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Abstract: FR-PO271

Etiology of the Elevated ΔAG/ΔHCO3 Ratio in Lactic Acidosis: Time for Another Delta?

Session Information

Category: Fluid and Electrolytes

  • 902 Fluid and Electrolytes: Clinical


  • Treger, Richard M., Veterans Affairs, Los Angeles, California, United States
  • Grogan, Tristan, UCLA, Los Angeles, California, United States
  • Rudkin, Scott, UCI, Orange, California, United States

The ratio of delta anion gap and delta bicarbonate (ΔAG/ΔHCO3) is used to detect co-exisiting acid-base disorders in patients with high AG metabolic acidosis. The ΔAG/ΔHCO3 ratio in lactic acidosis (LA) is 1.6-1.8, most commonly postulated to result from lactate anions remaining in the extracellular space while protons are buffered intracellularly. Others have proposed that hypochloremia, resulting from extrusion of cellular cations and resultant expansion of the extracellular compartment during the buffering process in LA, accounts for the increment in AG. This study examined the etiology of the elevated ΔAG/ΔHCO3 seen in LA.


Data were obtained prospectively from adult trauma patients at a level 1 trauma center. Venous samples were drawn prior to administration of intravenous fluids. The associations between ΔLactate and ΔAG, arterial pH and ΔAG/ΔHCO3, and serum chloride and ΔAG/ΔHCO3 were examined using Pearson’s correlations and linear regression models.


108 patients were included. 63 patients had normal serum lactate levels (< 2.1 mM) with a mean AG of 7.1 and a mean lactate level of 1.5 mM, the values used to calculate subsequent ΔAG and ΔLactate values. ΔAG/ΔHCO3 was calculated for 45 patients who had elevated serum lactate levels (>2.1 mM). The mean ΔAG/ΔHCO3 was 1.86. The mean ΔLactate/ΔHCO3 ranged between 0.95-1.21 and the ΔLactate only explained 24.6% of the observed variance in the ΔAG (Figure). There was no statistically significant association between arterial pH or serum chloride and the ΔAG/ΔHCO3 ratio (p = 0.52 and 0.33, respectively).


The high ΔAG that results in an increased ΔAG/ΔHCO3 ratio does not appear to be primarily a result of increased extracellular lactate, pH-dependent contribution of anions or cations to the AG, or hypochloremia. Therefore, the high ΔAG/ΔHCO3 seen in lactic acidosis is likely a result of unmeasured organic anions, possibly including Krebs cycle intermediates. Further work to identify them needs to be carried out.

Figure. Correlation between ΔLactate and ΔAG. r = 0.496, p = 0.001.


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