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      The origin and interpretation of hyperlactataemia during low oxygen delivery states

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      Author(s): 1 ,
      Publication date (Electronic):
      Journal: Critical Care
      Publisher: BioMed Central

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          Abstract

          The origin of hyperlactataemia during critical illness is complex but its presence can provide an indicator of inadequate tissue oxygen delivery. Cardiopulmonary bypass (CPB) represents a unique situation where systemic oxygen delivery can be directly measured and controlled. In the previous issue of Critical Care, Ranucci and colleagues use this phenomenon to identify independent variables associated with the development of hyperlactataemia during CPB. In doing so they highlight the complexity of interpreting hyperlactataemia during critical illness and provide further evidence of its association with worse postoperative morbidity.

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          Hyperlactatemia during cardiopulmonary bypass: determinants and impact on postoperative outcome

          Marco Ranucci, Barbara De Toffol, Giuseppe Isgrò … (2006)
          Introduction Hyperlactatemia during cardiopulmonary bypass is relatively frequent and is associated with an increased postoperative morbidity. The aim of this study was to determine which perfusion-related factors may be responsible for hyperlactatemia, with specific respect to hemodilution and oxygen delivery, and to verify the clinical impact of hyperlactatemia during cardiopulmonary bypass in terms of postoperative morbidity and mortality rate. Methods Five hundred consecutive patients undergoing cardiac surgery with cardiopulmonary bypass were admitted to this prospective observational study. During cardiopulmonary bypass, serial arterial blood gas analyses with blood lactate and glucose determinations were obtained. Hyperlactatemia was defined as a peak arterial blood lactate concentration exceeding 3 mmol/l. Pre- and intraoperative factors were tested for independent association with the peak arterial lactate concentration and hyperlactatemia. The postoperative outcome of patients with or without hyperlactatemia was compared. Results Factors independently associated with hyperlactatemia were the preoperative serum creatinine value, the presence of active endocarditis, the cardiopulmonary bypass duration, the lowest oxygen delivery during cardiopulmonary bypass, and the peak blood glucose level. Once corrected for other explanatory variables, hyperlactatemia during cardiopulmonary bypass remained significantly associated with an increased morbidity, related mainly to a postoperative low cardiac output syndrome, but not to mortality. Conclusion Hyperlactatemia during cardiopulmonary bypass appears to be related mainly to a condition of insufficient oxygen delivery (type A hyperlactatemia). During cardiopulmonary bypass, a careful coupling of pump flow and arterial oxygen content therefore seems mandatory to guarantee a sufficient oxygen supply to the peripheral tissues.
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            Outcome with high blood lactate levels during cardiopulmonary bypass in adult cardiac operation.

            Philippe Demers, Stephane Elkouri, Raymond Martineau … (2000)
            High blood lactate levels during cardiopulmonary bypass (CPB) are associated with tissue hypoperfusion and may contribute to postoperative complications or death. The objective of this study was to determine an association between blood lactate levels during CPB and perioperative morbidity and mortality. We reviewed 1,376 patients who underwent cardiac operation with CPB. Patients with abnormal preoperative blood lactate levels were excluded (n = 101). Blood lactate concentration during CPB, clinical data, and perioperative events were recorded. Peak blood lactate levels of 4.0 mmol/L or higher during CPB were present in 227 patients (18.0%). Postoperative mortality was higher in this group than in the patients who had peak blood lactate levels of less than 4.0 mmol/L during CPB (11.0% versus 1.4%; p < 0.001, relative risk [RR] = 9.0). Postoperative hemodynamic instability occurred in 29.5% of patients with elevated levels of lactate during CPB compared with 10.9% of patients with lower lactate levels (p < 0.001, RR = 3.4). Overall, major postoperative complications occurred in 43.2% and 21.8% of patients in each group, respectively (p < 0.001, RR = 2.7). Logistic regression analysis revealed that peak blood lactate levels of 4.0 mmol/L or higher during CPB were strongly associated with postoperative mortality (p = 0.0001) and morbidity (p = 0.013). Blood lactate concentration of 4.0 mmol/L or higher during CPB identifies a subgroup of patients with increased risk of postoperative morbidity and mortality.
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              Lactic acidosis in critical illness.

              Marni J. Falk, Barry A Mizock (1991)
              This article reviews the current body of knowledge regarding lactic acidosis in critically ill patients. The classification of disordered lactate metabolism and its pathogenesis are examined. The utility of lactate as a metabolic monitor of shock is examined and current therapeutic strategies in the treatment of patients suffering from lactic acidosis are extensively reviewed. The paper is designed to integrate basic concepts with a current approach to lactate in critical illness that the clinician can use at the bedside. Comprehensive review of the available, basic science, medical, surgical, and critical care literature. The severity of lactic acidosis in critically ill patients correlates with overall oxygen debt and survival. Lactate determinations may be useful as an ongoing monitor of perfusion as resuscitation proceeds. Therapy of critically ill patients with lactic acidosis is designed to maximize oxygen delivery in order to reduce tissue hypoxia by increasing cardiac index, while maintaining hemoglobin concentration. Buffering agents have not been shown to materially affect outcome from lactic acidosis caused by shock. The benefits of other specific therapies designed to reduce the severity of lactic acidosis remain unproven.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Crit Care
                Title: Critical Care
                Publisher: BioMed Central
                ISSN (Print): 1364-8535
                ISSN (Electronic): 1466-609X
                Publication date (Print): 2007
                Publication date (Electronic): 12 January 2007
                Volume: 11
                Issue: 1
                Page: 104
                Affiliations
                [1 ]Chelsea & Westminster Hospital, Imperial College London, 369 Fulham Road, London SW10 9NH, UK
                Article
                Publisher ID: cc5137
                DOI: 10.1186/cc5137
                PMC ID: 2151904
                PubMed ID: 17254315
                SO-VID: 81a5edaa-8296-4819-9251-bf3cc2df2a58
                Copyright © Copyright © 2007 BioMed Central Ltd
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                Subject: Commentary

                ScienceOpen disciplines: Emergency medicine & Trauma
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                ScienceOpen disciplines: Emergency medicine & Trauma

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