With great interest, we read the Clinical Focus Review on lactate by Pino and Singh.1  We strongly agree with the need to decouple an increased lactate level from the mandatory use of fluid infusions.

The authors argue, however, that lactate is a consequence rather than a cause of cellular acidosis and describe the lactate ion as a weak base (“that accepts some of the protons”). This latter statement would imply that increasing lactate levels per se would act to decrease acidity, which is in obvious conflict with ubiquitous clinical experience. In this context, we find the quantitative acid–base perspective as described by Stewart and others theoretically more satisfying and clinically useful.2  The core of the theory states that the concentration of protons (being weak ions) does not change primarily by processes adding or removing these ions (such as when producing lactic acid), but from processes changing the conditions for dissociation of water, which at a concentration of about 55 mol/l (sic) in plasma is a vast potential proton source. As shown by Stewart, the dissociation of water is influenced by carbon dioxide, weak acids, and the strong ion difference, the difference between the sums of strong cations and strong anions. Based on the cutoff value of 4 for the pK of strong electrolytes in biologic systems, lactate in plasma behaves as a strong anion.2  Therefore, an increase in lactate will decrease the strong ion difference and thereby increase water dissociation and thus increase proton concentration. Contrary to what the authors state, lactate (ion) and not the lactic acid per se is a direct cause of acidosis, and increased lactate concentration is reflected 1:1 as a change in base excess. Infusion of sodium lactate does not cause acidosis as the lactate is accompanied by the strong cation sodium, and when the lactate is metabolized (with sodium remaining), the strong ion difference increases, leading to decreased water dissociation and decreased acidity. This perspective on lactate also allows for rapid bedside differentiation of changes in base excess associated with changes in lactate.3 

The authors declare no competing interests.

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