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Pharm II > anti arrhythmic > Flashcards

anti arrhythmic Flashcards

1
Q

two gradients that influence energy requiring pumps

A

130-140 Na (high outside)

3.5-5 K

gradient

also creates electrical differential

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2
Q

two types of gates in the sodium channel

A

activation M

and inactivation h

inactivation contributes to the early repolorization of phase 1

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3
Q

inactivation gate is closed at what resting potential

A

-75– -55
but the activation gates are opened

this is important because during the activation

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4
Q

which nodes are more Ca dependent

A

SA and AV
more Ca dependent because of funny channel

no the non-dihydropyridine work here

(CLASS IV)

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5
Q

CLASS I arrhythmicss are

A

Na channel blockers

characterized by their ability to block these entry potins into the cell during depolarization

and decrease the rise of phase 0

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6
Q

no phase 1 or 2 in what AP

A

OF the pacemaker cells

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7
Q

how do cardiac muscle cells differ

A

resting membrane potential is at -90 due to constant leak of K

Na rushese in causing rapid depolarization

then K channels open (voltage gated)
leading to small dip that is phase 1

positive K ions leave and Ca go in
cause plateau of phase 2

then rapid depolarization of phase 3 of K leaving

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8
Q

abnormal automaticity

A

increased permeability to Na in phase 4

triggered activity
normal leakage of Ca ions that causes after dopolorization

and

rentry

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9
Q

This class of drugs slow the rate of rise of phase 0 and prolong the effective refractory period of the ventricle

A

Class 1a

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10
Q

these drugs shorten action potential duration and refractory period of purkinje fibers

A

1B

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11
Q

IC drugs work by

A

having the greates effect on the early depolarization and have less of an effect on the refractory period of ventricle

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12
Q

Class 1A 1B and 1C drugs

A

Class IA = Disopyramide, Quinidine, and Procainamide

Class IB = Lidocaine and Mexiletine

Class IC = Flecainide and Propafenone

Double Quarter Pounder
Lettece Mayo
Fries Please

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13
Q

class II drugs

A

LOL

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14
Q

class III drugs

A 
AIDS
A = amiodarone
 I = ibutilide
 D = dofetilide
 S = Sotalol
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15
Q

Class IV

A

• Class IV Antiarrhythmics are the

calcium channel blockers verapamil and diltiazem.

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16
Q

hyperkalemia effects

A

increases in serum K can depolarize the resting membrane potential

can inactivate Na channels resulting in increased refractory period duration and slowed impulse propagation

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17
Q

elevated potassium

A

slows a pacemaker

euthanasia
high doses dead

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18
Q

hypokalemia

A

make a pacemaker worse

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19
Q

inactivation gates close

A

-75 and -55
-55
and stimulation will have less Na here

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20
Q

what exacerbates arrhythmia

A 
ischemia
hypoxia
acidosis
electrolyte abnormalities 
excessive catecholamine
drug toxicity 
overstretching of cardiac tissue
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21
Q

MOA of procaniamide

A

blocks Na
prolongs QRS
increases refractory period
slow upstroke

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22
Q

procainamide can only be given ___ for

A

IV
WBW
VT

Afibb with others to slow HR

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23
Q

these drugs are used for rate control

A

digoxin
BB
CCB

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24
Q

when we talk about rhythm control

A

we are talking about turning quivering into normal depolarization

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25
Q

why can’t you use CCB with HFrEF

A

increase contractility

can only use BB or digoxin

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26
Q

anticholinergic effect of 1a is concerning

A

because it can increase the rate

has vagolytic effects

this is why they need to be used in conjunction with rate control

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27
Q

AE of procainamide

A 
hypotension 
lupus like 
depression
agranulocytosis 
PROLONGS QT
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28
Q

quinidine SE

A

tinnitius

HA

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29
Q

disopyramide ADE

A

very strong anticholinergic effects can cause sxs like urinary retention

can worsen HF

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30
Q

lidocaine is used for these three events

A

VENTRICULAR ARRHYTHMIAS ONLY:

PVC VT VF

or post MI

binds to both activated and inactivated
greater suppression in the tissues and long acting

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31
Q

need to reduce lidocaine in

A

liver failure and HF

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32
Q

lidocaine SE

A

seizures

CNS effects: drowsiness or aggitation

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33
Q

mexiletine is used

A

orally instead of topically or IV like lidocaine

more GI

34
Q

propafenone SE

A

also has some BB effect so you need to be worried about bronchospasms

CAN’T USE IN HF

35
Q

main effect of amiodarone

A

increasing APD (prolongs re-polorization through Na channel blockade)

BB and
Ca channel blockade so can be used for rate and rhythm

36
Q

what do we need to monitor with amiodarone

A

TSH can cause hypo hyperthyriod
CXR: pulmonary fibrosis
hepatotox: LFTs

37
Q

like procainamide (except no ganglion blockade

A

quinidine

38
Q

SE of quinidine

A 
•cinchonism: HA, vertigo, tinnitus (can decrease hearing)
altered color >5mcg
•hypotension
•hypersensitivity, diarrhea, nausea
•Prolongs QT (Torsades risk)
39
Q

quinidine adjustments needed with

A

Liver (80%) and renal. Reduce dose renal failure, liver dysfunction, HF.

40
Q
  • shortens AP, shortens refractory period
  • blocks activated and inactivated Na channels w/ rapid kinetics (the inactivated Na channel block ensures greater effect on Purkinje cells)
A

lidocaine

41
Q

Active ventric AR only. Can use in HF but high dose may cause hypotension.

A

lidocaine

42
Q

need normal heart inorder to take these medications

A

1C

think baby needs normal heart

43
Q

how to BB (propanolol, atenolol, metoprolol) Work to slow HR

A

decrease phase 4 and increase PR

44
Q

why can BB cause AV block

A

prolonged PR

45
Q

SE of BB

A

bronchospasm, masks hypoglycemia in DM

46
Q

when would you use a BB

A

rate control afib
SVT ST OF VT

Post MI!!!!
post-op afib rate control

47
Q

why can’t you use propafenone in HF

A

negative inotropic effect will increase mortality in pts who have HF or MI

48
Q

propafenone DDI

A

DI ritonovir and digoxin

as well as other drugs that prolong QT

49
Q

IV BB that is short acting

A

esmolol

50
Q

amidarone PK

A

good oral absorption

binds to a lot of tissues absorption is anywhere from 22-86%
gigantic Vd

1/2life is 40-113 days

steady state 200 days

51
Q

most troubling SE of amiodarone

A

pulmonary fibrosis and inflammation

will start with cough and shortness of breath

need CXR at baseline

52
Q

other than pulmonary fibrosis what do we worry about SE wise with amiodarone

A

photosens, blue-grey skin (permanent)

  • corneal microdeposits (halos around lights at night)
  • hypo/er thyroid: monitor TSHq6mos. HAS IODINE
  • hepatotoxic: monitor LFTs q6mos (dc or dec dose if LFTs 3x ULN or 2x baseline). Risk of fulminant liver failure.
  • pulm inflamm and fibrosis: do CXR and PFTs d6mos. Inquire about any new cough/dyspnea. Mortality 10%. May need steroids
  • Severe brady (CCB and BB effect)
  • Exacerbation ventricular ar (not as common as Class I agents)
  • Hypotension, phlebitis (IV >3mg/mL)

neurological: paresthesias, tremor, ataxia, HA

53
Q

DDI withamiodarone

A

increase dig levels
warfarin: need to reduce dose
increased risk of torsades with other prolonged QT: phenothiazines, FQ

ritonavir: large increases in serum amiodarone concentrations

54
Q

how often do you need to check LFTs for amiodarone

A

every 6 months

don’t forget to check TSH too

55
Q

dronedarone used

A

limited nonpermanent afib and flutter as well as rhythm control in structural heart dz

does not help with permanent HF or afib

56
Q

SE of dronedarone

A

similar to amiodarone but with less risls

still prolongs QTs brady arrhythmias

57
Q

Betablocker with class III properties

A

sotolol

58
Q

Sotolol compare anc contrast to regular BB as far as SE go

A

pro arrythmic effect but ortherwise same SE

will lower bP

59
Q

ibutilide is different that the other class III

A

does not affect K

60
Q

ibutilide would be seen

A

in hosp

61
Q

dofetilide mOA

A

block k current

conversion and maintenance of NSR

62
Q

dofetilide

A

HA main one can also be seen with dyspnea

63
Q

can use this K blocking drug in HF

A

doetilide

64
Q

You can not use these antiarrythmics in HF

A

disopyramide (1a)

properafone (Ia)
flecainaid (Ia)

dronedarone (III)
sotalol (III)

Verapamil (IV)
dilitiazem (IV)

65
Q

which class III can you use in HF

A

amiodarone
dofetilide

maybe ibutilide but that is used in the hospital

66
Q

adenosine receptors are in the

A

AV node

67
Q

digoxin works by

A

inhibiting Na/k pump

positive inotrope

68
Q

adenosine use

A

emergency rate controls
SVT reentry

not good for converting afibb or a flutter

SUPER SHORT HALF LIFE

69
Q

adenosine AE

A

facial flushing
SOB

can mimic angina

70
Q

Mg is used for

A

torssades and digoxin arrythmias

71
Q

Vasopressin

A

potent vasoconstrictor

72
Q

atropine

A

anticholinergic so it is used for bradycardia

73
Q

dopamine

A

can increase HR and positive inotropic effect

74
Q

isoproterenol

A

B1 and B2 agonist may cause tachycardia

75
Q

POST MI these two drugs have been shown to reduce arrhythmic death and improve survival

A

amiodarone and BB

76
Q

HF seen as sudden cardiac arrest or sustain VT is best treated with

A

ICD
amiodarone
sotalol or mexilitine

77
Q

AFIBB Rate control tx

A

for most casses can use BB or CCB except in LV dysfunction or HF
then use BB or dig
“][p-09

78
Q

negative inotropic

A

1c AND SOTALOL

79
Q

which classes are proarrythmis

A

1B
1c
III

80
Q

which drugs are CI in ptrs w/ prolonged QT

A

phase 3

Pharm II (16 decks)

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