Effects of cardiogenic shock on lactate and glucose metabolism after heart surgery

Détails

ID Serval
serval:BIB_45901308B524
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Effects of cardiogenic shock on lactate and glucose metabolism after heart surgery
Périodique
Critical Care Medicine
Auteur(s)
Chiolero  R. L., Revelly  J. P., Leverve  X., Gersbach  P., Cayeux  M. C., Berger  M. M., Tappy  L.
ISSN
0090-3493 (Print)
Statut éditorial
Publié
Date de publication
12/2000
Volume
28
Numéro
12
Pages
3784-91
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Dec
Résumé
BACKGROUND: Hyperlactatemia is a prominent feature of cardiogenic shock. It can be attributed to increased tissue production of lactate related to dysoxia and to impaired utilization of lactate caused by liver and tissue underperfusion. The aim of this prospective observational study was to determine the relative importance of these mechanisms during cardiogenic shock. PATIENTS: Two groups of subjects were compared: seven cardiac surgery patients with postoperative cardiogenic shock and seven healthy volunteers. METHODS: Lactate metabolism was assessed by using two independent methods: a) a pharmacokinetic approach based on lactate plasma level decay after the infusion of 2.5 mmol x kg(-1) of sodium lactate; and b) an isotope dilution technique for which the transformation of [13C]lactate into [13C]glucose and 13CO2 was measured. Glucose turnover was determined using 6,62H2-glucose. RESULTS: All patients suffered from profound shock requiring high doses of inotropes and vasopressors. Mean arterial lactate amounted to 7.8 +/- 3.4 mmol x L(-1) and mean pH to 7.25 +/- 0.07. Lactate clearance was not different in the patients and controls (7.8 +/- 3.4 vs. 10.3 +/- 2.1 mL x kg(-1) x min(-1)). By contrast, lactate production was markedly enhanced in the patients (33.6 +/- 16.4 vs. 9.6 +/- 2.2 micromol x kg(-1) x min(-1); p < .01). Exogenous [13C]lactate oxidation was not different (107 +/- 37 vs. 103 +/- 4 mmol), and transformation of [13C]lactate into [13C]glucose was not different (20.0 +/- 13.7 vs. 15.2% +/- 6.0% of exogenous lactate). Endogenous glucose production was markedly increased in the patients (1.95 +/- 0.26 vs. 5.3 +/- 3.0 mg x kg(-1) x min(-1); p < .05 [10.8 +/- 1.4 vs. 29.4 +/- 16.7 micromol x kg(-1) x min(-1)]), whereas net carbohydrate oxidation was not different (1.7 +/- 0.5 vs. 1.3 +/- 0.3 mg x kg(-1) x min(-1) [9.4 +/- 2.8 vs. 7.2 +/- 1.7 micromol x kg(-1) x min(-1)]). CONCLUSIONS: Hyperlactatemia in early postoperative cardiogenic shock was mainly related to increased tissue lactate production, whereas alterations of lactate utilization played only a minor role. Patients had hyperglycemia and increased nonoxidative glucose disposal, suggesting that glucose-induced stimulation of tissue glucose uptake and glycolysis may contribute significantly to hyperlactatemia.
Mots-clé
Acidosis, Lactic/*etiology/*metabolism Adult Aged Bilirubin/blood Cardiac Surgical Procedures/*adverse effects Case-Control Studies Female Glucose/*metabolism Glycolysis Hemodynamic Processes Humans Hydrocortisone/blood Hyperglycemia/*etiology/*metabolism Lactic Acid/*metabolism Liver/metabolism Male Middle Aged Oxidation-Reduction Prospective Studies Shock, Cardiogenic/*etiology/*metabolism/mortality/physiopathology Sodium Lactate/administration & dosage/pharmacokinetics Survival Analysis Tissue Distribution
Pubmed
Web of science
Création de la notice
24/01/2008 14:36
Dernière modification de la notice
03/03/2018 16:46
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