Myocardial Infarction Secondary to Prolong †Myassignmenthelp.Com

Question: Explanation Myocardial Infarction? Answer: Introducation Myocardial infarction, also known as heart attack is the irreversible death of myocardial cells secondary to prolonged lack of oxygen supply (ischaemia) (Berman et al., 2014). Myocardial infarction often results from imbalanced oxygen supply and demand, which is often as a result of rupturing of a plaque alongside thrombus formation in either coronary artery, leading to an acute reduction in the amount of blood supplied parts of the myocardium. Myocardial infarctions are primarily caused by coronary heart disease (CHD), also known as atherosclerosis (Bullock Hales, 2012). The condition causes hardening of arteries through the deposition of fatty calcified plaques. Heart attacks are typically triggered by a blood clot blocking a coronary artery (McCance Huether, 2014). Risk factors for myocardial infarction may be classified into either nonmodifiable risk factors or modifiable risk factors. Nonmodifiable risk factors include age, sex and family history of chronic heart disease, whereas modifiable ones include smoking and tobacco use, diabetes mellitus, obesity, hypertension, hypercholesterolemia and hypertriglyceridemia, excessive alcohol intake, poor diet, sedentary lifestyle and/or lack of exercise (Mehta, Wei, Wenger, 2015; Mendis S, Puska P, Norrving, 2011). Drawing on the current case study, the patient exhibits some of these signs which include a smoking history, alcohol drinking, obesity and elevated cholesterol le vel. Myocardial infarction is a common condition affecting over half a million Australians. It is one of the leading causes of morbidity and mortality accounting for at least 55,000 cases of heart attack per year, and an average of 9,286 deaths, as per 2012 statistics (Heart Research Australia, 2014). These figures translate to about one heart attack in every ten minutes, and an average of 25 deaths per day attributed to myocardial infarction. The incidence of the condition is claimed to be rising at about 1.98% annually, with an observed significant increase of incidence among those aged 50 to 80 years (Wong et al., 2013). Younger age groups have evidenced stable or increasing Myocardial infarction rates compared to stable or decreasing myocardial infarction rates among older age groups (Nedkoff et al., 2011). Myocardial infarction has an impact on both the patient and the entire family since its consequences are perpetuated through one's entire life, resulting in the need for permanent care. One of the primary impacts on the family is emotional disability by fear of death, disability, and fear of the unknown (Salminen-Tuomaala, stedt-Kurki, Rekiaro, Paavilainen, 2013). Mr. Tupa's wife and children may also experience difficult times as it affects the dynamics of the family by causing feelings of fear, anxiety, and distress after heart attack episodes. The possibility of losing a family member also triggers psychological distress. The patient's wife may have to strain economically so as to sustain the new financial demands. Signs and Symptoms Signs and Symptoms Link to pathophysiology Severe chest pain Severe chest pain presents as the primary symptom of myocardial infarction. The pain is often claimed to radiate to the left shoulder, neck, jaw or arm (Malik Khan, 2013). The pain is typically described as pressure-like, crushing or tight pain which may also radiate to other body parts aforementioned. The pain is as a result of acute blockage of a coronary artery as a result of ruptured plaques in the artery walls. Shortness of breath The heart and lungs have to function in together. Defective heart function often inhibits the transport of blood to tissues. Inadequate oxygen in the system is indicated by shortness of breath as a warning sign. In myocardial infarction, heart muscles are affected hence affected their contraction and as a result, impair blood flow and consequentially the transport of oxygen between lungs and the body. Dyspnoea is attributed to heart muscle damage causing a decline in pump function of the left ventricle, and as a result, left ventricular failure and pulmonary oedema occurs (Senecal, Caldera, Passeri, 2011). Fatigue Fatigue is reported to be a frequent precursor of heart attack (Mosca, Hammond, Mochari-Greenberger, Towfighi, Albert, 2013). Fatigue is evidenced by presentations such as excessive sleep during inappropriate times, reduced participation in social activities, reduced libido and overall slowing down. The involvement of fatigue in myocardial infarction is attributed to early left ventricular dysfunction. The early dysfunction is attributed to chronic heart disease due to the presence of an atrial gallop (Blakeman Booker, 2016). Light-headedness Light-headedness and dizziness are also reported in persons with myocardial infarction and other conditions such as high blood pressure (Jaffe, 2013). These symptoms are an indication of perturbation of spatial orientation and normal perception of balance. Light-headedness and dizziness may be as a result of reduced blood flow to the brain. Nausea, diaphoresis, palpitations, anxiety and vomiting Myocardial infarction episodes are also characterised by excessive sweating, nausea, vomiting, palpitation and anxiety (often felt like an impending doom) These presentations are attributed to the massive surge of adrenalin and noradrenalin from the sympathetic nervous system as a response to the pain and hemodynamic abnormities caused by cardiac dysfunction. Drugs for Myocardial Infarction Drug therapy for myocardial infarction aims at reducing morbidity and preventing complications associated with the condition. myocardial infarction can be treated using vasodilators, thrombolytics, anti-thrombolytics, antiarrhythmics, and analgesics (Lim McKenna, 2012). The current patient has been prescribed with morphine as the analgesic and sublingual glyceryl trinitrate as a nitrodilator. Vasodilators Vasodilators are used to relax smooth muscles of blood vessels hence causing dilation of blood vessels to achieve blood flow at much ease. Dilation of arteries leads to reduced systemic vascular resistance, which results in a drop in arterial blood pressure, whereas dilation of veins decreases venous blood pressure (Klabunde, 2012). There are various mechanisms of vascular smooth muscle relaxation. One of the mechanisms is to increase cyclic guanosine monophosphate (cGMP) which prevents the interaction of myosin with actin, the second mechanism is to decrease intracellular calcium ions, and the last mechanism is to prevent depolarization of cell membranes of vascular smooth muscles (Katzung, 2012). Vasodilators are classified according to the type of vessel they affect. The basic classification includes arterial dilators, venous dilators, and mixed dilators. Most dilators used are the mixed type since they have a wide spectrum of application. Arterial dilators reduce arterial pressure by reducing systemic vascular resistance, whereas venous dilators are used in dilation of venous capacitance for two primary purposes; a) to reduce preload on the heart and as a result, reduce cardiac output, and 2) decreasing proximal hydrostatic pressure to reduce edema formation (Klabunde, 2012). Mixed dilators on the other end have a balanced effect on both veins and arteries. Thrombolytics These drugs are used to lyse thrombi occurring in the vascular bed, coronary, pulmonary, or cerebral vessels, and in the case of myocardial infarction, lysis of thrombi of the coronary artery. Thrombolytics achieve the mechanism of thrombolysis by activating plasminogen to form plasmin. Plasmin is a proteolytic enzyme that breaks cross-links between fibrin molecules (the primary structural binder of blood clots) (OGara et al., 2013; (Anderson, 2016). Thrombolytics are classified into either urokinase, streptokinase, or tissue plasminogen activator, and they all have the clots dissolution abilities (Klabunde, 2012). Nursing Care Strategies The goals of treatment of a case presenting with myocardial infarction include relieving chest pain, reducing the cardiac workload, stabilizing heart rhythm, revascularization of the coronary artery, and preservation of myocardial tissue (Lippincott, 2012). Nursing management plays a critical role in this management. The following are some of the priority nursing care strategies for the first 24-hours post-emergency department. Administration of antiarrhythmics The first 48 hours are characterised by arrhythmias as the predominant problem (Lippincott, 2012). Management of the same stands out as a nursing priority, and it may require the administration of antiarrhythmic, and ultimately monitoring of the same with a pacemaker. Administration of thrombolytics The entire episode of myocardial infarction is attributed to an involvement of a thrombus. Hence, its management stands out as a nursing priority, and the same should be undertaken as early as possible into the treatment. Early administration of thrombolytics prevents any possibility of reinfarction. Monitoring and assessment of severity, location, duration and type of pain experienced by the patient, followed by the administration of analgesics as prescribed The administration of analgesics is of critical importance in the management of the myocardial infarction event. Pain management is a nursing priority as it helps the patient get relieve from severe pain, and also reduce reaction of the patient to pain in order to reduce patient anxiety. Avoid intramuscular administrations because absorption at the muscles is unpredictable and bleeding may also result if the patient is on thrombolytics. Monitor the patients blood pressure after administration of nitro-glycerine, especially after administration of the initial dose Monitor electrocardiograms before and after the administration of nitro-glycerine, alongside pulmonary artery catheter measurements and blood pressure. Monitor for tachypnoea, oedema, cough and crackles. Monitor these signs of fluid retention, which may be indicative of impending heart failure. In addition, monitor serum enzyme levels, and respirations. Also, perform periodic auscultation for adventitious breath sounds. Administration of clear fluid diets until nausea subsides This will also help maintain adequate hydration, provide the required energy, and also supply some of the required electrolytes (Lippincott, 2012). A low-cholesterol, low sodium, low fat, high fiber diet is recommended. Administration of stool-softener The aim of such is to prevent strain during defecation which leads to vagal stimulation, with the risk of slowing the heart rate (Lippincott, 2012). Provision of emotional support The nurse providing emotional support helps reduce stress and anxiety. It is also advisable to administer tranquilizers if need be. To provide support and show compassion, help the patient understand the position he is in. This can be achieved by explaining the procedures and answering any questions that the patient may pose. Also, explain the intensive care environment to help ease any anxiety. The patient's family has to be involved in the care as much as possible. Social support is essential for the maintenance of physical and psychological health. Nurses are expected to create a healing environment, which also encompasses social support (Huisman, Morales, Hoof, Kort, 2012). References Anderson, J. (2016). ST segment elevation acute myocardial infarction and complications of myocardial infarction. In L. Goldman, A. Schafer, Goldman's Cecil Medicine (p. 73). Philadelphia, PA: Elsevier Saunders. Berman, A., Snyder, S. J., Kozier, B., Erb, G. L., Levett-Jones, T., Dwyer, T., Stanley, D. (2014). Kozier Erbs Fundamentals of Nursing Australian Edition - Audry Berman, Shirlee J. 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