Effects of bicarbonate therapy on hemodynamics and tissue oxygenation in patients with lactic acidosis: a prospective, controlled clinical study

Abstract

Objective: To determine whether correction of acidemia using bicarbonate improves hemodynamic variables and tissue oxygenation in patients with lactic acidosis.

Design: Prospective, randomized, blinded, cross over study. Each patient sequentially received sodium bicarbonate and sodium chloride. The order of the infusions was randomized.

Patients: Ten patients with metabolic acidosis, increased arterial plasma lactate concentrations (greater than 2.45 mmol/L), and no severe renal failure (creatinine less than 250 mumol/L [less than 2.3 mg/dL]).

Method: Sodium bicarbonate (1 mmol/kg body weight) or equal volume of sodium chloride was injected iv at the beginning of two successive 1-hr study periods. Period order was randomized. Arterial and venous blood gas measurements, plasma electrolytes (sodium, potassium, chloride), osmolality and lactate, 2,3-diphosphoglycerate (DPG), and oxygen hemoglobin affinity, hemodynamic variables, oxygen delivery, and oxygen consumption measurements were obtained before and repeatedly during the 1-hr period after the injection of bicarbonate or sodium chloride.

Measurements and main results: Sodium bicarbonate administration increased arterial and venous pH, serum bicarbonate, and the partial pressure of CO2 in arterial and venous blood. Hemodynamic responses to sodium bicarbonate and sodium chloride were similar. Tissue oxygenation (as estimated by oxygen delivery, oxygen consumption, oxygen extraction ratio, and transcutaneous oxygen pressure) was not modified. No changes in serum sodium concentration, osmolality, arterial and venous lactate, red cell 2,3-DPG levels, or hemoglobin affinity for oxygen were observed.

Conclusion: Administration of sodium bicarbonate did not improve hemodynamic variables in patients with lactic acidosis, but did not worsen tissue oxygenation.