Very cool and succinct article by Josh Farkas on lactate and recommendations for sepsis

The article’s summary bullet points are

• Lactate production in septic shock is not due to anaerobic metabolism or low oxygen delivery.  It is largely driven by endogenous epinephrine stimulating aerobic glycolysis via beta-2 adrenergic receptors.
• Lactate may have a protective effect, serving as a metabolic fuel for the heart and brain under conditions of stress.
• Elevated lactate is useful to identify occult shock (patients who are being maintained by a robust endogenous catecholamine release).  These patients are at increased risk for deterioration and require more aggressive care.
• There is no clear evidence about what lactate adds to other resuscitation targets (e.g. blood pressure and urine output).  If lactate is trended during sepsis resuscitation, it should be interpreted carefully in clinical context.
• Administration of sodium lactate is safe and potentially beneficial.  This supports the use of lactated ringers as a resuscitative fluid.
• Epinephrine has often been avoided in the past due to concerns regarding lactate generation.  Given that lactate is potentially beneficial, epinephrine should be re-considered as a second-line vasopressor.  At low doses it works primarily as an inotrope, whereas at higher doses it also functions as a vasoconstrictor.

Source: Understanding lactate in sepsis & Using it to our advantage