Cardiovascular
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 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. The patient was transported to the ED of the nearest hospital and arrived within 30 minutes of the onset of chest pain. En route to the hospital, the patient was placed on a 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 2 Questions:
For patients at risk of developing coronary artery disease and patients diagnosed with acute myocardial infarction, describe the modifiable and non-modifiable risk factors.
What would you expect to see on Mr. W.G. EKG and which findings described in the case are compatible with the acute coronary event?
Having only the opportunity to choose one laboratory test to confirm the acute myocardial infarction, which would be the most specific laboratory test you would choose and why?
How do you explain that Mr. W.G’s temperature has increased after his Myocardial Infarction, when can that 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 Infarction. Elaborate and support your answer.
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Case Study 2: Cardiovascular
Introduction
Mr. W.G. is a 53-year-old man who presented with chest pain, which progressed to a crushing sensation in the sternal area. Upon arrival at the hospital, Mr. G. received aspirin, morphine, and NTG to manage the symptoms. In this case study, we will discuss the modifiable and non-modifiable risk factors for coronary artery disease (CAD), the expected EKG findings in Mr. W.G, the most specific laboratory test to confirm acute myocardial infarction (AMI), the reason behind Mr. W.G.’s increased temperature, and the explanation of his pain during his AMI.
Modifiable and Non-modifiable Risk Factors for CAD
CAD is a common cardiovascular disease that affects millions of people worldwide. Modifiable risk factors for CAD include smoking, high blood pressure, high cholesterol levels, physical inactivity, obesity, and unhealthy diet. Non-modifiable risk factors for CAD include age, family history of heart disease, male gender, and ethnic background (Lloyd-Jones et al., 2010).
EKG Findings in Mr. W.G.
In Mr. W.G.’s case, we would expect to see EKG changes such as ST-segment elevation, T-wave inversion, and the development of Q waves, which are indicative of an acute coronary event. ST-segment elevation suggests myocardial ischemia or injury, whereas T-wave inversion and the development of Q waves indicate myocardial infarction (Thygesen et al., 2012).
Most Specific Laboratory Test for Confirming AMI
The most specific laboratory test to confirm AMI is the troponin assay. Troponin is a protein that is released into the bloodstream following cardiac injury, and elevated levels of troponin are indicative of myocardial damage (Thygesen et al., 2012). This test is preferred over other cardiac markers, such as creatine kinase and myoglobin, due to its high sensitivity and specificity.
Increased Temperature after AMI
An increased temperature after an AMI is a common finding and can be observed for up to 72 hours following the event. This is due to the release of cytokines, which are inflammatory mediators that are produced in response to tissue damage (Garcia-Garcia et al., 2021). The release of cytokines causes an increase in body temperature and is known as a systemic inflammatory response.
Explanation of Pain during AMI
Mr. W.G.’s pain during his AMI was due to the lack of oxygen supply to the heart muscle. When the coronary arteries become narrowed or blocked, blood flow to the heart is reduced, leading to myocardial ischemia. This causes the heart muscle to become starved of oxygen, leading to the release of lactic acid and other metabolites, which stimulate pain receptors in the heart (American Heart Association, 2021). The resulting pain is described as a crushing sensation in the sternal area, which can radiate to the neck, back, or arms.
Conclusion
In conclusion, CAD is a common cardiovascular disease that can lead to an AMI, which is a medical emergency. Modifiable and non-modifiable risk factors for CAD should be identified and managed to prevent the development of the disease. EKG changes, troponin assay, increased temperature, and pain during AMI are important diagnostic findings that should be recognized and managed promptly to improve patient outcomes.
