NUM2306: Pathophysiology - Myocardial Infarction Case Study - Nursing Assignment Help

Assignment Task:

Introduction 

Between 2014 and 2015 there were 32, 388 individuals admitted to hospital due to an acute myocardial infarction (MI), between the ages of 35-84 (Australian Commission on Safety and Quality in Health Care, 2017). A myocardial infarction (MI) is clinically defined as an acute myocardial injury in the presence of abnormal cardiac biomarkers when it is observed that there is acute myocardial ischemia (Thygesen et al., 2018). This case study examines the presentation of Kath Harris to hospital due to a suspected MI. There will be an investigation into the pathophysiology of an MI, how it occurs and common causes. A review of Kath’s presenting condition and how that relates to an MI. There will also be a detailed overview of what management will occur upon Kath’s presentation as well as the medications routinely used. 

Pathophysiology 

An MI occurs when there is either complete or partial occlusion of the cardiac blood vessels to the myocardium, inhibiting blood flow and causing ischemia (Badimon, 2018). Kath’s MI is likely caused by the destabilization of the atherosclerotic plaque, and subsequent thrombus formation (Badimon, 2018; Montecucco et al., 2016). Atherosclerotic plaque formation occurs due to endothelial damage resulting in inflammation and low-density lipoprotein (LDL) oxidation within endothelial tissue (Shaffer et al., 2020). This process occurs due to adverse stimuli, in Kath’s case, this is likely due to her obesity, smoking, hypertension and diabetes (Andersson et al., 2017; Shaffer et al., 2020). When the plaque ruptures, clotting causes a thrombus to develop, inhibiting blood flow (Malecki-Ketchell, 2016). With minimized oxygen, anaerobic metabolism begins causing increased glycogen use (Buckley, 2017). The anaerobic metabolism explains Kath’s chest pain due to lactic-acid stimulating cardiac nociceptors in myocardium tissue (Malecki-Ketchell, 2016). Electrolyte changes are also observed, due to the change in blood flow, usually impacting contractility (Buckley, 2017). However, in Kath’s’ serum report, her potassium level is 4.9 mmol/L; this indicates hyperkalemia (Craft & Gordon, 2017). Hyperkalemia is often found with MI patients admitted to hospital (Grodzinsky et al., 2016). Kath’s hyperkalemia is potentially due to her diabetes and her beta-blocker, carvedilol (Carvedilol, n.d.; Grodzinsky, 2016). 

Once ischemia of the myocardial cells occurs, an arrhythmia may develop due to the release of catecholamines (Shaffer et al., 2020). Subsequently, glycogenolysis and lipolysis occur increasing glycogen in the bloodstream (Buckley, 2017; Shaffer et al., 2020). Kath’s serum findings evidence this; she had elevated glucose levels of 11.2 mmol/L (Craft & Gordon, 2017). 

Her hyperglycemia was concerning because she has diabetes and is on metformin (Metformin, n.d.). Kath’s history details she has unstable angina; this occurs when an occlusion lasts less than 20 minutes and is only partial (Buckley, 2017). An MI follows unstable angina in up to 20% of cases due to damaged endothelial tissue (Shaffer et al., 2020). In events longer than 20 minutes, the ischemia causes necrosis and develops into a MI (Buckley, 2017; Shaffer, 2020). When Kath presented, her symptoms were nausea, cold peripheries, pale skin, tachypnea and oxygen saturation (SpO2) of 91%. She also had a 6/10 chest pain, unrelieved by glycerin trinitrate (GTN), these are symptomatic of an MI (Shaffer et al., 2020). Kath’s nausea might be due to her hypotension or pain. However, her MI may be responsible if the ischemia triggers nearby autonomic receptors associated with the nausea centre of the brain (Malecki-Ketchell, 2016). The tachypnea is related to the reduced cardiac output and subsequent hypoxemia, evident by the SpO2 of 91% (Buckley, 2017). Kath’s peripheral temperature and skin pallor relate to the reduced cardiac output, or the stress of the situation impacting the sympathetic nervous system (Malecki-Ketchell, 2016). Another potentiator for Kath’s MI could be her iron levels or glycated haemoglobin (HbA1c); both are outside normal ranges (Craft & Gordon, 2017). Kath’s test revealed she was Iron deficient; this can predict non-fatal MI (Zeller et al., 2018). Meanwhile, Kath had HbA1c scores of 7.9%; studies show this increases the risk of cardiac events (Chen et al., 2017).

This NUM2306: Nursing Assignment has been solved by our Nursing Experts at My Uni Paper. Our Assignment Writing Experts are efficient to provide a fresh solution to this question. We are serving more than 10000+ Students in Australia, UK & US by helping them to score HD in their academics. Our Experts are well trained to follow all marking rubrics & referencing style.

Be it a used or new solution, the quality of the work submitted by our assignment experts remains unhampered. You may continue to expect the same or even better quality with the used and new assignment solution files respectively. There’s one thing to be noticed that you could choose one between the two and acquire an HD either way. You could choose a new assignment solution file to get yourself an exclusive, plagiarism (with free Turnitin file), expert quality assignment or order an old solution file that was considered worthy of the highest distinction.