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

Q wave/ ST segment/ T wave changes in V1-V2 with reciprocal changes in the inferior leads

A

septal MI caused by occlusion of the LAD

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26
Q

asymmetrical T wave inversion

A

RVH with strain

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27
Q

MI involving lead 1, aVL V5-V6

A

lateral

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28
Q

in an anterior STEMI (V1-V4), you would see reciprocal changes in

A

inferior leads (2, 3, aVF)

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29
Q

anteroseptal MI will involve

A

V1-V3

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30
Q

MI involving lead 2-3, aVF

A

inferior

31
Q

T wave inversion + ST depression

A

ischemia

32
Q

Q wave/ ST segment/ T wave changes in lead 1, aVL, and V5-V6 with reciprocal changes in the inferior leads

A

(left) lateral wall MI caused by occlusion of the left circumflex artery

33
Q

hyperacute T waves are ___ amplitude of the corresponding R wave amplitude

A

2/3

34
Q

which layer of heart tissue does ischemia typically appear first

A

sub-endocardial (b/c it’s furthest from the blood supply which originates from the coronary arteries on the epicardial surface)

35
Q

___ artery supplies the RA, RV, and inferior and posterior walls of the LV. As a result, infarct would cause abnormal arrhythmias

A

Right coronary artery

36
Q

how can you ID transmural ischemia

A

symmetric T wave inversion in 2+ contiguous precordial leads

37
Q

ST segment elevation 1+ mm over isoelectric baseline

A

myocardial injury

38
Q

in a posterior MI, a ____ may be noted which is ____ of a Q wave

A

in a posterior MI, a SEPTAL R WAVE may be noted which is the REVERSE of a Q wave

39
Q

Q wave/ ST segment/ T wave changes in V2-V4 with reciprocal changes in the inferior leads

A

anterior wall MI caused by occlusion of the LAD

40
Q

ST depression in V1-V3

A

have a high suspicion for posterior wall MI

41
Q

Q wave/ ST segment/ T wave changes in leads 2, 3, and aVF with reciprocal changes in the anterolateral leads

A

inferior MI caused by occlusion of the right coronary artery and its descending branch

42
Q

causes of MI (just look at a few times)

A

atherosclerosis, vasospasm, thrombosis/embolus, decreased ventricular filling time (tachycardia), decreased filling pressure in coronary arteries (severe hypotension/ aortic valve dz)

43
Q

in an anterospetal STEMI (V1-V2), you would see reciprocal changes in

A

inferior leads (2, 3, or aVF)

or

lateral leads (1, aVL, V5, V6)

44
Q

always suspect posterior MI in the presence of ___

especially ____

A

ST depression in leads 1 and 2

especially

in the absence of RAD or RVH

45
Q

indicates the presence of irreversible myocardial damage/ infarct

A

pathologic Q waves in 2+ contiguous leads (more than 0.04 secs, at least 1/3 the height of the R wave)

46
Q

lateral MI will involve

A

lead 1, aVL V5-V6

47
Q

death of myocardial cells, enzyme release

A

infarct

48
Q

pathologic Q wave + evolving ST segment and T wave changes + myocardial specific enzymes

A

transmural infarction

49
Q

which is reversible?

ischemia?

injury?

infarct?

A

which is reversible?

ischemia- YES

injury- YES

infarct- NO

50
Q

no Q wave but evolving ST segment and T wave changes + myocardial specific enzymes

A

subendocardial infarction (non-Q wave infarct)

51
Q

the ST segment shifts seen from a different angle or direction

A

reciprocal changes

52
Q

how do you determine that the ST segment is depressed (and significant)

A

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
Q

posterior MI abnormal R wave criteria

A

in V1 and V2:

  • more than 0.04 seconds
  • R bigger than S
  • pt over 30 y/o
  • no signs of RVH
54
Q

normal q wave criteria

A

less than 1/4 the R wave, less than 0.04 seconds

55
Q

when should you have a high degree of suspicion for posterior wall MI

A

ST depression in V1-V3

56
Q

downsloping ST segments (in ST depression) represents

A

a larger area of myocardium affected

57
Q

inferior MI will involve

A

lead 2-3, aVF

58
Q

T wave inversion is caused by ischemia and ____

A

strain (as in LVH or RVH with strain) because the thickened muscle doesnt relax as easily

59
Q

septal MI will involve

A

V1-V2

60
Q

ST elevation

A

injury

61
Q
A
62
Q

lack of O2 to the myocardium, reversible, no permanent damage

A

ischemia

63
Q

symmetrical peaked T waves + ST depression

A

ischemia

64
Q

after ___ hours in an acute MI, the T waves go from ___ to ___

A

after 2 hours in an acute MI, the T waves go from PEAKED to INVERTED

65
Q

which layer of the heart is the last to receive O2

A

endocardium

66
Q

ischemic T wave is more ____ than a normal T wave

A

symmetrical

67
Q

____ receptor stimulation of the coronary arteries causes vasodilation

A

beta

68
Q

in an lateral STEMI (lead 1, aVL, V5-6), you would see reciprocal changes in

A

inferior leads (2, 3, aVF)

sometimes V1-2, but that is more likely to be a posterior MI

69
Q

enlarging or new Q waves

A

infarct

70
Q

MI involving V1-V2

A

septal

71
Q

in an inferior STEMI (2, 3, aVF), you would see reciprocal changes in

A

lateral leads 1 and aVL

sometimes in V1-3, but that is more likely to be from a posterior MI

72
Q

flat ST segment depression

A

previous or completed subendocardial ischemia or infarct

73
Q

how long does it take for pathologic Q waves to develop and how long do they last

A

takes minutes to days to develop, last forever

74
Q

if looking for a posterior MI, where do you look for changes

A

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