Drugs Used in Cardiac Arrhythmias Lecture - Konorev Flashcards

1
Q

which cells have fast action potential

A

ventricular contractile cardiomyocytes
atrial cardiomyocytes
purkinje fibers

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2
Q

which cels have slow (pacemaker AP)

A

SA node cells

AV node cells

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3
Q

class 1a drugs

A

quinidine
procainamide
disopyramide

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4
Q

class 1B drugs

A

lidocaine

mexiletine

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5
Q

class 1C drugs

A

flecainide

propafenone

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6
Q

class 2 drugs- beta blockers

A

esmolol

propranolol

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7
Q

class 3 drugs

A

potassium channel blocking drugs

amiodarone
dronedarone
sotalol
dofetilide
ibutilide
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8
Q

class 4 drugs

A

cardioactive CCB

verapamil
diltiazem

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9
Q

miscelaneous agents

A

adenosine

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10
Q
class 1 drugs sodium channel blocker
-state dependent block
A

most useful drugs block open activated or inactivated Na+ channels, with very little affinity towards channels in a resting state

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11
Q

class 1A drugs and channels

A

block sodium channels, slow impulse conduction, reduce automatism of ectopic pacepaker

-use dependent block- preferentiallhy bind to open sodium channels (ectopics with faster rhythms targeted)

  • block postassium channels
    • prolong AP duration, prolong QRS and QT
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12
Q

class 1A drugs kinetics

A

dissociate with intermediate kinetics

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13
Q

class 1B drugs and channels

A

block sodium channels - bind to inactivated sodium channels (preferentially bind to depolarized cells)

-do not block potassium channels, no prolonged AP, QT, or ARS

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14
Q

class 1B drugs and kinetics

A

dissociate from channel with fast kinetics

-may shorten AP

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15
Q

class 1C drugs and channels

A

block sodium channels, slow impulse conduction (bind open/activated channels)

block certain potassium channels but not ones responsible for repol

  • no proloned AP, or QT
  • prolong QRS interval duration
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16
Q

class 1C drugs and kinetics

A

dissociate from channel with slow kinetics

17
Q

class 2 drugs effects

A

slow action potential
SA node decrease HR, increase RR

  • AV node - decrease AV conducatance (increase PR)
  • ventricular myocardium - decrease Ca2+ overload, prevent delayed afterdepol
18
Q

class 2 drug effects on ecg

A

decreased slope due to effects on If and T type ca chanels

increased threshold due to effect on L type Ca channels

19
Q

class 3 drugs

A

potassium channel blockers

inwardly rectifying K+ channels are open in resting state
no current in these channels
-limit frequency of AP (regulate duration of refractory period)

-prolong AP duration and QT

20
Q

class 4 drugs

A

block both activated and inactivated L type calcium channels

decrease slope of phase 0 depol

slow SA node depol
prolong AP duration and refractory period in AV node
prolong AV node conducation time

-may be effective in DAD-incuded ventricular arrhythmias