STEMI Case Study (Martha, 72): ST Elevation Pathophysiology, Fibrinolytics, Nitroglycerin, Oxygen and the Post-MI Inflammatory Response

Case study: Martha, 72, with ST-elevation myocardial infarction (STEMI)

Martha had just finished dinner with her husband, and they had just sat down to watch television. She is 72 years old and has had a history of angina. Shortly after they sat down, Martha said she had indigestion and went to take some antacid tablets. An hour later, she began to feel warm, restless and anxious. Her husband noticed she was looking pale and said he would take her to a nearby walk-in clinic. By the time they arrived, Martha said her left arm and shoulder were sore. Suspecting Martha was having a heart attack, her husband turned the car around and rushed her to the hospital. Three hours after the onset of her symptoms, Martha was receiving oxygen, fibrinolytic therapy and nitroglycerin in the emergency ward. Afterward, she was moved to the cardiac unit for STEMI.

1. An ECG of Martha’s heart demonstrated an elevated ST segment. What are the physiologic effects of myocardial ischemia that produce this finding? What variables affect the ECG tracing of a patient with ACS?
2. What are the benefits of administering fibrinolytic therapy, nitroglycerin and oxygen in the early management of STEMI?
3. What is the inflammatory response in the postinfarction recovery period? Why will Martha’s heart function be compromised after her STEMI?

Original example for study purposes (about 1,050 words). Add your pathophysiology textbook as a reference.

1. Myocardial Ischemia and ST-Segment Elevation

Physiologic effects. Most STEMIs begin when an atherosclerotic plaque ruptures or erodes, platelets aggregate and a thrombus completely blocks a coronary artery. Within seconds, the myocardium supplied by that artery shifts from aerobic to anaerobic metabolism. ATP production falls and lactic acid accumulates, and the sodium-potassium pump (Na⁺/K⁺-ATPase) begins to fail. Potassium leaks out of the cells and sodium and calcium accumulate inside, so the injured cells cannot maintain a normal resting membrane potential; they become partially depolarized and repolarize abnormally.

This creates a voltage difference between injured and healthy myocardium, called the current of injury. When ischemia extends through the full thickness of the ventricular wall (transmural ischemia), the injury current flows toward the leads facing the injured area during the ST segment, so those leads show ST-segment elevation. The leads with ST elevation localize the infarct and the blocked artery; for example, elevation in leads II, III and aVF suggests an inferior infarction, often involving the right coronary artery, while elevation in V1–V4 suggests an anterior infarction involving the left anterior descending artery. Leads facing the opposite wall may show reciprocal ST depression. Over time, if the artery stays closed, T waves invert and pathological Q waves develop as the tissue becomes necrotic and electrically silent.

Variables that affect the ECG in ACS.

• Time since symptom onset: hyperacute T waves appear first, followed by ST elevation, then Q waves and T-wave inversion.
• Location and size of the infarct: some areas, such as the posterior wall, are not well seen on a standard 12-lead ECG and may appear as ST depression in V1–V3 unless posterior leads are added; right ventricular infarction requires right-sided leads.
• Extent of ischemia: subendocardial ischemia (as in NSTEMI or unstable angina) typically produces ST depression or T-wave inversion rather than ST elevation, and some patients with ACS have a normal initial ECG, so serial ECGs and troponin levels are needed.
• Pre-existing conditions: left bundle branch block, paced rhythms, left ventricular hypertrophy, prior infarction and early repolarization can mask or mimic ST elevation.
• Other factors: electrolyte disturbances (especially potassium), medications such as digoxin, pericarditis, lead placement errors, body habitus and patient movement.

2. Benefits of Early Fibrinolytic Therapy, Nitroglycerin and Oxygen

Fibrinolytic therapy. Fibrinolytic drugs, such as tenecteplase, alteplase or reteplase, convert plasminogen to plasmin, which breaks down the fibrin in the clot and restores blood flow through the blocked artery. Reperfusion limits the size of the infarct, preserves left ventricular function and reduces mortality, and the benefit is greatest when it is given early because “time is muscle.” Primary percutaneous coronary intervention (PCI) is preferred when it can be performed promptly, but fibrinolysis is recommended for STEMI patients within 12 hours of symptom onset when timely PCI is not available, with a goal of administration within 30 minutes of arrival (Rao et al., 2025). Martha received fibrinolysis about three hours after symptom onset, within the window of greatest benefit. Before treatment, clinicians must screen for contraindications such as prior hemorrhagic stroke, recent major surgery or active bleeding, because bleeding, including intracranial hemorrhage, is the main risk, especially in older adults.

Nitroglycerin. Nitroglycerin releases nitric oxide, causing vascular smooth muscle relaxation. Venous dilation reduces preload, which lowers ventricular wall tension and myocardial oxygen demand, while coronary artery dilation and relief of vasospasm can improve blood flow to ischemic areas. Together, these effects relieve chest pain and can reduce pulmonary congestion. Nitroglycerin should be avoided in patients with hypotension, suspected right ventricular infarction or recent use of phosphodiesterase-5 inhibitors, because it can cause a dangerous drop in blood pressure. It relieves symptoms but has not been shown to reduce mortality.

Oxygen. Supplemental oxygen increases oxygen delivery to the ischemic myocardium when a patient is hypoxemic. However, current evidence shows that routine oxygen does not benefit patients with normal oxygen saturation; in a large randomized trial of patients with suspected myocardial infarction and normal oxygen saturation, routine oxygen did not reduce one-year mortality (Hofmann et al., 2017). Guidelines therefore recommend oxygen for patients with oxygen saturation below 90%, respiratory distress or other signs of hypoxemia (Rao et al., 2025). In Martha’s case, oxygen would be beneficial if her saturation was low or she showed signs of heart failure.

3. The Postinfarction Inflammatory Response and Compromised Heart Function

Inflammatory response. Myocardial necrosis triggers an inflammatory and repair process that occurs in overlapping phases (Frangogiannis, 2014):

• Inflammatory phase (first hours to several days): dying cardiomyocytes release danger signals that activate complement, cytokines (such as interleukin-1 and tumor necrosis factor) and chemokines. Neutrophils infiltrate the area within the first day, followed by monocytes and macrophages, which clear dead cells and debris. This phase explains fever, leukocytosis, elevated C-reactive protein and the risk of pericarditis after MI.
• Proliferative phase (several days to weeks): macrophages shift to reparative functions, releasing growth factors that stimulate fibroblasts and new blood vessels, forming granulation tissue. During roughly days 3 to 7, the infarcted wall is soft and weak, increasing the risk of complications such as ventricular free wall rupture, papillary muscle rupture or ventricular septal rupture.
• Maturation phase (weeks to months): fibroblasts become myofibroblasts and deposit collagen, forming a firm scar, usually by about two months.

Why Martha’s heart function will be compromised. Cardiomyocytes have very limited ability to regenerate, so the infarcted muscle is replaced by noncontractile scar tissue. The scar cannot contract, which reduces stroke volume and ejection fraction. Areas around the infarct may be “stunned,” temporarily depressed despite restored blood flow, or “hibernating” because of chronic reduced perfusion. Over time, ventricular remodeling occurs: the infarcted area thins and expands, the ventricle dilates and the remaining myocardium hypertrophies to compensate, which can lead to heart failure. Scar tissue also disrupts normal electrical conduction, creating a substrate for arrhythmias. Martha’s age, history of angina and possible underlying coronary disease further increase her risk of heart failure, recurrent ischemia and arrhythmias, making cardiac rehabilitation, medications such as beta-blockers, ACE inhibitors, statins and antiplatelet therapy, and risk factor management essential.

Clinical note. Martha’s initial “indigestion,” anxiety and restlessness illustrate that older women often present with atypical or vague symptoms, which can delay recognition. Her husband’s decision to go directly to the hospital likely saved heart muscle.

References

Frangogiannis, N. G. (2014). The inflammatory response in myocardial injury, repair, and remodelling. Nature Reviews Cardiology, 11(5), 255–265. https://doi.org/10.1038/nrcardio.2014.28

Hofmann, R., James, S. K., Jernberg, T., Lindahl, B., Erlinge, D., Witt, N., Arefalk, G., Frick, M., Alfredsson, J., Nilsson, L., Ravn-Fischer, A., Omerovic, E., Kellerth, T., Sparv, D., Ekelund, U., Linder, R., Ekström, M., Lauermann, J., Haaga, U., . . . Svensson, L. (2017). Oxygen therapy in suspected acute myocardial infarction. New England Journal of Medicine, 377(13), 1240–1249. https://doi.org/10.1056/NEJMoa1706222

Rao, S. V., O’Donoghue, M. L., Ruel, M., Rab, T., Tamis-Holland, J. E., Alexander, J. H., Baber, U., Baker, H., Cohen, M. G., Cruz-Ruiz, M., Davis, L. L., de Lemos, J. A., DeWald, T. A., Elgendy, I. Y., Feldman, D. N., Goyal, A., Isiadinso, I., Menon, V., Morrow, D. A., . . . Williams, M. S. (2025). 2025 ACC/AHA/ACEP/NAEMSP/SCAI guideline for the management of patients with acute coronary syndromes: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 151(13), e771–e862. https://doi.org/10.1161/CIR.0000000000001309

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