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

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 CO₂ pressure during the HCVR test, RR, V_t, Pdi, EAdi and V_E increased. The clinical ratio ΔV_E/ΔP_etCO₂ remained unchanged, but Pdi, EAdi and V_E were significantly lower after bicarbonate administration for similar levels of inspired CO₂.

This study demonstrates that in healthy subjects metabolic alkalosis decreases the neural respiratory drive and minute ventilation, as a response to inspiratory CO₂.