cardiovascular disorders
Overview of Acute Coronary Syndromes (ACS)
Pathophysiology of Acute Coronary Syndromes
Initial consequences vary with size, location, and duration of obstruction and range from transient ischemia to infarction. Measurement of newer, more sensitive markers indicates that some cell necrosis probably occurs even in mild forms; thus, ischemic events occur on a continuum, and classification into subgroups, although useful, is somewhat arbitrary. Sequelae of the acute event depend primarily on the mass and type of cardiac tissue infarcted. Ischemic (but not infarcted) tissue has impaired contractility and relaxation, resulting in hypokinetic or akinetic segments; these segments may expand or bulge during systole (called paradoxical motion). The size of the affected area determines effects, which range from minimal to mild Heart Failure (HF) to Acute Myocardial Infarction (MI) is myocardial necrosis resulting from abrupt reduction in coronary blood flow to part of the myocardium. Infarcted tissue is permanently dysfunctional; however, there is a zone of potentially reversible ischemia adjacent to infarcted tissue. MI affects predominantly the left ventricle (LV), but damage may extend into the right ventricle (RV) or the atria. Infarction may be Transmural: Transmural infarcts involve the whole thickness of myocardium from epicardium to endocardium and are usually characterized by abnormal Q waves on ECG. Nontransmural (subendocardial): Nontransmural infarcts do not extend through the ventricular wall and cause only ST-segment and T-wave (ST-T) abnormalities. Because the transmural depth of necrosis cannot be precisely determined clinically, infarcts are usually classified as STEMI or NSTEMI by the presence or absence of ST-segment elevation or Q waves on the ECG. Necrosis of a significant portion of the interventricular septum or ventricular wall may rupture, with dire consequences. A ventricular aneurysm or pseudoaneurysm may form. Electrical dysfunction can be significant in any form of acute coronary syndrome. Ischemic and necrotic cells are incapable of normal electrical activity, resulting in various ECG changes (predominantly ST-T abnormalities), arrhythmias, and conduction disturbances. ST-T abnormalities of ischemia include ST-segment depression (often downsloping from the J point), T-wave inversion, ST-segment elevation (often referred to as injury current), and peaked T waves in the hyperacute phase of infarction. Conduction disturbances can reflect damage to the sinus node, the atrioventricular (AV) node, or specialized conduction tissues. Most changes are transient; some are permanent. 