In this chapter, we integrate new and old knowledge on lactate metabolism and lactate monitoring that were obtained from experiments, sports physiology, and studies in critically ill patients.
An interesting aspect of lactate is that much of its behavior in physiology and pathophysiology can be explained from a few first principles. Rises of lactate during disease often result from the same effects as rises in lactate in physiology. Furthermore, at the very different spatial scales, from cellular to whole-body scales, lactate displays similar physiology.
For decades it has been recognized that circulating elevated lactate levels are strongly related with outcome in many acute critical conditions. Although hyperlactatemia was long thought to be related to tissue hypoxia in most ICU patients, we now know that in the most cases, stress is the main driver of increased lactate production. Since lactate itself in no way harms the body, lactate may be considered the clearest example of a marker and not a mediator of an acute critical condition.
In patients with hypotension resulting from sepsis, fundamental perfusion differences appear to exist between patients with and without hyperlactatemia.
Likewise, the ability of the liver to remove lactate during critical disease can be decreased through various mechanisms such as preexisting impairment, diminished flow, or endotoxin-induced damage.
The increased availability of point-of-care measurements has allowed lactate to emerge as a valuable marker to assess disease severity and facilitate differential diagnosis. With the short time scales on which lactate can change, it also constitutes a useful monitor of treatment.
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