Acute Myocardial Infarction

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Definition Myocardial infarction (MI) is defined as death of myocardial tissue. The extent and location of the infarction depend on the degree of ischemic burden, the availability of coronary collateral blood flow, the rapidity of reperfusion, and the location of the afflicted coronary artery.[1] Pathophysiology An increase in myocardial oxygen demand relative to the available myocardial oxygen supply or an acute decrease in myocardial oxygen delivery can precipitate acute myocardial ischemic injury. Episodes of ischemia that last more than 30 minutes usually cause MI. The involved area can be divided into three zones: the zone of infarction, the zone of injury, and the zone of ischemia . The infarction may be limited to the interior of the myocardium (subendocardial MI) or to a visceral layer of the pericardium (epicardial MI) or may extend through the full thickness of the myocardial wall (transmural MI). The most common cause of AMI is atherosclerosis of the coronary arteries, which narrows the coronary lumen and reduces myocardial blood supply. The terms athero and sclerosis are derived from the Greek words gruel and hard, respectively. The word gruel is similar to the rubbish located at the foundation of most formed plaques. Hard corresponds to the fibrotic cap of the lesion. The first noticeable sign of an atherosclerotic lesion is a fatty streak (yellow stripe) that runs parallel to the axis of the vessel. The lesion progresses to form a necrotic core composed primarily of lipids and cellular debris. Fibrous caps composed of smooth muscle and collagen cover the fatty streaks, leading to "vulnerable" lesions. Ulceration of the vulnerable lesion or regional changes in blood flow trigger platelet aggregation, leading to thrombosis and coronary occlusion. Platelet involvement in thrombus formation begins with vessel wall injury, followed by platelet adhesion, activation, and aggregation. Diabetes mellitus, high levels of low-density lipoprotein (LDL) cholesterol, increased levels of catecholamines, or other factors affecting blood flow can contribute to the formation of an intravascular clot.[2] Clinical Presentation and Diagnosis Signs and Symptoms A physical examination for AMI includes the following: * Vital signs, general observation * Pulmonary auscultation for rales * Presence or absence of stroke * Presence or absence of pulses * Presence or absence of systemic hypoperfusion (cool, clammy, pale, and ashen extremities)[3] Diagnosis [4] Main parameters considered for detection of AMI are, Total CPK CK-MB mass CK-MB mass Troponin 1 Treatment Oxygen Analgesics and Anxiolytics Nitrates Antiplatelet Agents Unfractionated Heparin Low-Molecular-Weight Heparin Direct Thrombin Inhibitors Reperfusion Therapy Thrombolytic Agents Primary Coronary Angioplasty With Stent Placement Facilitated PCI Rescue Coronary Angioplasty v-Adrenergic Blocking Agents Calcium-Channel Blockers ACE Inhibitors Magnesium Potassium Antiarrhythmics Anticoagulants Lipid-Lowering Therapy[5] REFERENCES : 1) 2) 3) 4) 5)

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Author: Swagat K. Soni

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