Case Study: Acute Myocardial Infarction

Posted: July 21st, 2023

Case Study: Acute Myocardial Infarction

Patient Presentation

Mr. R.T., a 62-year-old male, arrives at the emergency department at 10:30 AM reporting severe chest pain persisting for 90 minutes. He describes a crushing, tight sensation in the center of his chest, radiating to his left shoulder and jaw, which began while climbing stairs at work. Rest fails to alleviate the discomfort. Accompanying symptoms include nausea, excessive sweating, and mild shortness of breath. He denies recent trauma or injury, and his presentation prompts urgent evaluation for a cardiac event.

Medical history reveals hypertension, diagnosed eight years ago and managed with amlodipine 10 mg daily, and hyperlipidemia, treated with simvastatin 20 mg daily. A 30 pack-year smoking history, discontinued one year ago, also marks his profile. Socially, Mr. R.T. is divorced, works as a warehouse manager, consumes one to two beers weekly, and reports a sedentary lifestyle with a diet high in processed foods. He denies illicit drug use.

Physical examination shows a blood pressure of 170/95 mmHg, heart rate of 105 beats per minute, respiratory rate of 20 breaths per minute, temperature of 98.7°F, and oxygen saturation of 93% on room air. The patient appears pale, diaphoretic, and anxious. Cardiovascular assessment confirms a regular rhythm with normal S1 and S2 sounds, no murmurs, and no jugular venous distension. Lungs are clear bilaterally, the abdomen is soft and non-tender, and extremities show no edema with 2+ pulses bilaterally.

Diagnostic tests reveal critical findings. An electrocardiogram (ECG) displays ST-segment elevation in leads II, III, and aVF, suggesting an inferior wall myocardial infarction. Cardiac biomarkers indicate a troponin I level of 3.2 ng/mL (normal <0.04 ng/mL) and CK-MB of 7% (normal <5%). A basic metabolic panel shows sodium at 140 mM, potassium at 4.2 mM, and glucose at 115 mg/dL. The lipid profile reveals total cholesterol of 220 mg/dL, LDL of 150 mg/dL, and HDL of 30 mg/dL. Clinicians initiate immediate treatment with aspirin 325 mg chewed, nitroglycerin 0.4 mg sublingual (repeated twice), oxygen at 2 L/min via nasal cannula, and morphine 2 mg IV for pain, followed by urgent transfer to the cardiac catheterization lab for percutaneous coronary intervention (PCI).

Pathophysiology and Clinical Significance

Acute myocardial infarction (AMI) occurs when prolonged ischemia leads to myocardial tissue necrosis, typically due to coronary artery occlusion by a thrombus (Thygesen et al., 2018). This condition affects over 800,000 individuals annually in the United States, predominantly men aged 50–70 with cardiovascular risk factors (Gulati, Levy, and Mukherjee, 2021). Its significance lies in its high morbidity and mortality, necessitating prompt intervention to restore blood flow and minimize myocardial damage. Atherosclerotic plaque rupture, often triggered by hypertension or hyperlipidemia, is the primary cause, with smoking and inactivity as contributing factors. In Mr. R.T.’s case, occlusion of the right coronary artery likely explains the inferior wall infarction observed on ECG.

The pathophysiology involves disrupted oxygen supply to the myocardium, leading to ischemia and necrosis within hours. This process releases cardiac biomarkers, such as troponin and CK-MB, into the bloodstream. Inflammatory responses follow, increasing the risk of complications like arrhythmias or heart failure (Ibanez et al., 2018). Diagnosis relies on a triad: clinical symptoms (chest pain, nausea, dyspnea), ECG changes (ST-segment elevation in STEMI), and elevated biomarkers. Treatment prioritizes reperfusion, with PCI as the gold standard, alongside medications like aspirin, nitroglycerin, and beta-blockers. Long-term management includes antiplatelet therapy, statins, and lifestyle modifications to prevent recurrence (Collet et al., 2020).

Management and Nursing Considerations

Initial management of AMI focuses on rapid stabilization and reperfusion. Clinicians administer aspirin to inhibit platelet aggregation, nitroglycerin to reduce myocardial oxygen demand, and oxygen to improve saturation (Ibanez et al., 2018). Morphine alleviates pain and anxiety, which can exacerbate ischemia. PCI, performed urgently, restores coronary blood flow, significantly improving outcomes compared to thrombolytic therapy (Gulati, Levy, and Mukherjee, 2021). Nurses play a critical role in monitoring vital signs, assessing pain, and preparing the patient for catheterization.

Post-PCI, nurses must monitor for complications, including arrhythmias, bleeding, and heart failure. Continuous ECG monitoring detects ventricular tachycardia, particularly in inferior wall infarctions affecting the right coronary artery (Levine, Bates, and Blankenship, 2019). Bleeding risks arise from antiplatelet agents, requiring vigilant assessment of the catheterization site. Patient education on lifestyle changes, such as dietary improvements and smoking cessation, supports long-term recovery. With timely intervention, the 30-day mortality rate for STEMI is approximately 5–8% (Anderson and Morrow, 2019).

Critical Thinking and Problem-Solving Questions

I. What primary risk factors most significantly contributed to Mr. R.T.’s acute myocardial infarction?
II. Why did clinicians administer nitroglycerin in the emergency department?
III. What does ST-segment elevation in leads II, III, and aVF indicate about the myocardial infarction’s location?
IV. Which complications should nurses prioritize monitoring in the first 48 hours post-PCI?

Responses to Critical Thinking Questions

I. Primary Risk Factors for Acute Myocardial Infarction
Hypertension and hyperlipidemia stand as Mr. R.T.’s most significant risk factors. Hypertension accelerates atherosclerosis by damaging vascular endothelium, promoting plaque formation. Hyperlipidemia, evidenced by elevated LDL and low HDL, contributes to plaque buildup, increasing the likelihood of rupture and thrombosis (Thygesen et al., 2018). His prior smoking history, though ceased, likely exacerbated endothelial dysfunction over time. A sedentary lifestyle and poor diet further compound these risks, but hypertension and hyperlipidemia remain the dominant contributors due to their direct impact on coronary artery disease progression.

II. Rationale for Nitroglycerin Administration
Clinicians administered nitroglycerin to alleviate Mr. R.T.’s ischemic chest pain and reduce myocardial oxygen demand. Nitroglycerin dilates coronary arteries, enhancing blood flow to ischemic tissue, and reduces preload and afterload through systemic vasodilation (Ibanez et al., 2018). Sublingual delivery ensures rapid action, providing temporary relief until PCI restores coronary perfusion. This intervention stabilizes the patient, mitigating further myocardial damage during the critical pre-reperfusion period.

III. Significance of ST-Segment Elevation
ST-segment elevation in leads II, III, and aVF indicates an inferior wall myocardial infarction, resulting from occlusion of the right coronary artery (RCA) (Levine, Bates, and Blankenship, 2019). The RCA supplies the inferior left ventricle and portions of the right ventricle, and its blockage causes ischemia in these regions, reflected by ECG changes in the inferior leads. This finding guides urgent reperfusion to target the affected vessel.

IV. Post-PCI Complications to Monitor
Nurses should prioritize monitoring for ventricular arrhythmias and bleeding in the first 48 hours post-PCI. Arrhythmias, such as ventricular tachycardia, may arise from myocardial irritability or reperfusion injury, particularly in RCA-related infarctions affecting conduction pathways (Anderson and Morrow, 2019). Bleeding, either at the catheterization site or systemically, is a risk due to antiplatelet therapy, requiring close inspection and hemoglobin monitoring. These complications demand immediate intervention to ensure patient safety.

Conclusion

Acute myocardial infarction, as illustrated in Mr. R.T.’s case, underscores the critical need for rapid diagnosis and intervention. Nurses contribute significantly by recognizing symptoms, facilitating timely treatment, and monitoring for complications. Understanding risk factors, pathophysiology, and evidence-based management equips healthcare professionals to improve patient outcomes. Continued education on lifestyle modifications and adherence to therapy will support Mr. R.T.’s recovery, highlighting the importance of holistic care in cardiovascular nursing.

References

Anderson, J. L. and Morrow, D. A., 2019. Acute myocardial infarction. New England Journal of Medicine, 380(18), pp.1710–1720. https://doi.org/10.1056/NEJMra1808132
Collet, J. P., Thiele, H., Barbato, E., et al., 2020. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. European Heart Journal, 41(37), pp.3495–3568. https://doi.org/10.1093/eurheartj/ehaa575
Gulati, M., Levy, P. D. and Mukherjee, D., 2021. Management of acute coronary syndromes in the modern era. JAMA Cardiology, 6(7), pp.769–778. https://doi.org/10.1001/jamacardio.2021.0105
Ibanez, B., James, S., Agewall, S., et al., 2018. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. European Heart Journal, 39(2), pp.119–177. https://doi.org/10.1093/eurheartj/ehx393
Levine, G. N., Bates, E. R. and Blankenship, J. C., 2019. 2015 ACC/AHA/SCAI focused update on primary percutaneous coronary intervention for patients with ST-elevation myocardial infarction. Circulation, 133(11), pp.1135–1147. https://doi.org/10.1161/CIR.0000000000000336
Thygesen, K., Alpert, J. S., Jaffe, A. S., et al., 2018. Fourth universal definition of myocardial infarction. Journal of the American College of Cardiology, 72(18), pp.2231–2264. https://doi.org/10.1016/j.jacc.2018.08.1038

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Pathophysiology Case Study Assignment: Acute Myocardial Infarction

Introduction

Acute myocardial infarction (AMI), commonly known as a heart attack, remains a leading cause of mortality in the United States, affecting nearly one million individuals annually (Gulati, Levy, and Mukherjee, 2021). For nursing students, understanding AMI’s pathophysiology, clinical presentation, and management is critical to delivering effective patient care. This case study assignment, designed for Chamberlain University’s College of Nursing & Public Health, challenges students to apply pathophysiological principles to a clinical scenario. By analyzing a patient’s presentation and answering critical thinking questions, students will deepen their understanding of AMI and its implications for nursing practice. Evidence suggests that timely intervention significantly improves outcomes, making this exercise vital for developing clinical judgment.

Patient Case

Mr. Dylan Radin, a 55-year-old male, arrives at the emergency department (ED) via ambulance at 9:15 AM, reporting acute onset of midsternal chest pain radiating to his left arm and neck for the past two hours. He describes the pain as heavy and squeezing, unrelieved by rest, and accompanied by shortness of breath, diaphoresis, and nausea. The symptoms began while he was lifting heavy boxes at his construction job. He denies recent trauma. His medical history includes hypertension (managed with lisinopril 20 mg daily), hyperlipidemia (atorvastatin 40 mg daily), and a 25 pack-year smoking history (quit three years ago).

Physical examination reveals a blood pressure of 165/92 mmHg, heart rate of 110 beats per minute, respiratory rate of 26 breaths per minute, temperature of 98.6°F, and oxygen saturation of 92% on room air. Mr. Radin appears pale, cool, and diaphoretic, with an anxious demeanor. Cardiovascular assessment shows a regular rhythm, no murmurs, and normal S1 and S2 sounds. Lungs are clear bilaterally, and extremities exhibit no edema with 2+ pulses. An electrocardiogram (ECG) reveals ST-segment elevation in leads V1–V4, indicating an anterior wall ST-elevation myocardial infarction (STEMI). Laboratory results show troponin I at 2.8 ng/mL (normal <0.04 ng/mL) and CK-MB at 8% (normal <5%). Clinicians administer aspirin 325 mg chewed, nitroglycerin 0.4 mg sublingual, oxygen at 2 L/min via nasal cannula, and morphine 4 mg IV, then prepare Mr. Radin for percutaneous coronary intervention (PCI) within 60 minutes.

Pathophysiology Overview

Acute myocardial infarction results from prolonged ischemia causing irreversible myocardial necrosis, typically due to coronary artery occlusion by a thrombus (Thygesen et al., 2018). Atherosclerotic plaque rupture, often linked to risk factors like hypertension and hyperlipidemia, triggers thrombus formation, blocking blood flow and oxygen delivery to the myocardium (). This imbalance between oxygen supply and demand leads to cellular injury, releasing cardiac biomarkers like troponin and CK-MB. In Mr. Radin’s case, the anterior wall infarction suggests occlusion of the left anterior descending (LAD) artery, which supplies a significant portion of the left ventricle. Without prompt reperfusion, complications such as heart failure or arrhythmias may arise, underscoring the urgency of intervention (Ibanez et al., 2018).

Critical Thinking Questions

I. Which risk factors most significantly contributed to Mr. Radin’s acute myocardial infarction?
II. Why did clinicians prioritize PCI within 60 minutes of Mr. Radin’s arrival?
III. What does the ST-segment elevation in leads V1–V4 indicate about the location and severity of the infarction?
IV. Which complications should nurses monitor in the first 48 hours post-PCI, and what interventions can mitigate these risks?

Analysis and Answers to Critical Thinking Questions

I. Risk Factors Contributing to Acute Myocardial Infarction
Mr. Radin’s primary risk factors for AMI include hypertension and hyperlipidemia. Hypertension damages vascular endothelium, accelerating atherosclerosis, while hyperlipidemia promotes plaque buildup, increasing the risk of rupture and thrombosis (Thygesen et al., 2018). His 25 pack-year smoking history, though discontinued, likely contributed to endothelial dysfunction over time, compounding these risks. A sedentary lifestyle, inferred from his physically demanding job without regular exercise, further elevates his risk profile. Consequently, managing hypertension and lipids remains critical for preventing recurrent events.

II. Rationale for Urgent PCI
Clinicians prioritized PCI within 60 minutes to restore coronary blood flow and minimize myocardial damage, adhering to guidelines for STEMI management (Ibanez et al., 2018). The phrase “time is muscle” reflects the urgency, as prolonged ischemia leads to irreversible necrosis (). PCI, involving stent placement to open the occluded LAD artery, is the preferred reperfusion strategy when performed within 90–120 minutes of first medical contact. This rapid intervention improves survival rates and reduces complications like heart failure, making it critical for Mr. Radin’s anterior wall STEMI.

III. Significance of ST-Segment Elevation
ST-segment elevation in leads V1–V4 indicates an anterior wall myocardial infarction, caused by occlusion of the left anterior descending artery (Levine, Bates, and Blankenship, 2019). This artery supplies the anterior left ventricle, and its blockage causes significant ischemia, reflected by ECG changes in the precordial leads. The severity is underscored by the extent of myocardial tissue at risk, as anterior infarctions often involve a larger portion of the left ventricle, increasing the likelihood of complications like pump failure. Prompt recognition of these ECG findings guides urgent reperfusion.

IV. Post-PCI Complications and Nursing Interventions
Nurses should monitor for ventricular arrhythmias and bleeding in the first 48 hours post-PCI. Arrhythmias, such as ventricular tachycardia, may result from myocardial irritability or reperfusion injury, particularly in LAD-related infarctions (Anderson and Morrow, 2019). Continuous ECG monitoring and prompt administration of antiarrhythmic drugs, like lidocaine, can mitigate this risk. Bleeding, either at the femoral catheterization site or systemically due to antiplatelet therapy (e.g., aspirin, clopidogrel), requires vigilant inspection and hemoglobin monitoring. Nurses should apply pressure to the access site and report significant bleeding promptly to prevent hemodynamic instability.

Conclusion

This case study of Mr. Radin illustrates the complex interplay of risk factors, pathophysiology, and clinical management in acute myocardial infarction. Nurses play a pivotal role in recognizing symptoms, facilitating rapid intervention, and monitoring for complications. By understanding the underlying mechanisms of AMI, students can better anticipate patient needs and implement evidence-based care. For instance, educating patients on lifestyle modifications post-discharge can reduce recurrence risk. This assignment reinforces the importance of clinical reasoning in nursing practice, preparing students for real-world challenges in cardiovascular care.

References

Anderson, J. L. and Morrow, D. A., 2019. Acute myocardial infarction. New England Journal of Medicine, 380(18), pp.1710–1720. https://doi.org/10.1056/NEJMra1808132
Gulati, M., Levy, P. D. and Mukherjee, D., 2021. Management of acute coronary syndromes in the modern era. JAMA Cardiology, 6(7), pp.769–778. https://doi.org/10.1001/jamacardio.2021.0105
Ibanez, B., James, S., Agewall, S., et al., 2018. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. European Heart Journal, 39(2), pp.119–177. https://doi.org/10.1093/eurheartj/ehx393
Levine, G. N., Bates, E. R. and Blankenship, J. C., 2019. 2015 ACC/AHA/SCAI focused update on primary percutaneous coronary intervention for patients with ST-elevation myocardial infarction. Circulation, 133(11), pp.1135–1147. https://doi.org/10.1161/CIR.0000000000000336
Thygesen, K., Alpert, J. S., Jaffe, A. S., et al., 2018. Fourth universal definition of myocardial infarction. Journal of the American College of Cardiology, 72(18), pp.2231–2264. https://doi.org/10.1016/j.jacc.2018.08.1038
Virani, S. S., Alonso, A., Benjamin, E. J., et al., 2020. Heart disease and stroke statistics—2020 update: A report from the American Heart Association. Circulation, 141(9), pp.e139–e596. https://doi.org/10.1161/CIR.0000000000000757

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