Acute Myocardial Infarction

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1. Definition of acute myocardial infarction?

the early critical stage of necrosis of heart muscle tissue caused by blockage of a coronary artery. It is characterized by elevated S-T segments in the reflecting leads and elevated levels of cardiac enzymes

2. Pathophysiology of acute MI

Three pathologic phases of MI
MI can be categorized pathologically as acute, healing, or healed. Acute MI. In the first 6 hours after coronary artery occlusion, coagulation necrosis can be seen with no cellular infiltration. After 6 hours, polymorphonuclear leukocytes infiltrate the infarcted area, and this may continue for up to 7 days if coronary perfusion does not increase or myocardial demand does not decrease. Healing MI is characterized by mononuclear cells and fibroblasts and the absence of polymorphonuclear leukocytes. The entire healing process takes 5 to 6 weeks and can be altered by coronary reperfusion. Healed MI refers to scar tissue without cellular infiltration.

3. Treatment for patient with MI
Medical Options
* Antiplatelet Agents : Aspirin

Supplemental Oxygen
Oxygen should be administered to patients with symptoms or signs of pulmonary edema or with pulse oximetry less than 90% saturation.4 The rationale for using oxygen is the assurance that erythrocytes will be saturated to maximum carrying capacity. Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and by other tissues may be diminished. In some cases, elevated pulmonary capillary pressure and pulmonary edema can decrease oxygen uptake as a result of impaired pulmonary alveolar-capillary diffusion. Supplemental oxygen increases the driving gradient for oxygen uptake.1 Arterial blood that is at its maximum oxygen-carrying capacity can potentially deliver oxygen to myocardium in jeopardy during an MI via collateral coronary circulation. The recommended duration of supplemental oxygen administration in a MI is 2 to 6 hours, longer if congestive heart failure occurs or arterial oxygen saturation is less than 90%. However, there are no published studies demonstrating that oxygen therapy reduces the mortality or morbidity of an MI. Nitrates

Intravenous nitrates should be administered to patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI.4, 9 The primary benefit of nitrates is derived from its vasodilator effect. Nitrates are metabolized to nitric oxide in the vascular endothelium. Nitric oxide relaxes vascular smooth muscle and dilates the blood vessel lumen. Vasodilatation reduces cardiac preload and afterload and decreases the myocardial oxygen requirements needed for circulation at a fixed flow rate. Vasodilatation of the coronary arteries improves blood flow through the partially obstructed vessels as well as through collateral vessels. Nitrates can reverse the vasoconstriction associated with thrombosis and coronary occlusion. Pain Control

Pain from MI is often intense and requires prompt and adequate analgesia. The agent of choice is morphine sulfate, given initially IV at 5 to 15 minute intervals at typical doses of 2 to 4 mg.4 Reduction in myocardial ischemia also serves to reduce pain, so oxygen therapy, nitrates, and beta blockers remain the mainstay of therapy. Because morphine can mask ongoing ischemic symptoms, it should be reserved for patients being sent for coronary angiography. This was downgraded to a IIa recommendation in the latest STEMI guidelines. Beta Blockers

Beta blocker therapy is recommended within 12 hours of MI symptoms and is continued indefinitely.4, 9 Treatment with a beta blocker decreases the incidence of ventricular arrhythmias, recurrent ischemia, reinfarction, and, if given early enough, infarct size and short-term mortality. Beta blockade decreases the rate and force of myocardial contraction and decreases overall myocardial oxygen demand. In the setting of reduced oxygen supply in MI, the reduction in oxygen...
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