Primary Diagnosis
Based on the symptoms that the patient displays, one may assume that he suffers from heart failure (Ponikowski et al., 2016). By definition, heart failure implies that the patient’s heart cannot pump blood properly (Ponikowski et al., 2016). The specified condition may be caused by changes in the metabolic needs of the patient, as well as possible structural abnormalities (Ponikowski et al., 2016).
Patient Education Techniques
Determining the key difficulties that a healthcare provider faces when educating a STEMI patient, one must mention the lack of control over the threats to which a patient is exposed when leaving the hospital environment. Therefore, it is crucial to introduce simulations at the earliest stages of educating inpatients to ensure that the target population memorizes the essential steps for identifying a threat and contacting nearly healthcare services (Walsh, 2017). Particularly it is imperative to teach patients to seek medical attention at the earliest stages of the MI symptoms development so that the disease does not progress (Walsh, 2017). Teaching patients to use the MI emergency response system, thus, must be the essential point of the patient education process (Walsh, 2017). In addition, the patient must be aware of the key symptoms of an MI. Finally, the patient must be provided with exhaustive information about the means of communicating with healthcare providers and nurses. Thus, the foundation for continuous patient education can be created.
Differential Diagnosis
Given the symptoms that the patient has, myocardial infarction (MI) is most likely to be the differential diagnosis (Farshid et al., 2015). The specified assumption is justified by the fact that the patient’s cardiogram shows a significant ST-elevation (Farshid et al., 2015). The specified description aligns with the existing definition of “ST elevation (STEMI) myocardial infarction of unspecified site” (Centers for Medicare and Medicaid Services, n.d.).
MI and the Relevant Laboratory Findings
The electrocardiogram (ECG) is typically regarded as the tool for determining the presence of MI in patients (Farshid et al., 2015). The specified approach suggests that the locus of MI be detected efficiently. Moreover, the patient may have to be subjected to the laboratory test involving the use of cardiac biomarkers/enzymes as markers (Twerenbold et al., 2016). The levels of cardiac troponin will be measured to identify the presence of MI-related outcomes (Lyle, Woerkom, Tweet, Young, & Best, 2016). As a result, the presence of monoclonal antibodies in the patient’s blood will be located, which will help determine whether the patient suffers from MI. The outcomes of the coronary angiography carried out for this purpose, thus, will define the level of a threat to which the patient is exposed (Twerenbold et al., 2016).
Pathophysiological Responses
The pathophysiological mechanism launched by MI includes inflammatory cell infiltration with a further attack on the immune system. The latter responds by activating toll-like receptors (TLR) to prevent further inflammation and the launch of chemokine expression (Sayed, Abdel-Rahman, Esmat, & Nammas, 2015). M1 macrophages and CD4+ T- lymphocytes, in turn, block the patient’s infarct zone and drain their lymph nodes, causing the disease to affect the patient’s ability to breathe. The immune system, in turn, launches the production of anti-inflammatory cytokines and creates premises for phagocytosis and angiogenesis, therefore, preventing the patient’s condition from aggravating (Liu, Wang, & Li, 2016).
Because of the severity and fast pace of its progression, MI must be addressed immediately to prevent further aggravation of the patient’s condition. Therefore, apart from administering appropriate medications to the patient, one must consider educating him about the means of identifying the development of MI and contacting nearby healthcare facilities. Thus, a fatal outcome can be avoided.
References
Centers for Medicare and Medicaid Services. (n.d.). MDC 5 diseases & disorders of the circulatory system: Acute myocardial infarction. Web.
Farshid, A., Allada, C., Chandrasekhar, J., Marley, P., McGill, D., O’Connor, S.,… Shadbolt, B. (2015). Shorter ischaemic time and improved survival with pre-hospital STEMI diagnosis and direct transfer for primary PCI. Heart, Lung and Circulation, 24(3), 234-240. Web.
Liu, J., Wang, H., & Li, J. (2016). Inflammation and inflammatory cells in myocardial infarction and reperfusion injury: A double-edged sword. Clinical Medicine Insights: Cardiology, 10(1), 79-84. Web.
Lyle, M., Woerkom, R. C. V., Tweet, M., Young, P. M., & Best, P. J. (2016). Conus artery occlusion causing isolated right ventricular outflow tract infarction: Novel application of cardiac magnetic resonance in anterior STEMI. Cardiovascular Diagnosis and Therapy, 6(3), 262-266. Web.
Ponikowski, P., Voors, A. A., Anker, S. D., Bueno, H., Cleland, J. G., Coats, A. J.,… Jessup, M. (2016). 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) developed with the special contribution of the Heart Failure Association (HFA) of the ESC. European Heart Journal, 37(27), 2129-2200. Web.
Sayed, N. M., Abdel-Rahman, S. M., Esmat, I., & Nammas, W. (2015). CD4+ CD28null T cells in acute coronary syndrome: Lower with ST-elevation myocardial infarction. Scandinavian Cardiovascular Journal, 49(6), 325-330. Web.
Twerenbold, R., Jaeger, C., Gimenez, R. M., Wildi, K., Reichlin, T., Nestelberger, T.,… Pretre, G. (2016). Impact of high-sensitivity cardiac troponin on use of coronary angiography, cardiac stress testing, and time to discharge in suspected acute myocardial infarction. European Heart Journal, 37(44), 3324-3332. Web.
Walsh, J. (2017). A nurse led clinic’s contribution to patient education and promoting self-care in heart failure patients: A systematic review. International Journal of Integrated Care, 17(5), A492. Web.