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ST-Elevation Myocardial Infarction in the Presence of Septic Shock

Elevated cardiac enzymes are often seen in the setting of sepsis. The mechanism involves hypoperfusion and possible compromise to myocardial tissue. Electrocardiogram (ECG) changes in the setting of septic shock are less common and can vary widely. Rarely, ST-segment elevations can occur. This case...

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Autores principales: Ishmael, Leah, Zalocha, Joseph
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7450346/
https://www.ncbi.nlm.nih.gov/pubmed/32908714
http://dx.doi.org/10.1155/2020/8879878
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author Ishmael, Leah
Zalocha, Joseph
author_facet Ishmael, Leah
Zalocha, Joseph
author_sort Ishmael, Leah
collection PubMed
description Elevated cardiac enzymes are often seen in the setting of sepsis. The mechanism involves hypoperfusion and possible compromise to myocardial tissue. Electrocardiogram (ECG) changes in the setting of septic shock are less common and can vary widely. Rarely, ST-segment elevations can occur. This case describes a 54-year-old female who presented with septic shock secondary to pyelonephritis and Escherichia coli bacteremia. The patient was admitted to the intensive care unit on norepinephrine and required mechanical ventilation. A significant rise in troponin I (peak 19.8 ng/mL) was seen and ECG showed ST-segment elevations in leads I and aVL with reciprocal ST depressions in leads II, III, and aVF. The patient was taken urgently for left cardiac catheterization, which showed no evidence of obstructive coronary artery disease. When distinguishing between septic shock and cardiogenic shock, insertion of a pulmonary artery catheter may help with diagnosis and treatment of cardiogenic shock. Catheter hemodynamic monitoring can also confirm the diagnosis. In our patient's case, hemodynamic monitoring was initiated and was not consistent with cardiogenic shock. ST-segment elevations in the high lateral leads and elevated cardiac markers were likely due to severe transmural ischemia secondary to increased oxygen demand. The patient was continued on intravenous antibiotics for treatment of her septic shock. She was extubated and weaned off of norepinephrine within 48 hours. Repeat ECG performed after resolution of the infection showed normal sinus rhythm with no ST-segment changes. Cardiac dysfunction in the setting of septic shock is well described in medical literature; however, the mechanisms of dysfunction are not explicitly understood. Transient hypoperfusion, coronary vasospasm, and localized endothelial damage are possible components. It is important to think of varying etiologies, other than acute coronary syndrome when approaching patients in septic shock with acute ST-segment changes and elevated cardiac markers.
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spelling pubmed-74503462020-09-08 ST-Elevation Myocardial Infarction in the Presence of Septic Shock Ishmael, Leah Zalocha, Joseph Case Rep Crit Care Case Report Elevated cardiac enzymes are often seen in the setting of sepsis. The mechanism involves hypoperfusion and possible compromise to myocardial tissue. Electrocardiogram (ECG) changes in the setting of septic shock are less common and can vary widely. Rarely, ST-segment elevations can occur. This case describes a 54-year-old female who presented with septic shock secondary to pyelonephritis and Escherichia coli bacteremia. The patient was admitted to the intensive care unit on norepinephrine and required mechanical ventilation. A significant rise in troponin I (peak 19.8 ng/mL) was seen and ECG showed ST-segment elevations in leads I and aVL with reciprocal ST depressions in leads II, III, and aVF. The patient was taken urgently for left cardiac catheterization, which showed no evidence of obstructive coronary artery disease. When distinguishing between septic shock and cardiogenic shock, insertion of a pulmonary artery catheter may help with diagnosis and treatment of cardiogenic shock. Catheter hemodynamic monitoring can also confirm the diagnosis. In our patient's case, hemodynamic monitoring was initiated and was not consistent with cardiogenic shock. ST-segment elevations in the high lateral leads and elevated cardiac markers were likely due to severe transmural ischemia secondary to increased oxygen demand. The patient was continued on intravenous antibiotics for treatment of her septic shock. She was extubated and weaned off of norepinephrine within 48 hours. Repeat ECG performed after resolution of the infection showed normal sinus rhythm with no ST-segment changes. Cardiac dysfunction in the setting of septic shock is well described in medical literature; however, the mechanisms of dysfunction are not explicitly understood. Transient hypoperfusion, coronary vasospasm, and localized endothelial damage are possible components. It is important to think of varying etiologies, other than acute coronary syndrome when approaching patients in septic shock with acute ST-segment changes and elevated cardiac markers. Hindawi 2020-08-18 /pmc/articles/PMC7450346/ /pubmed/32908714 http://dx.doi.org/10.1155/2020/8879878 Text en Copyright © 2020 Leah Ishmael and Joseph Zalocha. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Case Report
Ishmael, Leah
Zalocha, Joseph
ST-Elevation Myocardial Infarction in the Presence of Septic Shock
title ST-Elevation Myocardial Infarction in the Presence of Septic Shock
title_full ST-Elevation Myocardial Infarction in the Presence of Septic Shock
title_fullStr ST-Elevation Myocardial Infarction in the Presence of Septic Shock
title_full_unstemmed ST-Elevation Myocardial Infarction in the Presence of Septic Shock
title_short ST-Elevation Myocardial Infarction in the Presence of Septic Shock
title_sort st-elevation myocardial infarction in the presence of septic shock
topic Case Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7450346/
https://www.ncbi.nlm.nih.gov/pubmed/32908714
http://dx.doi.org/10.1155/2020/8879878
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