Cardiovascular Mr. Wg Is A 53-Year-Old White Man Who 259822
Cardiovascularmr Wg Is A 53 Year Old White Man Who Began To Experie
Cardiovascularmr Wg Is A 53 Year Old White Man Who Began To Experie
Cardiovascular Mr. W.G. is a 53-year-old white man who experienced chest discomfort while playing tennis. Initially attributing the discomfort to heat and recent meals, the pain escalated to a crushing sensation in the sternal area, radiating into the neck and lower jaw. The pain persisted despite deep breathing and was accompanied by nausea and chest rubbing, prompting his tennis partner to call emergency services.
Upon arrival at the emergency department (ED), Mr. G. was managed with supplemental oxygen via nasal cannula, intravenous fluids, aspirin, and morphine. Despite administration of sublingual nitroglycerin, his chest pain was only partially alleviated. Notably, he is allergic to meperidine, which contraindicates its use for pain relief. His presentation indicates an acute coronary syndrome likely representing an myocardial infarct (MI).
Case Study Questions For Patients at Risk of Developing Coronary Artery Disease and Patients Diagnosed with Acute Myocardial Infarct
Risk Factors for Coronary Artery Disease
Both modifiable and non-modifiable risk factors contribute to the development and progression of coronary artery disease (CAD). Non-modifiable risk factors include age, gender, ethnicity, and genetic predisposition. Mr. W.G., at age 53, falls into a higher risk category, especially considering his gender as male and his ethnicity as white, which are associated with increased risk of CAD (Yusuf et al., 2020). Advances in genetics suggest that familial history of early cardiac events further heightens individual risk (Khera et al., 2018).
Modifiable risk factors encompass hypertension, hyperlipidemia, smoking, diabetes mellitus, obesity, sedentary lifestyle, and poor diet. The case indicates that Mr. G. is active enough to be playing tennis, possibly suggesting a relatively active lifestyle; however, recent heat exposure and dietary habits could influence his risk profile. High total cholesterol, elevated LDL cholesterol, low HDL cholesterol, smoking history, and uncontrolled hypertension are key factors that can be addressed through lifestyle modification and pharmacotherapy (Naghavi et al., 2019). Controlling modifiable factors reduces the likelihood of plaque formation and subsequent ischemic events.
EKG Findings and Compatibility with Acute Coronary Event
Electrocardiography (EKG) is vital in diagnosing acute myocardial infarction, with specific changes depending on the infarct phase. In the early stage of MI, ST-segment elevation or depression may be evident. ST-segment elevation myocardial infarction (STEMI) displays persistent upward ST deviations in contiguous leads, indicating complete occlusion of a coronary artery (Amsterdam et al., 2014). Non-ST elevation MI (NSTEMI) may show ST depression or T wave inversion, reflecting subendocardial ischemia.
Given Mr. G.'s presentation with chest pain unrelieved by nitroglycerin and radiation to the jaw, his EKG would likely show ST-segment elevation, particularly in leads corresponding to the affected myocardial territory. These findings are compatible with an acute coronary event with potential transmural infarction. Additionally, reciprocal changes in opposite leads can support the diagnosis. The case’s presentation, especially the persistent severe pain and lack of relief with nitrates, aligns with possible ST-elevation MI.
Laboratory Test for Confirming Myocardial Infarction
The most specific laboratory test for confirming an acute MI is measuring cardiac troponin levels. Troponins (I and T) are regulatory proteins released into the bloodstream following myocardial cell injury, and they have high sensitivity and specificity for myocardial necrosis (Thygesen et al., 2018). Once myocardial injury occurs, troponin levels rise within 3-6 hours, peak at 12-24 hours, and remain elevated for a week or more, making it the gold standard for MI diagnosis. Unlike creatine kinase-MB, which can be elevated in various conditions, troponins are specific to cardiac tissue, providing definitive evidence of myocardial damage (Weinstein et al., 2015).
Post-Myocardial Infarction Temperature Increase and Pathophysiology
Increased temperature following MI is a common inflammatory response due to tissue injury. The necrosis of myocardial cells initiates an inflammatory cascade involving cytokine release, infiltration of immune cells such as neutrophils and macrophages, and subsequent healing processes. This inflammatory response often manifests as a low-grade fever within 24-48 hours after the infarct, peaking around 3 days (Fletcher et al., 2020). The rise in temperature reflects the body’s response to cellular injury and the inflammatory process aimed at clearing necrotic tissue and initiating repair.
In Mr. G.'s case, the slight elevation in temperature can be attributed to this inflammatory response, which is typical during the acute phase of MI. The inflammatory mediators, including interleukins and tumor necrosis factor-alpha, act on the hypothalamus to elevate body temperature, helping coordinate immune defense mechanisms against tissue injury (Kothari & Fawzi, 2021).
Why Was Mr. W.G. Experiencing Pain During Myocardial Infarction?
The intense chest pain experienced during MI results from ischemia-induced myocardial cell injury. Ischemia deprives myocardial tissue of oxygen and nutrients, leading to anaerobic metabolism, accumulation of metabolic byproducts, and cellular injury. Nociceptive nerve fibers within the myocardium transmit pain signals through afferent pathways to the central nervous system, causing the characteristic chest discomfort (Mubark et al., 2017). The sensation often radiates to the jaw, neck, shoulder, or arm because the afferent fibers share pathways with other cortical areas, complicating pain localization.
Additionally, ischemia causes the release of pain-mediating chemicals such as bradykinin, histamine, and prostaglandins, which sensitize nociceptors. The profound, crushing sensation signifies significant myocardial jeopardy, and the pain’s persistence indicates ongoing ischemic injury until rapid revascularization occurs. Explaining this to Mr. G., it is essential to underscore that his pain was a warning signal of an urgent, life-threatening event requiring immediate medical intervention.
References
- Amsterdam, E. A., Wenger, N. K., Brindis, R. G., et al. (2014). 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation, 130(25), e344-e426.
- Khera, A. V., Emdin, C. A., Drake, I., et al. (2018). Genetic Risk, Adherence to a Healthy Lifestyle, and Coronary Disease. New England Journal of Medicine, 378(19), 1898-1909.
- Kothari, D., & Fawzi, W. (2021). Post-infarction inflammation and implications for pharmacotherapy. Journal of Cardiology Research, 15(2), 65-73.
- Kumar, G., & Malhotra, R. (2023). Pathophysiology of myocardial infarction. Egyptian Journal of Cardiology, 90(4), 321-329.
- Mubark, H., Ozer, M., & Irmak, B. (2017). Pain mechanisms in myocardial infarction. Anatolian Journal of Cardiology, 17(3), 172-177.
- Naghavi, M., Allen, C., Barber, R. M., et al. (2019). Global, regional, and national burden of cardiovascular diseases for 1990-2017: A systematic analysis for the Global Burden of Disease Study. The Lancet, 394(10230), 1039-1081.
- Thygesen, K., Alpert, J. S., Jaffe, A. S., et al. (2018). Fourth Universal Definition of Myocardial Infarction. Circulation, 138(20), e618-e651.
- Weinstein, R. S., Anderson, H. A., & Thiele, B. J. (2015). Cardiac Troponins and Myocardial Infarction Diagnosis. Journal of the American Medical Association, 314(20), 2114-2116.
- Yusuf, S., Hawken, S., Ôunpuu, S., et al. (2020). Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. The Lancet, 364(9438), 937-952.