Carlos Shared "MI Evolution" - 5 Picmonics

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MI Evolution

Early findings after MI (0- 4 hours)
Hypoxia leads to inversion of metabolsism to Anaerobic metabolism, this decreases ATP synthesis and increase Lactic Acid
Decrease in ATP disrupts function of Na+/K+ ATPase
This leads to increased Na+ intracelullarly, pulling in water, causing cellular edema
Increased K+ extracellularly, increasing risk for Arrhythmia
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Post MI changes after 4-24 hours
Early coagulative necrosis
Release of necrotic cell contents into blood from myocyte (LDH, CK-MB, Troponin, Inflammatory cytokines)
Dark mottling of heart that looks pale with tetrazolium stain
Tetrazolium binds to LDH, if there is no LDH, it means that the area is infarcted and has spilled its LDH.
Hypoxic environment stimulates HIF (hypoxic Induced factor) which leads to vascular prolypheration due to VEGF
Neutrophils start to respond to inflammatory trigger
Edema, hemorrhage and wavy fibers are seen histologically
Newly introduced oxygen (example: from a placed stent) is used by the netrophils leading to generation of free radicals that causes more damage. This is called Reperfusion Injury.
During reperfusion, Calcium (Ca2+) is introduced to recently damaged myocytes. Sarcomeres within the myocyte are exposed to the calcium, which leads to contraction. Since there is no ATP, myocin head cannot be uncocked (sarcomeres remain contracted)
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Post MI changes after 1-3 days
Extensive coagulative necrosis
Tissue surrounding infarct shows acute inflammation with neutrophils. Hyperemia can be seen (redness at infarct).
Postinfarction fibrinous pericarditis that presents as chest pain and friction rub
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Post MI changes after 3-14 days
Neutrophils call in Monocytes after their job is done. These Monocytes transform into Macrophages.
Hyperemic border; central yellow-brown softening maximally yellow and soft by 10 days. This border is due to VEGF from Hypoxia. Monocytes use these weak vessels to enter the infarct location so the macrophages can eat the dead tissue. The area is yellow
Softening of wall can lead to free wall rupture which causes cardiac tamponade due to flow going through gap and accumulating around the heart
LV pseudoaneurysm (risk of rupture). Known as False aneurysm because only one layer is involved.
Papillary muscle rupture leads to acute mitral regurgitation.
Interventricular septal rupture due to macrophage-mediated structural degradation can lead to shunt (VSD)
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Post MI changes after 2 weeks to several months
Contracted scar complete: After macrophages clear out debris in infarct location, they release many cytokines. They release TGF-Beta and PDGF which tell fibroblasts to start making collagen to replace the area previously occupied by healthy myocytes.
Scar appears gray-white in gross examination. Collagen stains pink.
Scar has no myocytes, making it hypocontractile/hypokinetic. This can lead to true ventricular aneurysm. No risk of rupture due to involving all 3 layers of the wall.
Risk of mural thrombus due to statis of blood in the hypocontractile area.
Dressler syndrome: Autoimmune phenomenon resulting in fibrinous pericarditis
Heart failure
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