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Fluid loading and norepinephrine infusion mask the left ventricular preload decrease induced by pleural effusion

BACKGROUND: Pleural effusion (PLE) may lead to low blood pressure and reduced cardiac output. Low blood pressure and reduced cardiac output are often treated with fluid loading and vasopressors. This study aimed to determine the impact of fluid loading and norepinephrine infusion on physiologic dete...

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Autores principales: Wemmelund, Kristian Borup, Ringgård, Viktor Kromann, Vistisen, Simon Tilma, Hyldebrandt, Janus Adler, Sloth, Erik, Juhl-Olsen, Peter
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer International Publishing 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5593801/
https://www.ncbi.nlm.nih.gov/pubmed/28895094
http://dx.doi.org/10.1186/s40635-017-0158-x
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author Wemmelund, Kristian Borup
Ringgård, Viktor Kromann
Vistisen, Simon Tilma
Hyldebrandt, Janus Adler
Sloth, Erik
Juhl-Olsen, Peter
author_facet Wemmelund, Kristian Borup
Ringgård, Viktor Kromann
Vistisen, Simon Tilma
Hyldebrandt, Janus Adler
Sloth, Erik
Juhl-Olsen, Peter
author_sort Wemmelund, Kristian Borup
collection PubMed
description BACKGROUND: Pleural effusion (PLE) may lead to low blood pressure and reduced cardiac output. Low blood pressure and reduced cardiac output are often treated with fluid loading and vasopressors. This study aimed to determine the impact of fluid loading and norepinephrine infusion on physiologic determinants of cardiac function obtained by ultrasonography during PLE. METHODS: In this randomised, blinded, controlled laboratory study, 30 piglets (21.9 ± 1.3 kg) had bilateral PLE (75 mL/kg) induced. Subsequently, the piglets were randomised to intervention as follows: fluid loading (80 mL/kg/h for 1.5 h, n = 12), norepinephrine infusion (0.01, 0.03, 0.05, 0.1, 0.2 and 0.3 μg/kg/min (15 min each, n = 12)) or control (n = 6). Main outcome was left ventricular preload measured as left ventricular end-diastolic area. Secondary endpoints included contractility and afterload as well as global measures of circulation. All endpoints were assessed with echocardiography and invasive pressure-flow measurements. RESULTS: PLE decreased left ventricular end-diastolic area, mean arterial pressure and cardiac output (p values < 0.001), but fluid loading (20 mL/kg) and norepinephrine infusion (0.05 μg/kg/min) restored these values (p values > 0.05) to baseline. Left ventricular contractility increased with norepinephrine infusion (p = 0.002), but was not affected by fluid loading (p = 0.903). Afterload increased in both active groups (p values > 0.001). Overall, inferior vena cava distensibility remained unchanged during intervention (p values ≥ 0.085). Evacuation of PLE caused numerical increases in left ventricular end-diastolic area, but only significantly so in controls (p = 0.006). CONCLUSIONS: PLE significantly reduced left ventricular preload. Both fluid and norepinephrine treatment reverted this effect and normalised global haemodynamic parameters. Inferior vena cava distensibility remained unchanged. The haemodynamic significance of PLE may be underestimated during fluid or norepinephrine administration, potentially masking the presence of PLE.
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spelling pubmed-55938012017-09-27 Fluid loading and norepinephrine infusion mask the left ventricular preload decrease induced by pleural effusion Wemmelund, Kristian Borup Ringgård, Viktor Kromann Vistisen, Simon Tilma Hyldebrandt, Janus Adler Sloth, Erik Juhl-Olsen, Peter Intensive Care Med Exp Research BACKGROUND: Pleural effusion (PLE) may lead to low blood pressure and reduced cardiac output. Low blood pressure and reduced cardiac output are often treated with fluid loading and vasopressors. This study aimed to determine the impact of fluid loading and norepinephrine infusion on physiologic determinants of cardiac function obtained by ultrasonography during PLE. METHODS: In this randomised, blinded, controlled laboratory study, 30 piglets (21.9 ± 1.3 kg) had bilateral PLE (75 mL/kg) induced. Subsequently, the piglets were randomised to intervention as follows: fluid loading (80 mL/kg/h for 1.5 h, n = 12), norepinephrine infusion (0.01, 0.03, 0.05, 0.1, 0.2 and 0.3 μg/kg/min (15 min each, n = 12)) or control (n = 6). Main outcome was left ventricular preload measured as left ventricular end-diastolic area. Secondary endpoints included contractility and afterload as well as global measures of circulation. All endpoints were assessed with echocardiography and invasive pressure-flow measurements. RESULTS: PLE decreased left ventricular end-diastolic area, mean arterial pressure and cardiac output (p values < 0.001), but fluid loading (20 mL/kg) and norepinephrine infusion (0.05 μg/kg/min) restored these values (p values > 0.05) to baseline. Left ventricular contractility increased with norepinephrine infusion (p = 0.002), but was not affected by fluid loading (p = 0.903). Afterload increased in both active groups (p values > 0.001). Overall, inferior vena cava distensibility remained unchanged during intervention (p values ≥ 0.085). Evacuation of PLE caused numerical increases in left ventricular end-diastolic area, but only significantly so in controls (p = 0.006). CONCLUSIONS: PLE significantly reduced left ventricular preload. Both fluid and norepinephrine treatment reverted this effect and normalised global haemodynamic parameters. Inferior vena cava distensibility remained unchanged. The haemodynamic significance of PLE may be underestimated during fluid or norepinephrine administration, potentially masking the presence of PLE. Springer International Publishing 2017-09-11 /pmc/articles/PMC5593801/ /pubmed/28895094 http://dx.doi.org/10.1186/s40635-017-0158-x Text en © The Author(s). 2017 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
Wemmelund, Kristian Borup
Ringgård, Viktor Kromann
Vistisen, Simon Tilma
Hyldebrandt, Janus Adler
Sloth, Erik
Juhl-Olsen, Peter
Fluid loading and norepinephrine infusion mask the left ventricular preload decrease induced by pleural effusion
title Fluid loading and norepinephrine infusion mask the left ventricular preload decrease induced by pleural effusion
title_full Fluid loading and norepinephrine infusion mask the left ventricular preload decrease induced by pleural effusion
title_fullStr Fluid loading and norepinephrine infusion mask the left ventricular preload decrease induced by pleural effusion
title_full_unstemmed Fluid loading and norepinephrine infusion mask the left ventricular preload decrease induced by pleural effusion
title_short Fluid loading and norepinephrine infusion mask the left ventricular preload decrease induced by pleural effusion
title_sort fluid loading and norepinephrine infusion mask the left ventricular preload decrease induced by pleural effusion
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5593801/
https://www.ncbi.nlm.nih.gov/pubmed/28895094
http://dx.doi.org/10.1186/s40635-017-0158-x
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