NUR 502 Cardiovascular Risk Factor and Heart Attacks Case Study
Mr. W.G. is a 53-year-old white man who began to experience chest discomfort while playing tennis with a friend. At first, he attributed his discomfort to the heat and having had a large breakfast. Gradually, however, discomfort intensified to a crushing sensation in the sternal area and the pain seemed to spread upward into his neck and lower jaw. The nature of the pain did not seem to change with deep breathing. When Mr. G. complained of feeling nauseated and began rubbing his chest, his tennis partner was concerned that his friend was having a heart attack and called 911 on his cell phone.
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The patient was transported to the ED of the nearest hospital and arrived within 30 minutes of the onset of chest pain. In route to the hospital, the patient was placed on nasal cannula and an IV D5W was started. Mr. G. received aspirin (325 mg po) and 2 mg/IV morphine. He is allergic to meperidine (rash). His pain has eased slightly in the last 15 minutes but is still significant; was 9/10 in severity; now7/10. In the ED, chest pain was not relieved by 3 SL NTG tablets. He denies chills.
Case Study Questions
- For patients at risk of developing coronary artery disease and patients diagnosed with acute myocardial infarct, describe the modifiable and non-modifiable risk factors.
- What would you expect to see on Mr. W.G. EKG and which findings described on the case are compatible with the acute coronary event?
- Having only the opportunity to choose one laboratory test to confirm the acute myocardial infarct, which would be the most specific laboratory test you would choose and why?
- How do you explain that Mr. W.G temperature has increased after his Myocardial Infarct, when that can be observed and for how long? Base your answer on the pathophysiology of the event.
- Explain to Mr. W.G. why he was experiencing pain during his Myocardial Infarct. Elaborate and support your answer.
NUR 502 Cardiovascular Risk Factor and Heart Attacks Case Study
AP2 Discussion 2b
In this case study, we examine Mr. W.G., a 53-year-old white man who encountered chest discomfort while playing tennis. Initially attributing it to the heat and a substantial breakfast, he soon experienced an escalating, crushing sensation in the sternal region, radiating to his neck and lower jaw. The pain persisted despite deep breathing, and as he felt nauseated, his tennis partner, concerned about a potential heart attack, promptly called 911. Mr. G. was transported to the nearest hospital’s Emergency Department (ED) within 30 minutes of symptom onset. En route, he received nasal cannula oxygen and an IV infusion of D5W. Upon arrival, he was administered aspirin (325 mg po) and 2 mg/IV morphine. Although the pain had slightly eased in the last 15 minutes, it remained significant, decreasing from 9/10 to 7/10. In the ED, 3 sublingual nitroglycerin (NTG) tablets failed to relieve the chest pain. The patient denies chills.
1. Modifiable and Non-Modifiable Risk Factors for Coronary Artery Disease and Acute Myocardial Infarction in At-Risk and Diagnosed Patients
Modifiable risk factors, including high blood cholesterol, depression, obesity, and physical inactivity, can be altered through behavioral changes, unlike non-modifiable risk factors such as race, gender, age, and genetics (Anderson & Morrow, 2017).
2. EKG Findings and Acute Coronary Event Compatibility in Mr. W.G.’s Case
Despite the lack of relief from chest pain following 3 sublingual NTG tablets, the reduction in pain severity from 9/10 to 7/10 suggests that slight ST-segment deviations may be observed on the electrocardiogram (EKG). The elevated electrical activity in the heart due to coronary artery blockage might also manifest as T wave inversion on the EKG.
3. Selection of a Specific Laboratory Test to Confirm Acute Myocardial Infarction
The most specific laboratory test for confirming myocardial infarction is Cardiac Troponin 1. This test, known for its sensitivity and specificity compared to Troponin T, is highly effective in indicating risks of composite cardiovascular events, including coronary heart attacks (Lu et al., 2015).
4. Explanation of Mr. W.G.’s Increased Temperature Post-Myocardial Infarct and Temporal Considerations
Within 30 minutes of being rushed to the hospital, the coronary artery blockage led to heart exhaustion, causing difficulties in blood pumping. This compromised blood circulation resulted in heat exhaustion and a subsequent increase in body temperature by more than 1°C (Lu et al., 2015).
5. Elucidating the Cause of Pain During Myocardial Infarction to Mr. W.G.
Myocardial infarction occurs when there is an abrupt blockage of blood flow to the heart muscle, causing tissue damage (Anderson & Morrow, 2017). The pain Mr. W.G. experienced was a direct result of this tissue damage caused by the blockage.
References
Anderson, J. L., & Morrow, D. A. (2017). Acute myocardial infarction. New England Journal of Medicine, 376(21), 2053-2064.
Lu, L., Liu, M., Sun, R., Zheng, Y., & Zhang, P. (2015). Myocardial infarction: Symptoms and treatments. Cell biochemistry and biophysics, pp. 72, 865–867.
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