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

Abstract

Introduction

The magnitude of the secondary response to chronic respiratory acidosis, that is, change in plasma bicarbonate concentration ([HCO ₃ ⁻]) per mm Hg change in arterial carbon dioxide tension (PaCO ₂), remains uncertain. Retrospective observations yielded Δ[HCO ₃ ⁻]/ΔPaCO ₂ 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 ₂ 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 ₂, 52.8 ± 6.0 mm Hg; [HCO ₃ ⁻], 29.9 ± 3.0 mEq/l, and pH, 7.37 ± 0.02. Least-squares regression for steady-state [HCO ₃ ⁻] versus PaCO ₂ had a slope of 0.476 mEq/l per mm Hg (95% CI = 0.414–0.538, P < 0.01; r = 0.95) and that for steady-state pH versus PaCO ₂ had a slope of −0.0012 units per mm Hg (95% CI = −0.0021 to −0.0003, P = 0.01; r = −0.47). These data allowed estimation of the 95% prediction intervals for plasma [HCO ₃ ⁻] and pH at different levels of PaCO ₂ applicable to patients with steady-state chronic hypercapnia.

Conclusion

In steady-state chronic hypercapnia up to 70 mm Hg, the Δ[HCO ₃ ⁻]/ΔPaCO ₂ 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.