Blood Lactate in the Critical Patient:
Where Are We Now?

Global, or whole-body hypo-perfusion has, for many years, been thought to be the most common pathological cause of elevated blood lactate in dogs and cats. Furthermore, it has also been postulated that plasma lactate rises proportionally to the severity of hypo-perfusion, with the magnitude of hyper-lactataemia being proportional to the severity of the insult (but not necessarily its reversibility).

However, studies over many years suggest that lactate production is more a function of adrenaline/epinephrine concentrations in body tissues, rather than primarily oxygen debt, with higher epinephrine concentration accelerating production of pyruvate above the capacity of mitochondria to process it into ATP, with subsequent diversion of pyruvate to lactate production instead. In fact, in studies of sepsis, most lactate in the body is produced in the lungs, which, even in severe ARDS, have oxygen concentrations in excess of those required for solely anaerobic metabolism. With this evidence in mind, it seems likely that lactate is a measure of disease severity, and not necessarily the magnitude of tissue hypoxia (although tissue hypoxia in regions of poor blood flow probably contributes). Regardless of the relative contributions of disease, or hypoxia, failure of blood lactate to return to normal over 24–28 hours is generally associated with a worse outcome – making lactate a useful prognostic indicator.