Lecture 7- MI Flashcards
sub-epicardial
entire thickness of cardiac wall is affected
sub-endocardial
partial thickness of cardiac wall is affected
ventricular remodeling
after MI
both infarcted and non-infarcted areas
changes in shape and thickness
is ischemia reversible?
yes
if EDV is higher, therefore
stroke volume is lower
sympathetic activation during MI (4)
increase HR and BP
constrict arterioles
venoconstriction
increased RAA
compensatory mechanisms during MI (3)
aren’t actually helping
sympathetic NS
hypertrophy
vasovagal response
vasovagal response
leads to bradycardia and hypertension
symptoms during MI
chest discomfort nausea dyspnea (difficulty breathing) diaphoresis (sweating) weak hypertension arrhythmia
biomarkers in MI
myoglobin CK-MB Trop 1 Trop 2 CK LDH
which biomarkers will remain elevated
trop 1 and 2 (best markers)
area of necrosis
tissue is dead
what causes changes in T wave?
ischemia prolongs repolarization
inversion or tall T wave- early sign
3 I’s
ischemia
injury
infarct
ischemia
T wave inversion or tall T
injury
ST elevation- subepicardial injury
ST depression- subendocardial injury
infarct
abnormal Q wave
J point
where ST segment begins
above baseline- elevation
below baseline- depression
smiley
in healthy pt, benign
frowny
myocardial damage
EKG changes during MI
onset of pain, normal EKG w/ tall T wave
1 hr- ST elevation means myocardial necrosis
if given drugs- ST reduces by 50%
24 hrs- ST returning to normal, T wave inverted
months- deep Q wave
what do leads II, III, aVF see?
RCA, inferior surface
what do leads V5, V6, I, aVL see?
LCX, lateral surface
what do leads V3, V4 see?
LAD, anterior surface
what do leads V1, V2 see?
LCA, septal
treatment for MI
reduce O2 demand, increase blood flow
how- O2, rest, beta blockers, calcium channel blockers
grafts used for bypass
internal mammary artery
radial artery
saphenous vein (most common)
gastroepipolic artery
