Half-molar sodium lactate infusion improves cardiac performance in acute heart failure: a pilot randomised controlled clinical trial
Identifieur interne : 001496 ( Pmc/Curation ); précédent : 001495; suivant : 001497Half-molar sodium lactate infusion improves cardiac performance in acute heart failure: a pilot randomised controlled clinical trial
Auteurs : Marek Nalos [Australie] ; Xavier Maurice Leverve [France] ; Stephen Joseph Huang [Australie] ; Leonie Weisbrodt [Australie] ; Ray Parkin [Australie] ; Ian Mark Seppelt [Australie] ; Iris Ting [Australie] ; Anthony Stuart Mclean [Australie]Source :
- Critical Care [ 1364-8535 ] ; 2014.
Abstract
Acute heart failure (AHF) is characterized by inadequate cardiac output (CO), congestive symptoms, poor peripheral perfusion and end-organ dysfunction. Treatment often includes a combination of diuretics, oxygen, positive pressure ventilation, inotropes and vasodilators or vasopressors. Lactate is a marker of illness severity but is also an important metabolic substrate for the myocardium at rest and during stress. We tested the effects of half-molar sodium lactate infusion on cardiac performance in AHF.
We conducted a prospective, randomised, controlled, open-label, pilot clinical trial in 40 patients fulfilling two of the following three criteria for AHF: (1) left ventricular ejection fraction <40%, (2) acute pulmonary oedema or respiratory failure of predominantly cardiac origin requiring mechanical ventilation and (3) currently receiving vasopressor and/or inotropic support. Patients in the intervention group received a 3 ml/kg bolus of half-molar sodium lactate over the course of 15 minutes followed by 1 ml/kg/h continuous infusion for 24 hours. The control group received only a 3 ml/kg bolus of Hartmann’s solution without continuous infusion. The primary outcome was CO assessed by transthoracic echocardiography 24 hours after randomisation. Secondary outcomes included a measure of right ventricular systolic function (tricuspid annular plane systolic excursion (TAPSE)), acid-base balance, electrolyte and organ function parameters, along with length of stay and mortality.
The infusion of half-molar sodium lactate increased (mean ± SD) CO from 4.05 ± 1.37 L/min to 5.49 ± 1.9 L/min (
Infusion of half-molar sodium lactate improved cardiac performance and led to metabolic alkalosis in AHF patients without any detrimental effects on organ function.
Clinicaltrials.gov
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DOI: 10.1186/cc13793
PubMed: 24666826
PubMed Central: 4057379
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id="I1">Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750</wicri:regionArea></affiliation></author><author><name sortKey="Parkin, Ray" sort="Parkin, Ray" uniqKey="Parkin R" first="Ray" last="Parkin">Ray Parkin</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750</wicri:regionArea></affiliation></author><author><name sortKey="Seppelt, Ian Mark" sort="Seppelt, Ian Mark" uniqKey="Seppelt I" 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2750</wicri:regionArea></affiliation></author><author><name sortKey="Mclean, Anthony Stuart" sort="Mclean, Anthony Stuart" uniqKey="Mclean A" first="Anthony Stuart" last="Mclean">Anthony Stuart Mclean</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">24666826</idno><idno type="pmc">4057379</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057379</idno><idno type="RBID">PMC:4057379</idno><idno type="doi">10.1186/cc13793</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">001636</idno><idno 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2750</wicri:regionArea></affiliation></author><author><name sortKey="Leverve, Xavier Maurice" sort="Leverve, Xavier Maurice" uniqKey="Leverve X" first="Xavier Maurice" last="Leverve">Xavier Maurice Leverve</name><affiliation wicri:level="1"><nlm:aff id="I2">LBFA, INSERM-U884, Université Joseph-Fourier Grenoble, BP 53 X 38041 Grenoble, cedex 9, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea>LBFA, INSERM-U884, Université Joseph-Fourier Grenoble, BP 53 X 38041 Grenoble, cedex 9</wicri:regionArea></affiliation></author><author><name sortKey="Huang, Stephen Joseph" sort="Huang, Stephen Joseph" uniqKey="Huang S" first="Stephen Joseph" last="Huang">Stephen Joseph Huang</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750</wicri:regionArea></affiliation></author><author><name sortKey="Weisbrodt, Leonie" sort="Weisbrodt, Leonie" uniqKey="Weisbrodt L" first="Leonie" last="Weisbrodt">Leonie Weisbrodt</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750</wicri:regionArea></affiliation></author><author><name sortKey="Parkin, Ray" sort="Parkin, Ray" uniqKey="Parkin R" first="Ray" last="Parkin">Ray Parkin</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750</wicri:regionArea></affiliation></author><author><name sortKey="Seppelt, Ian Mark" sort="Seppelt, Ian Mark" uniqKey="Seppelt I" first="Ian Mark" last="Seppelt">Ian Mark Seppelt</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750</wicri:regionArea></affiliation></author><author><name sortKey="Ting, Iris" sort="Ting, Iris" uniqKey="Ting I" first="Iris" last="Ting">Iris Ting</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750</wicri:regionArea></affiliation></author><author><name sortKey="Mclean, Anthony Stuart" sort="Mclean, Anthony Stuart" uniqKey="Mclean A" first="Anthony Stuart" last="Mclean">Anthony Stuart Mclean</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750, Australia</nlm:aff><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750</wicri:regionArea></affiliation></author></analytic><series><title level="j">Critical Care</title><idno type="ISSN">1364-8535</idno><idno type="eISSN">1466-609X</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Introduction</title><p>Acute heart failure (AHF) is characterized by inadequate cardiac output (CO), congestive symptoms, poor peripheral perfusion and end-organ dysfunction. Treatment often includes a combination of diuretics, oxygen, positive pressure ventilation, inotropes and vasodilators or vasopressors. Lactate is a marker of illness severity but is also an important metabolic substrate for the myocardium at rest and during stress. We tested the effects of half-molar sodium lactate infusion on cardiac performance in AHF.</p></sec><sec><title>Methods</title><p>We conducted a prospective, randomised, controlled, open-label, pilot clinical trial in 40 patients fulfilling two of the following three criteria for AHF: (1) left ventricular ejection fraction <40%, (2) acute pulmonary oedema or respiratory failure of predominantly cardiac origin requiring mechanical ventilation and (3) currently receiving vasopressor and/or inotropic support. Patients in the intervention group received a 3 ml/kg bolus of half-molar sodium lactate over the course of 15 minutes followed by 1 ml/kg/h continuous infusion for 24 hours. The control group received only a 3 ml/kg bolus of Hartmann’s solution without continuous infusion. The primary outcome was CO assessed by transthoracic echocardiography 24 hours after randomisation. Secondary outcomes included a measure of right ventricular systolic function (tricuspid annular plane systolic excursion (TAPSE)), acid-base balance, electrolyte and organ function parameters, along with length of stay and mortality.</p></sec><sec><title>Results</title><p>The infusion of half-molar sodium lactate increased (mean ± SD) CO from 4.05 ± 1.37 L/min to 5.49 ± 1.9 L/min (<italic>P</italic> < 0.01) and TAPSE from 14.7 ± 5.5 mm to 18.3 ± 7 mm (<italic>P</italic> = 0.02). Plasma sodium and pH increased (136 ± 4 to 146 ± 6 and 7.40 ± 0.06 to 7.53 ± 0.03, respectively; both <italic>P</italic> < 0.01), but potassium, chloride and phosphate levels decreased. There were no significant differences in the need for vasoactive therapy, respiratory support, renal or liver function tests, duration of ICU and hospital stay or 28- and 90-day mortality.</p></sec><sec><title>Conclusions</title><p>Infusion of half-molar sodium lactate improved cardiac performance and led to metabolic alkalosis in AHF patients without any detrimental effects on organ function.</p></sec><sec><title>Trial registration</title><p>Clinicaltrials.gov <ext-link ext-link-type="uri" xlink:href="http://www.clinicaltrials.gov/NCT01981655">NCT01981655</ext-link>. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Crit Care</journal-id><journal-id journal-id-type="iso-abbrev">Crit Care</journal-id><journal-title-group><journal-title>Critical Care</journal-title></journal-title-group><issn pub-type="ppub">1364-8535</issn><issn pub-type="epub">1466-609X</issn><publisher><publisher-name>BioMed Central</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">24666826</article-id><article-id pub-id-type="pmc">4057379</article-id><article-id pub-id-type="publisher-id">cc13793</article-id><article-id pub-id-type="doi">10.1186/cc13793</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research</subject></subj-group></article-categories><title-group><article-title>Half-molar sodium lactate infusion improves cardiac performance in acute heart failure: a pilot randomised controlled clinical trial</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes" id="A1"><name><surname>Nalos</surname><given-names>Marek</given-names></name><xref ref-type="aff" rid="I1">1</xref><email>mareknalos@gmail.com</email></contrib><contrib contrib-type="author" deceased="yes" id="A2"><name><surname>Leverve</surname><given-names>Xavier Maurice</given-names></name><xref ref-type="aff" rid="I2">2</xref><email>xavier.leverve@ujf-grenoble.fr</email></contrib><contrib contrib-type="author" id="A3"><name><surname>Huang</surname><given-names>Stephen Joseph</given-names></name><xref ref-type="aff" rid="I1">1</xref><email>stephen.huang@sydney.edu.au</email></contrib><contrib contrib-type="author" id="A4"><name><surname>Weisbrodt</surname><given-names>Leonie</given-names></name><xref ref-type="aff" rid="I1">1</xref><email>leonie.weisbrodt@sydney.edu.au</email></contrib><contrib contrib-type="author" id="A5"><name><surname>Parkin</surname><given-names>Ray</given-names></name><xref ref-type="aff" rid="I1">1</xref><email>parkinr@iinet.com.au</email></contrib><contrib contrib-type="author" id="A6"><name><surname>Seppelt</surname><given-names>Ian Mark</given-names></name><xref ref-type="aff" rid="I1">1</xref><email>ian.seppelt@sydney.edu.au</email></contrib><contrib contrib-type="author" id="A7"><name><surname>Ting</surname><given-names>Iris</given-names></name><xref ref-type="aff" rid="I1">1</xref><email>iris.ting@swahs.health.nsw.gov.au</email></contrib><contrib contrib-type="author" id="A8"><name><surname>Mclean</surname><given-names>Anthony Stuart</given-names></name><xref ref-type="aff" rid="I1">1</xref><email>anthony.mclean@sydney.edu.au</email></contrib></contrib-group><aff id="I1"><label>1</label>Department of Intensive Care Medicine, Sydney Medical School–Nepean, University of Sydney, Nepean Hospital, Penrith NSW 2750, Australia</aff><aff id="I2"><label>2</label>LBFA, INSERM-U884, Université Joseph-Fourier Grenoble, BP 53 X 38041 Grenoble, cedex 9, France</aff><pub-date pub-type="ppub"><year>2014</year></pub-date><pub-date pub-type="epub"><day>25</day><month>3</month><year>2014</year></pub-date><volume>18</volume><issue>2</issue><fpage>R48</fpage><lpage>R48</lpage><history><date date-type="received"><day>4</day><month>12</month><year>2013</year></date><date date-type="accepted"><day>12</day><month>3</month><year>2014</year></date></history><permissions><copyright-statement>Copyright © 2014 Nalos et al.; licensee BioMed Central Ltd.</copyright-statement><copyright-year>2014</copyright-year><copyright-holder>Nalos et al.; licensee BioMed Central Ltd.</copyright-holder><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/2.0"><license-p>This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/2.0">http://creativecommons.org/licenses/by/2.0</ext-link>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/publicdomain/zero/1.0/">http://creativecommons.org/publicdomain/zero/1.0/</ext-link>) applies to the data made available in this article, unless otherwise stated.</license-p></license></permissions><self-uri xlink:href="http://ccforum.com/content/18/2/R48"></self-uri><abstract><sec><title>Introduction</title><p>Acute heart failure (AHF) is characterized by inadequate cardiac output (CO), congestive symptoms, poor peripheral perfusion and end-organ dysfunction. Treatment often includes a combination of diuretics, oxygen, positive pressure ventilation, inotropes and vasodilators or vasopressors. Lactate is a marker of illness severity but is also an important metabolic substrate for the myocardium at rest and during stress. We tested the effects of half-molar sodium lactate infusion on cardiac performance in AHF.</p></sec><sec><title>Methods</title><p>We conducted a prospective, randomised, controlled, open-label, pilot clinical trial in 40 patients fulfilling two of the following three criteria for AHF: (1) left ventricular ejection fraction <40%, (2) acute pulmonary oedema or respiratory failure of predominantly cardiac origin requiring mechanical ventilation and (3) currently receiving vasopressor and/or inotropic support. Patients in the intervention group received a 3 ml/kg bolus of half-molar sodium lactate over the course of 15 minutes followed by 1 ml/kg/h continuous infusion for 24 hours. The control group received only a 3 ml/kg bolus of Hartmann’s solution without continuous infusion. The primary outcome was CO assessed by transthoracic echocardiography 24 hours after randomisation. Secondary outcomes included a measure of right ventricular systolic function (tricuspid annular plane systolic excursion (TAPSE)), acid-base balance, electrolyte and organ function parameters, along with length of stay and mortality.</p></sec><sec><title>Results</title><p>The infusion of half-molar sodium lactate increased (mean ± SD) CO from 4.05 ± 1.37 L/min to 5.49 ± 1.9 L/min (<italic>P</italic> < 0.01) and TAPSE from 14.7 ± 5.5 mm to 18.3 ± 7 mm (<italic>P</italic> = 0.02). Plasma sodium and pH increased (136 ± 4 to 146 ± 6 and 7.40 ± 0.06 to 7.53 ± 0.03, respectively; both <italic>P</italic> < 0.01), but potassium, chloride and phosphate levels decreased. There were no significant differences in the need for vasoactive therapy, respiratory support, renal or liver function tests, duration of ICU and hospital stay or 28- and 90-day mortality.</p></sec><sec><title>Conclusions</title><p>Infusion of half-molar sodium lactate improved cardiac performance and led to metabolic alkalosis in AHF patients without any detrimental effects on organ function.</p></sec><sec><title>Trial registration</title><p>Clinicaltrials.gov <ext-link ext-link-type="uri" xlink:href="http://www.clinicaltrials.gov/NCT01981655">NCT01981655</ext-link>. Registered 13 August 2013.</p></sec></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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