CASE PRESENTATIONA 58 year old male patient came in ED Emergence Department

CASE PRESENTATIONA 58 year old male patient came in ED (Emergence Department) with his workmate complaining of crushing chest pain in the middle of the chest (central). He is a taxi driver. (Gallagher) On arrival patient had dyspnoea, and had nausea, patient looked clammy and was sweating. Patient’s pain was radiating to the left arm in. Patient does not have any past medical history or family history apart from his dad who died from an unexpected Heart Attach. He is a smoker of 20–30 cigarettes every day and drink alcohol on Fridays, Saturdays and Sundays (Gallagher). Patient was placed in resuscitation bay directly after being triaged.PATIENT VITALSHeart rate: 94 bpm, Breathing rate: 18 bpm, SpO2: 95%, BP (Blood Pressure): 150/90 mmHg and the Temperature of 37ºC. A 12 Leads ECG (Electrocardiogram) was done and patient was found with an anterior STEMI (segment elevation myocardial infarction). Blood test was done (U&E: Urea and Electrolytes and FBP: Full Blood Picture) and also highly sensitive troponin T.(Gallagher, n.d.)INTRODUCTIONAcute coronary syndrome (ACS) is a serious medical condition that cause death in almost 30% of patient who suffers from it and did not go to the hospital as soon as possible, early recognition and early treatment improve the chain of survival. This disease causes extreme pain to the chest so a quick identification and management such as ameliorating the flow of blood to the coronary artery, to put a stop to further damage. Symptoms and signs differ from one person to another and can be determine by the patient’s other medical problems, their age group and their gender.in this MCR we will discuss: 1. The pathophysiology of STEMI, its signs and symptoms.2. patient treatments: the treatments of a patient presenting with STEMI3. the ECG and diagnosis4. the importance of taking a high-sensitivity troponin T5. the benefit of PCI in comparison to thrombolytic therapyDISCUSSION1. THE PATHOPHYSIOLOGY OF STEMIWhen the patient entered the ED was triaged using the Manchester Triage which is based on grouping the patients that are critically ill and to help nurses to know which patient should be given the priority to treatment including the ABCDE (Gallagher). ACS is generally caused by the plaque that forms in the of coronary arteries’ walls, which play a role of distributing O2 to cardiac muscles and nourishing it. When the plaque breaks blood start to create a thrombus and this will occlude the blood flow to the cardiac muscles. (MIYO CLINIC STUFF, 2017), when there is insufficient provision of O2 to the cells the cardiac muscles can die. When the cells die causing destruction to the tissues muscle we talk of myocardial infarction. (MIYO CLINIC STUFF, 2017)We speak of STEMI when there is a rupture in the plaque of the coronary artery called atherosclerosis, this plaque that break activate the gathering of platelet at the site and stimulate the plug formation of platelets causing a thrombus in the coronary artery which will occlude it (Gallagher).SIGNS AND SYMPTOMSCHEST PAINIn ACS patient Chest pain is among the dominant symptoms. This symptom is caused by the lack of O2 in the myocardium and also the obstruction of the coronary artery. Chest pain results from the inequality between the demand of O2 and the supply of O2. Blood will then try to squeeze or put its pressure to find a way out to pass the obstruction. So when there is elongation of ischemia myocardial infarction occurs, which will then result in destruction of cardiac muscle and will not be reversed (Gallagher). The occlusion of the coronary artery will cause the cardiac muscle not to get the blood that contains O2 so this also lead to the pain felt by the Patient. (Gallagher)SWEATY AND CLAMMY SENSATIONSerious arterial obstruction of the coronary will trigger the SNS (sympathetic nervous system).This SNS will stimulate the supply of noradrenaline and adrenaline resulting in tachycardia trying to conserve homeostasis, these 2 will also create vasoconstriction of the peripheries because of their impact on alpha- and beta-adrenergic receptors. The impact of these catechol-amines that happen naturally aim to produce sweat on the skin, feel a bit cold also clammy, as tachycardia happens trying to balance for a decrease in contractility, the BP will similarly increase. This explains why this patient has high BP.NAUSEAThe medullary vomiting centre being stimulated causes Nausea and is usually accompanied by vomiting (Gallagher). Hypoxia may cause a straight impact on the vomiting centre and can cause nausea and vomiting that happens in reduce CO (cardiac output) (Gallagher). Nausea is normally followed by the signs and symptoms of the autonomic nervous system suchlike sweating, a reduction in size of blood vessels, too much salivation and patient looking pale (Gallagher)SHORTNESS OF BREATHThis happens because of low blood flow to the heart muscle affected, oxygen supplies are quickly used, the consequence will be:” a change from aerobic to anaerobic metabolism” (Gallagher); this will cause remarkable diminution in function of myocardial contractile. The dyspnoea can be seen in high breathing rate (RR) and a decrease in SpO22. PATIENT TREATEMENTAll patient have right to relief of pain as a basic need, giving analgesia can decrease the anxiety of the patient, reduction of pain can also stop the demands of the autonomic nervous system. Practitioner should come and reassure the patient and explain to patient procedure using AIDET. When evaluating a patient who present with the signs and symptoms of ACS, it is important to do focus history using the OPQRSTUV mnemonic: O: on set of action: when did the pain started?P: provoking factures: what cause the pain? Does it happen at rest or on exertion, etc?Q: quality of pain: is it crushing pain, stubbing pain, or heavy pain?R: Radiation: is it radiation anywhere? Like radiating to his back, neck, jaw, arm usually left arm.S: severity of the pain: can he rate the pain out of 10? 1=least and 10=severe.T: time: for how long you got the pain?U: underlying factors: AMPLEV: vasodilator: did patient take any vasodilator in the 24 preceding hours?Patients with suspected ACS complaining of chest pain should be given MONA-RO: low dose of Oxygen if needed, by administering Oxygen bad impacts of hypoxemia on the heart and brain are eliminated and also on other vital organs (HPCSA , Netcare Education, 2018)A: Aspirin reduce the production of a chemical (a prostaglandin called thromboxane A2) thromboxane is a chemical that makes platelets to form on the injury site and cause clotting (Thrombus). (HPCSA , Netcare Education, 2018). Platelets are the primary contributors of the clotting process; aspirin stops the production of the precursor to Thromboxane and stop the clotting process and the tightness of the vessels surrounding the site (HPCSA , Netcare Education, 2018)that is why we use it in the patient with a clot (HPCSA , Netcare Education, 2018) (NB: give clopidogrel if allergy to aspirin)GTN: when you administer GTN the venous system will dilate, which will reduce venous return (pre-load) to the heart and reduce the myocardial wall tension, GTN decrease to coronary vasoconstriction/ spasm, this will boost sub-endocardial perfusion GTN dilates the coronary arteries. (HPCSA , Netcare Education, 2018). GTN create a reduction in systemic vascular resistance, so a decrease in cardiac output and Blood pressure may be present because of the decreased preload. (HPCSA , Netcare Education, 2018)MORPHINE: Intravenous morphine (or diamorphine) should be titrated to control the patient’s symptoms.REPERFUSION: At the hospital (PCI).3. THE ECG AND DIAGNOSISWith MI or STEMI patients it is important to do a 12-lead ECG which will help you in diagnosing the patient and to give the right treatment during the primary assessment; in saying this it does not mean that the ECG is perfect. Our patient ECG revealed an ST elevation in leads V2, V3, V4 and a not remarkable in V5. (Gallagher) This is generally a frontal STEMI meaning that our patient is supposed to be managed as soon as possible so reperfusion therapy should be highly considered (Gallagher). which include thrombolytic therapy or stent insertion. (Gallagher)

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