Secondary Response to Chronic Respiratory Acidosis in Humans: A Prospective Study.

INTRODUCTION

The magnitude of the secondary response to chronic respiratory acidosis, that is, change in plasma bicarbonate concentration ([HCO]) per mm Hg change in arterial carbon dioxide tension (PaCO), remains uncertain. Retrospective observations yielded Δ[HCO]/ΔPaCO slopes of 0.35 to 0.51 mEq/l per mm Hg, but all studies have methodologic flaws.

METHODS

We studied prospectively 28 stable outpatients with steady-state chronic hypercapnia. Patients did not have other disorders and were not taking medications that could affect acid-base status. We obtained 2 measurements of arterial blood gases and plasma chemistries within a 10-day period.

RESULTS

Steady-state PaCO ranged from 44.2 to 68.8 mm Hg. For the entire cohort, mean (± SD) steady-state plasma acid-base values were as follows: PaCO, 52.8 ± 6.0 mm Hg; [HCO], 29.9 ± 3.0 mEq/l, and pH, 7.37 ± 0.02. Least-squares regression for steady-state [HCO] versus PaCO had a slope of 0.476 mEq/l per mm Hg (95% CI = 0.414-0.538,  < 0.01;  = 0.95) and that for steady-state pH versus PaCO had a slope of -0.0012 units per mm Hg (95% CI = -0.0021 to -0.0003,  = 0.01;  = -0.47). These data allowed estimation of the 95% prediction intervals for plasma [HCO] and pH at different levels of PaCO applicable to patients with steady-state chronic hypercapnia.

CONCLUSION

In steady-state chronic hypercapnia up to 70 mm Hg, the Δ[HCO]/ΔPaCO slope equaled 0.48 mEq/l per mm Hg, sufficient to maintain systemic acidity between the mid-normal range and mild acidemia. The estimated 95% prediction intervals enable differentiation between simple chronic respiratory acidosis and hypercapnia coexisting with additional acid-base disorders.