Sodium bicarbonate causes dose-dependent increases in cerebral blood flow in infants and children with single-ventricle physiology

Background: Sodium bicarbonate (NaHCO 3 ) is a common treatment for metabolic acidemia; however, little definitive information exists regarding its treatment efficacy and cerebral hemodynamic effects. This pilot observational study quantifies relative changes in cerebral blood flow (ΔrCBF) and oxy- and deoxyhemoglobin concentrations (ΔHbO 2 and ΔHb) due to bolus administration of NaHCO 3 in patients with mild base deficits. Methods: Infants and children with hypoplastic left heart syndrome (HLHS) were enrolled before cardiac surgery. NaHCO 3 was given as needed for treatment of base deficit. Diffuse optical spectroscopies were used for 15 min postinjection to noninvasively monitor ΔHb, ΔHbO 2 , and ΔrCBF relative to baseline before NaHCO 3 administration. Results: Twenty-two anesthetized and mechanically ventilated patients with HLHS (aged 1 d to 4 y) received a median (interquartile range) dose of 1.1 (0.8, 1.8) mEq/kg NaHCO 3 administered intravenously over 10–20 s to treat a median (interquartile range) base deficit of −4 (−6, −3) mEq/l. NaHCO 3 caused significant dose-dependent increases in ΔrCBF; however, population-averaged ΔHb and ΔHbO 2 as compared with those of controls were not significant. Conclusions: Dose-dependent increases in cerebral blood flow (CBF) caused by bolus administration of NaHCO 3 are an important consideration in vulnerable populations wherein risk of rapid CBF fluctuations does not outweigh the benefit of treating a base deficit.