Acute sodium bicarbonate administration improves ventilatory efficiency in experimental respiratory acidosis: clinical implications.

Abstract

Administering sodium bicarbonate (NaHCO₃) to patients with respiratory acidosis breathing spontaneously is contraindicated because it increases carbon dioxide load and depresses pulmonary ventilation. Nonetheless, several studies have reported salutary effects of NaHCO₃ in patients with respiratory acidosis but the underlying mechanism remains uncertain. Considering that such reports have been ignored, we examined the ventilatory response of unanesthetized dogs with respiratory acidosis to hypertonic NaHCO₃ infusion (1 N, 5 mmol/kg) and compared it with that of animals with normal acid-base status or one of the remaining acid-base disorders. Ventilatory response to NaHCO₃ infusion was evaluated by examining the ensuing change in PaCO₂ and the linear regression of the PaCO₂ vs. pH relationship. Strikingly, PaCO₂ failed to increase and the ΔPaCO₂ vs. ΔpH slope was negative in respiratory acidosis, whereas PaCO₂ increased consistently and the ΔPaCO₂ vs. ΔpH slope was positive in the remaining study groups. These results cannot be explained by differences in buffering-induced decomposition of infused bicarbonate or baseline levels of blood pH, PaCO₂, and pulmonary ventilation. We propose that NaHCO₃ infusion improved the ventilatory efficiency of animals with respiratory acidosis, i.e., it decreased their ratio of total pulmonary ventilation to carbon dioxide excretion (V_E/V_CO2). Such exclusive effect of NaHCO₃ infusion in animals with respiratory acidosis might emanate from baseline increased V_D/V_T (dead space/tidal volume) caused by bronchoconstriction and likely reduced pulmonary blood flow, defects that are reversed by alkali infusion. Our observations might explain the beneficial effects of NaHCO₃ reported in patients with acute respiratory acidosis.