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      ST-Elevation Myocardial Infarction in the Presence of Septic Shock

      case-report
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      Case Reports in Critical Care
      Hindawi

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          Abstract

          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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          Mechanisms of sepsis-induced cardiac dysfunction.

          To review mechanisms underlying sepsis-induced cardiac dysfunction in general and intrinsic myocardial depression in particular. MEDLINE database. Myocardial depression is a well-recognized manifestation of organ dysfunction in sepsis. Due to the lack of a generally accepted definition and the absence of large epidemiologic studies, its frequency is uncertain. Echocardiographic studies suggest that 40% to 50% of patients with prolonged septic shock develop myocardial depression, as defined by a reduced ejection fraction. Sepsis-related changes in circulating volume and vessel tone inevitably affect cardiac performance. Although the coronary circulation during sepsis is maintained or even increased, alterations in the microcirculation are likely. Mitochondrial dysfunction, another feature of sepsis-induced organ dysfunction, will also place the cardiomyocytes at risk of adenosine triphosphate depletion. However, clinical studies have demonstrated that myocardial cell death is rare and that cardiac function is fully reversible in survivors. Hence, functional rather than structural changes seem to be responsible for intrinsic myocardial depression during sepsis. The underlying mechanisms include down-regulation of beta-adrenergic receptors, depressed postreceptor signaling pathways, impaired calcium liberation from the sarcoplasmic reticulum, and impaired electromechanical coupling at the myofibrillar level. Most, if not all, of these changes are regulated by cytokines and nitric oxide. Integrative studies are needed to distinguish the hierarchy of the various mechanisms underlying septic cardiac dysfunction. As many of these changes are related to severe inflammation and not to infection per se, a better understanding of septic myocardial dysfunction may be usefully extended to other systemic inflammatory conditions encountered in the critically ill. Myocardial depression may be arguably viewed as an adaptive event by reducing energy expenditure in a situation when energy generation is limited, thereby preventing activation of cell death pathways and allowing the potential for full functional recovery.
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            Cardiogenic shock: current concepts and improving outcomes.

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              Sepsis-associated myocardial dysfunction: diagnostic and prognostic impact of cardiac troponins and natriuretic peptides.

              Myocardial dysfunction, which is characterized by transient biventricular impairment of intrinsic myocardial contractility, is a common complication in patients with sepsis. Left ventricular systolic dysfunction is reflected by a reduced left ventricular stroke work index or, less accurately, by an impaired left ventricular ejection fraction (LVEF). Early recognition of myocardial dysfunction is crucial for the administration of the most appropriate therapy. Cardiac troponins and natriuretic peptides are biomarkers that were previously introduced for diagnosis and risk stratification in patients with acute coronary syndrome and congestive heart failure, respectively. However, their prognostic and diagnostic impact in critically ill patients warrants definition. The elevation of cardiac troponin levels in patients with sepsis, severe sepsis, or septic shock has been shown to indicate left ventricular dysfunction and a poor prognosis. Troponin release in this population occurs in the absence of flow-limiting coronary artery disease, suggesting the presence of mechanisms other than thrombotic coronary artery occlusion, probably a transient loss in membrane integrity with subsequent troponin leakage or microvascular thrombotic injury. In contrast to the rather uniform results of studies dealing with cardiac troponins, the impact of raised B-type natriuretic peptide (BNP) levels in patients with sepsis is less clear. The relationship between BNP and both LVEF and left-sided filling pressures is weak, and data on the prognostic impact of high BNP levels in patients with sepsis are conflicting. Mechanisms other than left ventricular wall stress may contribute to BNP release, including right ventricular overload, catecholamine therapy, renal failure, diseases of the CNS, and cytokine up-regulation. Whereas cardiac troponins may be integrated into the monitoring of myocardial dysfunction in patients with severe sepsis or septic shock to identify those patients requiring early and aggressive supportive therapy, the routine use of BNP and other natriuretic peptides in this setting is discouraged at the moment.
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                Author and article information

                Contributors
                Journal
                Case Rep Crit Care
                Case Rep Crit Care
                CRICC
                Case Reports in Critical Care
                Hindawi
                2090-6420
                2090-6439
                2020
                18 August 2020
                : 2020
                : 8879878
                Affiliations
                HCA Healthcare/USF Morsani College of Medicine GME Programs, Northside Hospital, St. Petersburg, FL, USA
                Author notes

                Academic Editor: Mehmet Doganay

                Author information
                https://orcid.org/0000-0003-4413-1339
                Article
                10.1155/2020/8879878
                7450346
                42315eab-9145-4258-be09-584608a01ddf
                Copyright © 2020 Leah Ishmael and Joseph Zalocha.

                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.

                History
                : 3 May 2020
                : 4 August 2020
                : 12 August 2020
                Funding
                Funded by: HCA
                Categories
                Case Report

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