Understanding the Acid-Base Response to Respiratory Derangements: Finding, and Clinically Applying, the In Vivo Base Excess.

Abstract

Objectives: To evaluate the base excess response during acute in vivo carbon dioxide changes.

Design: Secondary analysis of individual participant data from experimental studies.

Setting: Three experimental studies investigating the effect of acute in vivo respiratory derangements on acid-base variables.

Subjects: Eighty-nine (canine and human) carbon dioxide exposures.

Interventions: Arterial carbon dioxide titration through environmental chambers or mechanical ventilation.

Measurements and main results: For each subject, base excess was calculated using bicarbonate and pH using a fixed buffer power of 16.2. Analyses were performed using linear regression with arterial dioxide (predictor), base excess (outcome), and studies (interaction term). All studies show different baselines and slopes for base excess across carbon dioxide titrations methods. Individual subjects show substantial, and potentially clinically relevant, variations in base excess response across the hypercapnic range. Using a mathematical simulation of 10,000 buffer power coefficients we determined that a coefficient of 12.1 (95% CI, 9.1-15.1) instead of 16.2 facilitates a more conceptually appropriate in vivo base excess equation for general clinical application.

Conclusions: In vivo changes in carbon dioxide leads to changes in base excess that may be clinically relevant for individual patients. A buffer power coefficient of 16.2 may not be appropriate in vivo and needs external validation in a range of clinical settings.