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This is a challenging question that few people answer correctly! Most anesthesiologists do not know that in the Stewart approach, bicarbonate is NOT an independent determinant of pH. The Stewart approach to acid base, first described in 1981, is an alternative to the Henderson-Hasselbach approach taught to most medical students. The Henderson-Hasselbach equation describes the associative relationship between pH, HCO3-, and pCO2, but is NOT a causal relationship. It was developed approximately 100 years ago in order to give clinicians an easy way to estimate pH (which is relatively difficult to measure directly). The problem with the Henderson-Hasselbach equation is that, while mathematically correct, it is often misinterpreted to imply that pH is dependent on HCO3-. In fact, it can be proven (as Stewart did) that there are only three mathematically independent variables on which pH depends - the strong ion difference (SID), the total weak acid concentration, and pCO2. SID is equal to the difference between all completely associated cations (sodium, potassium, magnesium, calcium) and anions (chloride, lactate). The total weak acid is the sum of phosphate and albumin. There is a non-linear relationship between SID and pH. The reason that sodium bicarbonate increases pH is not because of the bicarbonate per se, but because the strong ion difference of sodium bicarbonate is positive (sodium is a strong cation, bicarbonate is a weak anion). Administration of any agent with a positive SID (e.g. calcium gluconate) will increase pH, whereas administration of any agent with an SID of zero or less (e.g. calcium chloride, sodium chloride) will decrease pH. The normal SID in a healthy person is 40-44 mEq/L. The kidneys respond to metabolic acidosis by attempting to increase the strong ion difference (which will increase pH). This can be accomplished by retaining sodium bicarbonate as well as by excreting ammonium (NH4+) chloride. Traditionally we are taught that NaHCO3 retention is the primary mechanism for combating a metabolic acidosis but this is limited by the important role that sodium plays in the regulation of intravascular volume (similarly, K+ is crucial from an electrophysiological standpoint, thus retention of KHCO3 is not an ideal means of maintaining pH). Chloride, by contrast, is a relatively unimportant ion and exists in large quantities, thus making it an ideal candidate to pair with a weak cation for the regulation of pH. The pKa of NH4+ is 9.25, thus it behaves as a weak cation. In the setting of a metabolic acidosis, the kidneys will excrete NH4Cl, which increases the serum SID and increases pH. The urine SID (also known as the urine anion gap [UAG]) is equal to urine sodium plus urine potassium minus urine chloride and urine and is an estimate of the amount of NH4+ excreted. Thus, in the setting of a metabolic acidosis with appropriate renal compensation, UAG will be negative (which reflects the NH4+ excreted). A positive UAG in the setting of metabolic acidosis suggests a renal component to the acid-base abnormality (e.g. renal tubular acidosis).