To evaluate the precision, bias and CO2 invariance of base excess as determined by the Van Slyke equation over a wide Pco2 range at normal and low hemoglobin concentrations.
Prospective in vitro study.
University research laboratory.
Normal human blood, both undiluted and diluted with plasma.
Two experiments were conducted. In the first, blood unmodified or after adding HCl or sodium bicarbonate was rendered hypercarbic (Pco2 >70 torr) by gas equilibration. Rapid Pco2 reduction in ≥10 steps to a final Pco2 ≤20 torr was then performed. In the second experiment, blood unmodified or diluted to a hemoglobin concentration of ∼4 G% was mixed anaerobically (9:1, vol:vol) with varying concentrations of lactic acid in saline (0–250 mmol/L).
Measurements and Main Results
In the first experiment, blood gas analysis at each step during the progressive Pco2 reduction revealed that base excess remained nearly constant (sd all specimens ≤0.6 mmol/L) whereas Pco2 changed by >80 torr. In the second experiment, simultaneous blood gas and plasma lactate analyses showed that changes in base excess correlated closely with changes in both plasma and whole blood lactate concentrations (r2 ≥ 0.91) despite concurrent Pco2 elevations as great as 200 torr. Quantification by base excess of change in whole blood lactate concentration was precise with slight negative bias (mean negative bias, 1.1 ± 1.9 mmol/L) in both diluted and undiluted blood. There was significant underestimation of change in plasma lactate concentration in undiluted blood, presumably because base excess is a whole blood variable.
Base excess calculated using the Van Slyke equation accurately quantifies metabolic (nonrespiratory) acid-base status in blood in vitro. This accuracy is little affected by large simultaneous alterations in Pco2, or by very low hemoglobin concentrations similar to that used to calculate standard base excess.