Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PMI AS > Basic ECG COPY > Flashcards

Basic ECG COPY Flashcards

1
Q

pacemaker cell

A

determine heart rate and initiate heart beats

SA and AV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

electrical conducting cell

A

deliver the impulse to the myocardial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

mycardial cells

A

contract and pump blood out of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

SA node

A

primary pacemaker of the heart (sets HR)

60-100 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

AV node

A

becomes the pacemaker if for some reason the SA node fails

AV node rate= 40-60bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

narrow QRS complex means what for conduction

A

rapid conduction

normal pathway of conductance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

do electrical conducting cells transmit current slow or fast?

A

quickly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

myocardial cells can initiate heat beats in what two situations?

A

1- SA and AV nodes fail

2- myocardium is irritated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what causes the myocardium to become irritated?

A

ischemia
electrolyte abnormality
acidosis
caffine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

electrical conducting cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Wide QRS complex means what for conductance

A

slow conductance

current travels through the muscle, not normal pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what do ECG leads detect?

A

the electrical difference (voltage) between two limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Lead I provides a picture from what angle?

A

180 degrees

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

lead II provides a picture from what angle?

A

60 degrees

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where are the leads on a 3 lead ecg?

A

right arm, left arm, left leg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the limitation for the 3 lead system?

A

not as sensitive for detecting myocardial ischemia in the left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

The green lead

A

neutral or ground lead

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

brown lead

A

additional precordial lead

more sensitive for detecting LV ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

ECG paper 1mV= ___ small boxes?

A

10small boxes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ECG paper 1 large box

A

200msec

5mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

1 small box= ____ mseconds

A

40 msec

1mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

5 large boxes

A

1 second

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

300 large boxes

A

1 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

do segments or intervals of the ECG have waves?

A

intervals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

P wave

A

atrial depolarization

duration <120msec (3 small boxes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

QRS complex

A

ventricular depolarization

duration <120msec (3 small boxes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

premature ventricular contractions are causes by what?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

ventricular escape rhythm

A

electrical conductance fails and ventricles take over as pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

T wave

A

ventricular repolarization

height <5mm in leads I,II,III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

U wave

A

follows t wave

not seen unless hypokalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

J point

A

point at which S wave returns to baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Delta wave

A

upward slurring of Q wave seen in WPW syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

J wave (osborne wave)

A

“bump” on the S wave

seen in hypothermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

PR interval start

A

beginning of p wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

PR interval end

A

start of Q wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

PR interval normal time

A

120-200msec (3-5 small boxes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

QT interval start

A

q wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

QT interval end

A

end of the t wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

PR segment start

A

end of p wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

PR segment end

A

beginning of Q wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

ST segment start

A

J point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

ST segment end

A

start of T wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

premature beat

A

heart beat that happens before it is expected to

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

examples of premature beats

A

premature atrial contraction
premature junctional contraction
premature ventricular contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

escape beat

A

heart beat that comes after a long pause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

examples of escape beats

A

ventricular escape beat

junctional escape beat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

During diastole what is and is not perfused?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is cardiac output determined by?

A

ventricular filling prior to contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

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

A

lower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what happens when atria contract too quickly?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What happens when ventricles contract too quickly?

A

dont have enough time to fill before contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Rapid heart rate leads to (3)

A

decreased cardiac output
hypotension
pulseless pt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

ECG description of sinus bradycardia

A

p wave present

HR <60bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

benefits of sinus bradycardia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

sinus brady cardia in healthy patients

A

higher stroke volume

maintains adequate cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

PMI AS (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions