Expected EKG Findings for Mr. W.G

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.

1. Modifiable and Non-Modifiable Risk Factors for Coronary Artery Disease (CAD):

   Modifiable Risk Factors:

   • Smoking: Smoking is a significant modifiable risk factor for CAD. It increases the risk by promoting atherosclerosis, raising blood pressure, and reducing oxygen delivery to the heart.
   • Diet and Lifestyle: Poor diet choices high in saturated and trans fats, excessive intake of processed foods, and a sedentary lifestyle can contribute to CAD.
   • Hypertension: High blood pressure is a modifiable risk factor that can be controlled through medication, dietary changes, and lifestyle modifications.
   • Diabetes: Proper management of diabetes through diet, exercise, and medication can mitigate the risk of CAD.
   • Obesity: Maintaining a healthy weight through diet and exercise can reduce the risk of CAD.
   • Stress: Chronic stress can lead to unhealthy behaviors and contribute to CAD risk. Stress management strategies can be employed.

   Non-Modifiable Risk Factors:

   • Age: As in Mr. W.G.’s case, age is a non-modifiable risk factor. The risk of CAD increases with age, especially after 45 for men.
   • Gender: Men are generally at a higher risk for CAD compared to women, but the risk for women increases post-menopause.
   • Family History: A family history of CAD increases the risk due to genetic factors.
   • Ethnicity: Certain ethnic groups, including African Americans, Hispanics, and Native Americans, are at a higher risk for CAD.
2. Expected EKG Findings for Mr. W.G.:

   Mr. W.G. is experiencing symptoms suggestive of an acute coronary event. On the EKG, you would expect to see:

   • ST-Segment Elevation: This is the hallmark of ST-segment elevation myocardial infarction (STEMI). It indicates that a significant portion of the heart muscle is not receiving adequate blood supply.
   • T-Wave Changes: T-wave inversion or flattening may also be present, indicating myocardial ischemia.
   • Q-Waves: Over time, Q-waves may develop, signifying irreversible damage to the myocardium.
   • Arrhythmias: Ventricular arrhythmias like ventricular tachycardia or ventricular fibrillation may occur in severe cases.

   The case description of Mr. W.G.’s chest discomfort, its progression, and the lack of relief with nitroglycerin tablets are compatible with an acute coronary event.

3. Most Specific Laboratory Test to Confirm Acute Myocardial Infarct:

   The most specific laboratory test to confirm an acute myocardial infarct is Troponin measurement. Troponin is a protein released into the bloodstream when there is damage to the heart muscle. Troponin levels rise within hours of a myocardial infarction and remain elevated for several days.

   Troponin is highly specific to cardiac muscle injury and provides a more accurate diagnosis than other cardiac biomarkers like creatine kinase (CK) or myoglobin. It allows for the detection of smaller myocardial infarctions, making it the preferred choice for diagnosing acute myocardial infarcts.

4. Increased Temperature After Myocardial Infarct:

   After a myocardial infarct, Mr. W.G.’s increased temperature can be observed. This is known as a post-myocardial infarction fever, and it typically occurs within the first few days following the event. The pathophysiology behind this fever includes:

   • Inflammatory Response: Myocardial infarction triggers an inflammatory response as the body attempts to repair the damaged tissue. This response includes the release of inflammatory cytokines and the recruitment of immune cells to the site of injury.
   • Release of Pyrogens: The inflammatory process can lead to the release of pyrogens, substances that stimulate the hypothalamus in the brain to raise the body’s temperature set point, resulting in a fever.
   • Stress Response: The body also undergoes a stress response during a myocardial infarct, which can lead to an elevated body temperature.

   Post-myocardial infarction fever is usually transient and self-limiting as the inflammatory process resolves. It is an expected part of the body’s healing response to the cardiac injury.

5. Explanation of Pain During Myocardial Infarct:

   Mr. W.G.’s pain during his myocardial infarct can be explained by the following factors:

   • Ischemia: The underlying cause of the pain is myocardial ischemia, which occurs when the blood supply to a portion of the heart muscle is compromised due to a blocked coronary artery. Ischemia results in oxygen deprivation to the heart tissue, leading to pain.
   • Chemical Mediators: Ischemia triggers the release of chemical mediators like bradykinin and adenosine, which stimulate pain receptors (nociceptors) in the heart. These mediators sensitize the nerve endings, amplifying the perception of pain.
   • Muscle Spasm: Ischemic muscle tissue can go into spasm, contributing to the chest pain.
   • Inflammatory Response: The inflammatory response associated with myocardial infarction can further exacerbate pain by irritating surrounding tissues.
   • Visceral Pain: Cardiac pain is often described as visceral pain, which is poorly localized and typically felt in the chest, neck, and jaw, as seen in Mr. W.G.’s case.

   It’s important to explain to Mr. W.G. that this pain is a warning sign of inadequate blood supply to his heart and requires immediate medical attention to minimize heart muscle damage.