The increase in CO2 production induced by NaHCO3 depends on blood albumin and hemoglobin concentrations

Objective:To evaluate the origin of HC ions participating in the generation of CO2 coming from sodium bicarbonate infusion during metabolic acidosis. We hypothesized that these H+ ions come from a back-titration of the main n on-bicarbonate buffers present in the blood, i.e. the hemoglobin and the al bumin, and thus postulated that the rate of CO2 release from a bicarbonate load is dependent on the concentration of these buffers. Design: Prospective clinical and experimental study. Setting: Surgical intensive care unit of a university hospital Patients and material: (1) Sixteen stable sedated and artificially ventilat ed critically ill patients with a mild base deficit. (2) Acidotic human blo od (bicarbonate 5 mM, pH 7.0) of hematocrit 5, 10, 20 and 40% regenerated f rom a mixture of frozen fresh plasma and packed red blood cells. Interventions: Patients: infusion of 1.5 mmol/kg sodium bicarbonate over 5 min. Regenerated blood: 25 mM sodium bicarbonate load. Measurements and results: Patients: continuous measurement of CO2 productio n (VCO2) on the expired gas using a metabolic monitor and arterial blood ga s analysis before (T0), at the end (T5) and at 10, 30 and 60 min after the beginning of the bicarbonate infusion. The increase in VCO` was 18 +/- 7% l eading to a rise in PaCO2 from 39.6 +/- 2.3 at T0 to 46.2 +/- 2.7 mmHg at T 5. The increases in VCO2 and in PaCO2 were significantly correlated to the albumin (r = 0.73, p < 0.005 and r = 0.70, p < 0.005, respectively) and to the hemoglobin (r = 0.51, p < 0.05 and r = 0.65, p < 0.01, respectively) co ncentrations. Regenerated blood: gas analysis 1 min after the bicarbonate l oad. The increase in PCO2 was closely related to the hematocrit (Ht) of the blood as it was 15.9 +/- 7.5 mmHg for Ht 5%, 29.0 +/- 9.6 for Ht 10%, 44.2 +/- 5.9 for Ht 20% and 71.0 +/- 3.5 for Ht 40% (n = 5 for each, p < 0.001) . Conclusions: The importance of the release of CO2 from a bicarbonate load i s dependent; on the concentration of the blood non-bicarbonate buffers. It is therefore likely that the adverse effects of bicarbonate therapy linked to the CO2 generation are more important in patients with high blood albumi n and hemoglobin concentrations.