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Common Congenital Heart Lesions - page 38 / 126





38 / 126

38 of 126

Early Changes (changes occurring at the time of acute infarction)

  • Cellular Changes:

As myocardial O2 levels fall:

  • Shift in aerobicÆanaerobic metabolism

  • Inability to oxidize fats & products of glycolysis

  • Accumulation of lactic acidÆlow intracellular pH

  • Decreased production of ATP

*These events all lead to impaired function myocytes as:

Decreased ATPÆimpaired Na/K ATPase activityÆincreased intracellular [Na] & Extracellular [K]Æaltered membrane potentialÆarrythmias

Increased intracellular [Na]Æimpaired Na/Ca exchanger activityÆincreased intracellular [Ca]Æintracellular edemaÆwavy myofibers

Increased intracellular [Ca]Æactivation of proteases & lipasesÆcell death & release of serum biomarkers

  • Decreases in myocardial function can occur as soon as 2 minutes following occlusive thrombosis

  • Without intervention, irreversible cell injury can occur within 20 minutes as indicated by membrane defects

  • Proteases & lipases leak across the altered membrane causing more damage and the subsequent release of serum biomarkers (of infarction)

Taken from Dr. Smith’s lecture…

Microscopic Features of Infarction

  • <4 hours - None, variable wavy fibers at border

  • 4-12 hours - Early ischemic necrosis, edema, hemorrhage

  • 12-24 hours - Coagulative necrosis, nuclear pyknosis, hypereosinophilia, contraction band necrosis, early PMNs

  • 1-3 days - Loss of nuclei and striations, interstitial PMNs

  • 3-7 days - Early disintegration of dead myocytes, dying PMNs, macrophages at border

  • 7-10 days - Phagocytosis of dead cells, early granulation tissue at margins

  • 10-14 days - Granulation tissue, new vessels, collagen

  • 2-8 weeks - Gradual loss of cellularity, increasing collagen

  • >2 months - Dense collagenous scar

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