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CV > 100814 antiarrthymic drugs > Flashcards

100814 antiarrthymic drugs Flashcards

1
Q

what inhibitors depolarization of fast response cells in the myocardium?

A

class I antiarrhythmics

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2
Q

inhibitors of depolariztion for slow response cells of myocardium?

A

calcium entry blockers (verapamil, diltiazem)

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3
Q

diff btwn fast and slow response cells

A

diastolic depolarization-in slow response cells usually

fast response cells-their level of resting membrane potential determines maximum upstroke or conduction velocity of the action potential

effective refractory period (minimum interval btwn two propagating impulses): slow response cells have delayed recovery

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4
Q

3 mechanisms of arrhythmias

A

increased automaticity

triggered automaticity (normal AP is interrupted or followed by an abnormal depoliariztion; afterdepolarizations)

reentry (abnormal impulse conduction)

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5
Q

what is early afterdepolarization exacerbated by?

A

long QT syndrome-Torsades de Pointes results

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6
Q

what is delayed afterdepolarization exacerbated by?

A

fast rates, high intracellular calcium, digitalis toxicity, catecholamines, ischemia

delayed afterdepolarizations occur AFTER repolarization

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7
Q

two types of reentry

A

functionally defined reentry (tissue with ischemia, hypoxia)

anatomic reentry (reentry in AV node)

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8
Q

four ways in which antiarrhyth drugs work

A

decrease phase 4 slope
increase threshold
increase maximum diastolic potential (making it more negative)
increase action potential duration

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9
Q

class IA drugs action

A

sodium channel blocker

moderate phase 0 depression and slowed conduction; prolong repolarization

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10
Q

examples of class IA drugs

A

quinidine
procainamide
disopyramide

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11
Q

class IB drugs action

A

sodium channel blocker

minimal phase 0 depression and slow conduction; shorten reploarization

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12
Q

ex of class IB drug

A

lidocaine

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13
Q

class IC drugs action

A

sodium channel blocker

marked phase 0 depression and slow conduction
little effect on repolarization

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14
Q

ex of class IC drug

A

flecainide

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15
Q

class II drug action

A

beta adrenergic blocker

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16
Q

ex of class II drugs

A

proproanolol, esmolol

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17
Q

class III drug action

A

K+ channel blocker-prolong repolarization

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18
Q

ex of class III drug

A

amiodarone
sotalol
dofetilide

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19
Q

class IV drug action

A

calcium channel blocker

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20
Q

ex of class IV drug

A

verapamil

diltiazem

21
Q

MOA of class I

A

reduce membrane responsiveness
increase threshold of AP firing
reduce Vmax (depress conduction velocity)
prolong effective refractive period

22
Q

what kind of cells do class I drugs act on

A

fast response cells

23
Q

uses of class IA drugs

A

atrial flutter or fibrillation

prevent ventricular tachycardia and fibrillation

24
Q

side effects of class IA drugs

A

block K channels so can get early afterdepolarizations

vagolytic effect (if used on atrial fibrillation, can decrease atrial firing but this may increase AV nodal firing due to giving AV node enough time to surpass refractory period)

severe GI

inhibits P450

proarrhythmic

reduces renal clearance of digitalis

metabolized by liver actually

SO MANY SIDE EFFECTS OVERALL

25
Q

class IB MOA

A

increase AP threshold

block Na+ channels at high HR (greater than 120, so it’s use dependent) and in depolarized cells (so could target disease ischemic cells)… binds preferably in Na+ inactivated channel state

decrease AP duration and ERP

26
Q

use of class IB

A

ventricular tachycardia
digitalis induced arrhythmias
safe for patients with long QT syndrome

27
Q

class IC MOA

A 
increase AP threshold
decrease Vmax (conduction velocity)

dissociates from Na channel slowly

28
Q

side effects of class IC

A

pro arrhythmic

29
Q

use of class IC

A

life threatening situations when supraventricular and ventricular arrhythmias are resistant to other drugs

30
Q

class II drugs act on what phase of AP?

A

phase 4–prolongs it in the slow response cells

31
Q

uses of beta blockers

A

all atrial arrhythmias, ventricular tachycardia and fibrillation

most useful antiarrhytmic drugs due to safety record and wide clinical applications

32
Q

side effects of beta blockers

A

negative inotropic effect
heart block
bradycardia
bronchospasm

33
Q

MOA of class III

A

prolong AP repolarization

34
Q

uses of amiodarone

A

ventricular tachyarrhytmias and fibrillation

prevention of recurrent paroxysmal atrial fibrillation or flutter

35
Q

side effects of amiodarone

A

triggered arrhthmias, but rarely associated with Torsades de Pointes

altered thyroid fxn

pulmonary fibrosis

36
Q

most serious side effect of sotalol

A

triggered arrhytmias, with Torsades de Pointes

37
Q

uses of sotalol

A

ventricular tachyarrhtmias and fibrillation

supraventricular tachycardias, atrial fibrillation

38
Q

class IV drugs act most on what type of cells

A

slow response cells

39
Q

MOA of calcium channel blockers

A

increase threhold for AP firing in nodal cells
increase nodal cell refractory period
depress conduction velocity in SA and AV nodes

40
Q

uses of calcium channel blockers

A

paroxysmal supraventricular tachycardia

note: rarely used for ventricular tachycardia

41
Q

side effects of calcium ch blockers

A

negative chronotropic effect (decreases automaticity of SA node, bradycardia)

negative inotropic effect (decreases calcium influx during plateau phase of ventricular AP)

hypotension (decreases calcium influx into vascular sm muscle cells)

constipation (verapamil)

interacts with digitalis to slow conduction velocity in AV node, leading to heart block (verapamil and diltiazem)

increase plasma digitalis levels for competing for renal excretion (verapamil and diltiazem)

42
Q

adenosine MOA

A

VERY RAPIDLY activates K channels to slow phase 4 depolarization AV node (half life of 10 seconds)

blocks cAMP enhanced Calcium channel activity at AV node

43
Q

uses of adenosine

A

supraventricular tachycardia-slows AV conduction and heart rate

44
Q

digoxin MOA

A

enhances vagal parasympathetic activity to slow conduction at the AV node

45
Q

uses of digoxin

A

atrial fibrillation and supraventircular tachycardia to control ventricular response rate

46
Q

what should you be careful of with flecainide?

A

increases risk of death in pts with CAD

47
Q

adenosine may be better than diltiazem and metoprolol for AV nodal reentrant tachycardia b/c

A

adenosine targets directly the AV node

although all three could be used

48
Q

what has been shown to be most effective for long QT syndrome?

A

propranolol

CV (34 decks)

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