Overview Of ST-Elevated Myocardial Ischemia
Disease Process
Cardiac muscles are made up of fibers which are arranged in series of cells called myocytes. Sarcolemma surrounds these fibers and make up tight junctions that increase electrical activity and enable rapid communication between the cells. When a thrombus or fatty plaques build up on arterial walls and occlude normal blood flow, cardiac cells do not receive oxygenated blood and there will be a buildup of carbon dioxide. Under these ischemic conditions, hypoxia occurs from the lack of oxygen and cells will depend of anaerobic metabolism to maintain ATP and survive. This can lead to an acidotic state and cells will compensate by removing excess H+ to extracellular space and take in Na+ intracellularly. The increase in Na+ leads to mitochondrial permeability transition pore (MPTP) opening, leading to cell apoptosis and death. Oxygen deprived cardiac muscle cells will produce troponin, a cardiac regulatory protein involved in controlling calcium levels during the interaction of myosin and actin, which is why a high troponin level in the blood indicates necrosis of cardiac tissue.
Etiology
ST elevated myocardial ischemia (STEMI) occurs due to increased myocardial metabolic demand, and lack of oxygen delivery to the area of infarct. Thrombus or an unstable atherosclerotic plaque occludes the arterial space, resulting in coronary vasospasm from the accumulation of CO2 and lack of O2. There are several conditions that precipitate an MI including hyperlipidemia, diabetes mellitus, severe hypertension, obstructive cardiomyopathy, and aortic valve stenosis. Coronary atherosclerosis is caused of high cholesterol, triglyceride, LDL, and low HDL levels. Atherosclerosis, or thickening and hardening of the arteries predisposes patients to an increased risk of myocardial infarct. Moreover, diabetes mellitus fluctuates lipid and glucose levels in the blood, which increases blood pressure and buildup of atherosclerosis. High blood pressure (hypertension) exerts force against the arterial walls, weakening the wall and increasing the workload of the heart, thereby increasing the risk of MI. Furthermore, tobacco and combustion gases damage blood vessel wall and facilitates the progression of atherosclerosis and precipitate MI. The male gender and family history are non-modifiable factors with an increased incidence of atherosclerosis and MI. Although genetic factors play some role in the etiological process, elements such as a high-fat, high-cholesterol diet, smoking, and alcohol abuse have significant effect on the progression of the disease.
Patient’s past medical history of HLD (hyperlipidemia), acute respiratory failure with hypoxia, hypertension, aphagia, chronic atrioventricular fibrillation is a big contributing factor to STEMI event. Patient claims of frequent consumption of high fat, high calorie diet, which could have contributed to atherosclerosis and hyperlipidemia, all of which increases the risk for STEMI. Patient is not particularly interested in any kind of exercises or muscle-strengthening activities. Lack of exercise is another contributing factor to STEMI that could have predisposed her to encounter this health deficit.
Epidemiology
Coronary artery disease is the leading cause of death in the United States, affecting both men and women. Myocardial infarction is a prevalent and life-threatening disease affecting over 500, 000 people annually and approximately 450, 000 people die from some form of coronary disease each year. Of the 120, 000 deaths in the U. S. due to a STEMI event, males had a 10% higher incidence in comparison to females in people over the age of 60. The prevalence rate increases for women who are post-menopause. At least 9 out of 10 people report risk factors pertaining of smoking, diabetes, atherosclerosis, hypertension, abdominal obesity and hyperlipidemia. Although the incidence rate of STEMI is higher in Western countries, African populations have a higher risk of hypertension and other cardiovascular diseases, and they are also at an increased risk of death from cardiac crisis. Globally, the overall risk of death from acute STEMI is 15%, with more than 50% of those deaths occurring within an hour of the onset of symptoms.
Pathophysiology/Clinical manifestations
Damage to the intimal lining of the coronary arteries increases permeability of the endothelial cell membranes. Platelets, fibrin, and white blood cells congregate at the injured site and cause narrowing of the lumen. The traditional signs and symptoms of myocardial infarction are not detectable until 70% or more of the arterial lumen is occluded. As the arterial lumen narrows, the increasing myocardial demand for oxygen puts stress on the heart. Myocardial metabolism shifts from aerobic to anaerobic, produces lactic acid and stimulates pain nerve endings. The lack of oxygen causes the oxygen-deprived myocardial cells to die, which results in decreased contractility, stroke volume, and blood pressure. Clinically manifested symptoms of the early stages include decreased blood pressure, tachycardia, cyanosis, confusion, dyspnea and arrhythmias. Decreased blood pressure stimulates baroreceptors and stimulates the sympathetic response which increases heart rate and vasoconstriction, further increasing myocardial oxygen demand, triggering arrhythmias, pulse abnormalities, decreased level of consciousness, and cold, sweaty skin.
Tissue damage in the left ventricle can impair the ventricle’s pumping ability, resulting in backflow of blood into left atrium and to pulmonary veins and arteries. The nurse may hear crackles on auscultation of the lungs, dyspnea, orthopnea, and increased pulmonary artery pressure. The patient can also have increased respiratory distress/hyperventilate from acidic pH level, increased PCO2 and buildup of fluid in the alveolar-capillary membrane.
Complications with Treatment Modalities
The therapeutic goal for STEMI patients is to quickly restore normal coronary blood flow and minimize myocardial workload. There are medicinal interventions that include the use of antiplatelet agents such as aspirin. Aspirin works by interfering with the enzyme cyclooxygenase and inhibiting thromboxane A2 formation as well as platelet adhesion. The adverse effect of this drug is increased bleeding tendencies, GI irritation and nausea. Furthermore, oxygen therapy should be utilized for patients with respiratory distress and oxygen saturation less than 90% to compensate for increased pulmonary capillary pressure. Nitrates are vasodilators which reduce cardiac preload and afterload and decreases myocardial oxygen demand. With nitroglycerin, it is important to watch for pounding, uneven heart rate, dry mouth, blurred vision, and severe hypotension, all of which can put patients into shock. Beta blockers such as metoprolol and bisoprolol are used as both acute and long-term management for STEMI patients. It blocks the effect of epinephrine thereby reducing blood pressure, contractility, heart rate, and reduce myocardial oxygen demand and workload. Common yet life-threatening side effects of beta blockers are development of arrhythmia, angina, and heart failure.
Patients of older age and kidney and liver damage, or hemodynamic instability are at a high risk of those potential serious effects and toxicity. Moreover, primary angioplasty is performed within 24 hours for STEMI patients to open occluded cardiac arteries, which was performed for patient S. S. within 4 hours of onset. A catheter is inserted through an open incision (usually start from femoral artery) to the occluded vessel of the heart, and a balloon opens up the occlusion and a stent is placed to maintain the opened blood vessel. Although primary/rescue angioplasty is a procedure that increases the chance of survival and decreases the risk of another STEMI event, there are risks associated with the procedure. Patients can have a hemorrhagic crisis from bleeding of the femoral artery, or it can cause arrhythmia or another infarct from a dislodged thrombus. It is rare that a catheter will tear or damage an artery, but it is a possibility that can be life-threatening because the patient can have internal bleeding and go into a state of shock.
