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Cardio > Arrhythmia overview > Flashcards

Arrhythmia overview Flashcards

1
Q

normal monocyte conduction

phase 0

A

initial, rapid depolarization of myocyte tissues; increase in Na+ influx; rapid depolarization overshoots electrical potential, brief period of repolarization

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2
Q

normal monocyte conduction

phase 1

A

transient active K+ efflux; Ca2+ influx

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3
Q

normal monocyte conduction

phase 2

A

calcium influx balanced by K+ efflux; plateau

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4
Q

normal monocyte conduction

phase 3

A

membrane permeable to K+ efflux; repolarization

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5
Q

normal monocyte conduction

phase 4

A

gradual depolarization; constant Na+ leak to intracellular space balanced K+ efflux (true resting membrane potential)

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6
Q

SA action potential

phase 0

A

depolarization is due to influx of fast Ca2+

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7
Q

SA action potential

phase 3

A

efflux of K to repolarize the cell (Ca2+ influx is halted)

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8
Q

SA action potential

phase 4

A

pacemaker current by leaking Na+, eventually leaks enough to cause cell activation

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9
Q

electrical activity initiated at

A

sinoatrial (SA) node

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10
Q

SA node

A
  • highest rate of spontaneous impulse generation

- largely influenced by ANS

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11
Q

t/f other cells outside SA node can spontaneously generate impulses

A

true but these are normally overridden by the SA node because rate of generation of impulse is lower in these cells

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12
Q

P wave

A

depolarization of atria in response to SA node triggering

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13
Q

T wave

A

ventricular repolarization

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14
Q

PR interval

A
  • atrial depolarization plus AV nodal delay of impulse

- normal is 120 to 200 msec (.12-.2 sec)

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15
Q

longer PR interval

A

heart block

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16
Q

QT interval

A
  • depolarization plus repolarization of ventricle
  • normal is 200-400 msec (0.2-0.4 sec)
  • dependent on HR
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17
Q

higher QT interval

A

greater risk of ventricular arrhythmias

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18
Q

automatic tachycardia

A
  • abnormal impulse generation

- tissues compete with SA node for cardiac rhythm dominance

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19
Q

automatic tachycardia typically occurs

A

when there is blockage at the AV node (prevents conduction from atria to ventricles) or in some bundle branch

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20
Q

do you see tachycardia or bradycardia in automatic tachycardia?

A

both

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21
Q

causes of automatic tachycardia

A
  • digitalis glycosides
  • catecholamines
  • electrolyte abnormalities (hypokalemia)
  • myocardial stretch (cardiac dilation)
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22
Q

hypokalemia and cardiac elevation lead to an increased

A

slop 4 so they recover faster than SA node cells

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23
Q

re-entrant tachycardia

A
  • abnormal pulse conduction
  • conducting pathway is stimulated prematurely by a previously conduction action potential leading to rapid cyclical reactivation
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24
Q

re-entrant tachycardia occurs when

A

the pathway branches and then rejoins at a later point. one branch conducts signal quickly, one branch has slow conduction (not fully repolarized)

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25
Q

is there an acceleration or deceleration phase in re-entrant tachycardia?

A

no. initiation and termination of tachycardia usually abrupt

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26
Q

examples of re-entrant tachycardia

A

atrial fibrillation, atrial flutter, av nodal or an reentrant tachycardia, recurrent VT

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27
Q

Vaughn Williams classification

A

drugs are classified by where they work in the action potential

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28
Q

class Ia

A

procainamide, disopyramide, quinidine

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29
Q

class Ib

A

lidocaine, mexiletine

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30
Q

class Ic

A

flecainide, propafenone

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31
Q

class II

A

beta blockers

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32
Q

class III

A

dofetilide, ibutilide, sotalol, dronedarone, amiodarone

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33
Q

class IV

A

non dhp ccbs

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34
Q

procainamide

A

procan

35
Q

procainamide used for

A

ventricular tachycardia, a fib

36
Q

procainamide SE

A

drug induced lupus; agranulocytosis; QT prolongation

37
Q

procainamide clinical pearls

A
  • active metabolite = NAPA

- monitor closely for renal disease

38
Q

lidocaine

A

xylocaine

39
Q

lidocaine uses

A

ventricular fibrillation, ventricular tachycardia

40
Q

lidocaine SE

A

hypotension and seizure at high doses

41
Q

lidocaine clinical pearls

A
  • iv only

- metabolized in the liver: reduce dose

42
Q

flecainide

A

tambacor

43
Q

flecainide uses

A

ventricular tachycardia, supraventricular tachycardia

44
Q

flecainide SE

A

new or worsened arrhythmias; heart block; QT prolongation

45
Q

flecainide interactions

A

2D6 substrate

46
Q

flecainide clinical pearls

A
  • po only
  • renal dose adjustment
  • worsens HF
47
Q

beta blockers are useful for

A
  • exercise related tachycardia or other tachycardias induced by high sympathetic tone
48
Q

beta blockers decrease

A

conduction velocity and shorten refractory period

49
Q

dofetilide

A

tikosyn

50
Q

dofetilide use

A
  • conversion of a fib to sinus rhythm

- maintenance of sinus rhythm after conversion

51
Q

dofetilide SE

A

HA; QT prolongation; bradycardia

52
Q

dofetilide interactions

A

3A4 substrate - black box warning

53
Q

dofetilide clinical pearls

A
  • renal dose adjustment

- pharmacy/MD must be registered to use

54
Q

sotalol

A

betapace

55
Q

sotalol uses

A

ventricular tachycardia, a fib, a flutter

56
Q

sotalol SE

A

QT prolongation; bradycardia; NVD; bronchospasms

57
Q

sotalol interactions

A

warning with low K and HF

58
Q

sotalol clinical pearls

A

renal dose adjustment

59
Q

dronedarone

A

multaq

60
Q

dronedarone uses

A

a fib, a flutter

61
Q

dronedarone SE

A

liver failure; QT prolongation; HF; heart block

62
Q

dronedarone interactions

A

3A4 substrate - black box warning; digoxin - decrease dose by 50%; warfarin - start at 2.5mg

63
Q

dronedarone clinical pearls

A

must stop all class I and III agents first; similar to amiodarone without iodine

64
Q

initial action of amiodarone

A

b-blockade

65
Q

predominant effect with chronic use of amiodarone

A

prolongation of repolarization

66
Q

amiodarone most commonly prescribed as

A

antiarrhythmic

67
Q

amiodarone used in

A

VT, VF, a fib, a flutter, PSVT

68
Q

amiodarone half life

A

extremely long; 15 to 100 days

69
Q

amiodarone inhibits

A

glycoprotein and most cyp-p450 enzymes

70
Q

SE with chronic use of amiodarone

A

pulmonary fibrosis, hypothyroidism, hyperthyroidism, optic neuritis/neuropathy; increased LFTs, tremors/ataxia/peripheral neuropathy; photosensitivity/ blue-gray skin discoloration

71
Q

monitoring for pulmonary fibrosis

A

chest radiograph
baseline, then every 12 months
pulmonary function tests

72
Q

monitoring for hypothyroidism and hyperthyroidism

A

thyroid functions test

baseline, then every 6 months

73
Q

monitoring optic neuritis/neuropathy

A

ophthalmologic exam

baseline, then every 12 months

74
Q

monitoring increased LFTs

A

LFTs

baseline, then every 6 months

75
Q

monitoring bradycardia/heart block

A

ECG

baseline, then every 3-6 months

76
Q

monitoring for tremors, ataxia, and peripheral neuropathy

A

history and physical examination

each office visit

77
Q

monitoring photosensitivity/blue-gray skin discoloration

A

history and physical examination

each office visit

78
Q

calcium channel blockade

A
  • slows conduction velocity

- prolongs repolarization = longer refractory period

79
Q

calcium channel blockers used for

A
  • effective for SA/AV node automatic or reentrant tachycardia
  • may slow ventricular response in supraventricular arrhythmia
80
Q

adenosine

A

adenocard

81
Q

adenosine use

A

psvt

82
Q

adenosine SE

A

flushing; chest burning; bronchospasm

83
Q

adenosine interactions

A

none, half life < 10 seconds

84
Q

adenosine clinical pearls

A
  • iv only

- asystole when given

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