Influence of bicarbonate on ventilatory drive in healthy subjects

Background Acute hypoventilation results in CO 2 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 CO 2 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 (V E ) and end-tidal CO 2 pressure (P et CO 2 ) 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 ΔV E /ΔP et CO 2 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 V E for each step of increasing inspiratory CO 2 . Akaike index on intra-individual fits showed a significant effect of bicarbonate on EAdi and a small effect on V E . 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.