Case Study Analysis

A 55-year-old high school teacher begins experiencing a cough after a parent-teacher conference. Initially, it was a mild cough, and the teacher thought nothing of it since he had a history of asthma. As he was driving home, the cough became more intense, and he began experiencing chest tightness. He used his rescue inhaler as usual but did not get any relief. Minutes later, he began experiencing chest pain, unlike the tightness that he experienced with his asthma. He began to sweat profusely and experience light-headedness and difficulty breathing. He attempted to pull into a park but passed out and struck the curve causing his vehicle to come to a stop. A passerby saw the incident and called 9-1-1. On the scene, the paramedic found the man unconscious. His EKG revealed ST segment elevation in the anterior leads (V3 and V4), his pulse was shallow, and respirations were 10 breaths/min. Upon arrival at the ER, a troponin level was 13ng/l, and his CK level was 265 U/L.

To prepare:

The Assignment

In your Case Study Analysis related to the scenario provided, explain the following.

  • The cardiovascular and cardiopulmonary pathophysiologic processes that result in the patient presenting these symptoms. (Acute Anterior Myocardial Infarction)
  • Any racial/ethnic variables that may impact physiological functioning.
  • How these processes interact affects the patient.

Please be sure you use the correct APA format, including cover sheet format, running header, etc.

Follow the rubric and use the section headings on the rubric. Delineate each area, please don’t run them together.

Most importantly, please review the readings and look at the cause and effects of disease processes. The materials in the course are to help to develop your critical thinking; your responses need to move from general to scientific. For example, to a layperson, fever occurs because of “germs,” however, as advanced providers, you should be able to explain the scientific reasoning for a fever.



Case Study Analysis

This week’s case study was about a 55-year-old high school teacher who started experiencing a cough after a parent-teacher conference. At first, the cough was mild, and the teacher did not think much of it due to his history of asthma. However, as he was driving home, the cough intensified and he experienced chest tightness. He used his rescue inhaler, but it did not provide relief. Soon after, the teacher experienced chest pain, which was different from the tightness he usually experienced with asthma. He also began sweating heavily, feeling lightheaded, and having difficulty breathing. He tried to pull over into a park but passed out and crashed his car. A passerby saw the incident and called 9-1-1. When the paramedic arrived, they found the man unconscious with ST-segment elevation on his EKG, a shallow pulse, and shallow breathing. Upon arriving at the emergency room, the man’s troponin level was 13 ng/l and his CK level was 265 U/L. This paper aims to describe the cardiovascular and cardiopulmonary pathophysiologic processes behind this patient’s presentation, how these processes interact to affect the patient, and finally explain the racial and ethnic variables that may impact the patient’s physiological functioning.

Cardiovascular and Cardiopulmonary Pathophysiologic Processes

This patient acute anterior myocardial infarction is a result of various cardiovascular pathogenetic processes. The outcome of this cardiac cell death can be multisystemic. The cardiovascular, pulmonary, renal, and central nervous systems would be the most affected (Saleh & Ambrose, 2018). However, the pulmonary and cardiovascular systems will be among the first systems to manifest the outcomes of this cardiac cell death. Acute myocardial infarction results from the abrupt cessation of blood flow to the cardiac muscles from the occlusion of coronary arteries. The process of occlusion of the coronary vessels can be gradual, but the actual cell death would result when the myocardial cells can no longer withstand the ischemia, usually from the rupture of an atherosclerotic plaque or embolization of a blood clot. Occlusion from coronary thrombosis and atherosclerosis are the commonest causes of acute MI (McCance & Huether, 2018). Thus, their significance in understanding this disease pathophysiology.

In acute myocardial infarction, the ischemia leads to mitochondrial dysfunction, the release of reactive oxygen species (ROS), alterations in calcium homeostasis, and cellular electrolyte alterations that ultimately lead to un-programmed cell death, which is called necrosis. In necrosis, the dead cells and the matrix debris trigger an inflammatory cascade (McCance & Huether, 2018). This inflammation serves to clear this debris from the myocardium. Acute inflammation is always associated with swelling and pain, among other signs. The process of acute inflammation triggers a cascade of prostaglandin production and plasma kinins that modulate pain. Inadequate perfusion of the myocardium also leads to lactate accumulation in the myocardium leading to pain due to anaerobic processes. Therefore, acute inflammation and inadequate myocardial respiration lead to the chest pain that was seen in this school teacher.

An ischemic myocardium cannot sufficiently pump blood to end organs and signs of hypoperfusion can kick in (Brener et al., 2020). Signs of cardiogenic shock can result from widespread infarction. Unconsciousness from brain hypoperfusion seen in this patient can result from early shock. Acute myocardial infarction can cause various respiratory changes. Hypoxia and alteration in breathing rates result from fluid buildup in the lungs and pulmonary edema.

Interaction Between Processes Interact to affect the Patient.

Compromised myocardium due to acute myocardial infarction can fail to adequately pump blood to the lungs leading to hypoxia. Decreased cardiac contractility in acute myocardial infarction in the left heart chambers leads to left ventricular insufficiency. Left ventricular insufficiency leads to pulmonary hypertension and a buildup of fluid in the lungs, described as pulmonary congestion. Pulmonary congestion can present with shortness of breath and signs of respiratory insufficiency. A decrease or increase in respiratory rates can be observed as a compensatory mechanism to prevent hypoxia. In the long term, infarcts heal through scar formation (Leoni & Soehnlein, 2018). This is because the human myocardial cells, as well as myocardial cells of other mammals, possess a very negligible regenerative potential and thus heal via fibrosis and scar formation

Racial/Ethnic Variables in Acute Myocardial Infarction (AMI)

AMI doesn’t not only result from atherosclerosis and thromboembolisms but also other disease conditions with racial predilections. Another disease that has ethnic and racial patterns can also cause AMI. Racial variations in risks also contribute to the difference in the incidence and prevalence of AMI. Social and economic variations that are sometimes associated with certain races and ethnic groups can lead to incidence and disease outcomes in patients with AMI. When comparing the races, the existing literature sources have documented that blacks, Hispanics, and Native Americans have higher risk factors for AMI, such as obesity, hypertension, and diabetes mellitus, than non-Hispanic whites. Lower socioeconomic status among these races also predisposes them to the development of poor outcomes such as mortality and morbidity from AMI (Chi et al., 2020; Graham et al., 2018; Rashid et al., 2021). Therefore, race and ethnicity play an essential role in understanding the patterns of this disease.


This patient’s AMI could be explained by cardiovascular and pulmonary pathophysiologic processes. Inadequate heart perfusion led to myocardial infarction and cell death. This cell death led to decreased cardiac contractility and acute inflammation, leading to chest pain and tightness. The cardiac insufficiency resulted in pulmonary congestion and edema, thus shortness of breathing. This teacher’s condition has underlying racial and ethnic variations that variations in familial conditions and socioeconomic status can explain. Overall, this evidence-based knowledge has significance in making a timely diagnosis to prevent mortality and morbidity outcomes.


Brener, M. I., Rosenblum, H. R., & Burkhoff, D. (2020). Pathophysiology and advanced hemodynamic assessment of cardiogenic shock. Methodist DeBakey Cardiovascular Journal16(1), 7–15.

Chi, G. C., Kanter, M. H., Li, B. H., Qian, L., Reading, S. R., Harrison, T. N., Jacobsen, S. J., Scott, R. D., Cavendish, J. J., Lawrence, J. M., Tartof, S. Y., & Reynolds, K. (2020). Trends in acute myocardial infarction by race and ethnicity. Journal of the American Heart Association9(5), e013542.

Graham, G. N., Jones, P. G., Chan, P. S., Arnold, S. V., Krumholz, H. M., & Spertus, J. A. (2018). Racial disparities in patient characteristics and survival after acute myocardial infarction. JAMA Network Open1(7), e184240.

Leoni, G., & Soehnlein, O. (2018). (re) solving repair after myocardial infarction. Frontiers in Pharmacology9, 1342.

McCance, K. L., & Huether, S. E. (2018). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Mosby.

Rashid, M., Timmis, A., Kinnaird, T., Curzen, N., Zaman, A., Shoaib, A., Mohamed, M. O., de Belder, M. A., Deanfield, J., Martin, G. P., Wu, J., Gale, C. P., & Mamas, M. (2021). Racial differences in management and outcomes of acute myocardial infarction during the COVID-19 pandemic. Heart (British Cardiac Society)107(9), 734–740.

Saleh, M., & Ambrose, J. A. (2018). Understanding myocardial infarction. F1000Research7, 1378.

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