HUMAN PACO2 AND STANDARD BASE EXCESS COMPENSATION FOR ACID-BASE IMBALANCE

Objectives: Renal and respiratory acid-base regulation systems interac t with each other, one compensating (partially) for a primary defect o f the other. Most investigators striving to typify compensations for a bnormal acid-base balance have reported their findings in terms of art erial pH, Paco(2), and/or HCO3-. However, pH and HCO3- are both altere d by both respiratory and metabolic changes, We sought to simplify the se relations by expressing them in terms of standard base excess (SBE in mM), which quantifies the metabolic balance and is independent of P aco(2). Design: Meta-analysis, Setting: Historical synthesis developed via the Internet, Patients: Arterial pH, Paco(2), and/or HCO3- data s ets were obtained from 21 published reports of patients considered to have purely acute or chronic metabolic or respiratory acid-base proble ms, Interventions: We used the same data to compute the typical compen satory responses to imbalances of SEE and Paco(2). Relations were expr essed as difference (Delta) from normal values for Paco(2) (40 torr [5 .3 kPa]) and SEE (0 mM). Measurements and Main Results: The data of pa tient compensatory changes conformed to the following equations, as we ll as to the traditional Paco(2) vs. HCO3- or H+ vs, Paco(2) equations : Metabolic change responding to change in Paco(2): Acute Delta SBE = 0 x Delta Paco(2) hence: SEE = 0 Chronic Delta SBE = 0.4 x Delta Paco< INF>2 Respiratory change responding to change in SEE: Acidosis Delta P aco?(2</INF> = 1.0 x Delta SBE Alkalosis Delta Paco(2) = 0.6 x Delta S BE Conclusion: Data reported by many investigators over the past 35 yr s on typical, expected, or ''normal'' human compensation for acid-base imbalance may be expressed in terms of the independent variables: Pac o(2) (respiratory) and SEE (metabolic).