Clinical meaning
Acute coronary syndrome results from atherosclerotic plaque disruption within coronary arteries, triggering a cascade of thrombotic events. Vulnerable plaques (thin fibrous cap, large lipid-rich necrotic core, abundant inflammatory macrophages) are most prone to rupture. Plaque rupture exposes subendothelial collagen and tissue factor to flowing blood. Platelet adhesion occurs via GP Ib-IX-V binding to von Willebrand factor on exposed collagen. Platelet activation follows through multiple agonists: collagen binding to GP VI, thrombin binding to PAR-1 and PAR-4 receptors, ADP binding to P2Y12 receptors, and TXA2 binding to TP receptors. Activated platelets undergo shape change, degranulation (releasing ADP, serotonin, TXA2), and surface expression of GP IIb/IIIa which binds fibrinogen to cross-link adjacent platelets. The coagulation cascade amplifies thrombin generation through the tissue factor-factor VIIa complex (extrinsic pathway) and contact activation (intrinsic pathway), converging at factor Xa which converts prothrombin to thrombin. Thrombin converts fibrinogen to fibrin monomers that polymerize and are cross-linked by factor XIIIa, creating a stable fibrin mesh. The degree of coronary occlusion determines the clinical presentation: non-occlusive thrombus produces unstable angina or NSTEMI, while complete occlusion produces STEMI. Ischemic myocytes switch to anaerobic metabolism within seconds, depleting ATP, accumulating lactate and hydrogen ions, causing intracellular calcium overload via failure of Na+/K+-ATPase and Na+/Ca2+ exchanger, ultimately leading to cell membrane disruption and necrosis. The wavefront of necrosis progresses from subendocardium to epicardium over 3-6 hours, defining the therapeutic window for reperfusion. The nurse independently interprets ECG findings, initiates protocol-based interventions, coordinates the catheterization team, and manages hemodynamic monitoring.