Oppersma E, Doorduin J, van der Hoeven J G, Veltink P H, van Hees H W H, Heunks L M A
MIRA - Institute for Biomedical Technology & Technical Medicine, University of Twente, Enschede, The Netherlands; Department of Critical Care Medicine, Radboud University Medical Center, Nijmegen, The Netherlands.
Department of Critical Care Medicine, Radboud University Medical Center, Nijmegen, The Netherlands; Department of Neurology, Radboud University Medical Center, Nijmegen, The Netherlands.
Respir Physiol Neurobiol. 2018 Feb;249:47-53. doi: 10.1016/j.resp.2018.01.002. Epub 2018 Jan 4.
Patients with acute respiratory failure may develop respiratory acidosis. Metabolic compensation by bicarbonate production or retention results in posthypercapnic alkalosis with an increased arterial bicarbonate concentration. The hypothesis of this study was that elevated plasma bicarbonate levels decrease respiratory drive and minute ventilation.
In an intervention study in 10 healthy subjects the ventilatory response using a hypercapnic ventilatory response (HCVR) test was assessed, before and after administration of high dose sodium bicarbonate. Total dose of sodiumbicarbonate was 1000 ml 8.4% in 3 days.
Plasma bicarbonate increased from 25.2 ± 2.2 to 29.2 ± 1.9 mmol/L. With increasing inspiratory CO pressure during the HCVR test, RR, V, Pdi, EAdi and V increased. The clinical ratio ΔV/ΔPCO remained unchanged, but Pdi, EAdi and V were significantly lower after bicarbonate administration for similar levels of inspired CO.
This study demonstrates that in healthy subjects metabolic alkalosis decreases the neural respiratory drive and minute ventilation, as a response to inspiratory CO.
