Organ dysfunction, injury, and failure in cardiogenic shock
Abstract Background Cardiogenic shock (CS) is caused by primary cardiac dysfunction and induced by various and heterogeneous diseases (e.g., acute impairment of cardiac performance, or acute or chronic impairment of cardiac performance). Main body Although a low cardiac index is a common finding in...
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| Format: | Article |
| Language: | English |
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BMC
2023-06-01
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| Series: | Journal of Intensive Care |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s40560-023-00676-1 |
| _version_ | 1797789949950427136 |
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| author | Akihiro Shirakabe Masato Matsushita Yusaku Shibata Shota Shighihara Suguru Nishigoori Tomofumi Sawatani Kazutaka Kiuchi Kuniya Asai |
| author_facet | Akihiro Shirakabe Masato Matsushita Yusaku Shibata Shota Shighihara Suguru Nishigoori Tomofumi Sawatani Kazutaka Kiuchi Kuniya Asai |
| author_sort | Akihiro Shirakabe |
| collection | DOAJ |
| description | Abstract Background Cardiogenic shock (CS) is caused by primary cardiac dysfunction and induced by various and heterogeneous diseases (e.g., acute impairment of cardiac performance, or acute or chronic impairment of cardiac performance). Main body Although a low cardiac index is a common finding in patients with CS, the ventricular preload, pulmonary capillary wedge pressure, central venous pressure, and systemic vascular resistance might vary between patients. Organ dysfunction has traditionally been attributed to the hypoperfusion of the organ due to either progressive impairment of the cardiac output or intravascular volume depletion secondary to CS. However, research attention has recently shifted from this cardiac output (“forward failure”) to venous congestion (“backward failure”) as the most important hemodynamic determinant. Both hypoperfusion and/or venous congestion by CS could lead to injury, impairment, and failure of target organs (i.e., heart, lungs, kidney, liver, intestines, brain); these effects are associated with an increased mortality rate. Treatment strategies for the prevention, reduction, and reversal of organ injury are warranted to improve morbidity in these patients. The present review summarizes recent data regarding organ dysfunction, injury, and failure. Conclusions Early identification and treatment of organ dysfunction, along with hemodynamic stabilization, are key components of the management of patients with CS. |
| first_indexed | 2024-03-13T01:57:56Z |
| format | Article |
| id | doaj.art-fbfaefd6f7a846fa8d7e350371fc6926 |
| institution | Directory Open Access Journal |
| issn | 2052-0492 |
| language | English |
| last_indexed | 2024-03-13T01:57:56Z |
| publishDate | 2023-06-01 |
| publisher | BMC |
| record_format | Article |
| series | Journal of Intensive Care |
| spelling | doaj.art-fbfaefd6f7a846fa8d7e350371fc69262023-07-02T11:09:03ZengBMCJournal of Intensive Care2052-04922023-06-011111910.1186/s40560-023-00676-1Organ dysfunction, injury, and failure in cardiogenic shockAkihiro Shirakabe0Masato Matsushita1Yusaku Shibata2Shota Shighihara3Suguru Nishigoori4Tomofumi Sawatani5Kazutaka Kiuchi6Kuniya Asai7Division of Intensive Care Unit, Nippon Medical School Chiba Hokusoh HospitalDivision of Intensive Care Unit, Nippon Medical School Chiba Hokusoh HospitalDivision of Intensive Care Unit, Nippon Medical School Chiba Hokusoh HospitalDivision of Intensive Care Unit, Nippon Medical School Chiba Hokusoh HospitalDivision of Intensive Care Unit, Nippon Medical School Chiba Hokusoh HospitalDivision of Intensive Care Unit, Nippon Medical School Chiba Hokusoh HospitalDivision of Intensive Care Unit, Nippon Medical School Chiba Hokusoh HospitalDepartment of Cardiovascular Medicine, Nippon Medical SchoolAbstract Background Cardiogenic shock (CS) is caused by primary cardiac dysfunction and induced by various and heterogeneous diseases (e.g., acute impairment of cardiac performance, or acute or chronic impairment of cardiac performance). Main body Although a low cardiac index is a common finding in patients with CS, the ventricular preload, pulmonary capillary wedge pressure, central venous pressure, and systemic vascular resistance might vary between patients. Organ dysfunction has traditionally been attributed to the hypoperfusion of the organ due to either progressive impairment of the cardiac output or intravascular volume depletion secondary to CS. However, research attention has recently shifted from this cardiac output (“forward failure”) to venous congestion (“backward failure”) as the most important hemodynamic determinant. Both hypoperfusion and/or venous congestion by CS could lead to injury, impairment, and failure of target organs (i.e., heart, lungs, kidney, liver, intestines, brain); these effects are associated with an increased mortality rate. Treatment strategies for the prevention, reduction, and reversal of organ injury are warranted to improve morbidity in these patients. The present review summarizes recent data regarding organ dysfunction, injury, and failure. Conclusions Early identification and treatment of organ dysfunction, along with hemodynamic stabilization, are key components of the management of patients with CS.https://doi.org/10.1186/s40560-023-00676-1Acute decompensated heart failureBiomarkerMortalityInflammation |
| spellingShingle | Akihiro Shirakabe Masato Matsushita Yusaku Shibata Shota Shighihara Suguru Nishigoori Tomofumi Sawatani Kazutaka Kiuchi Kuniya Asai Organ dysfunction, injury, and failure in cardiogenic shock Journal of Intensive Care Acute decompensated heart failure Biomarker Mortality Inflammation |
| title | Organ dysfunction, injury, and failure in cardiogenic shock |
| title_full | Organ dysfunction, injury, and failure in cardiogenic shock |
| title_fullStr | Organ dysfunction, injury, and failure in cardiogenic shock |
| title_full_unstemmed | Organ dysfunction, injury, and failure in cardiogenic shock |
| title_short | Organ dysfunction, injury, and failure in cardiogenic shock |
| title_sort | organ dysfunction injury and failure in cardiogenic shock |
| topic | Acute decompensated heart failure Biomarker Mortality Inflammation |
| url | https://doi.org/10.1186/s40560-023-00676-1 |
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