Throughout the whole of this assignment the writer will critically analyse discuss, and evaluate the case study, pathophysiology of the condition, two major investigations with their clinical features, and the impact of two scientific advances on the care of the client, who is a 60 year old gentleman whom from this time forward will only be known as Peter in accordance with the Nursing and Midwifery Council (NMC 2008).
Peter’s presenting symptoms were dyspnoea, nausea, vomiting and severe chest pain radiating down his left arm, neck and jaw. An electrocardiogram (ECG) showing marked ST elevation in inferior leads II III and aVF and reciprocal ST depression in the anterior leads. His initial cardiac enzymes (troponin) levels were 19.1 thus the prognosis was that Peter had suffered acute myocardial infarction (AMI).
Peter’s past medical history showed Ischemic Heart disease, Angina, and Aortic Valve Replacement. Following Acute Coronary Syndrome (ACS) protocol Peter was placed on the cardiac monitors and his vital signs observed half hourly. Observations showed sinus tachycardia 120 beats per minute (BPM), pyrexia (temperature of 39.6) and hypotension (systolic blood pressure 85mmHg) (SIGN 2007).
Myocardial infarction (MI) refers to necrosis of myocardial cells caused by cessation or severe reduction in the blood supply (Jowett and Thompson 1995). Following an MI irreversible necrosis of a portion of heart muscle results due to prolonged ischaemia (Lilly 1998). The prolonged, unrelieved ischaemia results in hypoxia and as the amount of oxygen to the cardiac cells diminishes cellular death ensues. However, cardiac cells can withstand ischaemic conditions for about 20 minutes even though they are metabolically altered and non-functional (McCance and Huether 1997). If oxygen supply is not resumed the death of a segment of heart muscle (i.e. a myocardial infarction) results.
Myocardial cell viability requires a certain level of blood flow,...