Basic ECG Flashcards
1
Q
pacemaker cell
A
determine heart rate and initiate heart beats
SA and AV
2
Q
electrical conducting cell
A
deliver the impulse to the myocardial cells
3
Q
mycardial cells
A
contract and pump blood out of the heart
4
Q
SA node
A
primary pacemaker of the heart (sets HR)
60-100 bpm
5
Q
AV node
A
becomes the pacemaker if for some reason the SA node fails
AV node rate= 40-60bpm
6
Q
narrow QRS complex means what for conduction
A
rapid conduction
normal pathway of conductance
7
Q
do electrical conducting cells transmit current slow or fast?
A
quickly
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
9
Q
myocardial cells can initiate heat beats in what two situations?
A
1- SA and AV nodes fail
2- myocardium is irritated
10
Q
what causes the myocardium to become irritated?
A
ischemia
electrolyte abnormality
acidosis
caffine
11
Q
Do myocardial cells or electrical conducting cells transmit current quickly and more effectively?
A
electrical conducting cells
12
Q
Wide QRS complex means what for conductance
A
slow conductance
current travels through the muscle, not normal pathway
13
Q
what do ECG leads detect?
A
the electrical difference (voltage) between two limbs
14
Q
Lead I provides a picture from what angle?
A
180 degrees
15
Q
lead II provides a picture from what angle?
A
60 degrees
16
Q
Where are the leads on a 3 lead ecg?
A
right arm, left arm, left leg
17
Q
what is the limitation for the 3 lead system?
A
not as sensitive for detecting myocardial ischemia in the left ventricle
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
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
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
21
Q
The green lead
A
neutral or ground lead
completes electrical circuit and doesn’t have anything to do with the EKG itself
22
Q
brown lead
A
additional precordial lead
more sensitive for detecting LV ischemia
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
24
Q
ECG paper 1mV= ___ small boxes?
A
10small boxes
25
ECG paper 1 large box
200msec
| 5mm
26
1 small box= ____ mseconds
40 msec
| 1mm
27
5 large boxes
1 second
28
300 large boxes
1 min
29
two ways to estimate the HR?
- 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
30
do segments or intervals of the ECG have waves?
intervals
31
P wave
atrial depolarization
| duration <120msec (3 small boxes)
32
QRS complex
ventricular depolarization
| duration <120msec (3 small boxes)
33
premature ventricular contractions are causes by what?
if the heart gets irritated and the ventricles start their own heart beat
34
ventricular escape rhythm
electrical conductance fails and ventricles take over as pacemaker
35
potential cause for wide QRS complex (not irritation or electrical failure)
current travels across myocardium instead of through purkinje fibers
Wolf Parkinson White Syndrome (WPW)
Right bundle branch block (RBBB)
Left bundle branch block (LBBB)
36
T wave
ventricular repolarization
| height <5mm in leads I,II,III
37
U wave
follows t wave
| not seen unless hypokalemia
38
J point
point at which S wave returns to baseline
39
Delta wave
upward slurring of Q wave seen in WPW syndrome
40
J wave (osborne wave)
"bump" on the S wave
| seen in hypothermia
41
PR interval start
beginning of p wave
42
PR interval end
start of Q wave
43
PR interval normal time
120-200msec (3-5 small boxes)
44
Why is the PR interval time important?
shows conduction is delayed in the AV node and allows atria to finish contract before ventricles contract
OPTIMAL VENTRICLE FILLING
45
QT interval start
q wave
46
QT interval end
end of the t wave
47
What medications prolong the QT interval? When should these be avoided?
Zofran and Phenergan (antiemetics)
| avoided in pts with prolonged QT syndrome
48
PR segment start
end of p wave
49
PR segment end
beginning of Q wave
50
ST segment start
J point
51
ST segment end
start of T wave
52
premature beat
heart beat that happens before it is expected to
53
examples of premature beats
premature atrial contraction
premature junctional contraction
premature ventricular contractions
54
escape beat
heart beat that comes after a long pause
55
examples of escape beats
ventricular escape beat
| junctional escape beat
56
during systole what is and is not perfused?
Perfused: organs of the body
| Not perfused: the heart (coronary arteries are closed by valve)
57
During diastole what is and is not perfused?
Perfused: the heart (coronary arteries drain blood from backflow)
Not perfused: everything else
58
Do patients with high or low heart rates have better coronary perfusion? why?
slower HR
- longer time coronary arteries open
- greater diastolic filling time
59
What is cardiac output determined by?
ventricular filling prior to contraction
60
What are the two ways that ventricular filling occurs and which is better?
```
active filling (atria contract)** BETTER
passive filling (atria dont contract)
```
61
If the ventricular filling is passive will the volume be lower or higher than active filling?
lower
62
factors that can reduce ventricular filling (3)
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)
63
what happens when atria contract too quickly?
not enough time to fulling contract so reduces amount of blood forced to ventricles
64
What happens when ventricles contract too quickly?
dont have enough time to fill before contraction
65
Rapid heart rate leads to (3)
decreased cardiac output
hypotension
pulseless pt
66
ECG description of sinus bradycardia
p wave present
| HR <60bpm
67
benefits of sinus bradycardia
normal/good for these patients:
healthy pt who exercises
CAD patients
68
sinus brady cardia in healthy patients
higher stroke volume
| maintains adequate cardiac output
69
sinus brady cardia in patients with CAD
increased oxygen supply (diastolic filling)
| decreased oxygen demand
70
What do patients with CAD normally take to maintain a slow HR?
beta blockers
71
what does the level of concern with sinus bradycardia depend on? (3)
1- age (children very bad)
2- severity (50 could be normal; 30 always concern)
3- how fast the drop in HR occured
72
treatment for bradycardia
1- drugs (glyco, atropine, epi)
| 2- if unresponsive to drugs then initiate cardiac pacing with pacemaker
73
temporary transcutaneous pacing
use defibrillator to pace the heart
| set a HR and it will stimulate at that pace
74
permanent implantable pacemaker
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
ECG description of sinus tachycardia
P wave present
| HR > 100 bpm
76
etiology (causes) of sinus tachycardia
hypovolemia/hypotension
| pain/light anesthesia
77
anesthetic concerns with sinus tachycardia (3)
increased cardiac oxygen demand (bad in CAD)
decreased cardiac oxygen supply (decreases diastolic filling; bad CAD)
indicates possible hypovolemia
78
treatment for sinus tachycardia
depends on cause:
1- fluids if bc hypovolemia
2- deepen anesthetic if light
3- consider beta blocker if not hypovolemic or light
79
ECG description of irregular sinus rhythm
looks like sinus but rate is irregular
faster during inspiration
slower during expiration
80
during spontaneous inspiration what happens to the intrathoracic pressure and preload
intrathoracic pressure decreases
preload increase
HR speeds up to pump excess out
81
during spontaneous expiration what happens to the intrathoracic pressure and preload?
intrathoracic pressure increases
preload decreases
HR slows does bc it doesnt have to pump out as fast
82
anesthetic concerns with irregular sinus rhythm
not as concerned
| seen in healthy pts with deep breaths
83
ectopy
any heart beat that originates outside the SA node
84
ectopy is activated where? (3)
AV node
atrial myocardium
ventricular myocardium
85
Supraventricular ectopy (6)
```
premature atrial contraction (PAC)
atrial flutter
atrial fibrillation (Afib)
Premature junctional contraction (PJC)
Junctional rhythm
junctional escape beat
```
86
ventricular ectopy (5)
```
premature ventricular contraction (PVC)
escape ventricular contraction
ventricular escape (idioventricular) rhythm
ventricular tachycardia (Vtach)
ventricular fibrillation (Vfib)
```
87
Premature Atrial Contraction (PAC) ECG
premature beat has:
upright p wave
normal/narrow QRS complex
88
physiology of PAC
artrial myocardium node got irritated and initiated a beat without signal from SA node
89
Anesthetic concerns with PACs
depends on the frequency
| associated with less ventricular filling and will cause problems if they happen often
90
Atrial flutter ECG
saw tooth pattern ~250-300 P waves/min
| more p waves than QRS complexes
91
physiology of atrial flutter
atrial myocardium contracts regularly ~250-300 times/min
decreased ventricular filling
AV node blocks some signals thus ventricular rate is much slower
92
anesthetic concerns with atrial flutter
ventricular filling and CO decreased
heart has higher oxygen metabolism
NO ELECTIVE SURGERIES
93
treatment for atrial flutter
medications (digoxin, amiodarone)
| unstable then use synchronized cardioversion
94
what does sychronized cardioversion treat?
"shocking" the heart (cardioversion or defibrillation) treats unstably fast rhythms
95
what does pacing treat?
unstably slow rhythms
96
fibrillate definition
quiver rapidly
97
Atrial fibrillation (afib)
electrical impulses originate from irregular spots in the atrium and radiate through the atrium walls in an uncoordinated manor
98
afib EKG
no p waves
irregularly irregular rhythm
(may look like junctional rhythm but the afib is irreg irreg)
99
physiology of afib
atria chaotically quivering up to 500 atrial impulses a minute
AV allows occasional impulse to pass
100
clinical implications of afib
risk of clot formation in left atrium increases
| cardiac output decreases 25-30%
101
what does afib cause in acute cases?
hypotension
102
anesthetic concerns with afib
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
treatment for afib
treatment the same as with atrial flutter:
medications
synchonized cardioversion
104
special concern for treatment of afib prior to cardioversion
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
premature junctional contraction (PJC) ECG
premature beat has:
missing or inverted p wave (some cases inverted p wave can come after QRS complex)
normal QRS complex
106
physiology of PJC
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
anesthetic concerns with PJC
level of concern proportional to the frequency of PJC
108
junctional rhythm
beat or rhythm originated in the AV node
109
junctional rhythm ECG
inverted or absent p wave
| normal QRS complex
110
normal junctional rhythm
40-60bpm
111
accelerated junctional rhythm
60-100bpm
112
junctional tachycardia
>100bpm
113
physiology of junctional rhythms
SA node not working
| AV node is primary pacemaker
114
do the atria contract during junctional rhythm?
yes but delayed
| atrial and ventricular contractions occur at similar times so decreases ventricular filling
115
anesthetic concerns with junctional rhythm
HR is slow and less ventricular filling; concerning if BP is low
**converts back to sinus rhythm after robinul
116
escape beat
a beat that comes after a long pause
117
junctional escape beat ECG
escape beat that has junctional properties
inverted or absent p wave
normal or narrow QRS
118
physiology of junctional escape beat
SA node temporarily failed
av node jumps in to initiate heat beat
SA node works again
¯\_(ツ)_/¯
119
anesthetic concerns with junctional escape beats
the frequency in which this occurs is proportional to level or concern
120
treatment for junctional escape beats
robinul, atropine, pacing if frequently or pauses are prolonged
121
premature ventricular contractions (PVC) EKG
no p wave
| a wide or bizarre or different QRS complex
122
physiology of PVC
ventricular myocardium initiates single beat prematurely
123
anesthetic concerns with PVC
concerning if frequent
| PVC dont produce pulse (if bigeminal then pulse is half of EKG rate)
124
bigeminy
cardiac rhythm where a normal beat is followed by irregular beat
125
What can PVCs develop into?
Vtach if their frequency continues to increase
126
treatment of PVC
antiarrhythmics (lidocaine, amiodarone)
| Robinul or atropine
127
what are the three types of premature beats?
premature atrial contraction (PAC)
premature junctional contraction (PJC)
premature ventricular contraction (PVC)
128
ventricular escape beat EKG
long pause followed by ventricular beat (wide QRS)
no p wave
similar to junctional escape beat but no p wave
129
physiology of ventricular escape beat
SA and AV node fail
ventricular myocardium initiates beat
SA node starts to work
¯\_(ツ)_/¯
130
anesthetic concerns with ventricular escape beats
concern increases as frequency increases
| consider robinul or atropine if it occurs frequently
131
what are the two types of escape beats?
junctional escape beat
| ventricular escape beat
132
ventricular escape rhythm (idioventricular) EKG
no pave
wide QRS complex
slow HR <60bpm
133
physiology of ventricular escape rhythms
SA and AV nodes failed
| ventricular myocardium starts initiating beats
134
anesthetic concerns with idioventricular rhythm
no active ventricular filling
HR slow
low CO
NO ELECTIVE CASE
135
treatment for ventricular escape rhythm
cardiac pacing
| epi if unstable
136
When should you avoid lidocaine?
ventricular escape rhythm
| 3rd degree AV node block
137
idoventricular rhythm pace
<60 bpm
138
accelerated idioventricular rhythm pace
60-100bpm
139
vtach
>100bpm
140
EKG ventricular tachycardia (Vtach)
no p wave
wide QRS complex
HR >100bpm
141
physiology of vtach
ventricular myocardium initiating beats at rapid rate
high oxygen consumption
minimal ventricular filling
142
anesthetic concerns with vtach
MEDICAL EMERGENCY
| immediate cardioversion/defibtrillation
143
what are the two treatments of vtach?
antiarrhythmics
| electrical cardioversion
144
ventricular fibrillation (vfib) EKG
just deflections from the baseline
| no p wave or QRS complex
145
physiology of vfib
ventricles are quivering at rapid rate
heart consuming a lot of oxygen
no pulse or cardiac output
146
anesthetic concerns with vfib
MEDICAL EMERGENCY
(more than vtach)
requires immediate defibrillation
147
treatment for vfib
defibrillation
| CPR until perfusing rhythm returns
148
1st degree AV block
long PR interval
| >1 large box
149
physiology of 1st degree AV block
conduction through the AV node is slower than normal
150
anesthetic concern with 1st degree AV block
don't need to worry
151
2nd degree AV block (mobitz)
dropped QRS complex (sometimes can be two in a row)
152
what are the two types of 2nd degree blocks?
mobitz type I (wenckebach)
| mobitz type II
153
mobitz type I 2nd degree block EKG
dropped QRS complex
| increasingly longer PR intervals before the ORS is dropped
154
physiology of mobitz type I 2nd degree block
wenckebach
| partial block in AV node that is bad enough to fully block sometimes
155
mobitz type II 2nd degree block EKG
dropped QRS complex
| constant PR interval before the QRS is dropped
156
physiology of mobitz type II 2nd degree block
block below the AV node thats bad enough to completely block some impulses
157
anesthetic concerns with 2nd degree AV block
NO ELECTIVE CASES
more concerning the more dropped beats
potentially require pacing
158
3rd degree AV block (complete heart block) EKG
have p waves and QRS complexes that are not associated with eachother
"atrioventricular dissociation"
159
what is the normal ventricular rate for 3rd degree AV block
~30-40bpm
160
physiology of 3rd degree AV block
atria are contracting no impulse goes through AV though
ventricles also initiate their own beats
contracting independently
161
For a 3rd degree AV block are the QRS complexes normal or wide?
they can be either
(we dont know why)
¯\_(ツ)_/¯
162
clinical effects of complete heart block
atria may try to empty into full ventricles
ventricles may contract when empty
serious reduction in cardiac output
163
anesthetic concerns with 3rd degree AV block
NO ELECTIVE CASES
| CO low
164
treatment for complete heart block
cardiac pacing
| epi if unstable
165
signs of ischemia/infarction (3)
ST segment changes
abnormal T waves
Abnormal Q waves
166
ST depression vs ST elevation (what does each indicate)
ST depression: ischemia
| ST elevation: infarction
167
what are the two abnormal T waves
peaked T wave
| T wave inversion
168
Myocardial ischemia treatment
increase oxygen supply
| decrease oxygen demand
169
ways to increase oxygen (5)
```
1-100% FiO2
2-decrease HR (beta blocker)
3-maintain normal BP
(avoid hypotension)
4-administer NTG
5-administer aspirin
```
170
ways to decrease oxygen demand (3)
1-decrease HR (beta blocker)
2-avoid pain /anxiety
/tachycardia (narcotics/sedatives)
3- avoid high afterload (Htn)
171
Why is it important to compare preoperative EKG to intraoperative EKG?
signs of ischemia and infarction can be present in an EKG due to an old MI
