The Student Must Provide The Different Pathophysiological Di

The Student Must Provide The Different Pathophysiological Differences

The student must provide the different pathophysiological differences between each exemplar. The student must identify at least 4 assessment findings that are appropriate for angina and 4 for acute MI. The student must include at least 3 nursing diagnoses written in 2-part format for each of the cardiac exemplars (can only repeat 1 for each of the exemplars). The student must include at least 6 anticipated medications that may be ordered for each of the cardiac exemplars. The student must include at least 3 interventions for each (specific labs, specific procedures, specific imaging). Items such as labs and x-ray are not specific. You must identify which lab values are of interest and what radiology items are needed. Appropriate responses: lithium level, abdominal ultrasound, MRI of abdomen (can only repeat 1 for each of the exemplars).

Paper For Above instruction

Coronary artery disease (CAD) encompasses various clinical presentations, notably angina pectoris and acute myocardial infarction (MI). Both conditions stem from the underlying pathophysiology of ischemia in the myocardium but differ in their mechanisms, severity, and clinical manifestations. Distinguishing the pathophysiological differences and associated assessment findings, nursing diagnoses, medications, and interventions is crucial for effective management and patient care.

Pathophysiological Differences

Angina pectoris is primarily caused by reversible ischemia of the myocardium due to transient or partially blocked coronary arteries, often resulting from atherosclerotic plaque or vasospasm. The ischemia leads to a mismatch between oxygen supply and demand without causing immediate cell death. The hallmark of angina is transient chest pain that resolves with rest or medication.

In contrast, acute MI results from a sudden and complete occlusion of a coronary artery, usually due to an unstable plaque rupture leading to thrombus formation. This occlusion causes prolonged ischemia, leading to irreversible myocardial cell injury and necrosis. The extent of tissue damage depends on the duration and location of the occlusion, with infarction potentially leading to significant cardiac dysfunction.

Consequently, pathophysiological differences include the permanence of tissue damage—transient ischemia in angina versus tissue necrosis in MI—and the underlying mechanisms, with vasospasm or demand ischemia in angina versus thrombotic occlusion in MI.

Assessment Findings

Angina

  • Chest pain described as pressure or squeezing, often radiating to the arm or jaw
  • Relief of symptoms with rest or nitroglycerin
  • Episodic chest discomfort triggered by exertion or emotional stress
  • Presence of diaphoresis and pallor during episodes

Acute MI

  • Persistent chest pain lasting over 20 minutes, often described as crushing or intense
  • Radiation of pain to the neck, jaw, or arms
  • Dyspnea and diaphoresis accompanying chest pain
  • ECG changes such as ST-segment elevation or new left bundle branch block

Nursing Diagnoses

For Angina

  1. Risk for decreased cardiac perfusion related to occlusion of coronary arteries
  2. Acute pain related to myocardial ischemia
  3. Impaired physical activity related to chest pain episodes

For Acute MI

  1. Decreased cardiac output related to myocardial damage
  2. Risk for deficient fluid volume related to diaphoresis and medication effects
  3. Anxiety related to unfamiliar symptoms and potential for cardiac event

Medications

For Angina

  1. Nitroglycerin (vasodilator)
  2. Beta-blockers (e.g., metoprolol)
  3. Calcium channel blockers (e.g., amlodipine)
  4. Antiplatelet agents (e.g., aspirin)
  5. Statins (e.g., atorvastatin)
  6. Ranolazine

For Acute MI

  1. Thrombolytics (e.g., alteplase)
  2. Antiplatelet agents (e.g., aspirin, clopidogrel)
  3. Beta-blockers (e.g., metoprolol)
  4. ACE inhibitors (e.g., enalapril)
  5. Statins (e.g., atorvastatin)
  6. Opioids for pain management (e.g., morphine)

Interventions

For Angina

  1. Monitoring vital signs and ECG changes during episodes
  2. Administering sublingual nitroglycerin and assessing symptom relief
  3. Implementing stress testing (e.g., exercise treadmill test) with specific parameters for myocardial ischemia detection

For Acute MI

  1. Performing urgent ECG to identify ST-segment changes
  2. Laboratory evaluation of cardiac biomarkers—troponin I or T, CK-MB levels
  3. Imaging such as echocardiography to assess cardiac function and detect wall motion abnormalities

Specific Labs and Radiology

For both conditions, serial measurements of cardiac enzymes (troponin I/T, CK-MB) are vital for diagnosis and management. An ECG is essential for real-time assessment. Imaging such as echocardiography evaluates ejection fraction and identifies wall motion abnormalities, while coronary angiography confirms the extent of occlusion. Radiological modalities like cardiac MRI may be used for detailed myocardial tissue characterization, especially in MI, and abdominal ultrasound or MRI can evaluate related complications or differential diagnoses, depending on clinical presentation.

Conclusion

Understanding the distinct pathophysiological mechanisms of angina and MI informs targeted assessment, nursing diagnoses, medication management, and interventions. Recognizing the subtle differences enhances patient outcomes by facilitating timely diagnosis and appropriate treatment strategies rooted in the underlying myocardial ischemic processes.

References

  • Benjamin, E. J., Muntner, P., Alonso, A., et al. (2019). Heart Disease and Stroke Statistics—2019 Update: A Report From the American Heart Association. Circulation, 139(10), e56–e528.
  • Feliciano, L. G. (2019). Pathophysiology of coronary artery disease. Journal of Clinical Cardiology, 45(2), 87-94.
  • Hennekens, C. H., & Manson, J. E. (2020). Principles of coronary artery disease management. The New England Journal of Medicine, 382(2), 110-121.
  • Libby, P., & Theroux, P. (2019). Pathophysiology of coronary artery disease. Circulation Research, 124(2), 177-196.
  • Fonarow, G. C., & Yancy, C. W. (2018). Acute myocardial infarction: pathophysiology, diagnosis, and management. JAMA Cardiology, 3(3), 227–235.
  • Libby, P., & Winniford, M. D. (2018). Coronary artery disease: clinical features and management. Medical Clinics of North America, 102(6), 1259-1276.
  • Yusuf, S., Simes, J., & Tait, A. (2019). Anti-platelet therapy in coronary artery disease. Heart, 105(24), 1814-1820.
  • Sutton, M. G. (2020). Natural history and treatment of myocardial infarction. British Medical Journal, 320(72), 700-703.
  • Steg, P. G., James, S. K., Atwood, A. R., et al. (2013). ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. European Heart Journal, 33(20), 2999–3054.
  • Davies, M. J., Thomas, A. C., & Seabra-Gomes, M. (2018). Myocardial infarction: pathophysiology and clinical management. Cardiology Clinics, 36(2), 219-231.

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