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Initially, PJ had shown clear symptoms of stable angina characterized by chest pain or a discomfort that results from minor activities. However, PJ’s current condition reflects symptoms of unstable angina.
Unstable angina often affects the shoulder, neck, jaws and arms. Tightness, burning, or choking signs in the chest also accompany the condition. PJ’s condition took place at rest and did not go away. In addition, the patient showed shortness of breath and sweating.
As opposed to stable angina, which only results from certain activities and is accompanied by mild pain lasting only few minutes, unstable angina is normally sudden and could become severe within a shorter period.
PJ’s symptoms will become more severe, appear more often and increase with minimal activities or during rest or sleep. The condition will last relatively longer time, more than 15 minutes and result from no cause, particularly when he is sleeping. PJ will respond poorly to medication (nitroglycerin) and develop low blood pressure.
Most important, unstable angina is an indication that a heart attack could occur to PJ soon and, therefore, he is advised to seek medical attention immediately.
Differential diagnoses for ST-segment elevation myocardial infarction (STEMI) include (1) “ST elevation that is straight or convex upward and blends with T to form a dome; (2) wide upright T or inverted T waves; (3) Q waves; (4) ST elevation or T waves that may approximate or exceed QRS height; and (5) reciprocal ST depression” (Hanna & Glancy, 2015, p. 373).
Laboratory Tests for MI
Several laboratory tests are available to determine MI in patients (Zimetbaum & Josephson, 2003). It is imperative to note that none of these tests is specific and sensitive to MI shortly after the onset of the condition. Thus, timing of intervention is vital.
The elevation of the total Creatine Kinase in the skeletal muscle could indicate MI. However, is not an absolute test because other non-cardiac conditions may coexist with MI.
MB fraction of Creatine Kinase from the isoenzymes is much more specific for the MI cardiac muscles. Hence, it is an excellent laboratory test for MI. In addition, the serum increases between 2 and 8 hours after the start of the MI condition.
Higher levels of Troponins I and T in the cardiac muscle show injuries to the muscles. The test is highly specific for MI, and it could assist to distinguish Creatine Kinase found in the muscles.
The laboratory tests also involve the CK-MB isoforms determination. The 2 to 1 ratio has been used to determine MI injury. The increase in myoglobin shows potential MI.
The lactate dehydrogenase test is conducted between 12 and 24 hours after the onset of the MI when it rises to the peak. Evaluation of the lactate dehydrogenase isoenzymes is performed because of high reliability for cardiac injury.
Pathophysiological Responses for MI
The response should be immediate, and it must aim to restore regular coronary blood flow and ensure optimal functional myocardium.
Pain management is necessary for PJ to reduce intense pain.
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For PJ, who has hypertension, needs intravenous nitrates. The administered nitrates would ensure vasodilator effect on the patient and control hypertension. In addition, beta blocker would be administered for PJ to control the rate and force of the MI and, therefore, lower the overall oxygen demand for the muscles (Sinert, Newman, Brandler, & Paladino, 2010). The response minimizes injuries and potential deaths.
Hanna, E. B., & Glancy, D. L. (2015). ST-segment elevation: Differential diagnosis, caveats. Cleveland Clinic Journal of Medicine, 82(6), 373-384.
Sinert, R., Newman, D., Brandler, E., & Paladino, L. (2010). Immediate ß-blockade in patients with myocardial infarctions: is there evidence of benefit? Annals of Emergency Medicine, 56(5), 571-7.
Zimetbaum, P. J., & Josephson, M. E. (2003). Use of the electrocardiogram in acute myocardial infarction. New England Journal of Medicine, 348(10), 933–940.