Abstract
Background: Acute hypoventilation results in CO2 retention and respiratory acidosis. Bicarbonate retention aims to restore pH level. However, after institution of mechanical ventilation metabolic alkalosis may develop, which could impair respiratory drive.
Aim: To investigate whether increased plasma bicarbonate reduces ventilatory drive and minute ventilation.
Methods: We enrolled 11 healthy volunteers. At baseline (t0), arterial blood gas (ABG) analysis and a hypercapnic ventilatory response (HCVR) test were performed while flow, diaphragm electrical activity (EAdi), and partial pressure of in- and expiratory CO2 were measured. 100 ml 8.4% sodium bicarbonate was administered for 10 times with 8 h interval. Subsequently, measurements were repeated (t1). Ratio between difference in start and end of minute ventilation (VE) and end-tidal CO2 pressure (PetCO2) was calculated.
Results: Bicarbonate levels increased from 25.2±2.2 mmol/L to 29.2±1.9 mmol/L. There was no difference in ΔVE/ΔPetCO2 between t0 (6.1±2.5 L·min-1/kPa) and t1 (6.3±2.6 L·min-1/kPa, p=0.76). Figure 1 shows mean EAdi and VE for each step of increasing inspiratory CO2. Akaike index on intra-individual fits showed a significant effect of bicarbonate on EAdi and a small effect on VE.
Conclusion: Increasing arterial bicarbonate reduces ventilatory drive in healthy subjects. The clinical importance is that it could be helpful to reduce plasma bicarbonate in selected difficult to wean patients.
Aim: To investigate whether increased plasma bicarbonate reduces ventilatory drive and minute ventilation.
Methods: We enrolled 11 healthy volunteers. At baseline (t0), arterial blood gas (ABG) analysis and a hypercapnic ventilatory response (HCVR) test were performed while flow, diaphragm electrical activity (EAdi), and partial pressure of in- and expiratory CO2 were measured. 100 ml 8.4% sodium bicarbonate was administered for 10 times with 8 h interval. Subsequently, measurements were repeated (t1). Ratio between difference in start and end of minute ventilation (VE) and end-tidal CO2 pressure (PetCO2) was calculated.
Results: Bicarbonate levels increased from 25.2±2.2 mmol/L to 29.2±1.9 mmol/L. There was no difference in ΔVE/ΔPetCO2 between t0 (6.1±2.5 L·min-1/kPa) and t1 (6.3±2.6 L·min-1/kPa, p=0.76). Figure 1 shows mean EAdi and VE for each step of increasing inspiratory CO2. Akaike index on intra-individual fits showed a significant effect of bicarbonate on EAdi and a small effect on VE.
Conclusion: Increasing arterial bicarbonate reduces ventilatory drive in healthy subjects. The clinical importance is that it could be helpful to reduce plasma bicarbonate in selected difficult to wean patients.
| Original language | English |
|---|---|
| Article number | PA5025 |
| Journal | European respiratory journal |
| Volume | 48 |
| Issue number | suppl 60 |
| DOIs | |
| Publication status | Published - 2016 |
| Event | ERS International Congress 2016 - London, United Kingdom Duration: 3 Sep 2016 → 7 Sep 2016 |