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Impact of fluid challenge increase in cardiac output on the relationship between systemic and cerebral hemodynamics in severe sepsis compared to brain injury and controls

BACKGROUND: Cognitive dysfunction and delirium after ICU are frequent and may partially result from brain ischemia episodes. We hypothesized that systemic inflammation (severe sepsis or septic shock) modifies the control of brain circulation and the relation between systemic and cerebral hemodynamic...

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Autores principales: Le Dorze, Matthieu, Huché, Florian, Coelembier, Clément, Rabuel, Christophe, Payen, Didier
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6023801/
https://www.ncbi.nlm.nih.gov/pubmed/29956057
http://dx.doi.org/10.1186/s13613-018-0419-1
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author Le Dorze, Matthieu
Huché, Florian
Coelembier, Clément
Rabuel, Christophe
Payen, Didier
author_facet Le Dorze, Matthieu
Huché, Florian
Coelembier, Clément
Rabuel, Christophe
Payen, Didier
author_sort Le Dorze, Matthieu
collection PubMed
description BACKGROUND: Cognitive dysfunction and delirium after ICU are frequent and may partially result from brain ischemia episodes. We hypothesized that systemic inflammation (severe sepsis or septic shock) modifies the control of brain circulation and the relation between systemic and cerebral hemodynamic after a positive response to fluid challenge (FC). METHODS: Three groups of patients were studied if they increased stroke volume (SV) > 10% after 250 or 500 ml of crystalloids: control group: patients free of comorbidity anesthetized for orthopedic surgery; sepsis group: patients with severe sepsis or septic shock (classic definition); brain injury (BI) group: trauma brain jury or hemorrhagic stroke with no detectable systemic inflammation. The measurements before and after FC were mean arterial blood pressure (MAP) (radial catheter); SV and cardiac output (CO; transesophageal Doppler); bilateral middle cerebral artery (MCAv) velocity with peak systolic (PSV) and end diastolic (EDV) values (transcranial Doppler); end-tidal CO(2). The role of MAP increase was investigated by an arbitrarily threshold increase of 5%, called responder in CO and MAP (RR). The remaining patients were call responders in CO and non-responders in MAP (RnR). Nonparametric tests were used for statistical analysis. RESULTS: Among the 86 screened patients, 66 have completed the protocol: 17 in control group; 38 in sepsis group; and 11 in BI group. All patients increased SV > 10% after FC. Only the sepsis group increased MAP [+ 12 (2–25%), p < 0.05] with a significant increase in PSV and EDV [(17 (3–30)% and 17 (12–42)%, respectively (p < 0.05)], which did not change in the two other groups. The septic RR or RnR had similar variations in MCAv after FC. The baseline MAP < or > baseline median MAP had similar MCAv. CONCLUSIONS: After a FC-induced increase in SV, MCAv (PSV and EDV) increased only in septic group, mostly independently from MAP increase and from baseline MAP level. Cerebral perfusion becomes passively dependent on systemic blood flow, suggesting a modification of the control of cerebrovascular tone in sepsis-induced systemic inflammation. This information has been considered in the clinical management of septic patients. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13613-018-0419-1) contains supplementary material, which is available to authorized users.
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spelling pubmed-60238012018-07-13 Impact of fluid challenge increase in cardiac output on the relationship between systemic and cerebral hemodynamics in severe sepsis compared to brain injury and controls Le Dorze, Matthieu Huché, Florian Coelembier, Clément Rabuel, Christophe Payen, Didier Ann Intensive Care Research BACKGROUND: Cognitive dysfunction and delirium after ICU are frequent and may partially result from brain ischemia episodes. We hypothesized that systemic inflammation (severe sepsis or septic shock) modifies the control of brain circulation and the relation between systemic and cerebral hemodynamic after a positive response to fluid challenge (FC). METHODS: Three groups of patients were studied if they increased stroke volume (SV) > 10% after 250 or 500 ml of crystalloids: control group: patients free of comorbidity anesthetized for orthopedic surgery; sepsis group: patients with severe sepsis or septic shock (classic definition); brain injury (BI) group: trauma brain jury or hemorrhagic stroke with no detectable systemic inflammation. The measurements before and after FC were mean arterial blood pressure (MAP) (radial catheter); SV and cardiac output (CO; transesophageal Doppler); bilateral middle cerebral artery (MCAv) velocity with peak systolic (PSV) and end diastolic (EDV) values (transcranial Doppler); end-tidal CO(2). The role of MAP increase was investigated by an arbitrarily threshold increase of 5%, called responder in CO and MAP (RR). The remaining patients were call responders in CO and non-responders in MAP (RnR). Nonparametric tests were used for statistical analysis. RESULTS: Among the 86 screened patients, 66 have completed the protocol: 17 in control group; 38 in sepsis group; and 11 in BI group. All patients increased SV > 10% after FC. Only the sepsis group increased MAP [+ 12 (2–25%), p < 0.05] with a significant increase in PSV and EDV [(17 (3–30)% and 17 (12–42)%, respectively (p < 0.05)], which did not change in the two other groups. The septic RR or RnR had similar variations in MCAv after FC. The baseline MAP < or > baseline median MAP had similar MCAv. CONCLUSIONS: After a FC-induced increase in SV, MCAv (PSV and EDV) increased only in septic group, mostly independently from MAP increase and from baseline MAP level. Cerebral perfusion becomes passively dependent on systemic blood flow, suggesting a modification of the control of cerebrovascular tone in sepsis-induced systemic inflammation. This information has been considered in the clinical management of septic patients. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s13613-018-0419-1) contains supplementary material, which is available to authorized users. Springer International Publishing 2018-06-28 /pmc/articles/PMC6023801/ /pubmed/29956057 http://dx.doi.org/10.1186/s13613-018-0419-1 Text en © The Author(s) 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Research
Le Dorze, Matthieu
Huché, Florian
Coelembier, Clément
Rabuel, Christophe
Payen, Didier
Impact of fluid challenge increase in cardiac output on the relationship between systemic and cerebral hemodynamics in severe sepsis compared to brain injury and controls
title Impact of fluid challenge increase in cardiac output on the relationship between systemic and cerebral hemodynamics in severe sepsis compared to brain injury and controls
title_full Impact of fluid challenge increase in cardiac output on the relationship between systemic and cerebral hemodynamics in severe sepsis compared to brain injury and controls
title_fullStr Impact of fluid challenge increase in cardiac output on the relationship between systemic and cerebral hemodynamics in severe sepsis compared to brain injury and controls
title_full_unstemmed Impact of fluid challenge increase in cardiac output on the relationship between systemic and cerebral hemodynamics in severe sepsis compared to brain injury and controls
title_short Impact of fluid challenge increase in cardiac output on the relationship between systemic and cerebral hemodynamics in severe sepsis compared to brain injury and controls
title_sort impact of fluid challenge increase in cardiac output on the relationship between systemic and cerebral hemodynamics in severe sepsis compared to brain injury and controls
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6023801/
https://www.ncbi.nlm.nih.gov/pubmed/29956057
http://dx.doi.org/10.1186/s13613-018-0419-1
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