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
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)
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).
- COMPLICATIONS
- Postinfarction fibrinous pericarditis that presents as chest pain and friction rub
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
- COMPLICATIONS
- 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.
- NEW MURMURS POST MI
- Papillary muscle rupture leads to acute mitral regurgitation.
- Interventricular septal rupture due to macrophage-mediated structural degradation can lead to shunt (VSD)
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.
- COMPLICATIONS
- 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
- Arrhythmias
