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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
is there an acceleration or deceleration phase in re-entrant tachycardia?
no. initiation and termination of tachycardia usually abrupt
26
examples of re-entrant tachycardia
atrial fibrillation, atrial flutter, av nodal or an reentrant tachycardia, recurrent VT
27
Vaughn Williams classification
drugs are classified by where they work in the action potential
28
class Ia
procainamide, disopyramide, quinidine
29
class Ib
lidocaine, mexiletine
30
class Ic
flecainide, propafenone
31
class II
beta blockers
32
class III
dofetilide, ibutilide, sotalol, dronedarone, amiodarone
33
class IV
non dhp ccbs
34
procainamide
procan
35
procainamide used for
ventricular tachycardia, a fib
36
procainamide SE
drug induced lupus; agranulocytosis; QT prolongation
37
procainamide clinical pearls
- active metabolite = NAPA | - monitor closely for renal disease
38
lidocaine
xylocaine
39
lidocaine uses
ventricular fibrillation, ventricular tachycardia
40
lidocaine SE
hypotension and seizure at high doses
41
lidocaine clinical pearls
- iv only | - metabolized in the liver: reduce dose
42
flecainide
tambacor
43
flecainide uses
ventricular tachycardia, supraventricular tachycardia
44
flecainide SE
new or worsened arrhythmias; heart block; QT prolongation
45
flecainide interactions
2D6 substrate
46
flecainide clinical pearls
- po only - renal dose adjustment - worsens HF
47
beta blockers are useful for
- exercise related tachycardia or other tachycardias induced by high sympathetic tone
48
beta blockers decrease
conduction velocity and shorten refractory period
49
dofetilide
tikosyn
50
dofetilide use
- conversion of a fib to sinus rhythm | - maintenance of sinus rhythm after conversion
51
dofetilide SE
HA; QT prolongation; bradycardia
52
dofetilide interactions
3A4 substrate - black box warning
53
dofetilide clinical pearls
- renal dose adjustment | - pharmacy/MD must be registered to use
54
sotalol
betapace
55
sotalol uses
ventricular tachycardia, a fib, a flutter
56
sotalol SE
QT prolongation; bradycardia; NVD; bronchospasms
57
sotalol interactions
warning with low K and HF
58
sotalol clinical pearls
renal dose adjustment
59
dronedarone
multaq
60
dronedarone uses
a fib, a flutter
61
dronedarone SE
liver failure; QT prolongation; HF; heart block
62
dronedarone interactions
3A4 substrate - black box warning; digoxin - decrease dose by 50%; warfarin - start at 2.5mg
63
dronedarone clinical pearls
must stop all class I and III agents first; similar to amiodarone without iodine
64
initial action of amiodarone
b-blockade
65
predominant effect with chronic use of amiodarone
prolongation of repolarization
66
amiodarone most commonly prescribed as
antiarrhythmic
67
amiodarone used in
VT, VF, a fib, a flutter, PSVT
68
amiodarone half life
extremely long; 15 to 100 days
69
amiodarone inhibits
glycoprotein and most cyp-p450 enzymes
70
SE with chronic use of amiodarone
pulmonary fibrosis, hypothyroidism, hyperthyroidism, optic neuritis/neuropathy; increased LFTs, tremors/ataxia/peripheral neuropathy; photosensitivity/ blue-gray skin discoloration
71
monitoring for pulmonary fibrosis
chest radiograph baseline, then every 12 months pulmonary function tests
72
monitoring for hypothyroidism and hyperthyroidism
thyroid functions test | baseline, then every 6 months
73
monitoring optic neuritis/neuropathy
ophthalmologic exam | baseline, then every 12 months
74
monitoring increased LFTs
LFTs | baseline, then every 6 months
75
monitoring bradycardia/heart block
ECG | baseline, then every 3-6 months
76
monitoring for tremors, ataxia, and peripheral neuropathy
history and physical examination | each office visit
77
monitoring photosensitivity/blue-gray skin discoloration
history and physical examination | each office visit
78
calcium channel blockade
- slows conduction velocity | - prolongs repolarization = longer refractory period
79
calcium channel blockers used for
- effective for SA/AV node automatic or reentrant tachycardia - may slow ventricular response in supraventricular arrhythmia
80
adenosine
adenocard
81
adenosine use
psvt
82
adenosine SE
flushing; chest burning; bronchospasm
83
adenosine interactions
none, half life < 10 seconds
84
adenosine clinical pearls
- iv only | - asystole when given

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