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Maddy - CPR I - some pharm > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

what part of the cardiac action potential do class 1 antiarrhythmic drugs affect

A

phase 0

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2
Q

what part of the cardiac action potential do class 3 antiarrhythmic drugs affect

A

phases 2 and 3

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3
Q

what part of the nodal action potential do class 2 antiarrhythmic drugs affect

A

prolongs phase 4 (delays progression to phase 0)

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4
Q 
what part of the nodal action potential do class 4 
 antiarrhythmic drugs affect
A

prolongs phase 4 (delays progression to phase 0)

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5
Q

describe phase 0 of the cardiac action potential

A

voltage-dependent fast Na+ channels open as a result of depolarization and Na+ enters the cells down its gradient

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6
Q

describe phase 1 of the cardiac action potential

A

K+ exits the cell down its gradient while fast Na+ channels close, causing some depolarization

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7
Q

describe phase 2 of the cardiac action potential

A

the plateau phase which results from K+ exiting the cells offset by Ca2+ entering the cells through slow voltage- dependent Ca2+ channels

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8
Q

describe phase 3 of the cardiac action potential

A

Ca2+ channels close and K+ begins to exit more rapidly, resulting in repolarization

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9
Q

describe phase 4 of the cardiac action potential

A

resting membrane potential is gradually restored by Na+/K+ ATPase and Na+/Ca2+ exchanger

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10
Q

describe phase 4 of the pacemaker action potential

A

slow spontaneous depolarization; pacemaker current (funny current) opens and lets Na+ into the cell

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11
Q

describe phase 0 of the pacemaker action potential

A

upstroke of action potential; Ca2+ influx through L-type Ca2+ channels

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12
Q

describe phase 3 of the pacemaker action potential

A

Repolarization; inactivation of Ca2+ channels with increased K+ efflux

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13
Q

describe resting state of sodium channels

A

channel closed but ready to generate an action potential

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14
Q

describe activated state of sodium channels

A

depolarization to the threshold opens m-gates which greatly increases sodium permeability

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15
Q

describe inactivated state of sodium channels

A

h-gates are closed, inward sodium flux is inhibited, channel not available for reactivation
–> responsible for the refractory period

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16
Q

describe the state-dependent block of class 1 antiarrhythmics

A

they block activated or inactivated Na+ channels with very little affinity toward channels in a resting state

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17
Q

class 1A antiarrhythmics:

  • state dependent block
  • binding strength
  • effect on ECG
A
  • preferentially bind to open (activated) channels
  • dissociate with intermediate kinetics (medium strength)
  • prolong QRS and QT
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18
Q

what does procainamide do in addition to Na+ channel block

A
  • directly depresses SA and AV node
  • antimuscarinic activity
  • reduces PVR and can cause hypotension
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19
Q

non-cardiac adverse effects procainamide

A
  • lupus-like syndrome (arthritis, pleuritis, hepatitis)

- nausea, diarrhea

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20
Q

non-cardiac adverse effects quinidine

A
  • GI stuff
  • tinnitus, dizziness, HA
  • thrombocytopenia
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21
Q

non-cardiac adverse effects disopyramide

A
  • urinary retention
  • dry mouth
  • blurred vision
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22
Q

cardiac adverse effects of all class 1A drugs

A
  • QT prolongation
  • torsades de pointes
  • excessive inhibition of conduction
23
Q

class 1B antiarrhythmics:

  • state dependent block
  • binding strength
  • effect on ECG
A
  • bind preferentially to inactivated Na+ channels
  • dissociate with fast kinetics (weak binding)
  • doesn’t block K+ so does not prolong QT or action potential on ECG
24
Q

how does lidocaine make damaged tissue “electrically silent”

A

it selectively blocks conduction in depolarized tissue

25
Q

why do class 1B drugs have no effect on cardiac conductivity in normal tissue

A

fast kinetics of dissociation from Na+ channels results in recovery from block between action potentials

26
Q

adverse effects lidocaine

A
  • hypotension in pts with heart failure

- paresthesias, tremor, slurred speech, convulsions

27
Q

adverse effects mexiletine

A
  • tremor
  • blurred vision
  • nausea
  • lethargy
28
Q

class 1C antiarrhythmics:

  • state dependent block
  • binding strength
  • effect on ECG
A
  • preferentially bind to activated sodium channels
  • dissociate from channel with slow kinetics (strong binding)
  • prolongs QRS, does not prolong action potential or QT on ECG
29
Q

which class 1 drugs also block K+ channels

A 
class 1A
class 1C
30
Q

adverse effects Flecainide

A

severe exacerbation of ventricular arrhythmias in pts with preexisting ventricular tacchyarrhyhtmias, previous MIs, or ventricular ectopic rhythms

31
Q

adverse effects Propafenone

A
  • exacerbation of ventricular arrhythmias
  • metallic taste (purple phone tastes like metal)
  • constipation
32
Q

sympathetic effect of beta blockers on funny channel and T-type Ca2+ channels in nodal AP

A

increased slope

33
Q

sympathetic effect of beta blockers on L type Ca2+ channels in nodal AP

A

reduced threshold

34
Q

effect of esmolol on SA and AV node and ECG

A

SA node: decreases HR (increase RR interval)

AV node: decreases AV conductance (increase PR interval)

35
Q

based on its half life, how must esmolol be administered

A

continuous IV infusion with rapid onset and termination of its action
(half life is 10 min b/c hydrolysis by blood esterases)

36
Q

contraindications beta blockers

A
  • asthma
  • PVD
  • Raynaud’s
  • type 1 DM on insulin
  • bradyarrhythmias and AV conductance abnormalities
37
Q

adverse effects beta blockers

A
  • reduced CO
  • bronchoconstriction
  • impaired liver glucose mobilization
  • increase VLDL and decreases HDL
  • sedation, depression
38
Q

effect of class 3 drugs on ECG

A

prolong QT

39
Q

effect of class 3 drugs on refractory period

A

prolong refractory period

40
Q

effects of amiodarone on Na+ and Ca2+ channels

A

blocks Ca2+ and inactivated sodium channels as well as K+ channels

41
Q

what is amiodarone metabolized by

A

CYP3A4

42
Q

effect of cimetidine or rifampin on amiodarone

A

they inhibit CYP3A4, which affects metabolism of amiodarone

43
Q

how does amiodarone affect metabolism of other drugs

A

it inhibits many CYP enzymes

44
Q

cardiac adverse effects amiodarone

A
  • AV block and bradycardia

- torsade de pointes

45
Q

extracardiac adverse effects amiodarone

A
  • fatal pulmonary fibrosis
  • hepatitis
  • photodermatitis (blue-gray skin)
  • deposits of drug in cornea
  • hypo or hyperthyroidism
46
Q

adverse effects sotalol

A
  • depression of cardiac function

- torsades de pointes

47
Q

adverse effects dofetilide and ibutilide

A

QT interval prolongation and increased risk of ventricular arrhythmias

48
Q

why are the effects of dofetilide and ibutilide more pronounced at lower heart rates

A

they specifically block the rapid component of the delayed rectifier potassium current

49
Q

effect of class 4 drugs on nodal action potential

A
  • decrease slope of phase 0
  • increase L-type Ca2+ channel threshold potential
  • prolong refractory period in AV node
50
Q

adverse effects of class 4 drugs

A
  • negative inotropy
  • AV block
  • SA node arrest
  • bradyarrhythmias
  • hypotension
51
Q

non-cardiac adverse effect verapamil

A

constipation

52
Q

effect of adenosine on nodal action potential

A
  • inhibits Ca2+ and funny currents
  • causes hyperpolarization and suppression of AP in slow cells
  • inhibits AV conduction
  • increases refractory period
53
Q

adverse effects adenosine

A
  • SOB
  • bronchoconstriction
  • chest burning
  • AV block
  • hypotension

Maddy - CPR I - some pharm (25 decks)

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