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Neurological Emergency: Pathophysiology of the Peri-Operative Myocardial Infarction - Assignment Example

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"Neurological Emergency: Pathophysiology of the Peri-Operative Myocardial Infarction" paper explains the A to E assessment of the patient, the pathophysiology of the provisional diagnosis, and identifies the urgency (or not) of transport and the type of healthcare facility which would be appropriate…
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Extract of sample "Neurological Emergency: Pathophysiology of the Peri-Operative Myocardial Infarction"

Case studies Name of student Institution Affiliation Date Case Study 1 1) History: The patient is 48 years old male, married and has no past medical history. He is not on any medication. The patient presents with complaints of chest pains, and on a rating scale the pain is 8 out of 10.the pain is crushing in nature Vital signs Pulse 148 and is irregular Respirations 28 Temperature 37.5 C Spo2 90% (Room air) 2) Provisional Diagnosis: A provisional diagnosis is a myocardial infarction or ischemia.it is because the patient presents with an elevation of the ST segment based on ECG results. Differential diagnosis: coronary artery disease CAD. It is because the patient is presenting with pain that is radiating to the jaw. 3) Assessment: Explain the A to E assessment of the patient Airway- the patient is hyperventilating since his respiratory rate is abnormal 28 breaths per minute. Breathing- the patient is presenting with respiratory acidosis with compensatory mechanisms. He also presents with low spo2 of 90% (Room air). The circulation-the patient is pressing with increased blood pressures of 172/90, =pulse of 148 beats per minute, and has central cyanosis. He also presents with a normal capillary refill of < 2 seconds. Disability- the patients present with normal glucose levels at 5.8mmol, and has a GCS of 15 with pupils that are equal and reactive. Exposure- the patient, does not require to be exposed for any examination. 4) Pathophysiology of the provisional diagnosis Atherosclerotic plaques develop gradually and begin with the accumulation of low-density lipoproteins cholesterols and saturated fats in the intima of blood vessels. Adhesion of leukocytes usually follows the process to the endothelium, diapedes follows and finally, entry into the intima ensues. In the intima, accumulation of these lipids leads to the formation of foam cells. The foam cells are rich in pro-inflammatory mediators (Biccard & Rodseth, 2010). The lesions are usually referred to as the fat steak and can be reversed up to a certain extent. Further evolution involves the migration of smooth muscles cells from the media, and their deposition of extracellular matrix and proliferating includes proteoglycans, elastin fibers, and interstitial collagen. Some of the smooth muscles exit apoptosis .plaques develop in areas of calcification as they continue to evolve. Initially, the plaques form with the artery remodeling in an outwards fashion followed by encroachment on the lumen of the artery (Biccard & Rodseth, 2010). Eventually, the stenosis can inhibit the flow due to increased demand thus causing angina. STEMI results from an unexpected catastrophic disruption of a cholesterol-laden plaque. This results in the exposure of substances that promotes the activation of platelets and aggregation. Generation of thrombin and the formation of a thrombus thus causes the interruption in blood flow. In the case of a severe occlusion, myocardial cell necrosis ensues. On interruption of blood flow in the coronary artery, the area around the myocardium supplied by that vessel loses the ability to shorten and carry out its contractile function (Biccard & Rodseth, 2010). Early hyperkinesia of the non-infarction zones occurs as a result if an acute compensatory mechanism that includes an increase in the frank-Starling mechanism and sympathetic activity .with the splitting of the necrotic myocytes leads to the thinning and elongation of the infarcted zones especially in anterior inaction and this leads to the expansion of infarction. 5) Investigations: Explain any further investigations you would carry out? (E.g. ECG) The ECG helps in monitoring the heart rate of the patient and evaluating the effects of the injury or disease on the funct6ioins of the heart. It helps in the evaluation of the functions of the pacemaker while at the same time evaluating response to medication by a patient.ir=t also helps in obtaining a baseline recording before, during, and after a certain medical procedure. Besides, an evaluation of the cardiac enzymes such as troponin I and CPK and a CT scan can help in diagnosing or carrying out further investigations on the patient (Mythili & Malathi, 2015). 6) Treatment: Explain the treatment (including procedures/medications) you would implement to treat the provisional diagnosis (can be in point form) The use of morphine to relieve pain not relieved by nitroglycerine helps in the management of MI. Point to note ism, remember to always check the vitals due to the side effects of constipation and hypotension. The patient should be put on oxygen therapy at 4 liters per minute so as to promote perfusion. Administration of aspirin and anticoagulant at 160-325 mg and the use of sublingual nitroglycerine act as an essential treatment .furthermore, it is important to check vital signs when using nitroglycerine since it is a vasodilator (Roncalli, 2013). 7) Transport: Identify the urgency (or not) of transport and the type of healthcare facility which would be appropriate Barrack Obama should be taken to the hospital with immediate effects so as to avoid potential complications of Myocardial Infarction. 8) References: Biccard, B. M., & Rodseth, R. N. (2010). The pathophysiology of peri-operative myocardial infarction. Anaesthesia, 65(7), 733-741. doi:10.1111/j.1365-2044.2010.06338.x Mythili, S., & Malathi, N. (2015). Diagnostic markers of acute myocardial infarction (Review). Biomedical Reports. doi:10.3892/br.2015.500 Roncalli, J. L. (2013). Future directions in the treatment of myocardial infarction. Advances in Myocardial Infarction Management, 134-147. doi:10.2217/ebo.13.93 Case study 2 1) History The patient is a 21-year-old female; she has a history of epilepsy based on the alert bracelet. Her vital signs are; a pulse of 120 beats per minute, blood pressure of 122/65 mmHg, Spo2 93%, respirations of 30 breaths per minute and a temperature of 36.4 C. 2) Provisional Diagnosis: Identify your provisional diagnosis and differential diagnoses Provisional; diagnosis; Epileptic seizure as the patient presents with a medic bracelet that indicate she has epilepsy. Furthermore, the patient has a tonic-clonic seizure that lasted for 2 minutes. Differential diagnosis; syncope- the patient is presenting with a difference in blood pressure. The patient also presents with loss of consciousness. 3) Assessment: Explain the A to E assessment of the patient (can be in point form) Airway- the patient is hyperventilating as she presents with abnormally high respirations of 30 breaths per minute. Breathing- the patient is presenting with respiratory acidosis with a compensatory mechanism. She also presents with low spo2 of 93% (Room air). The circulation-the patient is presenting with an elevated blood pressure of 122/65 mmHg, and she is pale indicating that there is an impairment in blood circulation. Her capillary refill is normal and is Read More
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