Base excess (BE) was introduced by Siggaard-Andersen in 1960 as an answer to the forty-year-long quest for a reliable, stand-alone marker of metabolic acidosis/alkalosis, independent from co-existing respiratory derangements, and able to quantify the severity of the disorder [1]. Previously, several parameters had been examined. The first was actual bicarbonate (HCO₃⁻) [2], which was quickly discarded due to its known dependency on the partial pressure of CO₂ (PCO₂). To eliminate the respiratory component, standard bicarbonate (HCO₃⁻(st)) was introduced, representing the plasma bicarbonate concentration after equilibration at a PCO₂ of 40 mmHg [3]. Although this was certainly a step forward, HCO₃⁻(st) does not take into account the buffer effect of weak non-carbonic acids, i.e. proteins, which normally contribute to buffering with 14–16 negative charges (A⁻) per liter. Indeed, when a strong acid is added to blood, both HCO₃⁻ and A⁻ concentrations will be reduced. In an open system, which is the case of a subject properly regulating PCO₂ through breathing, carbonic buffers have a predominant role (about 75–80%), however, non-carbonic buffers cannot be disregarded completely. Therefore, the difference between HCO₃⁻(st) and the ideal, “normal” bicarbonate value, slightly underestimates the acid/base added to the system (e.g. the addition of 10 mmol/L of a strong acid to blood with HCO₃⁻ of 24 mmol/L could result in an HCO₃⁻(st) of 16 mmol/L, instead of 24–10 = 14 mmol/L). To overcome this problem, Singer and Hastings introduced the buffer base (BB), the sum of all buffer anions.