Introduction/Etiology and Pathophysiology of STEMI
Myocardial infarction is a serious and potentially life threatening emergency. Rapid assessment and diagnosis is imperative to correctly treat a patient. It is essential for the nurse and healthcare team to understand the diagnostic procedures, lab tests, and treatments that can provide life -saving treatment for a patient presenting with chest pain. Myocardial infarctions can occur in different parts of the heart and can be given different classifications depending on the presenting symptoms. The most serious type of myocardial infarction is classified as an ST-elevation myocardial infarction or STEMI.
A STEMI is one type of heart ...view middle of the document...
Most of these people are not hospitalized and experience a sudden death from cardiac arrest (AHA, 2010). “Most myocardial infarctions are due to atherosclerosis of a coronary artery, rupture of the plaque, subsequent thrombosis, occlusion of blood flow, coronary artery spasm, platelet aggregation, or emboli from mural thrombi” (Ignatavicius & Workman, 2013, p. 829).
Myocardial infarctions often begin with infarction of the subendocardial layer of cardiac muscle, which has the longest myofibrils, greatest oxygen demand, and the poorest oxygen supply (Ignatavicius & Workman, 2013, p. 830). There are two other zones that surround the initial area of infarction. The first is the zone of injury, which is tissue that is injured but not necrotic. This is when the ST elevation will show on the ECG (Ignatavicius & Workman, 2013, p. 830). The second is the zone of ischemia, which is tissue that is oxygen deprived. This is when a T-wave inversion may show on the ECG (Ignatavicius & Workman, 2013, p. 830). It causes a decrease in oxygen in the heart, which may lead to local vasodilation of blood vessels, acidosis, and electrolyte imbalances (Ignatavicius & Workman, 2013, p. 830). In response to the decrease in oxygen, or hypoxia, and intense pain, epinephrine and norepinephrine are released, increasing the heart’s rate, contractility, and afterload (Ignatavicius & Workman, 2013, p. 830). This only leads to depriving the heart of even more oxygen.
Physical changes to the heart do not occur until six hours after the infarction, which is why the need for intervention in the first four to six hours is crucial to get the blood flow restored (Ignatavicius & Workman, 2013, p. 830). When the infarction only involves the subendocardium it is called a subendocardial MI, and when all three layers are involved, it is called a transdermal MI (Ignatavicius & Workman, 2013, p. 830). The infracted area of the heart goes from turning blue and swollen after six hours, to gray with yellow streaks after forty-eight hours (Ignatavicius & Workman, 2013, p. 830). Once eight to ten days has passed, granulation tissue begins to form on the edges of the necrotic tissue, which then develops into a firm scar in about two to three months (Ignatavicius & Workman, 2013, p. 830). The problem with this scar tissue is that it will not contract or conduct electricity, which many times will lead to ventricular dysrhythmias. How a person responds to a myocardial infarction all depends on which coronary artery or arteries were obstructed and which part of the left ventricle was damaged (Ignatavicius & Workman, 2013, p. 831).
Prevalence of the Disease and Risk Factors
According to the American Heart Society (2013), 250,000 Americans experience ST-elevated myocardial infarctions each year. This 250,000 Americans represents 25% to 40% of all 683,000 US patient diagnosed with acute coronary syndrome each year (AHA, 2013). Of the 250,000 patients who experience a STEMI,...