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Hyperlactaemia Without Acidosis - An Investigation Using an In Vitro Model

ABSTRACT

Objective:


To use an in vitro dilutional blood model to simulate aerobic hyperlactaemia, and to question whether base excess and anion gap distinguish aerobic from anaerobic lactate production.

Methods:

Cooled fresh blood was diluted (3:1) with nine different crystalloid solutions, each with a sodium concentration of 140 mmol/L but with strong ion difference values ranging from -5 mEq/L to 40 mEq/L due to varying concentrations of Cl-, HCO3- and lactate anions. Normocapnic pH and base excess values post-dilution were determined by gas equilibration. Strong ion difference and anion gap values were measured.

Results:

There was close correlation between the normocapnic pH and both the diluent strong ion difference and the final strong ion difference of the diluted specimens (R2 = 0.96 and 0.89 respectively). This was independent of lactate concentrations in diluent or in post-dilution plasma. Where lactate-containing crystalloid was added, base excess, normocapnic pH and anion gap were strongly correlated with the final plasma lactate concentrations (R2 > 0.99). However, only at final lactate concentrations of approximately 10 - 15 mmol/L did values of base excess, normocapnic pH or anion gap indicate metabolic acidosis.

Conclusions:

Hyperlactaemia from any source reduces strong ion difference and base excess and increases the anion gap, but values may remain in the normal range until hyperlactaemia is severe. Abnormal base excess and anion gap values do not distinguish aerobic from anaerobic lactate production. Normal values merely reflect low sensitivity to small lactate elevations (aerobic or otherwise). (Critical Care and Resuscitation 1999; 1: 354-359)

Key words:

Hyperactataemia, lactic acidosis, strong ion difference, dysoxia, blood dilution, aerobic glycolysis

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