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LANCE > Basic ECG > Flashcards

Basic ECG Flashcards

1
Q

pacemaker cell

A

determine heart rate and initiate heart beats

SA and AV

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2
Q

electrical conducting cell

A

deliver the impulse to the myocardial cells

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3
Q

mycardial cells

A

contract and pump blood out of the heart

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4
Q

SA node

A

primary pacemaker of the heart (sets HR)

60-100 bpm

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5
Q

AV node

A

becomes the pacemaker if for some reason the SA node fails

AV node rate= 40-60bpm

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6
Q

narrow QRS complex means what for conduction

A

rapid conduction

normal pathway of conductance

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7
Q

do electrical conducting cells transmit current slow or fast?

A

quickly

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8
Q

What is the electrical conducting cells pathway? (6)

A 
SA node
anterior, posterior, middle fascicles
AVN
Bundle of His
RBB and LBB
Purkinje fibers
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9
Q

myocardial cells can initiate heat beats in what two situations?

A

1- SA and AV nodes fail

2- myocardium is irritated

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10
Q

what causes the myocardium to become irritated?

A

ischemia
electrolyte abnormality
acidosis
caffine

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11
Q

Do myocardial cells or electrical conducting cells transmit current quickly and more effectively?

A

electrical conducting cells

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12
Q

Wide QRS complex means what for conductance

A

slow conductance

current travels through the muscle, not normal pathway

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13
Q

what do ECG leads detect?

A

the electrical difference (voltage) between two limbs

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14
Q

Lead I provides a picture from what angle?

A

180 degrees

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15
Q

lead II provides a picture from what angle?

A

60 degrees

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16
Q

Where are the leads on a 3 lead ecg?

A

right arm, left arm, left leg

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17
Q

what is the limitation for the 3 lead system?

A

not as sensitive for detecting myocardial ischemia in the left ventricle

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18
Q

What does Lead I detect? What is the color-to-color for Lead I?

A

detects electrical difference between the right arm (-) and left arm (+)
white to black

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19
Q

What does Lead II detect? What is the color-to-color for Lead II?

A

electrical difference between right arm (-) and left leg (+)

white to red

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20
Q

What does Lead III detect? What is the color-to-color for Lead III?

A

electrical difference between the left arm (-) and left leg (+)
black to red

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21
Q

The green lead

A

neutral or ground lead

completes electrical circuit and doesn’t have anything to do with the EKG itself

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22
Q

brown lead

A

additional precordial lead

more sensitive for detecting LV ischemia

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23
Q

what helps make higher quality signal for the ECG electrodes

A

better connection
conductive gel on electrode
can clean skin
try not to place on hair

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24
Q

ECG paper 1mV= ___ small boxes?

A

10small boxes

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25
Q

ECG paper 1 large box

A

200msec

5mm

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26
Q

1 small box= ____ mseconds

A

40 msec

1mm

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27
Q

5 large boxes

A

1 second

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28
Q

300 large boxes

A

1 min

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29
Q

two ways to estimate the HR?

A
  • count number of beats within a certain number of time (2 sec or 6 sec) and multiply to get number of beats in minute
  • count # large boxes between beats
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30
Q

do segments or intervals of the ECG have waves?

A

intervals

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31
Q

P wave

A

atrial depolarization

duration <120msec (3 small boxes)

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32
Q

QRS complex

A

ventricular depolarization

duration <120msec (3 small boxes)

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33
Q

premature ventricular contractions are causes by what?

A

if the heart gets irritated and the ventricles start their own heart beat

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34
Q

ventricular escape rhythm

A

electrical conductance fails and ventricles take over as pacemaker

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35
Q

potential cause for wide QRS complex (not irritation or electrical failure)

A

current travels across myocardium instead of through purkinje fibers

Wolf Parkinson White Syndrome (WPW)
Right bundle branch block (RBBB)
Left bundle branch block (LBBB)

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36
Q

T wave

A

ventricular repolarization

height <5mm in leads I,II,III

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37
Q

U wave

A

follows t wave

not seen unless hypokalemia

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38
Q

J point

A

point at which S wave returns to baseline

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39
Q

Delta wave

A

upward slurring of Q wave seen in WPW syndrome

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40
Q

J wave (osborne wave)

A

“bump” on the S wave

seen in hypothermia

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41
Q

PR interval start

A

beginning of p wave

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42
Q

PR interval end

A

start of Q wave

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43
Q

PR interval normal time

A

120-200msec (3-5 small boxes)

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44
Q

Why is the PR interval time important?

A

shows conduction is delayed in the AV node and allows atria to finish contract before ventricles contract
OPTIMAL VENTRICLE FILLING

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45
Q

QT interval start

A

q wave

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46
Q

QT interval end

A

end of the t wave

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47
Q

What medications prolong the QT interval? When should these be avoided?

A

Zofran and Phenergan (antiemetics)

avoided in pts with prolonged QT syndrome

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48
Q

PR segment start

A

end of p wave

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49
Q

PR segment end

A

beginning of Q wave

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50
Q

ST segment start

A

J point

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51
Q

ST segment end

A

start of T wave

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52
Q

premature beat

A

heart beat that happens before it is expected to

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53
Q

examples of premature beats

A

premature atrial contraction
premature junctional contraction
premature ventricular contractions

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54
Q

escape beat

A

heart beat that comes after a long pause

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55
Q

examples of escape beats

A

ventricular escape beat

junctional escape beat

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56
Q

during systole what is and is not perfused?

A

Perfused: organs of the body

Not perfused: the heart (coronary arteries are closed by valve)

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57
Q

During diastole what is and is not perfused?

A

Perfused: the heart (coronary arteries drain blood from backflow)
Not perfused: everything else

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58
Q

Do patients with high or low heart rates have better coronary perfusion? why?

A

slower HR

  • longer time coronary arteries open
  • greater diastolic filling time
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59
Q

What is cardiac output determined by?

A

ventricular filling prior to contraction

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60
Q

What are the two ways that ventricular filling occurs and which is better?

A 
active filling (atria contract)** BETTER
passive filling (atria dont contract)
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61
Q

If the ventricular filling is passive will the volume be lower or higher than active filling?

A

lower

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62
Q

factors that can reduce ventricular filling (3)

A

1- heart beat that occurs without an atrial contraction (no P wave; passive)
2- premature heart beats (ventricles contract before being filled)
3- rapid HR (atrial or ventricular)

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63
Q

what happens when atria contract too quickly?

A

not enough time to fulling contract so reduces amount of blood forced to ventricles

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64
Q

What happens when ventricles contract too quickly?

A

dont have enough time to fill before contraction

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65
Q

Rapid heart rate leads to (3)

A

decreased cardiac output
hypotension
pulseless pt

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66
Q

ECG description of sinus bradycardia

A

p wave present

HR <60bpm

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67
Q

benefits of sinus bradycardia

A

normal/good for these patients:
healthy pt who exercises
CAD patients

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68
Q

sinus brady cardia in healthy patients

A

higher stroke volume

maintains adequate cardiac output

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69
Q

sinus brady cardia in patients with CAD

A

increased oxygen supply (diastolic filling)

decreased oxygen demand

70
Q

What do patients with CAD normally take to maintain a slow HR?

A

beta blockers

71
Q

what does the level of concern with sinus bradycardia depend on? (3)

A

1- age (children very bad)
2- severity (50 could be normal; 30 always concern)
3- how fast the drop in HR occured

72
Q

treatment for bradycardia

A

1- drugs (glyco, atropine, epi)

2- if unresponsive to drugs then initiate cardiac pacing with pacemaker

73
Q

temporary transcutaneous pacing

A

use defibrillator to pace the heart

set a HR and it will stimulate at that pace

74
Q

permanent implantable pacemaker

A

permanent, under clavicle, delivers current to the pacing wires that are inside the heart
only works when the HR falls below a certain point

75
Q

ECG description of sinus tachycardia

A

P wave present

HR > 100 bpm

76
Q

etiology (causes) of sinus tachycardia

A

hypovolemia/hypotension

pain/light anesthesia

77
Q

anesthetic concerns with sinus tachycardia (3)

A

increased cardiac oxygen demand (bad in CAD)
decreased cardiac oxygen supply (decreases diastolic filling; bad CAD)
indicates possible hypovolemia

78
Q

treatment for sinus tachycardia

A

depends on cause:
1- fluids if bc hypovolemia
2- deepen anesthetic if light
3- consider beta blocker if not hypovolemic or light

79
Q

ECG description of irregular sinus rhythm

A

looks like sinus but rate is irregular
faster during inspiration
slower during expiration

80
Q

during spontaneous inspiration what happens to the intrathoracic pressure and preload

A

intrathoracic pressure decreases
preload increase
HR speeds up to pump excess out

81
Q

during spontaneous expiration what happens to the intrathoracic pressure and preload?

A

intrathoracic pressure increases
preload decreases
HR slows does bc it doesnt have to pump out as fast

82
Q

anesthetic concerns with irregular sinus rhythm

A

not as concerned

seen in healthy pts with deep breaths

83
Q

ectopy

A

any heart beat that originates outside the SA node

84
Q

ectopy is activated where? (3)

A

AV node
atrial myocardium
ventricular myocardium

85
Q

Supraventricular ectopy (6)

A 
premature atrial contraction (PAC)
atrial flutter
atrial fibrillation (Afib)
Premature junctional contraction (PJC)
Junctional rhythm
junctional escape beat
86
Q

ventricular ectopy (5)

A 
premature ventricular contraction (PVC)
escape ventricular contraction
ventricular escape (idioventricular) rhythm
ventricular tachycardia (Vtach)
ventricular fibrillation (Vfib)
87
Q

Premature Atrial Contraction (PAC) ECG

A

premature beat has:
upright p wave
normal/narrow QRS complex

88
Q

physiology of PAC

A

artrial myocardium node got irritated and initiated a beat without signal from SA node

89
Q

Anesthetic concerns with PACs

A

depends on the frequency

associated with less ventricular filling and will cause problems if they happen often

90
Q

Atrial flutter ECG

A

saw tooth pattern ~250-300 P waves/min

more p waves than QRS complexes

91
Q

physiology of atrial flutter

A

atrial myocardium contracts regularly ~250-300 times/min
decreased ventricular filling
AV node blocks some signals thus ventricular rate is much slower

92
Q

anesthetic concerns with atrial flutter

A

ventricular filling and CO decreased
heart has higher oxygen metabolism
NO ELECTIVE SURGERIES

93
Q

treatment for atrial flutter

A

medications (digoxin, amiodarone)

unstable then use synchronized cardioversion

94
Q

what does sychronized cardioversion treat?

A

“shocking” the heart (cardioversion or defibrillation) treats unstably fast rhythms

95
Q

what does pacing treat?

A

unstably slow rhythms

96
Q

fibrillate definition

A

quiver rapidly

97
Q

Atrial fibrillation (afib)

A

electrical impulses originate from irregular spots in the atrium and radiate through the atrium walls in an uncoordinated manor

98
Q

afib EKG

A

no p waves
irregularly irregular rhythm
(may look like junctional rhythm but the afib is irreg irreg)

99
Q

physiology of afib

A

atria chaotically quivering up to 500 atrial impulses a minute
AV allows occasional impulse to pass

100
Q

clinical implications of afib

A

risk of clot formation in left atrium increases

cardiac output decreases 25-30%

101
Q

what does afib cause in acute cases?

A

hypotension

102
Q

anesthetic concerns with afib

A

a lot of patients have afib thats unresponsive to therapy- their bodies compensate
developing acute afib then they suffer from decreases CO (more concerning)

103
Q

treatment for afib

A

treatment the same as with atrial flutter:
medications
synchonized cardioversion

104
Q

special concern for treatment of afib prior to cardioversion

A

if afib present for more than 2 days then clot can form in left ventricle and needs to be on anticoagulants for at least 3 weeks prior to cardioversion

105
Q

premature junctional contraction (PJC) ECG

A

premature beat has:
missing or inverted p wave (some cases inverted p wave can come after QRS complex)
normal QRS complex

106
Q

physiology of PJC

A

AV node gets irritated and initiated a heartbeat without signal from SA node
impulse travels retrograde direction for the atria (none or inverted p wave)

107
Q

anesthetic concerns with PJC

A

level of concern proportional to the frequency of PJC

108
Q

junctional rhythm

A

beat or rhythm originated in the AV node

109
Q

junctional rhythm ECG

A

inverted or absent p wave

normal QRS complex

110
Q

normal junctional rhythm

A

40-60bpm

111
Q

accelerated junctional rhythm

A

60-100bpm

112
Q

junctional tachycardia

A

> 100bpm

113
Q

physiology of junctional rhythms

A

SA node not working

AV node is primary pacemaker

114
Q

do the atria contract during junctional rhythm?

A

yes but delayed

atrial and ventricular contractions occur at similar times so decreases ventricular filling

115
Q

anesthetic concerns with junctional rhythm

A

HR is slow and less ventricular filling; concerning if BP is low

**converts back to sinus rhythm after robinul

116
Q

escape beat

A

a beat that comes after a long pause

117
Q

junctional escape beat ECG

A

escape beat that has junctional properties
inverted or absent p wave
normal or narrow QRS

118
Q

physiology of junctional escape beat

A

SA node temporarily failed
av node jumps in to initiate heat beat
SA node works again
¯_(ツ)_/¯

119
Q

anesthetic concerns with junctional escape beats

A

the frequency in which this occurs is proportional to level or concern

120
Q

treatment for junctional escape beats

A

robinul, atropine, pacing if frequently or pauses are prolonged

121
Q

premature ventricular contractions (PVC) EKG

A

no p wave

a wide or bizarre or different QRS complex

122
Q

physiology of PVC

A

ventricular myocardium initiates single beat prematurely

123
Q

anesthetic concerns with PVC

A

concerning if frequent

PVC dont produce pulse (if bigeminal then pulse is half of EKG rate)

124
Q

bigeminy

A

cardiac rhythm where a normal beat is followed by irregular beat

125
Q

What can PVCs develop into?

A

Vtach if their frequency continues to increase

126
Q

treatment of PVC

A

antiarrhythmics (lidocaine, amiodarone)

Robinul or atropine

127
Q

what are the three types of premature beats?

A

premature atrial contraction (PAC)
premature junctional contraction (PJC)
premature ventricular contraction (PVC)

128
Q

ventricular escape beat EKG

A

long pause followed by ventricular beat (wide QRS)
no p wave
similar to junctional escape beat but no p wave

129
Q

physiology of ventricular escape beat

A

SA and AV node fail
ventricular myocardium initiates beat
SA node starts to work
¯_(ツ)_/¯

130
Q

anesthetic concerns with ventricular escape beats

A

concern increases as frequency increases

consider robinul or atropine if it occurs frequently

131
Q

what are the two types of escape beats?

A

junctional escape beat

ventricular escape beat

132
Q

ventricular escape rhythm (idioventricular) EKG

A

no pave
wide QRS complex
slow HR <60bpm

133
Q

physiology of ventricular escape rhythms

A

SA and AV nodes failed

ventricular myocardium starts initiating beats

134
Q

anesthetic concerns with idioventricular rhythm

A

no active ventricular filling
HR slow
low CO
NO ELECTIVE CASE

135
Q

treatment for ventricular escape rhythm

A

cardiac pacing

epi if unstable

136
Q

When should you avoid lidocaine?

A

ventricular escape rhythm

3rd degree AV node block

137
Q

idoventricular rhythm pace

A

<60 bpm

138
Q

accelerated idioventricular rhythm pace

A

60-100bpm

139
Q

vtach

A

> 100bpm

140
Q

EKG ventricular tachycardia (Vtach)

A

no p wave
wide QRS complex
HR >100bpm

141
Q

physiology of vtach

A

ventricular myocardium initiating beats at rapid rate
high oxygen consumption
minimal ventricular filling

142
Q

anesthetic concerns with vtach

A

MEDICAL EMERGENCY

immediate cardioversion/defibtrillation

143
Q

what are the two treatments of vtach?

A

antiarrhythmics

electrical cardioversion

144
Q

ventricular fibrillation (vfib) EKG

A

just deflections from the baseline

no p wave or QRS complex

145
Q

physiology of vfib

A

ventricles are quivering at rapid rate
heart consuming a lot of oxygen
no pulse or cardiac output

146
Q

anesthetic concerns with vfib

A

MEDICAL EMERGENCY
(more than vtach)
requires immediate defibrillation

147
Q

treatment for vfib

A

defibrillation

CPR until perfusing rhythm returns

148
Q

1st degree AV block

A

long PR interval

>1 large box

149
Q

physiology of 1st degree AV block

A

conduction through the AV node is slower than normal

150
Q

anesthetic concern with 1st degree AV block

A

don’t need to worry

151
Q

2nd degree AV block (mobitz)

A

dropped QRS complex (sometimes can be two in a row)

152
Q

what are the two types of 2nd degree blocks?

A

mobitz type I (wenckebach)

mobitz type II

153
Q

mobitz type I 2nd degree block EKG

A

dropped QRS complex

increasingly longer PR intervals before the ORS is dropped

154
Q

physiology of mobitz type I 2nd degree block

A

wenckebach

partial block in AV node that is bad enough to fully block sometimes

155
Q

mobitz type II 2nd degree block EKG

A

dropped QRS complex

constant PR interval before the QRS is dropped

156
Q

physiology of mobitz type II 2nd degree block

A

block below the AV node thats bad enough to completely block some impulses

157
Q

anesthetic concerns with 2nd degree AV block

A

NO ELECTIVE CASES
more concerning the more dropped beats
potentially require pacing

158
Q

3rd degree AV block (complete heart block) EKG

A

have p waves and QRS complexes that are not associated with eachother
“atrioventricular dissociation”

159
Q

what is the normal ventricular rate for 3rd degree AV block

A

~30-40bpm

160
Q

physiology of 3rd degree AV block

A

atria are contracting no impulse goes through AV though
ventricles also initiate their own beats
contracting independently

161
Q

For a 3rd degree AV block are the QRS complexes normal or wide?

A

they can be either
(we dont know why)
¯_(ツ)_/¯

162
Q

clinical effects of complete heart block

A

atria may try to empty into full ventricles
ventricles may contract when empty
serious reduction in cardiac output

163
Q

anesthetic concerns with 3rd degree AV block

A

NO ELECTIVE CASES

CO low

164
Q

treatment for complete heart block

A

cardiac pacing

epi if unstable

165
Q

signs of ischemia/infarction (3)

A

ST segment changes
abnormal T waves
Abnormal Q waves

166
Q

ST depression vs ST elevation (what does each indicate)

A

ST depression: ischemia

ST elevation: infarction

167
Q

what are the two abnormal T waves

A

peaked T wave

T wave inversion

168
Q

Myocardial ischemia treatment

A

increase oxygen supply

decrease oxygen demand

169
Q

ways to increase oxygen (5)

A 
1-100% FiO2
2-decrease HR (beta blocker)
3-maintain normal BP
(avoid hypotension)
4-administer NTG
5-administer aspirin
170
Q

ways to decrease oxygen demand (3)

A

1-decrease HR (beta blocker)
2-avoid pain /anxiety
/tachycardia (narcotics/sedatives)
3- avoid high afterload (Htn)

171
Q

Why is it important to compare preoperative EKG to intraoperative EKG?

A

signs of ischemia and infarction can be present in an EKG due to an old MI

LANCE (17 decks)

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