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.
post should be at least 500 words for each case study, formatted and cited in the current APA Paper Writing Service by Expert Writers Pro Paper Help: Essay Writing Service Paper Writing Service by Essay Pro Paper Help: Essay Writing Service style with support from at least 2 academic sources

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Modifiable and Non-Modifiable Risk Factors for Coronary Artery Disease and Acute Myocardial Infarction

Coronary artery disease (CAD) and acute myocardial infarction (AMI) have several risk factors that can be classified as modifiable or non-modifiable. Modifiable risk factors are those that can be changed through lifestyle modifications or medical interventions, while non-modifiable risk factors are those that cannot be altered (Khera and Kathiresan, 2017).

Modifiable risk factors for CAD and AMI include:
1. Smoking: Cigarette smoking is a significant risk factor for CAD and AMI. It causes endothelial dysfunction, increases inflammation, and promotes thrombosis (Barua and Ambrose, 2013).
2. Hypertension: High blood pressure can damage the coronary arteries and increase the risk of CAD and AMI.
3. Dyslipidemia: Elevated levels of low-density lipoprotein (LDL) cholesterol and reduced levels of high-density lipoprotein (HDL) cholesterol are associated with an increased risk of CAD and AMI.
4. Diabetes mellitus: Uncontrolled diabetes can lead to endothelial dysfunction, increased inflammation, and accelerated atherosclerosis.
5. Obesity: Being overweight or obese increases the risk of CAD and AMI by promoting insulin resistance, inflammation, and dyslipidemia.
6. Physical inactivity: A sedentary lifestyle is associated with an increased risk of CAD and AMI.

Non-modifiable risk factors for CAD and AMI include:
1. Age: The risk of CAD and AMI increases with age, particularly after 45 years for men and 55 years for women.
2. Gender: Men have a higher risk of CAD and AMI compared to premenopausal women. However, the risk equalizes after menopause.
3. Family history: A family history of premature CAD (before 55 years in men and 65 years in women) increases the risk of developing the condition.
4. Race and ethnicity: Some racial and ethnic groups, such as South Asians and African Americans, have a higher risk of CAD and AMI compared to others.

Expected EKG Findings and Case Compatibility

In the case of Mr. W.G., the EKG findings that would be expected in an acute coronary event include:
1. ST-segment elevation: ST-segment elevation in two or more contiguous leads is a hallmark of ST-elevation myocardial infarction (STEMI) (Reed et al., 2017).
2. T-wave inversion: T-wave inversion may be present in the leads with ST-segment elevation or in other leads, indicating myocardial ischemia or injury.
3. Pathological Q waves: The development of pathological Q waves suggests myocardial necrosis and is often seen in the later stages of AMI.

The case description of Mr. W.G. is compatible with an acute coronary event, as he presents with:
1. Chest discomfort that intensified to a crushing sensation in the sternal area
2. Pain radiating to the neck and lower jaw
3. Nausea
4. Partial response to nitroglycerin and morphine

Most Specific Laboratory Test for Confirming AMI

The most specific laboratory test for confirming AMI is the cardiac troponin assay. Cardiac troponins (I and T) are highly sensitive and specific markers of myocardial necrosis (Thygesen et al., 2018). They are released into the bloodstream when myocardial cells are damaged during an AMI. Troponin levels begin to rise within 2-3 hours of symptom onset, peak at 24-48 hours, and remain elevated for 7-14 days. The high specificity of cardiac troponins makes them the preferred biomarker for diagnosing AMI.

Temperature Increase After Myocardial Infarction

Mr. W.G.’s temperature increase after his myocardial infarction can be explained by the inflammatory response that follows myocardial necrosis. When myocardial cells die during an AMI, they release damage-associated molecular patterns (DAMPs) that activate the innate immune system (Ong et al., 2018). This leads to the recruitment of inflammatory cells, such as neutrophils and macrophages, to the site of injury. The inflammatory response is essential for clearing necrotic debris and initiating the repair process. However, it also contributes to the development of a systemic inflammatory response, which can manifest as fever.

The fever associated with AMI is typically low-grade and occurs within 24-48 hours of the event. It may persist for several days, depending on the extent of myocardial damage and the individual’s inflammatory response. In most cases, the fever resolves spontaneously as the inflammatory process subsides and the healing process begins.

Explanation of Pain During Myocardial Infarction

The pain experienced by Mr. W.G. during his myocardial infarction is a result of myocardial ischemia and necrosis. When a coronary artery becomes occluded by a thrombus, the myocardial tissue supplied by that artery is deprived of oxygen and nutrients. This leads to ischemia, which causes the release of various mediators, such as adenosine, bradykinin, and hydrogen ions, that stimulate nociceptors (pain receptors) in the myocardium (Leach et al., 2017).

As the ischemia progresses, myocardial cells begin to die, releasing additional pain-inducing substances, such as potassium ions and prostaglandins. The pain signal is transmitted via afferent nerve fibers to the spinal cord and then to the brain, where it is perceived as a deep, visceral pain. The pain is often described as a crushing, squeezing, or pressing sensation in the chest, and may radiate to the neck, jaw, arms, or back.

The pain associated with AMI is typically severe and persistent, lasting more than 20 minutes. It may be accompanied by other symptoms, such as shortness of breath, nausea, and diaphoresis. The pain may be partially relieved by nitroglycerin, which dilates the coronary arteries and improves myocardial perfusion. However, complete relief of pain often requires reperfusion therapy, such as thrombolysis or percutaneous coronary intervention, to restore blood flow to the affected myocardium.

In summary, the pain experienced during an AMI is a direct result of myocardial ischemia and necrosis, which stimulate nociceptors and trigger a cascade of inflammatory and neurohormonal responses that contribute to the perception of pain.

References:
Barua, R.S. and Ambrose, J.A., 2013. Mechanisms of coronary thrombosis in cigarette smoke exposure. Arteriosclerosis, Thrombosis, and Vascular Biology, 33(7), pp.1460-1467.

Khera, A.V. and Kathiresan, S., 2017. Genetics of coronary artery disease: discovery, biology and clinical translation. Nature Reviews Genetics, 18(6), pp.331-344.

Leach, R., Jhund, P. and McMurray, J., 2017. Angina pectoris and myocardial ischaemia in the absence of obstructive coronary artery disease: the role of diagnostic tests. Heart, 103(7), pp.533-542.

Ong, S.B., Hernández-Reséndiz, S., Crespo-Avilan, G.E., Mukhametshina, R.T., Kwek, X.Y., Cabrera-Fuentes, H.A. and Hausenloy, D.J., 2018. Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities. Pharmacology & Therapeutics, 186, pp.73-87.

Reed, G.W., Rossi, J.E. and Cannon, C.P., 2017. Acute myocardial infarction. The Lancet, 389(10065), pp.197-210.

Thygesen, K., Alpert, J.S., Jaffe, A.S., Chaitman, B.R., Bax, J.J., Morrow, D.A., White, H.D. and Executive Group on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction, 2018. Fourth universal definition of myocardial infarction (2018). Journal of the American College of Cardiology, 72(18), pp.2231-2264.

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