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Chest Pain in a Patient: Differential Diagnosis Case Study

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Updated: Jun 30th, 2022

STEMI

The first differential diagnosis for Frank is ST-elevation myocardial infarction (STEMI). It is a type of MI, where the coronary artery is fully blocked (Mesas et al., 2018). The infarction extends from the endocardium to the pericardium, causing chest pain, dyspnea, dizziness, nausea, sweating, and anxiety (Kingma, 2018). The movement of the pain from the chest area to the left arm is another symptom of infarction, as there exist neuronal connections to intercostobrachial nerves (Kingma, 2018). The physical examination shows tachycardia and the presence of jugular venous distention (JVD), which suggests the setting of a right ventricular infarction (Kingma, 2018). The patient’s complaints align with the description of STEMI.

NSTEMI

The diagnosis of a non-ST segment elevation myocardial infarction (NSTEMI) is also possible, as it appears similar to STEMI in symptoms. During an NSTEMI, the patient may experience shortness of breath, chest pain and tightness and its movement to other body parts, dizziness and nausea, and sweating (Kingma, 2018). An electrocardiogram (ECG) distinguishes STEMI and NSTEMI, as the latter shows ST depression and T-wave inversion (Mesas et al., 2018). This condition is characterized by the partial blockage of the coronary artery, where the infarction occurs closer to the endocardium (McCance & Huether, 2018). However, due to the elevated pulse and JVD, the risk of STEMI is increased, making the diagnosis of NSTEMI less suitable.

Acute Coronary Syndrome

The third differential diagnosis for the case is Acute Coronary Syndrome. According to McCance and Huether (2018), ACS occurs when the plaque that partially obstructs coronary blood flow is unstable or with rupture or ulceration (Zègre‐Hemsey et al., 2018). ACS is a range of conditions that include transient ischemia and unstable angina. In this case, unstable angina is a precursor to MI, and it is a result of reversible myocardial ischemia. The pathophysiology of ACSs implies that the thrombus occludes the vessel temporarily before irreversible damage (myocardial necrosis) occurs. The symptoms include chest pain, discomfort, dyspnea, and sweating. Low blood pressure is also an indicator of unstable angina, but it is also characteristic of both STEMI and NSTEMI (Kingma, 2018; Zègre‐Hemsey et al., 2018). Thus, acknowledging the severity of the patient’s symptoms, this differential diagnosis is not the first one.

Myocytes

During the progression of MI, myocytes die in the ischemic zone, as the thrombus causes the stoppage of blood flow, which leads to myocardial necrosis (Wang et al., 2018). Moreover, many myocytes die due to apoptosis, a regulated process of removing damaged cells (Wang et al., 2018). This death is followed by inflammation and subsequent risk of blockage (Wang et al., 2018). The symptoms of chest pain, inflammation, and edema suggest that myocytes were affected.

Blood Pressure

The renin-angiotensin-aldosterone system responds to low blood pressure by releasing renin into the bloodstream (Ames et al., 2019). Then, renin splits angiotensin into angiotensin I and II, the latter of which causes arterioles’ muscular walls to constrict. This increases blood pressure, while the hormone also causes a reaction with aldosterone and vasopressin for the kidneys to retain more sodium and fluids (Ames et al., 2019). As a result, the blood volume and pressure increase further. This process might be harmful to the patient if he experienced MI, as it can contribute to ischemia (Ames et al., 2019).

Decompensated Congestive Heart Failure

Decompensated heart failure (DHF) is characterized by dyspnea, swelling of the lower extremities, and fatigue (Tripoliti et al., 2017). The patient’s physical examination shows jugular venous distension, 3+pitting edema bilaterally, as well as crackles in the lungs, which aligns with the symptoms of DHF – MI may have led to DCH. Finally, the complaints of nausea, weakness, and distress also connect to heart failure, although they are common in infarction (Tripoliti et al., 2017).

References

Ames, M. K., Atkins, C. E., & Pitt, B. (2019). . Journal of veterinary internal medicine, 33(2), 363-382. Web.

Kingma, J. G. (2018). . World Journal of Cardiovascular Diseases, 8(11), 498-517. Web.

McCance, K. L., & Huether, S. E. (2018). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier Health Sciences.

Mesas, C. E., Rodrigues, R. J., Mesas, A. E., Feijó, V. B., Paraiso, L. M., Bragatto, G. F., Moron, V., Bergonso, M.H., Uemura, L., & Grion, C. M. C. (2018). . BMC Health Services Research, 18(1), 490. Web.

Tripoliti, E. E., Papadopoulos, T. G., Karanasiou, G. S., Naka, K. K., & Fotiadis, D. I. (2017). . Computational and Structural Biotechnology Journal, 15, 26-47. Web.

Wang, X., Guo, Z., Ding, Z., & Mehta, J. L. (2018). Journal of the American Heart Association, 7(9), e008024. Web.

Zègre‐Hemsey, J. K., Burke, L. A., & DeVon, H. A. (2018). . Research in Nursing & Health, 41(5), 459-468. Web.

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