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      Whither the Bicarbonate Era

      1 , *

      American Journal of Respiratory and Critical Care Medicine

      American Thoracic Society

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          Abstract

          To the Editor: For metabolic acidosis, beyond treating the underlying cause, correcting hypoxemia, and establishing good perfusion, sodium bicarbonate is often given at variable arbitrary thresholds of depressed blood pH. Recently, Zanella and colleagues (1) employed extracorporeal removal of chloride by electrodialysis in healthy pigs made acidemic by either lactic acid infusion or hypoventilation (CO2 retention). By physically drawing off chloride and establishing a local separation of charge, blood electroneutrality at the membrane is immediately reestablished by the hydrolysis of water to yield a hydroxyl ion that instantly combines with CO2 to form bicarbonate. The authors show the feasibility of quantitatively increasing bicarbonate in this fashion for both forms of acidosis without the associated and unwanted hypernatremia and volume loading that can occur with intravenous sodium bicarbonate administration. The accompanying editorialists (2) proclaim the postbicarbonate era with this study that illustrates a major tenet of the Stewart approach to acid–base chemistry and its superiority over other approaches to understanding acid–base physiology and pathophysiology. In Stewart’s paradigm, H+, OH−, HCO3 −, and CO3 2− are relegated to the status of dependent variables; that is, they can only be formed from the differential movements and exchanges of independent strong ions (Na+, K+, and Cl−) that disturb electroneutrality, which is immediately corrected by the hydrolysis of water and reaction with CO2. Although the heuristics of the Stewart analysis are valid, I remain unconvinced by the claim that what the mathematics of this approach reveal demands that physiology must follow these rules and conclusions. The assumption that only strong ions and their differential movement from one space to another alters H+ and HCO3 − concentrations because the math is consistent with it goes against all we know about numerous cell-membrane transporters that use H+, HCO3 −, or CO3 2− as coions or counterions with Na+, K+, and Cl− (3). There has been no identification of a Na+/Cl− antiporter or an electrogenic Na+-Cl cotransporter that will alter local electroneutrality to create or consume the supposed dependent variables. Simply because one can electrodialyze chloride by brute force, as Zanella and colleagues (4) report, does not mean it happens in vivo at the microscopic level. Clinical adoption of the Stewart approach has shown no superiority to conventional approaches (4–6), and the measurement of all the strong ions repeatedly is wasteful and costly, risks measurement errors that beget more testing, contributes to anemia in many patients, contributes to more transfusions, and is very difficult to teach to trainees and even seasoned clinicians.

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          Most cited references 6

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          Comparison of three different methods of evaluation of metabolic acid-base disorders.

          The Stewart approach states that pH is primarily determined by Pco2, strong ion difference (SID), and nonvolatile weak acids. This method might identify severe metabolic disturbances that go undetected by traditional analysis. Our goal was to compare diagnostic and prognostic performances of the Stewart approach with a) the traditional analysis based on bicarbonate (HCO3) and base excess (BE); and b) an approach relying on HCO3, BE, and albumin-corrected anion gap (AGcorrected). Prospective observational study. A university-affiliated hospital intensive care unit (ICU). Nine hundred thirty-five patients admitted to the ICU. None. The Stewart approach detected an arterial metabolic alteration in 131 (14%) of patients with normal HCO3- and BE, including 120 (92%) patients with metabolic acidosis. However, 108 (90%) of these patients had an increased AGcorrected. The Stewart approach permitted the additional diagnosis of metabolic acidosis in only 12 (1%) patients with normal HCO3, BE, and AGcorrected. On the other hand, the Stewart approach failed to identify 27 (3%) patients with alterations otherwise observed with the use of HCO3-, BE, and AGcorrected (16 cases of acidosis and 11 of alkalosis). SID and BE, and strong ion gap (SIG) and AGcorrected, were tightly correlated (R2 = .86 and .97, p < .0001 for both) with narrow 95% limits of agreement (8 and 3 mmol/L, respectively). Areas under receiver operating characteristic curves to predict 30-day mortality were 0.83, 0.62, 0.61, 0.60, 0.57, 0.56, and 0.67 for Sepsis-related Organ Failure Assessment (SOFA) score, SIG, AGcorrected, SID, BE, HCO3-, and lactates, respectively (SOFA vs. the rest, p < .0001). In this large group of critically ill patients, diagnostic performance of the Stewart approach exceeded that of HCO3- and BE. However, when AGcorrected was included in the analysis, the Stewart approach did not offer any diagnostic or prognostic advantages.
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            Acid-base analysis: a critique of the Stewart and bicarbonate-centered approaches.

            When approaching the analysis of disorders of acid-base balance, physical chemists, physiologists, and clinicians, tend to focus on different aspects of the relevant phenomenology. The physical chemist focuses on a quantitative understanding of proton hydration and aqueous proton transfer reactions that alter the acidity of a given solution. The physiologist focuses on molecular, cellular, and whole organ transport processes that modulate the acidity of a given body fluid compartment. The clinician emphasizes the diagnosis, clinical causes, and most appropriate treatment of acid-base disturbances. Historically, two different conceptual frameworks have evolved among clinicians and physiologists for interpreting acid-base phenomena. The traditional or bicarbonate-centered framework relies quantitatively on the Henderson-Hasselbalch equation, whereas the Stewart or strong ion approach utilizes either the original Stewart equation or its simplified version derived by Constable. In this review, the concepts underlying the bicarbonate-centered and Stewart formulations are analyzed in detail, emphasizing the differences in how each approach characterizes acid-base phenomenology at the molecular level, tissue level, and in the clinical realm. A quantitative comparison of the equations that are currently used in the literature to calculate H(+) concentration ([H(+)]) is included to clear up some of the misconceptions that currently exist in this area. Our analysis demonstrates that while the principle of electroneutrality plays a central role in the strong ion formulation, electroneutrality mechanistically does not dictate a specific [H(+)], and the strong ion and bicarbonate-centered approaches are quantitatively identical even in the presence of nonbicarbonate buffers. Finally, our analysis indicates that the bicarbonate-centered approach utilizing the Henderson-Hasselbalch equation is a mechanistic formulation that reflects the underlying acid-base phenomenology.
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              Extracorporeal Chloride Removal by Electrodialysis. A Novel Approach to Correct Acidemia

              Rationale: Acidemia is a severe condition among critically ill patients. Despite lack of evidence, sodium bicarbonate is frequently used to correct pH; however, its administration is burdened by several side effects. We hypothesized that the reduction of plasma chloride concentration could be an alternative strategy to correct acidemia.Objectives: To evaluate feasibility, safety, and effectiveness of a novel strategy to correct acidemia through extracorporeal chloride removal by electrodialysis.Methods: Ten swine (six treated and four control animals) were sedated, mechanically ventilated and connected to an extracorporeal electrodialysis device capable of selectively removing chloride. In random order, an arterial pH of 7.15 was induced either through reduction of ventilation (respiratory acidosis) or through lactic acid infusion (metabolic acidosis). Acidosis was subsequently sustained for 12-14 hours. In treatment pigs, soon after reaching target acidemia, electrodialysis was started to restore pH.Measurements and Main Results: During respiratory acidosis, electrodialysis reduced plasma chloride concentration by 26 ± 5 mEq/L within 6 hours (final pH = 7.36 ± 0.04). Control animals exhibited incomplete and slower compensatory response to respiratory acidosis (final pH = 7.29 ± 0.03; P < 0.001). During metabolic acidosis, electrodialysis reduced plasma chloride concentration by 15 ± 3 mEq/L within 4 hours (final pH = 7.34 ± 0.07). No effective compensatory response occurred in control animals (final pH = 7.11 ± 0.08; P < 0.001). No complications occurred.Conclusions: We described the first in vivo application of an extracorporeal system targeted to correct severe acidemia by lowering plasma chloride concentration. Extracorporeal chloride removal by electrodialysis proved to be feasible, safe, and effective. Further studies are warranted to assess its performance in the presence of impaired respiratory and renal functions.
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                Author and article information

                Journal
                Am J Respir Crit Care Med
                Am. J. Respir. Crit. Care Med
                ajrccm
                American Journal of Respiratory and Critical Care Medicine
                American Thoracic Society
                1073-449X
                1535-4970
                15 September 2020
                15 September 2020
                15 September 2020
                15 September 2020
                : 202
                : 6
                : 906-907
                Affiliations
                [ 1 ]University of Washington

                Seattle, Washington
                Author notes
                [* ]Corresponding author (e-mail: eswenson@ 123456uw.edu ).
                Article
                202005-1544LE
                10.1164/rccm.202005-1544LE
                7491393
                Copyright © 2020 by the American Thoracic Society

                This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial No Derivatives License 4.0 ( http://creativecommons.org/licenses/by-nc-nd/4.0/). For commercial usage and reprints, please contact Diane Gern ( dgern@ 123456thoracic.org ).

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