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ischemia and infarct Flashcards

1
Q

the LAD supplies the

A

septum, bundle branches, and anterior and lateral left ventricle

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2
Q

anterolateral MI will involve

A

V4-V6

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3
Q

prolonged lack of O2 to the myocardium, beginning of cellular damage, no tissue necrosis

A

injury

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4
Q

MI involving V1-V3

A

anteroseptal

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5
Q

evolution of an acute MI

A

normal ECG >>> peaked (hyperacute) T wave >>> ST elevation + peaked T wave >>> pathologic Q wave + decrease in ST elevation + T wave inversion >>> just pathologic Q waves + T wave inversion >>> just pathologic Q waves + upright T waves

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6
Q

what causes symmetrical T wave inversion

A

the reversed direction of repolarization (becomes endo to epi) b/c the subepicardial layers take longer

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7
Q

____ T waves aka hyperacute T waves seen in the early stages of acute MI are ___ mm in limb leads and ___ mm in precordial leads

A

PEAKED T waves aka hyperacute T waves seen in the early stages of acute MI are MORE THAN 5 mm in limb leads and MORE THAN 10 mm in precordial leads

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8
Q

for subendocardial ischemia, there will be new onset angina and the ST segment will be ____

A

depressed

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9
Q

best leads for evaluating T wave changes

A

precordial

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10
Q

MI involving V2-V4

A

anterior

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11
Q

how do you differentiate T wave inversion due to strain vs ischemia

A

in strain, you will see R or L VH and the inverted T will be ASYMMETRICAL

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12
Q

the left circumflex artery supplies the

A

left atrium, lateral, and posterior aspects of the heart

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13
Q

symmetrical T wave inversion

A

transmural ischemia

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14
Q

Q wave without ST elevation or T wave abnormality

A

prior/ healed/ old infarction

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15
Q

MI involving V4-V6

A

anterolateral

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16
Q

anterior MI will involve

A

V2-V4

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17
Q

tall R waves with ST depression and reciprocal changes in V1-V2,

A

posterior MI caused by occlusion of the right coronary artery

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18
Q

Q wave/ ST segment/ T wave changes in V1-V3 with reciprocal changes in the inferior leads

A

anteroseptal MI caused by occlusion of the LAD

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19
Q

___ receptor stimulation of the coronary arteries causes vasoconstriction

A

alpha

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20
Q

for transmural ischemia, there will be variable angina and the ST segment will be ____

A

elevated

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21
Q

___ artery divides into the ___ and the ___ branches whihc supply the LA, LV, and septum

A

LEFT MAIN CORONARY ARTERY artery divides into the LAD and the LEFT CIRCUMFLEX branches whihc supply the LA, LV, and septum

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22
Q

rapidly upsloping ST segments (in ST depression) represent

A

a smaller area of myocardium affected

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23
Q

at high HR, O2 demand is ____, but O2 delivery is ___

A

at high HR, O2 demand is HIGHEST, but O2 delivery is REDUCED (due to decreased diastole)

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24
Q

non Q wave infarction aka

A

subendocardial MI

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25
Q wave/ ST segment/ T wave changes in V1-V2 with reciprocal changes in the inferior leads
septal MI caused by occlusion of the LAD
26
asymmetrical T wave inversion
RVH with strain
27
MI involving lead 1, aVL V5-V6
lateral
28
in an anterior STEMI (V1-V4), you would see reciprocal changes in
inferior leads (2, 3, aVF)
29
anteroseptal MI will involve
V1-V3
30
MI involving lead 2-3, aVF
inferior
31
T wave inversion + ST depression
ischemia
32
Q wave/ ST segment/ T wave changes in lead 1, aVL, and V5-V6 with reciprocal changes in the inferior leads
(left) lateral wall MI caused by occlusion of the left circumflex artery
33
hyperacute T waves are ___ amplitude of the corresponding R wave amplitude
2/3
34
which layer of heart tissue does ischemia typically appear first
sub-endocardial (b/c it's furthest from the blood supply which originates from the coronary arteries on the epicardial surface)
35
\_\_\_ artery supplies the RA, RV, and inferior and posterior walls of the LV. As a result, infarct would cause abnormal arrhythmias
Right coronary artery
36
how can you ID transmural ischemia
symmetric T wave inversion in 2+ contiguous precordial leads
37
ST segment elevation 1+ mm over isoelectric baseline
myocardial injury
38
in a posterior MI, a ____ may be noted which is ____ of a Q wave
in a posterior MI, a **SEPTAL R WAVE** may be noted which is the **REVERSE** of a Q wave
39
Q wave/ ST segment/ T wave changes in V2-V4 with reciprocal changes in the inferior leads
anterior wall MI caused by occlusion of the LAD
40
ST depression in V1-V3
have a high suspicion for posterior wall MI
41
Q wave/ ST segment/ T wave changes in leads 2, 3, and aVF with reciprocal changes in the anterolateral leads
inferior MI caused by occlusion of the right coronary artery and its descending branch
42
causes of MI (just look at a few times)
atherosclerosis, vasospasm, thrombosis/embolus, decreased ventricular filling time (tachycardia), decreased filling pressure in coronary arteries (severe hypotension/ aortic valve dz)
43
in an anterospetal STEMI (V1-V2), you would see reciprocal changes in
inferior leads (2, 3, or aVF) or lateral leads (1, aVL, V5, V6)
44
always suspect posterior MI in the presence of \_\_\_ especially \_\_\_\_
ST depression in leads 1 and 2 especially in the absence of RAD or RVH
45
indicates the presence of irreversible myocardial damage/ infarct
pathologic Q waves in 2+ contiguous leads (more than 0.04 secs, at least 1/3 the height of the R wave)
46
lateral MI will involve
lead 1, aVL V5-V6
47
death of myocardial cells, enzyme release
infarct
48
pathologic Q wave + evolving ST segment and T wave changes + myocardial specific enzymes
transmural infarction
49
which is reversible? ischemia? injury? infarct?
which is reversible? ischemia- YES injury- YES infarct- NO
50
no Q wave but evolving ST segment and T wave changes + myocardial specific enzymes
subendocardial infarction (non-Q wave infarct)
51
the ST segment shifts seen from a different angle or direction
reciprocal changes
52
how do you determine that the ST segment is depressed (and significant)
compare it to the PR segment (at 0.04 secs from the J point): more than 1 mm (1 tiny box) below baseline in 2+ contiguous leads
53
posterior MI abnormal R wave criteria
in V1 and V2: * more than 0.04 seconds * R bigger than S * pt over 30 y/o * no signs of RVH
54
normal q wave criteria
less than 1/4 the R wave, less than 0.04 seconds
55
when should you have a high degree of suspicion for posterior wall MI
ST depression in V1-V3
56
downsloping ST segments (in ST depression) represents
a larger area of myocardium affected
57
inferior MI will involve
lead 2-3, aVF
58
T wave inversion is caused by ischemia and \_\_\_\_
strain (as in LVH or RVH with strain) because the thickened muscle doesnt relax as easily
59
septal MI will involve
V1-V2
60
ST elevation
injury
61
62
lack of O2 to the myocardium, reversible, no permanent damage
ischemia
63
symmetrical peaked T waves + ST depression
ischemia
64
after ___ hours in an acute MI, the T waves go from ___ to \_\_\_
after 2 hours in an acute MI, the T waves go from PEAKED to INVERTED
65
which layer of the heart is the last to receive O2
endocardium
66
ischemic T wave is more ____ than a normal T wave
symmetrical
67
\_\_\_\_ receptor stimulation of the coronary arteries causes vasodilation
beta
68
in an lateral STEMI (lead 1, aVL, V5-6), you would see reciprocal changes in
inferior leads (2, 3, aVF) sometimes V1-2, but that is more likely to be a posterior MI
69
enlarging or new Q waves
infarct
70
MI involving V1-V2
septal
71
in an inferior STEMI (2, 3, aVF), you would see reciprocal changes in
lateral leads 1 and aVL sometimes in V1-3, but that is more likely to be from a posterior MI
72
flat ST segment depression
previous or completed subendocardial ischemia or infarct
73
how long does it take for pathologic Q waves to develop and how long do they last
takes minutes to days to develop, last forever
74
if looking for a posterior MI, where do you look for changes
reciprocal changes in V1 and V2 hold EKG paper upside down and look through it in a posterior MI, septal lead depressions become elevations, and elevations become depressions

EKG (8 decks)

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