Acute Coronary Syndrome (ACS)

Acute coronary syndrome (ACS) encompasses a spectrum of clinical presentations resulting from acute myocardial ischemia: unstable angina, non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). The underlying mechanism involves rupture or erosion of a vulnerable atherosclerotic plaque within a coronary artery, exposing the lipid-rich necrotic core and thrombogenic subendothelial matrix to circulating blood. This triggers platelet adhesion via glycoprotein Ib-IX-V receptor binding to von Willebrand factor, followed by platelet activation through thromboxane A2 (TXA2) and adenosine diphosphate (ADP) release, and platelet aggregation mediated by glycoprotein IIb/IIIa receptor cross-linking with fibrinogen. The tissue factor pathway simultaneously activates the coagulation cascade, generating thrombin that converts fibrinogen to fibrin, stabilizing the platelet-rich thrombus. In unstable angina the thrombus is non-occlusive causing ischemia without necrosis (troponin negative). In NSTEMI partial occlusion causes subendocardial necrosis (troponin elevated, ST depression). In STEMI complete occlusion causes transmural necrosis (troponin elevated, ST elevation). Myocardial cell death begins within 20 minutes of sustained ischemia in the subendocardium, progressing toward the epicardium over 3-6 hours. The practical nurse monitors vital signs, recognizes chest pain characteristics using PQRST, administers prescribed...