Luciano Gattinoni1, Francesco Vasques2,3, Luigi Camporota2,3, Jennifer Meessen4, Federica Romitti1, Iacopo Pasticci1, Eleonora Duscio1, Francesco Vassalli1, Lui G Forni5,6, Didier Payen7, Massimo Cressoni8, Alberto Zanella9,10, Roberto Latini4, Michael Quintel1, John J Marini11,12. 1. Department of Anaesthesiology, Emergency and Intensive Care Medicine, University of Göttingen, Göttingen, Germany. 2. Department of Adult Critical Care, Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom. 3. Health Centre for Human and Applied Physiological Sciences, King's College London, London, United Kingdom. 4. Dipartimento di Ricerche Cardiovascolari, Istituto di Ricovero e Cura a Carattere Scientifico Istituto di Ricerche Farmacologiche "Mario Negri," Milan, Italy. 5. Department of Intensive Care Medicine, Royal Surrey County Hospital NHS Foundation Trust, Guildford, United Kingdom. 6. Faculty of Health Sciences, University of Surrey, Guildford, United Kingdom. 7. Department of Anaesthesiology and Critical Care, Lariboisière University Hospital, Public Assistance-Paris Hospital, University Paris Diderot, Paris, France. 8. Dipartimento di Scienze della Salute, Università degli Studi di Milano Bicocca, Milan, Italy. 9. Anaesthesia and Critical Care, Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy. 10. Dipartimento di Anestesia, Rianimazione ed Emergenza, Fondazione Istituto di Ricerca e Cura a Carattere Scientifico Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy. 11. Regions Hospital, St. Paul, Minnesota; and. 12. University of Minnesota, St. Paul, Minnesota.
Abstract
Rationale: Hyperlactatemia in sepsis may derive from a prevalent impairment of oxygen supply/demand and/or oxygen use. Discriminating between these two mechanisms may be relevant for the early fluid resuscitation strategy. Objectives: To understand the relationship among central venous oxygen saturation (ScvO2), lactate, and base excess to better determine the origin of lactate. Methods: This was a post hoc analysis of baseline variables of 1,741 patients with sepsis enrolled in the multicenter trial ALBIOS (Albumin Italian Outcome Sepsis). Variables were analyzed as a function of sextiles of lactate concentration and sextiles of ScvO2. We defined the "alactic base excess," as the sum of lactate and standard base excess.Measurements and Main Results: Organ dysfunction severity scores, physiologic variables of hepatic, metabolic, cardiac, and renal function, and 90-day mortality were measured. ScvO2 was lower than 70% only in 35% of patients. Mortality, organ dysfunction scores, and lactate were highest in the first and sixth sextiles of ScvO2. Although lactate level related strongly to mortality, it was associated with acidemia only when kidney function was impaired (creatinine >2 mg/dl), as rapidly detected by a negative alactic base excess. In contrast, positive values of alactic base excess were associated with a relative reduction of fluid balance.Conclusions: Hyperlactatemia is powerfully correlated with severity of sepsis and, in established sepsis, is caused more frequently by impaired tissue oxygen use, rather than by impaired oxygen transport. Concomitant acidemia was only observed in the presence of renal dysfunction, as rapidly detected by alactic base excess. The current strategy of fluid resuscitation could be modified according to the origin of excess lactate.
RCT Entities:
Rationale: Hyperlactatemia in sepsis may derive from a prevalent impairment of oxygen supply/demand and/or oxygen use. Discriminating between these two mechanisms may be relevant for the early fluid resuscitation strategy. Objectives: To understand the relationship among central venous oxygen saturation (ScvO2), lactate, and base excess to better determine the origin of lactate. Methods: This was a post hoc analysis of baseline variables of 1,741 patients with sepsis enrolled in the multicenter trial ALBIOS (Albumin Italian Outcome Sepsis). Variables were analyzed as a function of sextiles of lactate concentration and sextiles of ScvO2. We defined the "alactic base excess," as the sum of lactate and standard base excess.Measurements and Main Results:Organ dysfunction severity scores, physiologic variables of hepatic, metabolic, cardiac, and renal function, and 90-day mortality were measured. ScvO2 was lower than 70% only in 35% of patients. Mortality, organ dysfunction scores, and lactate were highest in the first and sixth sextiles of ScvO2. Although lactate level related strongly to mortality, it was associated with acidemia only when kidney function was impaired (creatinine >2 mg/dl), as rapidly detected by a negative alactic base excess. In contrast, positive values of alactic base excess were associated with a relative reduction of fluid balance.Conclusions: Hyperlactatemia is powerfully correlated with severity of sepsis and, in established sepsis, is caused more frequently by impaired tissue oxygen use, rather than by impaired oxygen transport. Concomitant acidemia was only observed in the presence of renal dysfunction, as rapidly detected by alactic base excess. The current strategy of fluid resuscitation could be modified according to the origin of excess lactate.
Entities:
Keywords:
base excess; lactic acidosis; sepsis; venous oxygen saturation
Authors: Ulrik Winning Iepsen; Ronni R Plovsing; Klaus Tjelle; Nicolai Bang Foss; Christian S Meyhoff; Camilla K Ryrsø; Ronan M G Berg; Niels H Secher Journal: Exp Physiol Date: 2021-06-18 Impact factor: 2.858
Authors: Sebastien Preau; Dominique Vodovar; Boris Jung; Steve Lancel; Lara Zafrani; Aurelien Flatres; Mehdi Oualha; Guillaume Voiriot; Youenn Jouan; Jeremie Joffre; Fabrice Uhel; Nicolas De Prost; Stein Silva; Eric Azabou; Peter Radermacher Journal: Ann Intensive Care Date: 2021-07-03 Impact factor: 6.925