Survival, but not the severity of hypoxic-ischemic encephalopathy, is associated with higher mean arterial blood pressure after cardiac arrest: a retrospective cohort study.

brain autopsy cardiac arrest (CA) cumulative vasopressor index hypoxic–ischemic encephalopathy (HIE) mean arterial pressure (MAP) prognosis

Journal

Frontiers in cardiovascular medicine
ISSN: 2297-055X
Titre abrégé: Front Cardiovasc Med
Pays: Switzerland
ID NLM: 101653388

Informations de publication

Date de publication:
2024
Historique:
received: 12 11 2023
accepted: 15 04 2024
medline: 22 5 2024
pubmed: 22 5 2024
entrez: 22 5 2024
Statut: epublish

Résumé

This study investigates the association between the mean arterial blood pressure (MAP), vasopressor requirement, and severity of hypoxic-ischemic encephalopathy (HIE) after cardiac arrest (CA). Between 2008 and 2017, we retrospectively analyzed the MAP 200 h after CA and quantified the vasopressor requirements using the cumulative vasopressor index (CVI). Through a postmortem brain autopsy in non-survivors, the severity of the HIE was histopathologically dichotomized into no/mild and severe HIE. In survivors, we dichotomized the severity of HIE into no/mild cerebral performance category (CPC) 1 and severe HIE (CPC 4). We investigated the regain of consciousness, causes of death, and 5-day survival as hemodynamic confounders. Among the 350 non-survivors, 117 had histopathologically severe HIE while 233 had no/mild HIE, without differences observed in the MAP (73.1 vs. 72.0 mmHg, Although a higher MAP was associated with survival in CA patients treated with a vasopressor-supported MAP target above 65 mmHg, the severity of HIE was not. Awakening from coma was associated with less vasopressor requirements. Our results provide no evidence for a MAP target above the current guideline recommendations that can decrease the severity of HIE.

Sections du résumé

Background UNASSIGNED
This study investigates the association between the mean arterial blood pressure (MAP), vasopressor requirement, and severity of hypoxic-ischemic encephalopathy (HIE) after cardiac arrest (CA).
Methods UNASSIGNED
Between 2008 and 2017, we retrospectively analyzed the MAP 200 h after CA and quantified the vasopressor requirements using the cumulative vasopressor index (CVI). Through a postmortem brain autopsy in non-survivors, the severity of the HIE was histopathologically dichotomized into no/mild and severe HIE. In survivors, we dichotomized the severity of HIE into no/mild cerebral performance category (CPC) 1 and severe HIE (CPC 4). We investigated the regain of consciousness, causes of death, and 5-day survival as hemodynamic confounders.
Results UNASSIGNED
Among the 350 non-survivors, 117 had histopathologically severe HIE while 233 had no/mild HIE, without differences observed in the MAP (73.1 vs. 72.0 mmHg,
Conclusions UNASSIGNED
Although a higher MAP was associated with survival in CA patients treated with a vasopressor-supported MAP target above 65 mmHg, the severity of HIE was not. Awakening from coma was associated with less vasopressor requirements. Our results provide no evidence for a MAP target above the current guideline recommendations that can decrease the severity of HIE.

Identifiants

pubmed: 38774664
doi: 10.3389/fcvm.2024.1337344
pmc: PMC11106407
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1337344

Informations de copyright

© 2024 Preuß, Multmeier, Stenzel, Major, Ploner, Storm, Nee, Leithner and Endisch.

Déclaration de conflit d'intérêts

JM works at Ada Health GmbH. CL reports institutional fees from Bard Medical, Pfizer, and Zoll and personal fees from Edwards Lifesciences outside the submitted work. CL is further supported by a clinical fellowship from the Berlin Institute of Health (BIH) at Charité Universitätsmedizin Berlin. CE received a research fellowship grant from the Laerdal Foundation. However, the research grants had no role in the study concept, data collection and analysis, publishing decision, or manuscript preparation. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Auteurs

Sandra Preuß (S)

Department of Neurology, AG Emergency and Critical Care Neurology, Campus Virchow Klinikum, Charité Universitätsmedizin Berlin, Berlin, Germany.
Department of Cardiology and Angiology, Charité Campus Mitte, Charité Universitätsmedizin Berlin, Berlin, Germany.

Jan Multmeier (J)

Department of Neurology, AG Emergency and Critical Care Neurology, Campus Virchow Klinikum, Charité Universitätsmedizin Berlin, Berlin, Germany.
Ada Health GmbH, Berlin, Germany.

Werner Stenzel (W)

Department of Neuropathology, Charité Campus Mitte, Charité Universitätsmedizin Berlin, Berlin, Germany.

Sebastian Major (S)

Center for Stroke Research, Charité Universitätsmedizin Berlin, Berlin, Germany.

Christoph J Ploner (CJ)

Department of Neurology, AG Emergency and Critical Care Neurology, Campus Virchow Klinikum, Charité Universitätsmedizin Berlin, Berlin, Germany.

Christian Storm (C)

Department of Nephrology and Intensive Care Medicine, Cardiac Arrest Center of Excellence Berlin, Campus Virchow Klinikum, Charité Universitätsmedizin Berlin, Berlin, Germany.

Jens Nee (J)

Department of Nephrology and Intensive Care Medicine, Cardiac Arrest Center of Excellence Berlin, Campus Virchow Klinikum, Charité Universitätsmedizin Berlin, Berlin, Germany.

Christoph Leithner (C)

Department of Neurology, AG Emergency and Critical Care Neurology, Campus Virchow Klinikum, Charité Universitätsmedizin Berlin, Berlin, Germany.

Christian Endisch (C)

Department of Neurology, AG Emergency and Critical Care Neurology, Campus Virchow Klinikum, Charité Universitätsmedizin Berlin, Berlin, Germany.

Classifications MeSH