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Global end-diastolic volume increases to maintain fluid responsiveness in sepsis-induced systolic dysfunction

BACKGROUND: Sepsis-induced cardiac dysfunction may limit fluid responsiveness and the mechanism thereof remains unclear. Since cardiac function may affect the relative value of cardiac filling pressures, such as the recommended central venous pressure (CVP), versus filling volumes in guiding fluid l...

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Autores principales: Trof, Ronald J, Danad, Ibrahim, Groeneveld, AB Johan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3698117/
https://www.ncbi.nlm.nih.gov/pubmed/23799933
http://dx.doi.org/10.1186/1471-2253-13-12
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author Trof, Ronald J
Danad, Ibrahim
Groeneveld, AB Johan
author_facet Trof, Ronald J
Danad, Ibrahim
Groeneveld, AB Johan
author_sort Trof, Ronald J
collection PubMed
description BACKGROUND: Sepsis-induced cardiac dysfunction may limit fluid responsiveness and the mechanism thereof remains unclear. Since cardiac function may affect the relative value of cardiac filling pressures, such as the recommended central venous pressure (CVP), versus filling volumes in guiding fluid loading, we studied these parameters as determinants of fluid responsiveness, according to cardiac function. METHODS: A delta CVP-guided, 90 min colloid fluid loading protocol was performed in 16 mechanically ventilated patients with sepsis-induced hypotension and three 30 min consecutive fluid loading steps of about 450 mL per patient were evaluated. Global end-diastolic volume index (GEDVI), cardiac index (CI) and global ejection fraction (GEF) were assessed from transpulmonary dilution. Baseline and changes in CVP and GEDVI were compared among responding (CI increase ≥10% and ≥15%) and non-responding fluid loading steps, in patient with low (<20%, n = 9) and near-normal (≥20%) GEF (n = 7) at baseline. RESULTS: A low GEF was in line with other indices of impaired cardiac (left ventricular) function, prior to and after fluid loading. Of 48 fluid loading steps, 9 (of 27) were responding when GEF <20% and 6 (of 21) when GEF ≥20. Prior to fluid loading, CVP did not differ between responding and non-responding steps and levels attained were 23 higher in the latter, regardless of GEF (P = 0.004). Prior to fluid loading, GEDVI (and CI) was higher in responding (1007 ± 306 mL/m(2)) than non-responding steps (870 ± 236 mL/m(2)) when GEF was low (P = 0.002), but did not differ when GEF was near-normal. Increases in GEDVI were associated with increases in CI and fluid responsiveness, regardless of GEF (P < 0.001). CONCLUSIONS: As estimated from transpulmonary dilution, about half of patients with sepsis-induced hypotension have systolic cardiac dysfunction. During dysfunction, cardiac dilation with a relatively high baseline GEDVI maintains fluid responsiveness by further dilatation (increase in GEDVI rather than of CVP) as in patients without dysfunction. Absence of fluid responsiveness during systolic cardiac dysfunction may be caused by diastolic dysfunction and/or right ventricular dysfunction.
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spelling pubmed-36981172013-07-02 Global end-diastolic volume increases to maintain fluid responsiveness in sepsis-induced systolic dysfunction Trof, Ronald J Danad, Ibrahim Groeneveld, AB Johan BMC Anesthesiol Research Article BACKGROUND: Sepsis-induced cardiac dysfunction may limit fluid responsiveness and the mechanism thereof remains unclear. Since cardiac function may affect the relative value of cardiac filling pressures, such as the recommended central venous pressure (CVP), versus filling volumes in guiding fluid loading, we studied these parameters as determinants of fluid responsiveness, according to cardiac function. METHODS: A delta CVP-guided, 90 min colloid fluid loading protocol was performed in 16 mechanically ventilated patients with sepsis-induced hypotension and three 30 min consecutive fluid loading steps of about 450 mL per patient were evaluated. Global end-diastolic volume index (GEDVI), cardiac index (CI) and global ejection fraction (GEF) were assessed from transpulmonary dilution. Baseline and changes in CVP and GEDVI were compared among responding (CI increase ≥10% and ≥15%) and non-responding fluid loading steps, in patient with low (<20%, n = 9) and near-normal (≥20%) GEF (n = 7) at baseline. RESULTS: A low GEF was in line with other indices of impaired cardiac (left ventricular) function, prior to and after fluid loading. Of 48 fluid loading steps, 9 (of 27) were responding when GEF <20% and 6 (of 21) when GEF ≥20. Prior to fluid loading, CVP did not differ between responding and non-responding steps and levels attained were 23 higher in the latter, regardless of GEF (P = 0.004). Prior to fluid loading, GEDVI (and CI) was higher in responding (1007 ± 306 mL/m(2)) than non-responding steps (870 ± 236 mL/m(2)) when GEF was low (P = 0.002), but did not differ when GEF was near-normal. Increases in GEDVI were associated with increases in CI and fluid responsiveness, regardless of GEF (P < 0.001). CONCLUSIONS: As estimated from transpulmonary dilution, about half of patients with sepsis-induced hypotension have systolic cardiac dysfunction. During dysfunction, cardiac dilation with a relatively high baseline GEDVI maintains fluid responsiveness by further dilatation (increase in GEDVI rather than of CVP) as in patients without dysfunction. Absence of fluid responsiveness during systolic cardiac dysfunction may be caused by diastolic dysfunction and/or right ventricular dysfunction. BioMed Central 2013-06-22 /pmc/articles/PMC3698117/ /pubmed/23799933 http://dx.doi.org/10.1186/1471-2253-13-12 Text en Copyright © 2013 Trof et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Trof, Ronald J
Danad, Ibrahim
Groeneveld, AB Johan
Global end-diastolic volume increases to maintain fluid responsiveness in sepsis-induced systolic dysfunction
title Global end-diastolic volume increases to maintain fluid responsiveness in sepsis-induced systolic dysfunction
title_full Global end-diastolic volume increases to maintain fluid responsiveness in sepsis-induced systolic dysfunction
title_fullStr Global end-diastolic volume increases to maintain fluid responsiveness in sepsis-induced systolic dysfunction
title_full_unstemmed Global end-diastolic volume increases to maintain fluid responsiveness in sepsis-induced systolic dysfunction
title_short Global end-diastolic volume increases to maintain fluid responsiveness in sepsis-induced systolic dysfunction
title_sort global end-diastolic volume increases to maintain fluid responsiveness in sepsis-induced systolic dysfunction
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3698117/
https://www.ncbi.nlm.nih.gov/pubmed/23799933
http://dx.doi.org/10.1186/1471-2253-13-12
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