Modifiable and Non-Modifiable Risk Factors for Coronary Artery DiseaseModifiable and Non-Modifiable Risk Factors for Coronary Artery Disease

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

  1. For patients at risk of developing coronary artery disease and patients diagnosed with acute myocardial infarct, describe the modifiable and non-modifiable risk factors.
  2. 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?
  3. 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?
  4. 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.
  5. Explain to Mr. W.G. why he was experiencing pain during his Myocardial Infarct. Elaborate and support your answer.

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.

 

Modifiable and Non-Modifiable Risk Factors for Coronary Artery Disease (CAD) and Acute Myocardial Infarction (AMI)

Modifiable Risk Factors:

  1. Smoking: Mr. W.G.’s case doesn’t mention smoking history, but it’s a significant risk factor. Quitting smoking is crucial for reducing the risk of CAD.
  2. Hypertension: There is no information about Mr. W.G.’s blood pressure, but it’s a modifiable risk factor that requires management.
  3. Hyperlipidemia: Elevated levels of cholesterol and triglycerides contribute to CAD. Lifestyle modifications and medications can help control lipid levels.
  4. Diabetes: Poorly controlled diabetes increases the risk of CAD. Lifestyle changes and medication management are essential.
  5. Obesity: Excess weight, especially around the abdomen, is a modifiable risk factor. Weight loss through diet and exercise is beneficial.
  6. Physical Inactivity: Regular exercise helps maintain cardiovascular health. It’s important to encourage physical activity tailored to the patient’s condition.

Non-Modifiable Risk Factors:

  1. Age: Mr. W.G. is 53 years old, and age is a non-modifiable risk factor for CAD and AMI.
  2. Gender: Being male increases the risk, although women are also at risk, particularly after menopause.
  3. Family History: There is no mention of family history, but genetics plays a role in CAD. Knowing family history helps assess risk.
  4. Race/Ethnicity: Being of white ethnicity doesn’t eliminate the risk; certain ethnic groups have a predisposition.

EKG Findings for Mr. W.G. and Compatibility with Acute Coronary Event

An EKG is crucial for diagnosing AMI. Expected findings might include:

  1. ST-Segment Elevation: Indicates myocardial injury or infarction.
  2. T-wave Changes: Inverted or flattened T-waves suggest ischemia.
  3. Pathological Q-waves: A sign of previous infarction.

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.

Most Specific Laboratory Test for Confirming 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.

Increased Temperature and the Pathophysiology of AMI

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.

Explanation of Pain During AMI to Mr. W.G.

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.

Complete Answer:

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