ACS Flashcards
ACS triggers
physical activity, emotional stress, SNS activation
endogenous anti thromotics
antithrombin III (enhanced w/ heparin), protein C and S (degrade Va and VIIIa), tissue factor inhib, tPA, prostacyclin (ups platelet cAMP and inhibits activation), NO
how much ischemia can cause infarct
20-30 min
how long to dissolve thrombus
12-24 hours
transmural infarct vs subendocardial
spans entire thickness of myocardium vs only innermost layers (more susceptible to ischemia)
factors determining amount of tissue death
mass perfused, magnitude/duration of ischemia, oxygen demand, collateral coronary flow, amount of reperfusion, inflammatory response
LAD occlusion
anterior LV, anterior 2/3 septum, apical LV
LCx occlusion
lateral LV, poserolateral LV
RCA occlusion
posterior LV, posterior 1/3 septum, posterior pap muscle, inferior
when does irreversible injury occur
in 20 mins
describe early changes during MI
shift to anaerobic, lactic acid accumulates, ATP drops, high Na causes cellular edema, abnormal electrolytes causes risk for arrhythmia (VT and V fib)
when does dark mottling of myocardium begin
4-12 hours
tan necrotic center forms?
1-3 days
when is injury maximally yellow tan, depressed red tan borders
3-14 days
when gray white scar forming
2-8 weeks
mature scar from MI?
more than 2 months
micro of MI less than 4 hours
no change, some wavy fibers
micro MI 4-12 hrs
early coag necrosis, edema, wavy fibers
micro MI 12-24 hrs
coag necrosis, pyknosis, contraction bands, early PMNs
micro MI 1-3 days
extensive coag necrosis, loss of nuclei, interstitial PMNs
micro MI 3-14 days
dying PMNs, disintegrating dead myocytes, macros and granulation tissue at border
micro MI 2-8 weeks
loss of cells, more collagen
micro MI over 2 months
dense collagenous scar
contrast hypokinesis, akinesis, dyskinesis
in order: reduced contraction, no contraction, local region bulging outward
diastolic dysfn from MI
impaired relaxation, less compliance and elevated filling pressue
stunned myocardium
prolonged but reversible contractile dysfn
ischemic preconditioning
brief ischemia renders tissue more resistant to future ischemia
functional changes w/ MI
ventricular remodeling of infarcted and non-infarcted myocardium
Sx of MI
angina; nausea vomiting weakness (PSNS, vagal); diaphoresis, cool skin (SNS), fever (inflammatory), SOB
look for ___ in physical exam
breathing airway, circulation, systemic hypoperfusion, HF (S4, rales, IJV)
importance of dynamic T wave inversions
w/ T wave inversions that resolve after nitro tx, more likely ischemia
MI defined as rise in troponin and…
at least one: sx of acute ischemia, new ECG finding, imaging findings, ID of thrombus w/ angiography
CK-MB and dx of MI
CK-MB more than normal and more than 2.5% of total CK
meaning of initial negative biomarkers
doesnt rule out MI, can take time for elevation
w/ angina and ST elevations, dont wait for biomarkers to tx
some other causes of Tn elevation
acute HF, PE, shock, dissection, myocarditis, trauma, ICD discharge
MI dx w/ ECG
more than 1mm ST elevation in 2 contiguous leads or 2 mm in contiguous precordial leads or new LBBB (treated like STEMI, hard to tell apart)
ST in II, III, aVF
inferior, RCA (some LCx if left dominant)
ST in V2-V4
anterior, LAD
ST in V1-V4
anteroseptal, LAD
ST in I, aVL, V5V6
lateral, LCx
LBBB
anterior, LAD
ST in V4R
RV, RCA
ST depressions in V1 and V2
posterior, RCA (LCx if left dominant)
electrically silent MI
LCx
pathologic Q waves
more than 1 mm wide, 25% amplitude of QRS, 2 or more contiguous lead
variant angina/prinzmetal
coronary artery spasm, transient ST elevations
risk factor and dx/ tx for variant angina
risk w/ smoking, dx w/ cardiac cath, tx w/ nitrates, CCBs
UA vs NSTEMI
UA has negative Tn, no infarction
ECG of UA/NSTEMI
ST depression or T wave inversion, no pathologic Qs chronically
TIMI criteria
over 65, known CAD, 3 or more CAD risk factors, ASA use w/i 7days, 2 or more angina episodes w/i 24 hours, ST changes above .5 mm, elevated Tn or CK-MB
other ACS causes
Supply: hypotension from shock, anemia, dissection/embolus
demand: rapid tachy, acute HTN, severe aortic stenosis