• Patricia G Rosenstein, Brett S Tennent-Brown, and Dez Hughes.
• Department of Veterinary Clinical Sciences, Faculty of Veterinary and Agricultural Sciences, University of Melbourne, Werribee, Victoria, Australia.
• J Vet Emerg Crit Care (San Antonio). 2018 Mar 1; 28 (2): 85-105.

ObjectiveTo review the current literature with respect to the physiology, pathophysiology, and measurement of lactate.Data SourcesData were sourced from veterinary and human clinical trials, retrospective studies, experimental studies, and review articles. Articles were retrieved without date restrictions and were sourced primarily via PubMed, Scopus, and CAB Abstracts as well as by manual selection.Human And Veterinary Data SynthesisLactate is an important energy storage molecule, the production of which preserves cellular energy production and mitigates the acidosis from ATP hydrolysis. Although the most common cause of hyperlactatemia is inadequate tissue oxygen delivery, hyperlactatemia can, and does occur in the face of apparently adequate oxygen supply. At a cellular level, the pathogenesis of hyperlactatemia varies widely depending on the underlying cause. Microcirculatory dysfunction, mitochondrial dysfunction, and epinephrine-mediated stimulation of Na+ -K+ -ATPase pumps are likely important contributors to hyperlactatemia in critically ill patients. Ultimately, hyperlactatemia is a marker of altered cellular bioenergetics.ConclusionThe etiology of hyperlactatemia is complex and multifactorial. Understanding the relevant pathophysiology is helpful when characterizing hyperlactatemia in clinical patients.© Veterinary Emergency and Critical Care Society 2018.

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