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. 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
Instructions:
Your initial post should be at least 500 words, formatted and cited in current APA style with support from at least 2 academic sources.
Non-Modifiable Risk Factors:
An EKG is crucial for diagnosing AMI. Expected findings might include:
Considering Mr. W.G.’s symptoms and the unrelieved chest pain after nitroglycerin, the EKG may show ST-segment elevation, supporting the diagnosis of AMI.
The most specific test is the Troponin assay. Troponins are proteins released when myocardial cells are damaged. Troponin levels rise within a few hours of injury, peaking at around 24 hours. Serial troponin measurements can confirm and assess the extent of myocardial damage.
Post-myocardial infarction, a low-grade fever may occur due to the inflammatory response. The damaged myocardium releases cytokines, triggering an immune response. Fever typically peaks within 48 hours and subsides within a week.
The chest pain during AMI is primarily due to ischemia and subsequent tissue damage. Ischemia results from an imbalance between oxygen supply and demand in the myocardium. As coronary arteries narrow or become obstructed (in this case, possibly due to atherosclerosis), blood flow is restricted, leading to tissue hypoxia. The pain is often described as a crushing sensation because the heart muscle is under stress. Radiation of pain to the neck and jaw is common due to shared neural pathways.
The pain’s persistence despite nitroglycerin could be indicative of a more severe and prolonged ischemic event. Morphine helps alleviate pain and reduces anxiety, but the relief may not be complete.
In summary, addressing modifiable risk factors, interpreting EKG findings, utilizing troponin assays, understanding post-MI fever, and explaining the pathophysiology of pain are essential aspects of managing and educating a patient like Mr. W.G. in the context of acute myocardial infarction.