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Cardio 2 > anti-arrythmics > Flashcards

anti-arrythmics Flashcards

1
Q

class Ia NaCh Blockers

A

Double Quarter Pounder
disopyramide
quinidine
procainamide

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2
Q

class Ib NaCh blockers

A

lettuce, tomato, mayo
lidocaine
tocainide
mexiletine

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3
Q

class Ic NaCh blockers

A

more fries please
moricizine
Flecainide
propafenone

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4
Q

class II beta blockers

A

esmolol
metoprolol
propranolol

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5
Q

class III KCh blockers

A 
a big dog is scary 
amidarone
bretylium
dofetilide
ibutilide
sotalol
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6
Q

class IV CCBs

A

verapamil

diltiazem

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7
Q

other ACLS drugs

A 
adenosine
atropine
MgSO4
anticoagluants
digoxin
naloxone
vasopressors
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8
Q

vassopressors

A

Epi
NE
vasopressin
dopamine

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9
Q

Na concentrations

A

intracellular 5-15

extracellular 135-142

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10
Q

K concentrations

A

intracelluarl 135-140

extracellular 3-5

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11
Q

factors which may precipitate or exacerbate an arrythmia

A

ischemia, hypoxia, acidosis, alkalosis, electrolyte abnormalities, excessive catecholamine exposure, autonomic influences, durg toxicity, over stretching of cardiac fiber

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12
Q

duration of diastolic interval

A

determined by slope of phase 4

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13
Q

early after depolarizations

A

transient deplarization that interrupts phase 3

exacerbated at slow heart rates contributes to long QT

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14
Q

delayed afterdepolarization

A

interrupts phase 4
often occurs when intracellular Ca is increased
exacerbated by fast HR
responsible for some arrhytmias related to excess digitalis, catecholamines, and myocardial ischemia

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15
Q

abnormal impulse conduction: severe depressed conduction

A

may result in simple block (AV, bundle branch)

b/c parasympathetic control of AC conduction is significant partial AV block sometimes relieved by atropine

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16
Q

abnormal impulse conduction: reentry

A

impulse reenters and excited areas of heart more then once
3 conditions:
-must be obstacle, thus establishing a circuit
-must be unidirectional
-conduction time must be long enough that retrograde impluse does not encounter refractory period

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17
Q

depress autonomic properties of abnormal pacemaker cell

A

decrease slope of phase 4 and/or elevate threshold potential

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18
Q

alter conduction characteristics of pathways of reentry - facilitate conduction

A

(shorten refractoriness) of area of unidirectional block -> anterograde conduction can proceed

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19
Q

-depress conduction

A

(prolong refractoriness) in area of unidirectional block or in pathway w/slowed conduction and short refractory period -> retrograde propagation of impluse no permitted causing bidirectional block

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20
Q

type I

A

NaCh Blockers

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21
Q

Ia

A

prolong action potential duration, dissociate from channel w/intermediate kinetics

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22
Q

Ia effects

A
  • decrease conduction velocity
  • increase refractoriness
  • decrease autonomic properties of Na dependent conduction
  • unidirectional block transformed to bidirectional
  • some K blocking properties
  • effective in supraventricular and ventricular arrhythmias
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23
Q

Ib

A

shorten AP duration in some tissues in heart and dissociate rapidly

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24
Q

Ib effects

A

decrease refractoriness w/no effect on conduction velocity -> improces anterograde conduction, eliminating area of unidirectional block
in diseased tissue refractoriness prolonged leading to bidirectional block
clinically effective in ventricular arrhythmias > suprventricular

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25
Q

Ic

A

minimal effects on AP duration and dissociate slowly

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26
Q

Ic effects

A

profoundly decreased conduction velocity while leaving refractoriness
theroretically eliminate reentry by slowing conduction to point where impulse is extinguished
clinically effective in supraventricular and ventricular arrhythmias, but ventricular limited due to risk of proarrhythmias

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27
Q

II

A 
sympatholytic beta blockers
decrease conduction velocity
increase refractoriness
decrease automaticity in nodal tissues
anti-adrenergic actions
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28
Q

III

A

KCh blockers
prolong AP duration
prolong refractoriness in atrial and ventricular tissues
delay repolarization by blocking KChs

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29
Q

IV

A

CCBs
slows conduction where AP dependent on Ca (SA and AV nodes)
decreases conduction, increases refractoriness, decreases automacity in Ca dependent tissues

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30
Q

procainamide

A

Ia
slows upstroke of AP, slows conduction, prolongs QRS, prolongs APD (due to some KCh block), direct depressant effects on SA and AV nodes

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31
Q

procainamide extracardiac effects

A

ganglion blocking -> decreased TPR -> hypotension

32
Q

procainamide toxicity

A 
excessive prolongation
induction of TdP
new arrythmias
reversible lupus like syndrome
nausea, diarrhea
rash, fever, hepatits, agranulocytosis
33
Q

procainamide dosage

A

IV, IM, PO

reduction required in renal failure

34
Q

NAPA

A 
metabolite of procainamide 
had class III activity associated w/ TdP especially in renal failure
35
Q

uses of procainamide

A

atrial and ventricular arrythmias

long term therapy avoided

36
Q

quinidine

A

Ia
like procainamide
can cause GI issues, headache, dizziness, tinnitus, rare immunologic rxns
rarely used

37
Q

disopyramide

A

Ia
much more pronounced antimuscarinic effects, (should beadministered w/drug that slows AV conduction) precipitates HF, urinary retention, dry mouth, blurred vision, constipation

38
Q

lidocaine

A

blocks activated and inactivated NaChs w/rapid kinetics

39
Q

lidocaine toxicity

A

least cardiotoxic of NaCh blockers
SA node arrest, worsening of imparied conduction, ventricular arrhythmias uncommon
large does -> hypotension
most common- neurologic (parasthesias, tremors, nausea, hearing, speech, convulsions)
dose related

40
Q

use of lidocaine

A

termination of ventircular tachycardia and prevention of V fib after cardioversion in setting of acute ischemia

41
Q

mexiletine

A

orally active congener of lidocaine
also has neuro side effects
used for ventirucalr arrythmias, off label use for chronic pain

42
Q

flecainide

A

potent blocker of Na and KChs but does not prolong AP or OT interval

43
Q

flecainide toxicity

A

severe exacerbation of arrhythmia in patients w/preexisting Vtach or previous MI

44
Q

flecainide uses

A

supraventricular arrythmias

45
Q

propafenone

A

similar to Flecainide, but wea beta-blocking activity, does not porlong AP

46
Q

propafenone toxicity

A

metallic taste, constipation, arrhythmia exacerbation

47
Q

propafenone uses

A

supraventircular arrythmias

48
Q

amiodarone

A

markedly prolongs AP and OT interval by blocking Ikr
chronic uses -> Iks blockage
also blocks NaChs, weak adrenergic and CCB activity

49
Q

amiodarone extracardiac effects

A

peripheral vasodilation

50
Q

amiodarone toxicity

A

symptomatic bradycardia
heart block in preexisting sinus of AV node disease
accumulates in heart, lung, liver, skin, and concentrates in tears
pulmonary toxicity, fetal pulmonary fibrosis, skin and corneal lesions, may cause hypo or hyperthyroidism

51
Q

amiodarone PK

A

after discontinuation affects may last 1-3 months

many drugs interactions ) increases statins, digoxin, and warfarin levels)

52
Q

use of amiodarone

A

Afib, prevention of recurrent Vtach, not associated w/increased mortality in CAD or HF, used as adjunct w/ICD

53
Q

dronedarone

A

analog of amiodarone w/iodine removed to eliminate thyroid adverse effects
works on Ikr, Iks, Ica, Ina, and beta Rs

54
Q

dronedarone toxicity

A

black box warning against use in acute decompensated or advanced (class IV) HF

55
Q

dronedarone uses

56
Q

sotalol

A

both beat blocking and AP prolonging actions
L-isomer- beta blocker (not cardioselective)
D and L isomers prolong AP

57
Q

sotalol toxicity

A

dose related incidence of TdP

further depression of LV function in patients w/HF

58
Q

uses of sotalol

A

life-threatening ventricualr arrhythmias, maintenance of sinus rythem in Afib, supraventriuclar and ventriucalr arrhythmias in peds

59
Q

dofetilide

A

dose-dependent blockage of rapid component of delayed rectifier K current increasing hypokalemia
slow recovery from blockade

60
Q

dofetilide toxicity

A

OT prolongation and risk of ventricular arrythmias

61
Q

dofetilide relative contraaindications

A

OTc> 450ms
bradycardia <50bpm
hypokalemia

62
Q

uses of dofetilide

A

maintencance of NSR is Afib and restoring NSR in Afib

63
Q

verapamil

A

blocks both activated and inactivated L-type CaChs
effect more marked in tissues that fire frequently, those that are less completely polarized at rest, and those in which actiation depends exclusively on Ca current (SA&AV nodes)
AV node conduction and effective refractory period prolonges
SA node conduction dlowed, but hypotensive action may result in reflex increase in SA node
suppresses both early and delayed after depolarizations

64
Q

extracardiac effects of verapamil

A

peripheral vasodilation

65
Q

verapamil toxicity

A

hypotension and Vfib if IV in Vtach misdiagnosed as supraventricular tachycardia
can induce AV blcok
constipation, lassitude, nervousness, peripheral edema

66
Q

verapamil uses

A

supraventricular tachycardia,
Afib, Aflutter
angina, HTN

67
Q

diltiazem toxicity

A

edema and headache

AV block, bradycardia, hypotension

68
Q

uses of diltiazem

A

supraventricualr tachycardia, angina, HTN

69
Q

adenosine

A

activates inward rectifying K current and blocks Ca current -> marked hyperpolarization
inhibits AV node conduction and increases refractory period

70
Q

adenosine toxicity

A 
flushing
SOB
chest burnign
high grade AV block
Afib
headache
hypotension
nausea
paresthesias
71
Q

uses of adenosine

A

drug of choice for conversion of paroxysmal supraventricular tachycardia

72
Q

atropine

A

blocks actions of Ach at parasympathetic sites increasing CO

73
Q

atropine toxicity

A

arrhythmias, tachycardia, dizziness, constipation, urinary retention

74
Q

atropine uses

A

bradycardia, neuromucular blockade reversal, cholinergic poisoning

75
Q

magnesium

A

may influence Na/K ATPase, NaChs, KChs, CaChs,

anti-arrhythmic effects in patients w/normal Mg levels

76
Q

uses of Mg

A

digitalis induced arrhythmias if hypomagnesemia present

TdP even in Mg normal

Cardio 2 (17 decks)

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