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IM 7 Test 1 > Cardiac Rhythm Analysis > Flashcards

Cardiac Rhythm Analysis Flashcards

1
Q

automaticity

A

ability to initiate impulse spontaneously and continuously

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2
Q

excitability

A

ability to be electrically stomulated

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3
Q

conductivity

A

ability to transmit impulses along a membrane in an orderly manner

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4
Q

contractility

A

the mechanical response to an impulse

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5
Q

SA node

A

where the beat starts (P wave)

pacemaker of the heart

60-100 bpm normally

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6
Q

AV node

A

fires 40-60 bpm normally

escape beat

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7
Q

parasympathetic nervous system effect on SA node

A

decreases rate

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8
Q

sympathetic nervous system effect on SA node

A

increases rate

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9
Q

dysrhythmias

A

disorder of impulse formation, conduction of impulses or both

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10
Q

P wave

A

depolarization of the atria

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11
Q

QRS complex

A

depolarization of the ventricles

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12
Q

T wave

A

repolarization of the whole heart

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13
Q

artifact

A

electrodes are not secre, muscle interference or electrical interference

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14
Q

How fast is normal sinus

A

60-100 BPM

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15
Q

where does normal sinus start

A

SA node and follows normal conduction pathways

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16
Q

when can sinus brady be normal

A

aerobically trained athletes and during sleep

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17
Q

what nervous system contributes to sinus brady

A

parasympathetic

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18
Q

S/s sinus brady X7

A 
hypotension
pale, cool skin
weakness
angina
dizziness or syncope
confusion or disorientation
SOB
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19
Q

sinus brady tx X3

A

atropine
pacemaker
stopping offending drugs

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20
Q

atropine class

A

anticholinergic

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21
Q

atropine MOA

A

raises HR

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22
Q

how much atropine can you give without an order

A

max of 3 mg titrating up from 0.5

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23
Q

what class of drugs can cause sinus brady

A

beta blockers

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24
Q

how fast is sinus tachy

A

101-200 bpm

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25
Q

what causes sinus tachy X3

A

vagal inhibition
sympathetic stimulation
drugs

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26
Q

sinus tachy s/s X6

A 
dizziness
dyspnea
hypotension
angina r/t CAD
diaphoresis
SOB
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27
Q

sinus tachy treatment X3

A

treat by cause
vagal maneuver
beta blockers

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28
Q

SVT HR

A

150-220 bpm

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29
Q

what is SVT assosicated with X7

A 
overexertion
stress
deep inspiration
stimulants
disease
dig toxicity
30
Q

what does SVT over 180 lead to

A

decreased cardiac output and stroke volume

31
Q

SVT s/s 4

A

hypotension
dyspnea
angina
chest pain

WILL BE SYMPTOMATIC

32
Q

SVT Tx X6

A 
vagal stimulation
Adenosine
beta blockers
ca channel blockers
amiodarone
cardioversion
33
Q

IV adenosine half life

A

10 seconds

34
Q

adenosine admin rate

A

1-2 second fast push followed immediately by fast 20 mL flush

35
Q

adenosine dosage

A

6 mg first dose

12 mg second dose

36
Q

a fib treatment X6

A 
amiodarone
ibutilide
cardioversion
anticoag
ablation
maxe procedure
37
Q

what does a flutter increase the risk of

A

stroke

38
Q

a flutter tx X3

A

drugs
cardioversion
ablation

39
Q

what are PVC’s associated with X4

A

stimulants
electrolyte imbalances
hypoxia
heart disease

40
Q

are PVC’s harmful

A

not in normal heart

41
Q

PVC tx X2

A

correct cause

antidysrhythmics

42
Q

V tach rate

A

150-200 BPM

43
Q

why is v tach bad

A

life threatening d/t decreased CO and possibility of moving to v fib

44
Q

torsades de points

A

v tach with different sized waves

45
Q

what is v tach associated with X4

A

heart disease
electrolyte imbalances
drugs
CNS disorder

46
Q

V tach symptoms X4

A

hypotension
pulmonary edema
decreased cerebral blood flow
cardiopulmonary arrest

47
Q

stable v tach tx X2

A

antidysrhythmics

cardioversion

48
Q

unstable v tach tx X2

A

CPR

rapid defibrillation

49
Q

what is v fib associated with X5

A 
MI
ischemia
disease
procedures
electrolyte imbalances
50
Q

v fib s/sx X3

A

unresponsive
pulseless
apneic

51
Q

v fib tx X3

A

CPR
defibrillation
ACLS drug protocol

52
Q

asystole s/sx X3

A

unresponsive
pulseless
apneic

53
Q

what is asystole the result of X3

A

cardiac disease
severe conduction disturbance
end-stage HF

54
Q

asystole tx X3

A

CPR
ACLS drug protocol
Intubation

55
Q

pulseless electrical activity

A

electrical activity is observed on the EKG

56
Q

PEA causes (H’s and T’s

A 
Hypovolemia
Hypoxia
Hydrogen ion (acidotic)
Hyper/hypo kalemia
Hypoglycemia
Hypothermia
Toxins
Tamponade
Thrombosis
Tension pneumothorax
Trauma
57
Q

PEA tx X4

A

CPR
intubation
ACLS

fix underlying cause

58
Q

1st degree Heart block s/sx

A

not symptomatic

59
Q

1st degree heart block tx

A

no tx

60
Q

third degree heart block tx X2

A

pacemaker

drugs to increase HR

61
Q

when is ST elevation significant

A

if 1 mm over the isoelectric line

62
Q

initial biphasic defibrillation

A

120-200 Joules

63
Q

initial monophasic defibrillation

A

360 joules

64
Q

when does CPR begin with defibrillation

A

immediately after

65
Q

where shoul dyou never put defibrillator pads

A

over a pacemaker or implantable cardioverter/defibrillator

66
Q

what is cardioversion ideal for X2

A

stable v tach

SVT

67
Q

what is cardioversion

A

shock is given on the R wave

68
Q

initial biphasic cardioversion

A

70-75 joules

69
Q

initial monophasic cardioversion

A

100 joules

70
Q

what do you do if patient goes pulseless during cardioversoin

A

turn sync button off and defibrillate

IM 7 Test 1 (5 decks)

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