Myocardial Infarction

A heart attack, also known as a myocardial infarction, usually occurs when a blood clot forms inside a coronary artery at the site of an atherosclerotic plaque. The blood clot severely limits or completely cuts off blood flow to part of the heart. In a small percentage of cases, blood flow is cut off when the muscles in the artery wall contract suddenly, constricting the artery. This constriction, called vasospasm, can occur in an artery that is only slightly narrowed by atherosclerosis or even in a healthy artery.

Regardless of the cause of a heart attack, the oxygen deprivation is so severe and prolonged that heart muscle cells begin to die for lack of oxygen. About 1. 1 million people in the United States have a heart attack every year; the heart attacks prove fatal for about 40 percent of these people (Microsoft Encarta, 2004). ETIOLOGY The most common cause of acute myocardial infarction (AMI) is complete or nearly complete occlusion of a coronary artery usually precipitated by rupture of the vulnerable atherosclerotic plaque and subsequent thrombus formation.

Plaque rupture can be precipitated by both internal and external factors. Internal factors include plaque characteristics, such as the size and consistency of the lipid core and the thickness of the fibrous cap, as well ac conditions to which it is exposed, such as coagulation status and degree of arterial vasoconstriction. Vulnerable plaques most frequently occur in areas with less than 70% stenosis and are characterized by an eccentric shape with an irregular border, a large, thin lipid core, and a thin, fibrous cap. External factors result from actions of the client or from external conditions that affect the client.

Strenuous physical activity and severe emotional stress, such as anger, increased sympathetic activity, which in turn, increases hemodynamic stress that may lead to plaque rupture. At the same time, sympathetic activity increases myocardial oxygen demand. Scientists have reported that external factors, such as exposure to cold and time of day, also affect plaque rupture. Acute coronary events occur more frequently with exposure to cold and during the morning hours. Researchers hypothesize that the sudden increases in sympathetic activity associated with these factors may contribute to plaque rupture.

The role of inflammation in triggering plaque rupture is currently being studied. Regardless of the cause, rupture of the atherosclerotic plaque results in •Exposure of the plaque’s lipid-rich core to flowing blood. •Seepage of blood into the plaque, casing it to expand. •Triggering of thrombus formation. •Partial or complete occlusion of the coronary artery. Unstable angina is associated with short term partial occlusion of a coronary artery. Whereas AMA results from significant or complete occlusion of a coronary artery that last more than one hour. When blood flow ceases abruptly, the myocardial tissue supplies by that artery dies.

Coronary artery spasm can also cause acute occlusion (Black & Hawks, 2004). CLINICAL MANIFESTATIONS The clinical manifestation result from ischemia of the heart muscle and the decrease in function and acidosis associated with it. The major clinical manifestation is chest pain, which is similar to angina pectoris but more severe and unrelieved by nitroglycerin. The pain may radiate to the neck, jaw, shoulder, back or left arm. The pain also may present near the epigastrium, stimulating indigestion. AMI may also be associated with less common clinical manifestation including the following: •Atypical chest, stomach, back or abdominal pain. Nausea and dizziness •Shortness of breath and difficulty breathing. •Unexplained anxiety, weakness or fatigue. •Palpitations, cold sweat or paleness (Black & Hawks, 2004). PATHOPHYSIOLOGY Myocardial infarction, or ischemic necrosis of the myocardium, results from prolong ischemia to the myocardium with irreversible cell damage and muscle death. The time between onset of ischemia and myocardial muscle death is approximately 20-40 minutes, although this varies with the vessels that is occluded and the amount of collateral circulation that has developed.

The result signs on 1) extent, severity and duration of episode; 2) the amount of collateral circulation; and 3) the metabolic needs of the myocardium at the time of event. Myocardial infarction almost always occurs in the left ventricle and often significantly depresses left ventricular function. The larger the infracted area, the greater the loss of contractility. Functionally, MI causes the following: 1) reduced contractility with abnormal wall motion; 2) altered left ventricular compliance; 3) reduced stroke volume; 4) reduced ejection fraction; and 5) elevated left ventricular end-diastolic pressure.

Alteration in function depends not only on the size but also on the location of an infarct. An anterior left ventricular infarct often results from occlusion of the left anterior descending coronary artery. Posterior left ventricular infarcts often arise from right coronary artery obstruction, whereas lateral wall infarct usually arise from circumflex artery obstruction. This distribution varies because of individual differences in coronary artery supply. The infarct is also describe in terms of where it occurs on the myocardial surface.

The transmural infarct extends from endocardium to epicardium. The subendocardial type is located on the endocardial surface, extending varying distances into the myocardial muscle. Intramural infarction is often seen in patchy areas of the myocardium and is also usually associated with long standing angina pectoris. These terms have been largely replaced by the terms Q wave infarction and non-Q-wave infarction, which reflect the ECG appearance of Q waves in association with the clinical picture in MI. n the pathogenesis in the initiating events are coronary occlusion, but the Q wave infarction usually results from sustained coronary occlusion and extensive necrosis, whereas the non-Q-wave type may have early spontaneous reperfusion for at least a part of the affected area. All acute MIs have a central area of necrosis or infarction that is surrounded by an area of injury; the area of injury is surrounded by a ring of ischemia. The amount of myocardial dysfunction that results depends not only the size of the necrotic lesion, but also on the amount injury and ischemia in the area.

Each area emits characteristic ECG patterns that help to localize and determine the extent of the infarct of a 12-lead ECG. When myocardial muscles cells die, they liberate the intramyocardial cellular enzymes. These enzymes can be used to date and infarct and partially to judged its severity. Because the affected myocardial muscle does not regenerate after an infarction, healing requires the formation of scar tissue that replaces the necrotic myocardial muscle. This involves a series of morphologic changes ranging from no apparent cellular change in the first six hours to total replacement by scar tissue.

Scar tissue inhibits contractility, and the significance of this depends of the amount of the scar tissue form. As contractility falls heart failure ensues and the body begins to use the compensatory mechanisms. In an attempt to maintain cardiac output. Arteriolar vascular constriction, heart rate increases, and renal retention of sodium and water all help to regulate cardial output. Ventricular dilatation is commonly seen. A large amount of ventricular myocardium is lost, contractility may be greatly compromised, and cardiogenic shock may ensue.

Right ventricular infarction may occur with occlusion of the right coronary artery. With infarct affect the posterior wall of the left ventricle and the posterior interventricular septum, they extend to the right ventricular wall in 15 to 30% of cases. The central venous pressure may be elevated markedly if acute right ventricular failure develops. Low right ventricular output causing shock often responds well to vigorous fluid therapy but poorly to vasodilators. Infusions raise both right and left ventricular filling pressures.

The diagnosis of right ventricular infarction is difficult but may be established by right sided ECG leads and echocardiographic studies (Bullock, 1996). PRINCIPLES OF MANAGEMENT The goal of medical management is to minimized myocardial damage, preserve myocardial function, and prevent complications. These goals are achieved by reperfusing the area by emergency use of Percutaneous Transluminal Coronary Angioplasty (PTCA) or thrombolytic medication. Minimizing myocardial damage is also accomplished by reducing myocardial oxygen demand and increasing oxygen supply with medications, oxygen administration, and bed rest.

The resolution of pain and ECG changes are the primary clinical indicators that demand and supply are in equilibrium; they may also indicate reperfusion (Smeltzer & Bare, 2000). Emergent PTCA PTCA may be used to open the occluded coronary artery in an acute MI and promote reperfusion to the area that has been deprived of oxygen. PTCA treats the underlying atherosclerotic lesion. The time from the patient’s arrival to the emergency room to the time of vessel access should be less than 60 minutes because the duration of the lack of oxygen is directly related to the number of cells that die.

To perform an emergent PTCA within that short time, a cardiac catheterization laboratory and staff must be available. Pharmacologic Therapy An acute MI patient receives thrombolytics, analgesics, and ACE inhibitors. Thrombolytics These are medications that are usually administered intravenously, but some may also be given directly into the coronary artery in the cardiac catheterization laboratory. The purpose of thrombolytics is to dissolve and lyse the thrombus in the coronary artery so that blood will flow in to the coronary artery again, minimizing the size of the infarction and preserving ventricular function.

Though it dissolves the thrombus, it does not affect the underlying atherosclerotic lesion. Thus, the patient is referred to a cardiac catheterization and other invasive interventions if needed at a later time. To be effective, thrombolytics must be administered as early as possible after the onset of symptoms that indicate an acute MI. They are not to be given to patients with unstable angina, monitor these medications within 30 minutes from the time the patients arrives in the emergency room, this is referred to as “door to needle” time. Streptokinase – the most often thrombolytic agents used.

It increases the amount of plasminogen activator, which then increases the amount of both circulating and clot bound plasminogen. This medication is not to be used for patient who has been exposed to a recent streptococcus infection or has received streptokinase in the past 6 – 12 months. Tissue – type Plasminogen Activator – it activates the plasminogen on the clot more than the circulating plasminogen. Heparin is used with t-PA to prevent another clot from forming at the same site because it does reduce the clotting factors as much as streptokinase does.

Analgesics- the drug of choice remains the use of Morphine Sulfate through intravenous boluses. Not only does to reduce pain and anxiety but it also reduces the preload, which in turn decreases the workload of the heart and relaxes bronchioles to enhance oxygenation. Angiotensin – Converting Enzyme Inhibitor – A substance found in the lumen of all blood vessels, ACE converts angiotensin I to angiotensin II. Angiotensin is formed when the kidneys release rennin in response to decrease blood flow (Smeltzer & Bare, 2000). NURSING DIAGNOSES and INTERVENTIONS

Nursing Diagnosis: Pain /t tissue ischemia secondary to coronary artery occlusion. Nursing Interventions: ?Monitor and document the characteristics of the chest pain as described by the patient. ?Note nonverbal signs of pain as well as hemodynamic changes such as heart rate, respiratory rate and blood pressure as the pain changes. ?Instruct the patient to report any chest pain immediately. ?Explain the medications and procedures that are used to relieve pain ? Provide a calm and quiet environment and comfort measures to ensure effectiveness of the pain medications. Teach the patient to use relaxation technique to reduce pain and to relieve anxiety ? Approach the patient in a calm and confident manner ?Check vital signs before administering medications for pain ? Administer oxygen by nasal cannula as indicated to promote oxygen perfusion of the myocardium. Nursing Diagnosis: Anxiety r/t change in health status, possible death, or loss of social economic status Nursing Interventions: ?Acknowledge the patient’s anxiety and the perception of the threat of the situation. ?Encourage expression of feeling of anger, fear and grief. Orient the patient to routine procedures, and explain all the activities that occur in the patient’s room ? Allow the family to express feelings and asks question ?Keep both the patient and the family apprised of changes in the patient’s status or treatment plan. ?Seek assistance from clergy or significant others if necessary to help allay the patient’s anxiety. ?Answer all questions factually, and provide consistent reinforcement, because the ability to understand and remember maybe temporarily impaired. ?Accept but to not reinforce the use of denial. Support grieving behavior, and let the patient know it is a normal response. ?Encourage independent, self care and decision making. Nursing Diagnosis: Decrease cardiac output r/t changes in cardiac rate, rhythm or electrical conduction. Nursing Interventions: ?Promptly treat life threatening dysrhythmias. ?Provide a bedside commode to decrease expenditure of energy that is required when using a bed pan or ambulating to the bathroom. ?Administer supplemental oxygen as indicated. ?Elevate the head of the bed to allow for maximum lung expansion to increase xygen intake. ?Place needed utensils near the patient to save energy from excessive movement ? Feed the patient if necessary, when allowed to eat, to conserve energy. ?Allow the patient time to rest between treatment, and limit visitors and extra activity in the room. Nursing Diagnosis: Knowledge deficit: nature of myocardial infarction and coronary artery disease treatment, expected outcomes, and potential lifestyle changes Nursing Interventions: ?Explain the cause, effects, and clinical course of artery disease and the resulting MI to the patient ?

Allow time for question from patient ?Allow the patient, to verbalize concerns and fears ?Evaluate discharge needs of the patient and family ?Alert the patient to signs and symptoms of MI for future and the complications ? Teach the patient to use safety measures or to ask for assistance when out of bed or when ambulating until strength and endurance improves ? Instruct the patient about dietary modifications needed to reduce risk or to prevent complications of the disorder. If the patient is obese, explain the need for weight reduction diet. Give the patient meal plans based on the predetermined caloric limitations. ?Explain the need for decreases in dietary fats and cholesterol to prevent the effects of the disease and increased in protein and vitamins to pro mote good health and healing. ?Initiate counseling with a dietitian to assist with meal planning if needed. ?Teach the patient about the effects of smoking and the importance of quitting. ?Refer the patient to a smoking cessation program. Plan a post-discharge exercise regimen that gradually increases the intensity and endurance of the exercise as prescribed by the physician. Teach patient dosage, route, time, frequency, side effects and toxic effects of any medication prescribed. ?Explain the diagnosis studies completed and the need for any follow up studies after discharge. Include the family in any of the teaching sessions when applicable (Monahan, et. al. , 1994). SOURCES: •Bullock, B. L. (1996). Pathophysiology: Adaptations and alterations in functions. (4th ed). Philadelphia, Pennsylvania: J. B. Lippincott Company. •Monahan, et. al. (1994). Nursing Care for Adults. USA: W. B. Saunders Company. •Smeltzer & Bare •Black & Hawks •Microsoft Encarta •Bucher & Melander

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