心肌梗死-护士讲课.pptVIP

0 5 10 15 20 25 30 % 死亡率 CCU前 CCU 溶栓 PCI 30 15 8 4 AMI 预后 小 结 心肌梗死是冠心病的一种 心肌梗死分为STEMI和NSTEMI 心肌梗死的机制是斑块破裂 心肌梗死的诊断 严重而持久的胸骨后疼痛 心肌坏死标记物升高 心电图进行性改变 心肌梗死的治疗可以归结为三大类 一般治疗 药物治疗 血运重建治疗 PCI和/或CBAG 郑大一附院 预祝我们的护士姐妹常吃不胖 —到60岁的年龄时 　　 拥有20岁的心脏！ * * Slide 4 Pathophysiology of ACS Various factors affect the risk that an atherosclerotic plaque will rupture, including the tensile strength of the fibrous cap and the shear stresses to which it is subjected. Unstable plaques at high risk of rupture typically have a large lipid core, a thin cap and contain large numbers of macrophages but relatively few smoothmuscle cells. Rupture or fissure of the plaque exposes the thrombogenic core of the lesion and leads to adhesion and aggregation of platelets and thrombus formation. A large fissure typically results in the formation of a large thrombus that completely occludes the coronary artery, causing acute MI, characterized by persistent ST-segment elevation and subsequent development of new Q-waves on the electrocardiogram (ECG). A smaller fissure may result in a mural thrombus that partially or transiently occludes the artery, causing acute myocardial ischemia without persistent ST-segment elevation. The clinical diagnosis is unstable angina, or if thereis biochemical evidence of myocardial damage, non-Q-wave MI. ACS is a classic example of atherothrombosis (plaque rupture and thrombus formation). References Fuster V, Badimon L, Badimon JJ et al. N Engl J Med 1992;326:310–318. Davies MJ. Circulation 1990;82(Suppl 3):II38–46. * 初发心绞痛原有性质发生变化，发作时恶心呕吐大汗，明显心动过缓，疼痛血压大幅度波动，伴有心力衰竭。ECG明显ST-T改变。 * 标记物 升高时间 高峰时间 恢复时间 肌红蛋白 2h 12h 24~48h cTnI 3~4h 11~24h 7~10d cTnT 3~4h 24~48h 10~14d CK-MB 4h 16~24h 3~4d CK 6h 24h 3~4d AST 6~12h 24~48h