Standard base excess is the concentration of titrable base when the blood is titrated back to a normal plasma pH of 7.40, at a normal pCO2 ( 40 mmHg) and 37° C, at the actual oxygen saturation, AND at an "anaemic" haemoglobin concentration, to account for the buffering of extravascular fluid by haemoglobin. It is reported as cBase(Ecf), to reflect the fact that the entirety of the extracellular fluid is under investigation here.
In summary, it is the actual base excess adjusted to a Hb level of around 50g/L.
This equation takes the actual base excess, and modifies it to incorporate a "dilute" haemoglobin concentration (in mmol/L).
Recall the nightmarish swamp of mathematics required for the calculation of actual base excess:
Now, for the calculation of standard base excess, the ctHb level is supplied rather than measured. It is artificially set as 3mmol/L by the local unit.
The utility of this stems from the clinical need for an accurate estimation of buffering.
After all, the blood represents only a fraction of the body fluid, and is therefore an inaccurate representation of whole-body buffering. Who cares what goes on there? You want to know what buffer is available in the fluid which actually surrounds the cells. An estimate of extracellular buffering capacity is thus estimated by using a dilute haemoglobin value in the equation; after all haemoglobin is not present in the extracellular fluid. One needs to compensate for the presence of all that extra water sloshing around.
The haemoglobin level is selected as an accurate representation of the "dilution" of haemoglobin when all the extracellular fluid is taken into account. Obviously, this all falls apart in the ICU. Our patients have wildly deranged fluid compartments, usually grossly distended with an abnormally enlarged extravascular volume. The normal correction factor for haemoglobin dilution is never going to be accurate in such a setting.
Furthermore, the CO2 tends to equilibrate into the extracellular fluid, and the equation does not account for this distribution. With this, the Van Slyke method tends to produce slight errors as the pCO2 changes.
That said, the SBE, unlike actual base excess (ABE), is extremely stable over wide ranges of PCO2.
Additionally, the Van Slyke equation does not factor in the concentrations of phosphate and albumin, which play a role in the acid-base balance. The concentration of phosphate and albumin are frequently abnormal in the ICU; in fact it is unusual to see somebody with a totally normal albumin there. Various others have proposed modifications to the Van Slyke equation which would incorporate correction factors for these discrepancies, but thus far this has not percolated into the ABG machine algorithms.
So, what is the point, one might ask? Specifically, why would it matter whether one has an actual base excess measurement, or a standard base excess measurement? Surely the ABE is good enough?
Well. There is a specific bedside use for the SBE for which the ABE is not validated, and that is the assessment of compensation using Copenhagen rules. The ABE cannot be used to determine whether the CO2 level is appropriate for a given metabolic acid-base disturbance; the papers on this topic were all published with the SBE in mind.
The issues involved in using various bedside rules to assess compensation are the topic of the next chapter.