ANSWER
ase Research: Acute Myocardial Infarction and Cardiovascular Disease
Presenting with chest pain, a classic sign of acute myocardial infarction (MI), more usually known as a heart attack, Mr. W.G. is 53 years old. His symptoms—which include nausea, discomfort not improved with deep breathing, and crushing chest pain spreading to the neck and jaw—point to a cardiovascular event. The modifiable and non-modifiable risk factors for coronary artery disease (CAD) and acute myocardial infarction will be discussed in this post together with the expected results on an electrocardiogram (EKG), the laboratory test most specific for verifying MI, and the pathophysiological explanation for his symptoms and temperature changes following MI.
Risk factors, both modifiable and non-modifiable, for acute myocardial infarction and coronary artery disease
Age: 53 years old Mr. W.G. is more likely to have coronary artery disease since age is a major determinant of cardiovascular health.
Gender: Though this risk rises for women post-menopause, men are more likely to have CAD and MI.
Key non-modifiable risk factor is a family history of CAD or early MI. Should Mr. W.G. have a family history, his risk would be much increased.
Development of CAD is influenced in part by genetics. Heart disease can be caused in individuals by genetic elements affecting blood pressure, cholesterol, and vascular condition.
Modifiable risk factors are:
Although not specifically mentioned in the case, smoking is a key modifiable risk factor that speeds up atherosclerosis and raises MI risk.
Diet and Obesity: Mr. W.G.’s big breakfast could point to eating patterns that lead to poor nutrition or weight gain—both of which raise CAD risk.
Although his tennis playing points to some activity, sedentary behaviour can cause obesity and high cholesterol—risk factors for CAD.
One of the main causes of CAD and a factor influencing MI probability is high blood pressure. Although Mr. W.G.’s blood pressure is not mentioned, if he has hypertension this would increase his risk.
Diabetes: Particularly when uncontrolled, diabetes is a major changeable risk factor for CAD. Again, Mr. W.G.’s risk would rise should he have diabetes.
Low high-density lipoprotein (HDL) cholesterol and raised low-density lipoprotein (LDL) cholesterol accelerate the production of plaque in coronary arteries, therefore causing CAD and MI.
Forepected EKG Results for Acute Myocardial Infarction
Several important results on Mr. W.G.’s EKG would probably show themselves, in line with an acute myocardial infarction:
Common indication of STEMi (ST-Elevation Myocardial Infarction), linked with total blockage of a coronary artery, is ST elevation. This would show up as a ST segment’s upward deflection in one or more leads.
T-wave inversion may be present, suggesting cardiac tissue ischemia—a lack of oxygen.
Pathological Q Waves: In cases of major myocardial injury, pathological Q waves could show up as evidence of cardiac tissue death brought on by the infarction.
Based on the clinical description of Mr. W.G.’s symptoms—crushing chest pain extending to the neck and jaw—a significant blockage in a major coronary artery seems most likely to cause ST-segment elevation on the EKG.
Acute Myocardial Infarction Laboratory Test Confirmation
A troponin level is the most particular laboratory test available to confirm an acute myocardial infarction. Highly sensitive and specific markers of myocardial damage, troponins are proteins expelled from injured heart muscle. Though it happens many hours after symptom start, troponin I and T levels rise within 3-4 hours of myocardial damage and remain high for up to 1-2 weeks, making them a great diagnostic tool for MI detection.
Other tests, including creatine kinase (CK-MB), might also be employed, but troponins are more specific and offer a more consistent signal of heart muscle injury.
Temperature Variations Following Cardiac Infarction
Usually occurring during the first 24 hours, people following a myocardial infarction often have a little fever. This can be ascribed to the inflammatory response the infarction sets off. Heart tissue’s ischemia and consequent necrosis generate inflammatory mediators including cytokines, which can cause fever and general inflammation. Usually low-grade, the fever can continue many days and peaked over the first 24 to 48 hours.
In Mr. W.G.’s instance, this inflammatory reaction—which is part of the body’s healing mechanism as it tries to mend the injured cardiac tissue—probably accounts for the temperature rise following his MI.
Description of Pain During Myocardial Infarction
The pathophysiology of ischemia and infarction helps one to understand Mr. W.G.’s suffering during his myocardial infarction. Blood high in oxygen cannot reach the heart muscle when a coronary artery is blocked. Myocardial ischemia, or a shortage of oxygen, follows from this and causes pain. The heart muscle is under great stress and starts to perish without enough oxygen, so the pain is sometimes characterised as a crushing or squeezing sensation.
Furthermore aggravating the pain is the production of several biochemical compounds, such lactic acid, from the ischemic tissue, which triggers pain receptors. The common neurological pathways between the heart and other parts of the body, especially the left side of the chest, neck, and jaw, which are serviced by the same spinal cord segments, produce the radiation of pain to the neck, mouth, and arms.
Last Thought
The symptoms and clinical presentation of Mr. W.G. point to an acute myocardial infarction; his EKG results and laboratory testing will most certainly support this diagnosis. Diagnosing and controlling cardiovascular events such as MI depends on an awareness of the modifiable and non-modifiable risk factors, identification of the predicted EKG variations, and knowledge of the suitable laboratory test. Furthermore, knowing the pathophysiology of the pain and fever connected with MI allows one to understand why Mr. W.G. felt the way he did during this life-threatening episode.
Consultations
The American Heart Association, 2023 Factors of coronary artery disease risk. www.heart.org
Mayo Clinic [2023] heart attack, or myocardial infarction). https://www.mayoclinic.org/diseases- Conditions/heart-attack
QUESTION
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 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
- 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.
Submission Instructions:
- Include both case studies in your post.
- Your initial post should be at least 500 words, formatted and cited in current APA style with support from at least 2 academic sources. Your initial post is worth 8 points.