The diagnosis and treatment of stemi in the emergency department gas x while pregnant


Acute myocardial infarction (MI) is the leading cause of death in the United States 1 and in much of the developed world. It is also a rising threat in developing countries. 2 Rapid diagnosis and treatment of MI is one of the hallmark specializations of emergency medicine (EM) because emergency departments (EDs) are a common health care entry point for patients experiencing MI-associated symptoms, MI is a life-threatening condition, and the emergency medical system has developed tools to manage it effectively. A patient whose MI is missed on evaluation has a 25% likelihood of a very poor outcome, which makes this a "can’t miss" diagnosis for the EM clinician. It is worth noting that missed MI has long been the most common justification for monetary awards in EM litigation. 3

Acute coronary syndrome (ACS) is one of many causes of MI and describes cardiac ischemia that results when a blood clot, or thrombus, acutely narrows an artery supplying myocardial cells with blood. Specifically, ACS is ischemia due to atherosclerotic plaque rupture. Blood clotting factors interact with the plaque’s contents and trigger the formation of a superimposed blood clot that narrows or, in the case of an ST-segment elevation myocardial infarction (STEMI), fully occludes the blood vessel lumen. ACS includes unstable angina and non-ST segment elevation myocardial infarction (UA/NSTEMI) as a combined phenomenon, as well as STEMI, but it is differentiated from other forms of cardiac ischemia such as demand ischemia or coronary vasospasm.

In UA/NSTEMI, a clot narrows the lumen enough to limit blood flow and cause myocardial ischemia. This ischemia often leads to chest pain or chest pain-equivalent symptoms (see the Emergency Department Evaluation: History section) of a different pattern from the patient’s baseline experience. This can be chest pain of a different quality or frequency for a patient with a history of angina or new chest pain in a patient who has never experienced these symptom before. ECG changes may or may not be seen with ischemia alone. Ischemia may lead to infarction that involves the myocardial tissue but falls short of affecting the full thickness of the myocardial wall as is the case with STEMI. The infarction is evidenced by eventual elevation of cardiac enzymes (troponin and/or creatine kinase isoenzyme MB [CK-MB]) and ECG changes including ST-segment depressions, inverted T waves, or (the most common finding) non-specific ST-segment changes. (See Figure 1.) In contrast, a STEMI typically occurs when this same process leads to complete occlusion of a coronary artery with transmural, or full thickness, myocardial wall infarction. (See Figure 1.)The ECG will show ST-segment elevations in the area of the heart fed by the affected blood vessel. Any ST-segment elevation is suggestive of a STEMI. However, ECG changes must meet STEMI criteria (see the Emergency Department Evaluation section) in order for this diagnosis to be made. 4-6 In all cases of cardiac ischemia, treatment objectives are to increase the delivery of blood to myocytes beyond the obstructive lesion and to limit the myocytes’ demand for oxygen-carrying and metabolite-removing blood. What differentiates STEMI therapy from treatment of other cardiac ischemic conditions is the primary focus on immediate reperfusion with percutaneous coronary intervention (PCI) performed in a cardiac catheterization laboratory or with fibrinolytic agents given intravenously. 7