正确诊断和治疗.ppt

AMI治疗误区（2） 用太多的中药制剂加大量静脉补液，促进心室扩大重构，产生心衰。 对AMI和心室重构的防治认识不足，为将来心衰埋下了隐患。对AMI RV梗死认识不足，血压能维持时也大量补液，导致重构和心衰。 对低血压休克时，血管活性药物用的不到位，缩血管药量太少，未用硝普钠等血管扩张剂，不能改善组织灌注和心功能，疗效差。 AMI治疗误区（3） 反对AMI恢复期常规做冠造和血运重建（PCI或CABG），带着隐患出院，再梗，心衰等MACE高。对冠造和PCI太积极，AMI后一周即做PCI，无复流和MACE发生率高，不安全。 对AMI恢复，只求4周未死亡，未能达成“彻底康复”的高标准。 AMI PCI只注重大血管开通，达TIMI III级血流，对心肌微血管灌注缺乏认识和研究，对微血管扩张药的应用、增加心肌灌注尚未形成共识。 小 结 个人观点 不太成熟 需要验证 多数正确 请批评指正 * This graphic illustrates the history of plaque formation. Early lesions in the form of isolated macrophage foam cells may occur in infancy. Lipid accumulation can then lead to a fatty streak. Next, lipids accumulate in the extracellular space within the vessel wall. After age 30, an atheroma or visible lipid core may develop. Note that at this point, plaque growth is marked primarily by lipid accumulation. From age 40 on, we can see more fibrous plaques, which depend on the growth of a matrix of smooth muscle cells and collagen over the atheromatous core. Finally, if unstable, plaques may erode or rupture. Once the contents of the plaque are exposed to blood, platelet activation and thrombosis may occur. Stary, et al. Circulation. 1995;92:1355-1374. * * Slide 3 In patients with chronic stable angina pectoris, blood flow to the myocardium is reduced as a result of stenoses in one or more coronary arteries. These stenoses result from stable atherosclerotic plaques that encroach upon the lumen. When the patient is at rest, myocardial oxygen supply usually meets demand. If myocardial oxygen consumption increases significantly, however, myocardial ischemia and angina can occur in patients who have a critical degree of coronary stenosis; this angina is usually relieved by rest. By contrast, in the majority of patients with acute coronary syndromes, there is an acute increase in coronary obstruction. This may occur at rest, and is due to rupture of an unstable fibrous plaque covering an atheroma with consequent platelet adhesion [1]. Reference 1. Braunwald E et al. J Am