Human PaCO2 and standard base excess compensation for acid-base imbalance.

Objectives: Renal and respiratory acid-base regulation systems interact with each other, one compensating (partially) for a primary defect of the other. Most investigators striving to typify compensations for abnormal acid-base balance have reported their findings in terms of arterial pH, PaCO2, and/or HCO3-. However, pH and HCO3- are both altered by both respiratory and metabolic changes. We sought to simplify these relations by expressing them in terms of standard base excess (SBE in mM), which quantifies the metabolic balance and is independent of PaCO2.

Design: Meta-analysis.

Setting: Historical synthesis developed via the Internet.

Patients: Arterial pH, PaCO2, and/or HCO3- data sets were obtained from 21 published reports of patients considered to have purely acute or chronic metabolic or respiratory acid-base problems.

Interventions: We used the same data to compute the typical compensatory responses to imbalances of SBE and PaCO2. Relations were expressed as difference (delta) from normal values for PaCO2 (40 torr [5.3 kPa]) and SBE (0 mM).

Measurements And Main Results: The data of patient compensatory changes conformed to the following equations, as well as to the traditional PaCO2 vs. HCO3- or H+ vs. PaCO2 equations: Metabolic change responding to change in PaCO2: Acute deltaSBE = 0 x deltaPaCO2, hence: SBE = 0, Chronic deltaSBE = 0.4 x deltaPaCO2. Respiratory change responding to change in SBE: Acidosis deltaPaCO2 = 1.0 x deltaSBE, Alkalosis deltaPaCO2 = 0.6 x deltaSBE.

Conclusion: Data reported by many investigators over the past 35 yrs on typical, expected, or "normal" human compensation for acid-base imbalance may be expressed in terms of the independent variables: PaCO2 (respiratory) and SBE (metabolic).