The effect of metabolic alkalosis on the ventilatory response in healthy subjects

E. Oppersma, J. Doorduin, J. G. van der Hoeven, P. H. Veltink, H. W. H. van Hees, L. M. A. Heunks

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Background: 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. Methods: 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. Results: Plasma bicarbonate increased from 25.2 ± 2.2 to 29.2 ± 1.9 mmol/L. With increasing inspiratory CO2 pressure during the HCVR test, RR, Vt, Pdi, EAdi and VE increased. The clinical ratio ΔVE/ΔPetCO2 remained unchanged, but Pdi, EAdi and VE were significantly lower after bicarbonate administration for similar levels of inspired CO2. Conclusion: This study demonstrates that in healthy subjects metabolic alkalosis decreases the neural respiratory drive and minute ventilation, as a response to inspiratory CO2.
Original languageEnglish
Pages (from-to)47-53
JournalRespiratory physiology & neurobiology
Volume249
DOIs
Publication statusPublished - 2018

Cite this

Oppersma, E. ; Doorduin, J. ; van der Hoeven, J. G. ; Veltink, P. H. ; van Hees, H. W. H. ; Heunks, L. M. A. / The effect of metabolic alkalosis on the ventilatory response in healthy subjects. In: Respiratory physiology & neurobiology. 2018 ; Vol. 249. pp. 47-53.
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abstract = "Background: 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. Methods: 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. Results: Plasma bicarbonate increased from 25.2 ± 2.2 to 29.2 ± 1.9 mmol/L. With increasing inspiratory CO2 pressure during the HCVR test, RR, Vt, Pdi, EAdi and VE increased. The clinical ratio ΔVE/ΔPetCO2 remained unchanged, but Pdi, EAdi and VE were significantly lower after bicarbonate administration for similar levels of inspired CO2. Conclusion: This study demonstrates that in healthy subjects metabolic alkalosis decreases the neural respiratory drive and minute ventilation, as a response to inspiratory CO2.",
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The effect of metabolic alkalosis on the ventilatory response in healthy subjects. / Oppersma, E.; Doorduin, J.; van der Hoeven, J. G.; Veltink, P. H.; van Hees, H. W. H.; Heunks, L. M. A.

In: Respiratory physiology & neurobiology, Vol. 249, 2018, p. 47-53.

Research output: Contribution to journalArticleAcademicpeer-review

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AU - Oppersma, E.

AU - Doorduin, J.

AU - van der Hoeven, J. G.

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AU - van Hees, H. W. H.

AU - Heunks, L. M. A.

PY - 2018

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N2 - Background: 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. Methods: 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. Results: Plasma bicarbonate increased from 25.2 ± 2.2 to 29.2 ± 1.9 mmol/L. With increasing inspiratory CO2 pressure during the HCVR test, RR, Vt, Pdi, EAdi and VE increased. The clinical ratio ΔVE/ΔPetCO2 remained unchanged, but Pdi, EAdi and VE were significantly lower after bicarbonate administration for similar levels of inspired CO2. Conclusion: This study demonstrates that in healthy subjects metabolic alkalosis decreases the neural respiratory drive and minute ventilation, as a response to inspiratory CO2.

AB - Background: 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. Methods: 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. Results: Plasma bicarbonate increased from 25.2 ± 2.2 to 29.2 ± 1.9 mmol/L. With increasing inspiratory CO2 pressure during the HCVR test, RR, Vt, Pdi, EAdi and VE increased. The clinical ratio ΔVE/ΔPetCO2 remained unchanged, but Pdi, EAdi and VE were significantly lower after bicarbonate administration for similar levels of inspired CO2. Conclusion: This study demonstrates that in healthy subjects metabolic alkalosis decreases the neural respiratory drive and minute ventilation, as a response to inspiratory CO2.

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