Clinical Approach to Assessing Acid-Base Status: Physiological vs Stewart

Arterial Blood Gases and Acid–Base Regulation

“…The base excess (BE) concept was developed in response to some of above limitations, since it includes nonbicarbonate buffering and deals with the effects of PCO 2 changes (respiratory acid-base changes) on bicarbonate. 7 It estimates how much strong acid or alkali must be added to titrate fully oxygenated blood to a pH of 7.4 at 37°C and at the hemoglobin concentration in that sample. The "standard" BE uses a hemoglobin value of 5 g/dL (one-third of a normal hemoglobin of 15 g/dL) since buffering by hemoglobin occurs throughout the entire extracellular space (intravascular and interstitial) not just the intravascular compartment, which is only one-third of the total extravascular space.…”

Acid–Base Analysis in the Operating Room: A Bedside Stewart Approach

“…In contrast, bicarbonate-based approaches cannot easily explain this inverse relationship between plasma albumin and bicarbonate despite advocates recommending correcting the anion gap for decreased albumin. 10 Further, studies of ICU patients, including postoperative patients, conclude that the Stewart approach can be superior in detecting important acid-base changes despite patient pH being in the reference range (7.35 to 7.45) [11][12][13] and no apparent acid-base disorder using bicarbonate or base excess analysis (example 4 in Box 4). In this review focusing on clinical anesthesia, I am proposing a simplified Stewart approach that incorporates base excess because it is associated with greater insight into the underlying causes including some masked by other processes.…”

“…The Stewart acid-base approach challenges the mainstream bicarbonate paradigm and is viewed by some as almost heretical. 10 Unfortunately, limitations of Stewart's original work include underreferencing, unfamiliar ideas such as strong ion difference, and an intimidating fourthorder polynomial equation derived from six simultaneous equations that combines all the factors to describe acidbase status in a fluid compartment, which is unsuitable for easy clinical application. 2 In line with concepts proposed George Box, the aim of our group and others 14,24 Added conclusion: relative hyperchloremic acidosis with added acidosis from hyperalbuminemia, both consistent with 5% albumin therapy.…”

“…7 Like the Stewart approach, the anion gap relies on the principle of plasma electroneutrality: sum of cations = sum of anions. For the last 30 yr, many have recommended correcting the anion gap for decreased albumin 10,34 when analyzing metabolic acidosis (examples 1 and 3 in Boxes 1 and 3).…”

“…In the presence of hypoalbuminemia, the correction calculation for the anion gap is the same as estimating for the albumin effect on base excess: 0.25 × (42 – albumin, g/l). 10,27,29 A less apparent point is that due to effects on both base excess and the anion gap, hypoalbuminemia can mask acidosis 13 from causes including relative hyperchloremia, increased lactate, and other ions (example 2 in Box 2). For any patient with hypoalbuminemia, the severity of acidifying strong ion and weak acids changes is masked.…”