This essay covers the Myocardial Infarction Case Study of a 65-year old woman, who is presented at an emergency department feeling sick. The essay covers mainly, the pieces of assessment data in support of a diagnosis of acute myocardial infarction…
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Four pieces of assessment data The key pieces of assessment data include: the elevation of serum cardiac troponin levels (cTnT) diagnosed by collecting and testing of the blood; breathlessness, diagnosed by the observation of shortness of breath; appearing pale and tired, diagnosed by observing the patients feeling; patient feeling tired, fatigued, weak and nausea; the detection of heart sound S3 with no adventitious lung sounds or peripheral oedema; and prior history of heart failure as diagnosed by her doctor earlier; and the data of the 12- lead ECG which shows 2mm elevation in anterior leads of V1-V4 with the Q waves in inferior leads 11, 11 and a VF. McCaffery does not complain of chest pain, which is a symptom of acute myocardial infarction the reason for not having chest pain stems from her age and that she is diabetic. Davidson (2008) states that old and diabetic patients experience silent or non-pain myocardial infarction. Pathophysiology of the data pieces of assessment The pathophysiology of the Electrocardiograph (ECG) and the elevation of serum cardiac troponin (TP) piece data. ...
he changes in plasma concentration of these markers bring out the diagnostic value; however, confusion may arise for the diagnoses of Angina which when damaged does produce troponins. The difference is that angina with minimal myocardial damage releases troponins to a minor degree. Electrocardiography (ECG) is difficult to interpret unless there exists a previous evidence of myocardial infarction. The first change is the serum troponin elevation followed by a diminution of the size of R wave and an occurrence of infarction of a Q wave develops. The Q wave develops because the myocardial infarct acts as an electrical window that transmits the changes from within the ventricular cavity to allow the electrocardiography (ECG) to see the reciprocal R wave from the walls of the ventricle (Hutchison’s, 2007). Therefore, McCaffery’s 12 lead show 2mm segment elevation with leads v1-v4 with the Q wave reciprocal changes of 11, 111, and a VF which leads to no other conclusion but to that of myocardial infarction. Electrocardiography recorded from a 70- year old man who had an acute infarct 2 days ago and had treatment for myocardial infarction 11 months before showed Q waves in the inferior leads (11, 111, and a VF) and serum troponin (ST) elevation on the anterior leads (1 and V2-V6) (Davidson’s, 2008). This diagnosis resembles that of McCaffery so it can rightly be inferred that McCaffery is suffering from myocardial infarction. The other reason for the pathophysiology of the electrocardiography is that one cannot rely on these results unless there is a prior diagnosis of myocardial infarction. This is overcome by the fact that, McCaffery was diagnosed with heart failure by her doctor and drugs prescribed.
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