10 Cardiac Ischemia
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Angina vs MI:
Angina: Symptoms relieved by NG; MI not relieved by NG
stable: unruptured plaque, blocking blood flow. RBC squeeze through. Symptoms with exertion. May have ST depression during symptoms
unstable angina: ruptured plaque, clot, subendothelial (ST depression) ischemia (no markers)
prinzmetal: transmural (ST elevation) ischemia (no markers)
NSTEMI: subendothelial necrosis, clot not completely obstruct artery (not transmural yet)
STEMI: transmural necrosis, clot completely obstructs artery, transmural
coronary ischemia most cause of sudden death, except with HCM in young people
angina: squeezing type of chest pain
lavigne sign: patient place hand over chest
vagus run along inferior wall of heart, can be stimulated with inferior MI
angina, MI in past highest risks
other very high risks
1 hour after chest pain: no cardiac marker, nl biomarkers
pt with rhabdo will have very high CK, but mostly MM
liver enzyme
blue: small area of subendocardial ischemia
endocardium can get blood from ventricle. Subendo receive blood from epicardial vessels, most vulnerable to ischemia
in mild ischemia: subendo ischemic first
ischemic tissues create electric current going away from it
T: EKG lead looking at LV
At baseline: T sees current heading towards it (elevated ST baseline)
Heart depolarize: everything at normal baseline
repolarize: elevated baseline again
Appears to have ST depression, in reality, baseline elevation
normally: subendo repolarizes first, current goes to T, create upward T wave from current heading towards it
subendo ischemia: subendocardium repolarizes last, reversing wave of repolarization, going away from T, inverted T
transmural ischemia, current away from it
baseline: T sees current heading away, depressed baseline
depolarizes: everything at baseline
repolarizes: depressed baseline again
ST elevation = baseline ST depression
transmural MI progression
Q wave after a few hours, but also represent old infarction
T wave invert after few days
normal ST
T wave normal, Q wave remain
tell which leads ischemic with transmural infarct
anterior wall
Overview:
1st thing: coagulative necrosis: removed nucleus from cells
2nd: acute inflammation with neutrophils/macrophages
3rd: healing, granulation, then conversion to scars
< 4 hours:
congestive heart failure: blood back up and can’t pump
arrythmia from damaged conduction
1-7 days:
WBC gives yellow pallor gross color
complication depends on whether neutrophil or macrophages
neutrophil: transmural inflammation, exudate leak to pericardium, pericarditis. Only with transmural inflammation
macrophage: eat up all dead debris, wall = weakest, rupture
1-3 weeks:
granulation: blood vessels, red border from outside, from normal tissues
months:
scar: not as strong as myocardium, not good movement, stasis, aneurysm/thrombus
1 day, 1 week, 1 month
1st day: coagulative necrosis
after 1st day: inflammation up to 1 week, neutrophil then macrophage
after 1 week: granulation
1 month: scar
subendo, mottled color
coagulation necrosis
inflammation
pericarditis
rupture
papillary muscle
scar
collagen, CT, type 1
aneurysm
return of blood flow: contraction band
return blood flow, Ca inflow into dead cells, contraction of muscle fibers, dense contraction bands
reperfusion: free radicals from O2 coming back. Cardiac enzyme continue to rise after open up clot
VTACH, can deteriorate into cardiac arrest
can cause tamponade if accumulation of fluid
inferior wall: papillary muscle with single supply from RCA
thrill: feel with hand
hypotension: blood leaks from left to right
US: apex with akinetic tissue, aneurysm with stasis of blood on left side
can have stroke if a piece breaks off
anterior infection: most common
EKG with pericarditis
diffuse ST elevation
PR depression, down going
autoimmune
like sand paper
extension of inflammation into pericardium
dye with fluoroscope
put in stent
balloon first to push the plaque, then leave stent (chickenwire) in
PCI: going across skin to access artery
PTCA: lumen of artery to get to coronary artery
PCI: within 90 min of symptoms onset
more than 90 min: tpa
PCI unsuccessful: emergency CABG
systolic dysfunction: cardiomyopathy with reduced LV EF
hibernating myocardium: myocardium so little flow that going into hibernation
in valve surgery: treat blocked artery at same time
bypass backup option
trigger inflammation when put in
drug: sirolimus/tacrolimus to prevent stenosis
thrombosis: complete closure of stent by blood clot inside
endothelialization: scar tissue grew over stent
1: catheter
time it takes: door to balloon or needle
inferior MI: bradycardia and AV block already from parasympathetic stimulation. Adding beta blocker make it worse
usually LV infarct, RV sometimes can be infarcted
hypotension and then cardiac arrest
No intRUDIN: bivaliRUDIN is a direct thrombin inhibitor
Big GATOR: arGATROban and dabiGATRAN are direct thrombin inhibitors
ABC sportscaster grabbing fries: abciximab blocks the GP IIb/IIIa receptor preventing platelet aggregation
Antibody-shaped microphones: abciximab is a monoclonal IgG antibody
Tied game: eptifibatide and tirofiban block the GP IIb/IIIa receptor to prevent platelet aggregation
Broken plates: GP IIb/IIIa inhibitors can cause thrombocytopenia
Ketchup time: antiplatelet therapy increases bleeding time (measure of platelet function)
damage to heart tissues but absence of EKG elevation
not important
treated just like NSTEMI
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