This topic is for some reason the subject of one frequently repeated question. Notable duplicates include the following:
So the lactate in sepsis is raised. What of it?
The college seems to favour this concept as an exam topic. It has come up repeatedly in the past papers. It seems important for the trainees to understand that in septic shock the lactate elevation is not purely a feature of tissue hypoperfusion, but rather the outcome of complex metabolic changes.
The mechanism of lactate elevation in sepsis is discussed in greater detail in a chapter dedicated to these metabolic changes. Instead of revisiting that elaborate explanation, I will instead produce some references, and this confusing flowchart diagram:
There, now that's all clear.
Jones, Alan E., and Michael A. Puskarich. "Sepsis-induced tissue hypoperfusion." Critical care clinics 25.4 (2009): 769.
Crouser, Elliott D. "Mitochondrial dysfunction in septic shock and multiple organ dysfunction syndrome." Mitochondrion 4.5 (2004): 729-741.
Levy, Bruno. "Lactate and shock state: the metabolic view." Current opinion in critical care 12.4 (2006): 315-321.
Bateman, Ryon M., Michael D. Sharpe, and Christopher G. Ellis. "Bench-to-bedside review: microvascular dysfunction in sepsis-hemodynamics, oxygen transport, and nitric oxide." CRITICAL CARE-LONDON- 7.5 (2003): 359-373.
Jansen TC, van Bommel J, Schoonderbeek J, et al: Early lactate-guided therapy in ICU patients:
A multicenter, open-label, randomized, controlled trial. Am J Respir Crit Care Med 2010 May 12
Ince, Can, and Michiel Sinaasappel. "Microcirculatory oxygenation and shunting in sepsis and shock." Critical care medicine 27.7 (1999): 1369-1377.