EKG Flashcards
1
Q
Precordial lead placement:
A
V1: 4th ICS R sternal border
V2: 4th ICS L sternal border
V3: between V2 + V4
V4: 5th ICS mid clavicular line
V5: between V4 + V6
V6: 5th ICS mid axillary line
2
Q
12 lead ekg (site of heart, leads, reciprocal leads, vessel/s involved)
Lateral
A
Lateral wall
leads: I and aVL (high lateral), V5 and V6 (low lateral)
reciprocal leads: II, III, aVF
vessels: LAD (LCx + Diag)
3
Q
12 lead ekg (site of heart, leads, reciprocal leads, vessel/s involved)
Inferior
A
Inferior Wall
leads: II, III, aVF
reciprocal: I and aVL
vessels: RCA or LCx
4
Q
12 lead ekg (site of heart, leads, reciprocal leads, vessel/s involved)
Anterior / septal
A
Anterior Wall
leads: V1+V2 (septal), V3+ V4 (anterior)
reciprocal: NONE
vessel: LAD
5
Q
12 lead ekg (site of heart, leads, reciprocal leads, vessel/s involved)
Posterior
A
Posterior wall
leads: NONE
reciprocal: V1-V4
vessel: RCA (PDA)
6
Q
Atrial enlargement
RAE criteria
A
TALL symmetric p wave (P pulminale)
leads II, III, aVF >2.5mm
lead V1+V2 >1.5mm, biphasic
7
Q
Atrial enlargement
LAE criteria
A
wide, notched P wave (P mitrale) > 0.1s in ANY lead
leads II, III, aVL notches + > 0.12s
lead V1 downward deflection + 1mm amplitude + 0.04s
V1 + V2 biphasic
8
Q
Best lead to look for atrial enlargement?
A
V1
9
Q
RVH criteria
A
can have peaked P wave (RAE)
II, III, V1 tall R wave (>7mm V1)
V1: R>S wave
V1-V6 R gets smaller
Deep S wave: I, V4-V5, wave persists in V5 + V6
ST segment: down sloping depression >1mm in II, III, aVF, and V1
T wave: inversion in II, III, aVF, and V1
RAD, slight wide QRS
10
Q
LVH criteria
A
can have wide, notched P wave (LAE)
-V1 S wave + V5 R wave > 35mm
-tall R wave I(>20mm), aVL(>11mm), V5-V6 (>30mm)
-deep S wave III (>20mm), V1 + V2 (>30mm)
-ST seg: I, aVL, V5+ V6 (1mm+ depress), V1-V3 (1mm+ elevation)
-inverted T wave I, aVL, V5 + V6
11
Q
Axis - simple way
Lead I = +
Lead aVF = +
A
normal
12
Q
Axis - simple way
Lead I = -
Lead aVF = +
A
RAD
13
Q
Axis - simple way
Lead I = +
Lead aVF = -
A
LAD
14
Q
Axis - simple way
Lead I = -
Lead aVF = -
A
northwest axis / extreme RAD
15
Q
Determine axis rotation in horizontal plane ( find most isoelectric lead)
-V1 or V2
A
rightward
16
Q
Determine axis rotation in horizontal place (find most isoelectric lead)
-V3 or V4
A
normal
17
Q
Determine axis rotation in horizontal plane (find most isoelectric lead)
-V5 or V6
A
leftward
18
Q
Coronary arteries: LCA
-branches
-what they supply
A
LCA > LAD + LCx
LAD = LV anterior + inferior, RBB + LBB(anterior fascicle), septum
LCx = LA + LV posterior + lateral
19
Q
Coronary arteries: RCA
-what it supplies
A
RA
RV
septum
LBB (posterior fascicle)
Electrical areas
20
Q
T/F the LBB is supplies by 2 arteries, so if there is a block there isa lot of damage/ ischemia
A
true
21
Q
Coronary artery: area of LV + artery supply
-Inferior LV (apex)
A
LAD
22
Q
Coronary arter: area of LV + artery supply
-Anterior
A
LAD
23
Q
Coronary artery: area of LV + artery supply
-Lateral
A
LCx
24
Q
Coronary artery: area of LV+ artery supply
-Posterior
A
PDA (80-85%)
Circ (10-15%)
25
Coronary artery: area of LV + artery supply
-Septum
Anterior 2/3 of LAD
Posterior 1/3 of RCA
26
Which membrane of heart is most vulnerable to ischemia?
EPICARDIUM not endocardium
27
CPP(coronary) =
aortic DBP - LVEDP
-low BP or increased LVEDP = reduced coronary perfusion
28
coronary blood flow =
250mL/min @ rest
29
T/F Tachycardia increases coronary perfusion.
false. they perfuse during diastole and if less time in diastole, less time for perfusion
30
Myocardium regulates blood flow between pressures of _ - _
50-120, beyond these pressures, blood flow is PRESSURE dependent
31
Infarcted areas of myocardium are _ shaped and have the wider side along the _
wedge
endocardium
32
T/F Ischemia, injury, and infarction are reversible.
False. ischemia + injury are reversible NOT infarction (cell death)
33
How does heart protect itself from ischemia?
-overlapped areas of perfusion (collateral)
-O2 from ventricles can diffuse into cells in nearby tissue
-some vessels, "thebesian veins" arise directly from ventricle
34
Main mechanism of ischemia/ injury:
demands of heart > than blood
supply
-increased demand OR decreased supply
35
Things that cause increased O2 demand in heart:
-tachycardia
-HTN
-big heart/CM
36
Things that cause decreased O2 supply in heart
-low Hgb
-low pO2
-fixed narrowing
-growing obstruction
-coronary spasm
37
Basic mechanism to relieve ischemia:
lessen demand, increase O2/blood supply
38
Acute Coronary Syndromes
-3 types
-unstable angina (+/- ekg s/s ST depress + T wave invert, NROMALY cardiac enzymes)
-NSTEMI (ST depress or T wave inversion + ELEVATED enzymes)
-STEMI (transmural injury occurs often, coronary occlusion is usualy cause)
39
Criteria of STEMI:
STE in 2+ contiguous leads and > 2mm V1-V3 or >1mm in other leads
-some YA can have 1mm STE in V1-V3 so need more
40
MI progression
-T wave inversion
ischemia
41
MI progression
-STE
infarction
42
MI progression
-pathologic Q wave
infarction (late)
43
Ischemia affects a wedge shaped portion of the heart and is thinner along the _ and wider along the _
endocardium
epicardium
44
Area of ischemia on heart is more _ (pos/neg) causing ST _ (ele/depression) and T wave inversion, causing repolarization to take an abnormal path.
negative
depression
45
T/F A normal T wave is symmetrical
false! asymmetrical
an inverted T wave is usually symmetrical
46
T/F T wave inversion is more often seen in precordial leads
True
47
T/F T wave inversion is NORMAL in lead II and Avf
FALSE
III and aVR!!!!!
48
Which is more specific to ischemia, T wave inversion or ST depression?
ST depression
-T wave inversion is cell running out of energy at END of repolarization
-ST depress is cell running out of energy at START of repolarization
49
Wellens warning/syndrome warns for stenosis of the _ artery.
LAD
50
Wellen's Warning/Syndrome ekg changes
marked T wave inversion in V2-V6
-alerts for critical stenosis of LAD, may have no pain and no elevation in enzymes at time of EKG but high risk of extensive anterior wall MI in days/wks
-may be biphasic T wave and have 0 or minimal STE
51
Ischemic injury remains more _ (pos/neg) than surrounding tissue causing ST (elev/depression)
positive
elevation
-T wave stays flipped bc abnormal repolarization
52
ST elevation tells us there has been a/an (recent/old) injury
recent
-will return to baseline as time passed
53
ST elevation
-patho
-atherosclerosis + thrombus
-transmural MI = STEMI, affecting more than just subendocardium
54
ST elevation in _ or more contiguous leads = _ % occlusion
2+
100% occlusion
55
J point
end of QRS and beginning of ST seg
-measure ST elevation here
56
J point elevation
not a big deal normally
-if elevation in inferior leads = riskier
-not the same as ST elevation technically
57
NSTEMI aka non _ _ MI
non Q wave MI
58
Pericarditis ekg =
WIDESPREAD STE + PR depression
concave STE
-**not in V1 and aVR**
reciprocal ST depression and PR elevation
59
T/F infarcted tissue is electrically neurtral
T
-doesnt generate any APs
-like an electrical "window" in the wall of myocardium
-unopposed positive vector > Q wave
60
Q wave is considered significant when: (2 criteria)
> 0.04s OR 1/3 ht of QRS
-never significant in aVR
-QS wave in V1 usually benign
-I and aVL normally show Q wave from septal depolarization
-benign Q waves found in pregnant pt or obese pts in lead III (horizontal placement of heart)
61
Necrotic myocardial tissue cannot depolarize so you can't see _ (toward/away) vectors, only _ (toward/away vectors)
toward
away
62
Give 4 situations Q waves don't matter:
1. never significant in aVR
2. QS wave in V1 usually benign
3. I and aVL normally show Q wave from septal depolarization
4. benign Q waves found in pregnant pt or obese pts in lead III (horizontal placement of heart)
63
_ (RAE /LAE) is often precursor to afib
LAE
64
P - _ happens when depolarization of R and L atrium are both seen in the P wave
MITRALE
65
T/F P wave is normally biphasic in V2
false, V1
66
Causes of BIatrial enlargement
-by itself
MITRAL STENOSIS
67
Causes of BI atrial enlargement
-WITH LVH
-HTN
-AS
-mitral incompetence
-hypertrophic CM
68
Biatrial enlargement criteria:
-MUST meet criteria of both RAE + LAE
lead II:
-notch p wave, amp >2.5, >0.12s
lead V1:
-biphasic p wave, initial pos deflection >1.5mm, terminal neg deflection >1mm deep, terminal neg deflection >0.4s
69
LVH leading cause:
HTN
-also valve dz
70
Bumper sticker for RVH:
BIG R in V1
-V1 sits above RV
71
T/F LVH often have some STE or depression with it
true, not always an AMI
72
Unstable angina definition:
severe ischemic state WITHOUT progression to permanent cell damage yet
73
Unstable angina
-3 subtypes
-new onset
-rest
-crescendo
74
Unstable angina
-s/s
cp @ rest or in crescendo pattern
SOB
diaphoresis
palps
N/V
75
Unstable angina
-ekg
-enzymes
EKG: normal OR ST depression AND/OR T wave inversion
enzymes: negative
76
NSTEMI definition:
severe ischemic state w/ typical s/s of MI
77
Main difference between NSTEMI and unstable angina =
lab tests confirming myocardial cell damage
78
NSTEMI
-ekg
-enzymes
EKG: ST depression or T wave inversion
enzymes: positive
79
STEMI criteria on EKG
-STE on 2+ contiguous leads
-STE must be > 2mm in V1, V2, and V3 and >1mm in other leads
79
STEMI definition
ischemic syndrome assoc w ST elevations and coronary occlusions
-typically caused by transmural ischemia/ infarction
80
"Contiguous leads" means:
leads that are anatomically next to each other, same area of heart
81
T/F Presence of a Q wave confirms a transmural infarct
false, may be from noncontiguous parts of myocardium
82
_ (Q wave/ non Q wave) infarcts associated with higher rate of acute mortality, tissue damage, and CHF where _ (Q wave/ non Q wave) infarcts have higher rate of long-term mortality if tx not taken
Q wave = acute mortality, damage, CHF
non Q wave = long term mortality
83
ACS: cp, EKG changes, enzymes
-unstable angina
-NSTEMI
-STEMI
UA: cp, possible EKG change, neg
NSTEMI: cp, ekg changes, enzymes
STEMI: cp, ekg changes, enzymes
84
Which wall of heart can have Q waves disappear possibly?
inferior wall
85
Inferior wall MI often involve _ infarction and some develop bradycardia from _ or _ degree AVB
RV
2nd or 3rd AVB
BRADY!!!!!!!
86
STE leads: pattern of elevation, injury location, and coronary artery involved
-I and aVL
I, aVL = lateral = Cx
87
STE leads: pattern of elevation, injury location, and coronary artery involved
-I, II, aVF
I, II, aVF = apical = LAD
88
STE leads: pattern of elevation, injury location, and coronary artery involved
-V1 and V2
V1 and V2 = septal = LAD, PDA
89
LCA normally supplies the _, the intraventricular _, and _ (septal, anterior, and lateral walls)
LA
intraventricular septum
LV
90
LCA branches
-LAD
septal + diag branches
supplies:
-anterior 2/3 of intraventricular septum
-RBB + LBB
-anterior + posterior papillary muscles of MV
-anterior + apical walls of LV
collateral circulation of anterior wall of RV
91
LCA branches
-L Cx
supplies:
-LA wall
-lateral LV (sometimes posterior LV)
92
Most important DETERMINANT of coronary blood flow:
myocardial O2 demand
93
Coronary blood flow is CONTROLLED primarily via:
variations in coronary arterial tone
94
What is pseudo-normalization of T wave inversion?
pt has normally flipped T waves, ischemia causes them to become normal
**compare old EKGs**
95
T/F T wave inversion is diagnostic for infarction
false
-dx for ischemia only
96
Pericarditis s/s
cp (pleuritic, retrosternal, tachy, worse laying flat, dyspnea
97
Why does infarction cause Q waves?
window effect - area of infarct is necrotic and doesn't depolarize and has no vectors. positive lead closest to this only sees "away" vectors on opposite walls
-
can happen with injuries that don't go all the way thru the heart, depolarization reverts back to cell-cell transmission , when this happened Q wave briefly appears to be unopposed
98
Anterior wall MI
-leads
-area of heart
-s/s
V3 + V4
infarcts of septum, lateral wall or both
HD compromise + shock
**may not have Q waves but lose normal R wave progression**
99
Anteroseptal wall MI
-leads
-vessel
V1-V4: STE + T wave invert, QS complex
LAD
100
Inferior Wall MI
-leads
-vessel
-s/s
II, III, aVF
recip: I and aVL
RCA
-**q waves may disappear
-often come with RV infarction > BRADYCARDIA (AVB)**
101
Lateral wall MI
-leads
-vessel
-s/s
I, aVL, V5 and V6 Q waves
-I and aVL Q waves may be "normal septal Q waves"
recip: ST depress in II, III, and aVF
L Cx
often occur in combos (inferolateral, anterolateral, posterolateral, etc)
102
T/F BBB is wide bc there are basically 2 QRS's, one for each ventricle
T
103
T/F PVC is aberrantly conducted since conception whereas BBB starts normal until reaching BB
T
104
T/F May be easier to check for BBB in LIMB leads, bc precordial leads can be larger
T
105
RBBB causes a _ (faster/slower) depolarization time
slower, >0.12s QRS = an additional wave or abberation of existing wave
106
RBBB is seen in right precordial leads of _ and _ as a RSR' complex
**V1 and V2
-doesn't always have rabbit ear appearance**
107
R' in a RBBB is a sign of slow conduction thru the _ _ and _
intraventricular septum and RV
108
1st _ (up/down) deflection after P wave is the R wave
upward = R wave
109
Main criteria for RBBB:
QRS > 0.12s (even just one lead)
**SLURRED S WAVE IN I AND V6**
-various morphologies but all prolonged + slow
RSR' pattern in V1 with R' taller than R (all predominantly positive)
110
Normally _ ventricle gives rise to the QRS complex, but in late innervation of septum and RBBB, the _ creates a new, slower vector
LV
RV
111
T/F 1st half of QRS is irrelevant in dxing RBBB
true
main criteria = slurred S wave V6 and I
112
Why is RSR' in V1 not enough to dx RBBB?
bc it is seen in anteroseptal MI too
-LOOK FOR SLURRED S IN I and V6!!!!!
113
RBBB can have other weird RSR' morphologies but always look for =
slurred S wave V6 and I
114
With RBBB you can only dx _ ventricular hypertrophy but not the other.
LVH
**bc RBB only affects the terminal portion of the complex**
115
T/F You can dx atrial enlargement with their normal criteria with RBBB
true
116
_ BBB is usually composed of monomorphic complexes (all + or all -) and are uglier
LBBB
117
_ BBB have ST depression or elevation and broad, discordant T waves associated with them
LBBB
-t wave goes in opposite direction of end of QRS
118
LBBB is either from:
-block of LB
-block of BOTH fascicles of LB
119
Depolarization occurs from L > R by cell-cell transmission in _ BBB
LBBB
120
Which complexes appear sharper, RBBB or LBBB
RBBB
-BROAD MONOMORPHIC COMPLEXES IN LBBB
121
LBBB: Complexes in V1 and V2 are _ (pos/neg) and in V5 and V6 they are _ (pos/neg)
V1+2 = NEGATIVE
V5+6 = POSITIVE
122
3 main criteria for LBBB:
- QRS > 0.12s
-broad, monomorphic R wave in I and V6 with NO Q WAVE
-broad, monomorphic S wave in V1, maybe small R wave
-others: LBBB notched in V6, no rabbit ears, LAD
123
Look for BBB in which leads mainly?
I, V1, V5 or V6
124
Common causes of LBBB:
**HTN
CAD**
dilated CM
HD
Infiltrative diseases
may be 1st clue to other serious dz:
-advanced CAD, CM, valve dz, HTN dz
125
Can you dx LVH or RVH with LBBB?
NO!
126
Can you dx LVH or RVH with RBBB?
LVH, not RVH bc true size of complex can't be assessed bc beats are abberent
127
Can you dx an infarction with a L or R BBB?
yes, both. Same with AE
128
T/F A localized intraventricular conduction delay is > 0.12s for QRS
false
-looks like QRS with many peaks
-GENERALIZED ICD is >0.12s without BBB criteria
129
Localized Intraventricular conduction delays are often seen in lead _
III
130
When noting a generalized intraventricular conduction delay with >0.12s QRS without BBB criteria you should anticipate _ abnormalities
electrolyte
-HYPERKALEMIA
131
4 possibilities of wide QRS complexes:
-LBBB
-RBBB
-IVCD (hyper K)
-ventricular or aberrantly conducted beats (VT?)
132
Most LBBB have a _ or _ axis
normal or LAD
133
Which type of BBB can you dx ventricular hypertrophy in?
RBBB and only LVH
-can also do atrial enlargement
134
Intraventricular conduction delays
-Localized will have a _ (normal/prolonged) QRS
-Generalized will have a _ (normal/prolonged) QRS
Local = normal
Generalized = prolonged
135
Hemiblock is half of _ BBB is blocked after splitting into _ and _ fascicles
LBBB
anterior and posterior fascicles
136
The left _ fascicle has organized, thin fibers and give rise to Purkinje fibers.
anterior
137
The left _ fascicle has loose, fanning fibers.
posterior
138
The left anterior fascicle innervated the _ and _ wall of the LV
anterior and lateral
139
The left posterior fascicle innervated the _ and _ walls of LV
inferior and posterior
140
Which fascicle innervates the anterior + lateral LV wall
LAF
141
Which fascicle innervates the inferior + posterior LV wall
LPF
142
Hemiblocks alter vectors produced by the _ ventricle
L
143
Hemiblocks will cause _ _ and _ (will/will not) prolong the QRS.
axis dev
will NOT prolong QRS
-look at LIMB leads for dx
144
Look at _ leads to dx hemiblocks
limb
145
Single most useful lead to distinguish RBBB and LBBB is _. With RBBB last segment of QRS will always be _ (pos/neg) and LBBB will always be _ (pos/neg)
V1!!!!
RBBB last seg QRS = positive
LBBB last seg QRS = negative
146
Which is more common, L anterior fascicle block or L posterior fascicle block?
LAFB
147
LAFB causes _ axis dev
LAD -30 to -90
148
L anterior hemiblock criteria:
- LAD (-30 to -90)
-qR complex or R wave in lead I
-rS complex in lead III, possibly II and aVF
**SHORTCUT: QRS complex is positive in I and negative in aVF and II**
149
T/F LPH is rare because hard to block from wide range fibers so lesion would have to be huge
t
150
LPH criteria:
-**Axis of 90-180 in R quadrant (RAD)**
-s wave in I and q wave in III
-**exclude RAE (tall P wave >2.5mm in limbs) and/or RVH (R>S in V1 and S>R in V6)**
151
Most common cause of RAD is
RVH
152
If there is RAD but no signs of RAE or RVH what is it most likely?
L posterior hemiblock!
-dx of exclusion!
153
P waves are normally positive in leads (5 total):
Negative in lead _
Commonly biphasic in lead _
Positive: I, II, V4, V5, V6
**Negative: aVR**
Biphasic: V1
154
Which lead NORMALLY has a negative P wave?
aVR
155
Which lead has a NORMALLY biphasic p wave?
V1
156
Best leads to look for atrial enlargement?
II and V1
-II is parallel to mean vector of atrial depolarization
-V1 perpendicular to mean vector of atrial depolarization and closest to atria (MAYBE SINGLE BEST LEAD TO LOOK AT FOR THIS)
157
RAE criteria:
-tall/narrow
P wave in inferior leads (II,III, aVF) >2.5mm
P wave in V1 or V2 >1.5mm
R rotation
158
Main cause of RAE
COPD, pulm HTN
159
P pulmonale is mainly found in leads _ and _
II and III
160
P wave in p pulmonale must be _ mm tall
2.5
161
P pulmonale is a sign of _ atrial enlargement
RAE
162
T/F peaked P wave <2.5mm is assoc with RAE
false
**can be less than this in precordial leads**
163
T/F P Pulmonale is seen in precordial leads
false
164
LAE criteria:
-prolonged (>0.11s), notches P with 0.04s between waves in II
-term portion of p wave >1mm below isoelectric line in V1
-**term portion of pwave >0.04s in width**
165
T/F LAE seen best in inferior leads
t
166
Most reliable dx for LAE is:
Terminal portion of p wave > 0.04s wide (look in inferior leads II, III, aVF)
167
P mitrale is assoc with _ AE
L
168
P mitrale width of notched p must be at least _ s
0.04
169
T/F P mitrales are a common finding
F
170
Notching of P wave in P mitrale is due to slower conduction thru the _ atrium
LA
171
LAE causes:
severe systemic HTN
aortic or mitral valve dz
restrictive CM
LV failure
172
T/F Obstructive CM is a cause of LAE
false, RESTRICTIVe
173
LVH effect on EKG:
more mass/cells = more APs generated = larger vector = increased amp (esp in precordials!)
pushed heart closer to CW = larger QRS complexes!!
174
LVH criteria:
**(S in V1 or V2) + (R in V5 or V6) = or > 35mm
any precordial lead QRS >45mm**
R in aVL >11mm
R in I >12mm
R in aVF >20mm
175
RVH criteria:
Limb leads:
-RAD (axis >100)
-lead I more negative than positive
Precordial:
-R wave prog disrupted
-V1 = largest, R>S wave
-V5 and V6 = smallest S>R wave
176
Hexaxial system: leads + degrees
I
I = 0deg
177
Hexaxial system: leads + degrees
II
II = 60deg
178
Hexaxial system: leads + degrees
III
III = 120deg
179
Hexaxial system: leads + degrees
aVR
aVR = -150deg
180
Hexaxial system: leads + degrees
aVL
aVL = -30deg
181
Hexaxial system: leads + degrees
aVF
aVF = 90deg
182
What is Einthovens Law and why do we care?
size of QRS in lead I + QRS in lead III = QRS in lead II
-if EKG taken simultaneous with limb leads (I,II,III), potential in lead II = sum of I and III
We care bc if leads are placed wrong, this will not be true so abnormal ekg may just be bad lead placement
183
Axis Dev:
Normal, RAD, LAD, Extreme RAD
N: 0-90deg
RAD: 90-180deg
LAD: 0-(-90deg)
Extreme RAD: 180 - (-90deg)
184
Axis Dev:
Lead I +
Lead aVF +
normal
185
Axis Dev:
Lead I -
Lead aVF +
RAD
186
Axis Dev:
Lead I+
Lead aVF -
LAD
187
Axis Dev:
Lead I -
Lead aVF -
extreme RAD
188
Axis Dev:
Lead I +
Lead aVF biphasic/=
borderline N/LAD
189
Axis Dev:
Lead I biphasic/=
Lead aVF +
borderline N/RAD
190
EKG truths:
impulse moving toward + electrode = _ (pos/neg) complex
positive
191
EKG truths:
impulse moving away from + electrode = _(pos/neg) complex
negative
192
EKG truths: impulse moving perpendicularly to + electrode = _ complex
isoelectric
193
T/F Only one isoelectric limb lead is on EKG bc only one ventricular axis
T
194
Precise axis:
look for most biphasic LIMB lead
look perpendicular to that (two directions)
determine axis from I and aVF then use perpendicular line to see precise quadrant
