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29 Cards in this Set

  • Front
  • Back
ischemic hrt disease
imbalance of tissue perfusion and oxygen requirement
decreased coronary blood flow
exercise induced ischemia
50-75% narrowing of coronary cross section, adequate at rest
critical stenosis
>75% narrowing of coronary flow, problem at rest
4 ischemic syndromes
MI
Angina Pectoris
Sudden Cardiac Death
Chronic ischemic Heart Disease
12 hrs after MI
Gross: no change
micro: wavy fibers, coagulation necrosis, edema
24-48 hrs after MI
gross: yellow
micro: hypereosinophilic, PMNs at border
3-5 days after MI
gross: tan yellow soft center, hyperemic borders
micro:lots of PMS, coag necr, loss of nuclei
Changes of serum in MI
increased creatine kinase MB CK2
lactic acid dehydrogenase (LDH-1)
cardiac troponin contractile proteins released from injured muscle
What are the major coronary events leading to MI
1)abrupt change or rupture in a stenosing atheroma (already more than 75% reduction)
2) platelets aggregate, activate, release ADP which further builds up aggreg
3) tissue thromboplastin is released activating extrinsic coag
4) platelets relase TXA2, serotonin, PF 3 and 4 causing coag and vasospasm
5) thrombus may become occlusive causing transmural AMI
6-10 days after MI
gross: yellow, depressed central, tan red margins
micro: GRANULATION TISSUE AT BORDER, mummified in center, MO at border
10-14 days after MI
gross: grey red borders, central tan yellow
micro: GRANULATION EVERYWHERE, collagen dep
What are the factors that determine the location and size of MI,
CA involvement (LAD, RCA, LCCA), existance of vascular collaterals, underlying coronary disease
Complications
Arrhythmias, within first few hours,
heart block, AV nodal PostMI, BBB LAS
LV Failure
Progressive infarct
Pericarditis within 2-3 days, pain, rub
Embolism from mural thrombis when endocardium is involved
Rupture (5%)
ventricular Aneurysm
Why is a primary right ventricular infarct rare
because it is thin walled and can be perfused directly from cahmber
when it happens is part of massive LV infarct
Difference between mural and subendocardial infarct
Mural full thickness is most common, wave front phen
subendocardial most vulnerable least well perfuse, inner third of LV wall, multifocal or circumferential depending on coronary involvement
LAD infarct
50%
anterior wall LV; anterior 2/3 septum
RCA infarct
30%
posterior wall LV; post 1/3 of septum
LCCA
20%
lateral wall LV
coronary abnormalities
>75% reduction of cross sectional area of one major
typically wihin first 2-4 cm of LAD and LCCA, and proximal distal thirds of RCA
Systemic Changes after Mi
fever
PMN up
fibrinogen and hepoglobin up (Acute phase reactants)
Electrocardial Changes after Mi
inverted T
elevated ST segment
abnormal Q
When does pericarditis occur
after 2-3 days
when can you rupture
5-7 day is the weakest
when is ventricular aneurysm risk high
2weeks to several months
Hemopericardium
cardiac tamponade
interventrculare septal rupture
L to R shunt, Acute RV failure
rupture of papillary muscles
acute mitral incompetence
what is prinztmetals angina
angina at rest, due to coronary spasm often ST elevated
Sudden cardiac death
dfined as unexpected death within an hour of onset of acute symptoms