Invited commentary: Putting standard base excess to the test

Abstract

The interface between acid-base physiology and blood gas interpretation is historically both stimulating and turbulent [1]. In 2009, most clinicians accept a bimodal categorization of acid-base disorders as either “respiratory” or “metabolic,” with arterial PCO2 (PaCO2) as the primary index of respiratory acid-base status. However, even today, there is no agreed method of defining and quantifying the metabolic component. An important milestone was passed nearly 50 years ago with the advent of “base excess” (BE), introduced by Siggaard-Andersen and Engel [2] after a series of experiments on the blood of Danish volunteers. Base excess was promoted as the ultimate measure of metabolic acid-base status. The subsequent debate was divisive [3], with practitioners separating into 2 “schools,” Boston or Copenhagen. Base excess became the flagship of the Copenhagen school. Base excess is determined from measurements of plasma pH, blood PCO2, and hemoglobin concentration. It can be defined as the concentration of titratable hydrogen ion required to return the pH of in vitro whole blood to 7.4 at 37°C, with PCO2 held at 40 mm Hg. For the first 17 years, BE was calculated empirically from the Danish nomogram. Then, Siggaard-Andersen [4] published a new equation, derived from expressions linking plasma and intraerythrocytic buffering and associated Gibbs-Donnan ionic distributions. He named it the Van Slyke equation, in honor of the American clinical chemist and acid-base pioneer, Donald Dexter Van Slyke. A prerequisite for any stand-alone metabolic acid-base parameter is “CO2 invariance.” By this, we mean that pure respiratory acid-base fluctuations have no distorting effect. Unfortunately, although the Van Slyke equation displays admirable CO2 invariance when applied to blood ex vivo [5], it falls short in the living patient [6]. The problem is that neither the nomogram nor the subsequent Van Slyke