Clinical acid-base disorders: Traditional versus “new” analytical models

Abstract

To the Editor: I have taught acid-base physiology to medical students, residents, fellows, and practicing clinicians for many years. Although this is often an initially confusing topic for many of these individuals, after several lectures, a few case examples, and some practical experience, most are soon able to successfully dissect even very complex mixed acid-base disorders. Measurements of arterial pH, pCO2, and calculated or measured HCO3, together with calculation of the anion gap and knowledge of several empiric compensation rules, allows most clinicians to fully explain virtually all acid-base perturbations. Over the past few decades a number of “new” approaches have been proposed, including “whole-blood buffer base” of Singer and Hastings and “standard bicarbonate” and “base excess” of Astrup. In a recent perspective discussion, Corey [1.Corey H.E. Stewart and beyond: New models of acid-base balance.Kidney Int. 2003; 64: 777-787Abstract Full Text Full Text PDF PubMed Scopus (141) Google Scholar] claims that a now classic editorial by Schwartz and Relman [2.Schwartz W.B. Relman A. A critique of the parameters used in the evaluation of acid-base disorders. “Whole-blood buffer base” and standard bicarbonate” compared with blood pH and plasma bicarbonate concentration.N Engl J Med. 1963; 268: 1382-1388Crossref PubMed Scopus (85) Google Scholar] concluded “… base excess has conquered its rivals to form the cornerstone of standard clinical acid-base chemistry.” The editorial actually says the opposite! Indeed, it concludes that “the traditional measurements of pH, pCO2, and plasma bicarbonate concentration continue to be the most reliable biochemical guides in the analysis of acid-base disturbances.” More recently, a number of clinicians, including Corey, have suggested we adopt the “Stewart” approach, which analyzes three “independent variables:”“strong ion difference,”“total weak acids,” and pCO2. The Stewart approach may be mathematically correct but I believe it adds little to the clinical interpretation of acid-base disorders and markedly increases complexity. It is claimed that the “Stewart” approach elucidates certain complex disorders, yet I have still not encountered a case where this is true. For example, Corey presents the following case: “a critically ill patient with septic shock and multiple organ failure … on cardiopressors, mechanical ventilation, antibiotics, and large volumes of normal saline. Na 130, K 3.0, Cl 111, albumin 1.5 g%, phosphate 2.0 mg%, HCO3= 9.25, pCO2= 30, pH = 7.1.” My interpretation is—metabolic acidosis with inadequate respiratory compensation (respiratory acidosis). The anion gap is about 10 (I prefer the equation AG = Na – (HCO3+ Cl)). His albumin is reduced to 1.5 g% so his “baseline” anion gap should be about 4. The AG is therefore increased by about 6 and would account for a portion of the fall in HCO3 (from 24 to about 18). His chloride concentration is also increased relative to sodium and explains the rest of the fall in HCO3 (from 18 to 9). The “traditional” approach therefore says the patient has an anion gap metabolic acidosis (probably lactic), a hyperchloremic metabolic acidosis (possibly diarrhea, renal tubular, and/or a component of “NaCl expansion”), and respiratory acidosis due to lung and/or brain dysfunction. Therefore, I strongly disagree with Corey's statement “… that the traditional model offers no further insight into the mechanism of the acid-base disorder.” Indeed, what does the “Stewart” approach add to my analysis? It may be mathematically correct, but it is bound to introduce further confusion to an already confusing area of medicine. Einstein said “Make everything as simple as possible, but not simpler,” and I would add a corollary, “Don't needlessly make things more complex than they need to be.”