreted?
renally - get CrCl
46
ADR of sotalol
QTc prolongation (should be \<500ms) could cause Tdp
47
When is sotalol contraindicated?
heart block
48
What is dronedarone?
same as amiodarone except no thyrotoxicity, increased mortality (no longer used)
49
Why are CCBs used to treat arrhythmias??
slows ventricular response to Afib/flutter, terminates PSVT
50
ADR for CCB as antiarrhytmics
bradycardia, HOTN
51
When are CCB as antiarrhymics contraindicated?
WPW and Afib, avoid in HOTN or advanced heart disease
52
Why can diltiazem only be given for 24 hours?
pts become refractory after 24 hours
53
What does adenosine treat?
PSVT associated with WPW
54
ADR of adenosine
chest pressure, flushing, tightness in throat
55
Contraindications of adenosine?
second/third degree heart block
56
half life of adenosine?
8seconds, give in left arm with .9% NaCl (pt might flatline for 8 seconds)
57
What are the 2 major factors in Afib?
the initiation of the arrhythmia and the maintenance of it by the muscle
58
What is the highest risk in a pt who has Afib?
stroke
59
Acute and long-term therapy for SVT
Acute: adenosine, BB or CCB long-term: Propafenone or flecainide
60
effects of class I antiarrhythmics?
proarrhythmic effect
61
Effect of class II antiarrhythmics
efficacy in reducing morbidity and mortality
62
effects of class III antiarrhytmics
efficacy with lower proarrhythmic effect than class IA agents
63
effects of class IV antiarrhythmics
no effect on conduction velocity or repolarization and tend to increase sympathetic activation
64
What drugs should/should not be used in HF?
amiodarone: yes (no increased risk of sudden death), class IA and IC: no