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PMI > 11. Basic ECG > Flashcards

11. Basic ECG Flashcards

1
Q

Cardiac conduction pathway

A

SA node
internodal fascicles
bachmann’s bundle
AV node
Bundle of His
Right Bundle branch
Left bundle branch
purkinje fibers

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2
Q

where does the electrical current slow down in the heart

A

AV node

allows for atria to fully contract before the ventricles contract
maximizes ventricular filling

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3
Q

pacemaker cells

A

initiate heart beat
set heart rate

SA node
AV node

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4
Q

primary pacemaker of heart

A

SA node

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5
Q

SA node beats per min

A

60-100 bpm

sinus beats

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6
Q

AV node beats per min

A

40-60 bpm

junctional beats

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7
Q

ventricular muscle beats per min

A

30-40 bpm

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8
Q

p wave

A

atrial contraction

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9
Q

QRS

A

ventricular contraction

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10
Q

premature atrial contractions

A

heartbeats initiated by atrial myocardium

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11
Q

retrograde current is seen in

A

junctional beats initiated by AV node

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12
Q

retrograde current on ecg

A

inverted p wave

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13
Q

upright p wave

A

heartbeat originated from SA node or atria

ategrade conduction

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14
Q

inverted p wave

A

heartbeat originated from AV node

retrograde conduction

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15
Q

wide QRS

A

slow ventricular depolarization

heartbeat initiated by ventricular myocardium

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16
Q

1 large box

A

0.2 sec

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17
Q

1 small box

A

0.04 sec

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18
Q

1 second

A

5 large boxes

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19
Q

1 min

A

300 large boxes

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20
Q

RR interval

A

heart rate

300/#lg boxes

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21
Q

intervals include

A

a wave

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22
Q

normal p wave

A

3 small boxes
<0.12s

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23
Q

normal QRS

A

<0.12s
1.5-3 sm boxes

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24
Q

T wave

A

ventricular repolarization

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25
Q

normal T wave

A

<5mm height

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26
Q

U wave indicates

A

hypokalemia

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27
Q

J point

A

point where S wave returns to baseline

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28
Q

Delta wave

A

upward slurring Q wave
wollff parkinson white syndome

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29
Q

J wave

A

hypothermia

bump on S wave

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30
Q

PR interval

A

beginning of P to start of Q

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31
Q

normal PR interval

A

0.12-0.2s

3-5 sm boxes

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32
Q

long PR interval

A

indicates delayed conduction in AV node

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33
Q

QT interval

A

begining of Q wave to end of T wave

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34
Q

what prolongs QT interval

A

zofran
phenergan
subarachnoid hemorrhage

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35
Q

PR segment

A

end of P wave to beginning of Q wave

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36
Q

ST segment

A

J point to start of T wave

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37
Q

premature beat

A

heartbeats happens before expected
“fast”

PAC
PVC
PJC

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38
Q

escape beat

A

heartbeat that comes oafter long pause
“slow”

ventricular
junctional

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39
Q

systole

A

heart contraction
heart is not perfusing
organs are perfused

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40
Q

diastole

A

heart relaxation
heart is perfused
organs are not perfused

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41
Q

slower heart rate

A

increases coronary perfusion

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42
Q

faster heart rate

A

worse coronary perfusion

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43
Q

ventricular filling

A

amount of blood that fills the ventricles prior to ventricular contraction
preload

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44
Q

decrease ventricular filling

A

decreased SV
decreases CO

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45
Q

active ventricular filling

A

during atrial contraction
incr preload
normal SV
normal CO

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46
Q

passive ventricular filling

A

when atria dont contract
decr preload
decr SV
decr CO

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47
Q

heart conditions that reduce ventricular filling

A
  1. heartbeat w/o atrial contraction (no p wave)
  2. premature heartbeat
  3. rapid heart rate
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48
Q

do premature heartbeats produce a pulse

A

no

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49
Q

ECG leads detect

A

electrical difference (voltage) between 2 limbs

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50
Q

3 lead ECG limitation

A

not as sensitive for detecting myocardial ischemia occuring in left ventricle

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51
Q

lead 1

A

white to black
(-): RA
(+): LA

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52
Q

lead 2

A

white to red
(-): RA
(+): LL

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53
Q

lead 3

A

black to red
(-): LA
(+): LL

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54
Q

what additional leads are in 5 lead ECG?

A

green
brown (V5)

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55
Q

green lead

A

neutral grounding lead

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56
Q

brown lead

A

V5
precordial lead
helps detect left ventricular ischemia

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57
Q

lead locations

A

white - right
green - below green
black - left
brown - below black
red - below brown

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58
Q

how to get best ECG connection

A

cleanse site of application w/alcohol
exfoliate skin layer
avoid placing over hair

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59
Q

irregular sinus

A

HR fluctuating w/inspiration and expiration

inspiration: faster
expiration: slower

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60
Q

why is inspriation HR faster

A

decrease intrathoracic pressure
increases preload
increases HR

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61
Q

why is expiration HR slower

A

increase intrathoracic pressure
decreases preload
decreases HR

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62
Q

sinus tachy

A

P wave
HR>100 bpm

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63
Q

sinus tachy etilogies

A

hypovolemia
hypotension
pain/light anesthesia

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64
Q

sinus tachycardia causes

A

incr cardiac O2 demand
decr cardiac O2 supply
hypovolemia

65
Q

sinus tachy treatment

A

give fluids
deepen anesthetic
beta blocker

66
Q

sinus brady

A

p wave
HR <60bpm

67
Q

sinus brady is good for what pts

A

healthy pts who exercise
pts w/CAD

68
Q

lower HR

A

incr O2 supply
decr O2 demand

69
Q

bradycardia is bad in what pt population

A

kids

70
Q

what heart rate is always a cause for concern

A

<=30bpm

71
Q

bradycardia treatment

A

robinul
atropine
epinephrine
cardiac pacing (unresponsive to meds)

72
Q

temporary transcutaneous pacing

A

SA node pacing pads via defibrillator

73
Q

pacemaker

A

implantable device to act as artificial SA node

74
Q

ectopy

A

any heartbeat that orginates outside the SA node

  • AV node
  • atrial myocardiaum
  • ventricular myocardium
75
Q

PAC

A

premature beat
upright p wave
normal/narrow QRS

76
Q

when are PACs concerning

A

when they start occuring frequently

77
Q

PJC

A

premature beat
missing/inverted p wave
normal QRS

retrograde

78
Q

when are PJCs concerning

A

when they start occuring frequently

79
Q

PVC

A

premature beat
no p wave
wide/bizarre/different QRS

80
Q

what can trigger PVC

A

ischemia
pH imbalance
electrolyte abnormalities
caffeine
stress
abnormal electrical pathways

81
Q

do PVCs produce a pulse

A

no

82
Q

what is the pulse rate for bigeminal PVCs

A

half of what the ECG says the pulse rate is

83
Q

bigeminal PVC

A

every other beat

84
Q

unifocal PVC

A

same shape = same origin

85
Q

multifocal PVC

A

different shape = different origin

86
Q

what is more concerning: unifocal or multifocal PVC?

A

multifocal

87
Q

couplet PVC

A

2 in a row

88
Q

salvo PVC

A

3 in a row

89
Q

PVC treatment

A

antiarrythmics
- lidocaine (100mg)
- amiodarone
robinul (speed HR up)

90
Q

junctional escape beat

A

escape beat
inverted/missing p wave
normal QRS

91
Q

junctional escape beat physiology

A

SA node failed
AV node starts heartbeat
SA node starts working again

92
Q

when should we be concerned w/junctional escape beats

A

if they occur frequently

treat w/robinul/atropine/pacing

93
Q

junctional escape beat treatment

A

robinul/atropine
pacing

94
Q

ventricular escape beat

A

long pause
wide QRS
no p wave

95
Q

ventricular escape beat physiology

A

SA and AV node fail
ventricular myocardium initiates beat
SA node works again

96
Q

atrial flutter

A

sawtooth p waves (250-350/min)
wide p waves

97
Q

atrial flutter physiology

A

decr ventricular filling
decr CO
incr O2 demand

98
Q

when are we concerned about atrial flutter

A

would not do an elective case until pt has been evaluated by a cardiologist

99
Q

type 1 atrial flutter

A

<350bpm

100
Q

type 2 atrial flutter

A

> 350bpm

101
Q

atrial flutter treatment

A

amiodarone, sotalol, digoxin
synchronized cardioversion (for hypotensive pts)

102
Q

shocking heart

A

treats unstable fast rhythms

103
Q

pacing heart

A

treats unstable slow rhythms

104
Q

Afib

A

no p waves
narrow QRS
may or may not have fibrillation waves
irregularly irregular rhythm

105
Q

Afib physilogy

A

atria quivering w/500 atrial impulses/min

106
Q

Afib risks

A

clot formation in LA (blood pooling)
CO decr
hypotension

107
Q

Afib CO decreases by

A

25-50%

108
Q

what type of afib is more concerning: chronic or acute?

A

acute afib is more concerning
suffer significant drop in CO

109
Q

controlled afib

A

ventricular rate <100bpm

110
Q

uncontrolled afib

A

ventricular rate >100bpm\
rapid ventricular response

111
Q

afib treatment

A

medications
synchronized cardioversion

112
Q

how long should a pt be anticoagulated prior to cardioversion

A

3 weeks prior
4 week post

113
Q

junctional rhythm

A

inverted/absent P
normal QRS

114
Q

normal junction

A

40-60bpm

115
Q

accelerated junctional

A

60-100 bpm

116
Q

junctional tachycardia

A

> 100bpm

117
Q

junctional rhythm concerns

A

slower HR
reduced ventricular filling

118
Q

junctional rhythm treatment

A

robinul to incr HR

119
Q

SVT

A

HR >150bpm
normal QRS
may or may not have P waves

120
Q

SVT concerns

A

decr ventricular filling
decr CO

121
Q

SVT treatment

A

vagal maneuvers
adenosine (slows SA/AV)
synchronized csrdioversion
antiarrythmics

122
Q

ventricular escape rhythm (idoventricular)

A

no p wave
wide WRS
slow HR <60bpm

123
Q

ventricular escape physiology

A

SA and AV node failed
ventricular myocardium is beating

124
Q

ventricular escape concerns

A

no active ventricular filling
HR is low
low CO

125
Q

ventricular escape treatment

A

cardiac pacing
epinephrine

avoid lidocaine (suppresses ventricular beat)

126
Q

accelerates idivoentricular rhythm

A

60-100bm

127
Q

Vtach

A

> 100bpm
no p waves
wide QRS (same shape)

128
Q

polymorphic Vtach

A

torsades de pointes
twisting

129
Q

Vtach physiology

A

ventricular myocardium initiates heart beat at rapid rate
high O2 consumption
minimal ventricular filling

130
Q

does vtach have a pulse?

A

potentially

131
Q

Vtach treatment

A

electrical cardioversion

132
Q

monomorphic vtach treatment

A

amiodarone
lidocaine

133
Q

polymorphic vtach

A

magnesium

134
Q

amiodarone does what to QT interval

A

prolongs it

135
Q

Vfib

A

no real p waves or QRS complexes
shorter deflections

136
Q

Vfib physiology

A

quivering ventricles
rapid rate
high O2 consumption
no pulse
no CO

137
Q

Vfib treatment

A

defibrillation
CPR

138
Q

agonal rhythm

A

slow complex rhythm immediately preceding asystole

139
Q

do agonal rhythms produce cardiac output

A

nope

140
Q

asystole

A

cardiac arrest
CPR
epinephrine
do not defibrilate

141
Q

pulseless electrical activity (PEA)

A

pt has no pulse
ECG shows electrical activity

142
Q

PEA is most likely seen with what rhythms

A

sinus
bradycardish
ventricularish
AV blockish
slowish type

143
Q

cause of PEA

A

heart does not contract
insufficient cardiac output to generate pulse and supply blood to organs

144
Q

PEA treatment

A

CPR
epinephrine

NO defibrillation

145
Q

1st Deg AV block

A

long PR interval
>200msec (1 lg box)

146
Q

2d Deg AV block

A

dropped QRS complex

147
Q

2d Deg AV Type 1

A

dropped QRS
increasingly long PR intervals

148
Q

2d Deg AV Type 2

A

dropped QRS
unchanging PR intervals

149
Q

where is the block in 2d deg type 2

A

below the AV node
in bundle of his or bundle branches

150
Q

3d deg AV block

A

wandering P waves
slow ventricular rate

151
Q

3d deg AV block physiology

A

AV node completely blocekd
ventricles must initiate heart beat
atria and ventricals are not synchronized

decreased CO

152
Q

treatment for complete heart block

A

cardiac pacing
epinephrine

AVOID lidocaine

153
Q

pacemaker atrial lead

A

sense when atria is contracting

154
Q

pacemaker ventricular lead

A

paces 120-200msec after each atrial beat

155
Q

Ischemia/Infarction ECG indications

A

ST segment changes
abnormal T waves
abnormal Q waves

156
Q

ST depression indicates

A

ischemia

157
Q

ST elevation indicates

A

infarction

158
Q

myocardial ischemia treatment: increase O2 supply

A
  1. 100% FiO2
  2. decrease HR
    –give beta blockers
  3. mx normal BP
    —avoid hypotension
  4. give NTG
  5. give aspirin
159
Q

myocardial ischemia treatment: decrease O2 demand

A
  1. decr HR
    –give beta blockers
  2. avoid pain/anxiety/tachycardia
    –give narcs/sedatives
  3. avoid high afterload
    –avoid HTN

PMI (18 decks)

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