Integration of acid-base and electrolyte disorders.

Copyright © 2014 Massachusetts Medical Society. This review describes a method of analyzing acid–base disorders that incorporates insights from the traditional, bicarbonate-centered model and the Stewart (or strong ion) model (Table 1).1-6 Acid–base balance and electrolyte homeostasis are intricately connected at the cellular level and in clinical disorders. This article emphasizes the integration of the principles of mass balance and electroneutrality — which are prominently featured in the strong ion model (also known as the physicochemical model) — for interpretation of acid–base phenomena. Most acid–base abnormalities can be diagnosed and interpreted with the use of the traditional approach. Why, then, should the strong ion theory be incorporated into teaching about acid–base balance? Although the Stewart model is not primarily a mathematical expression of a confirmed reality, it is relevant because it is a powerful construct that can shed light on an important biologic system. Included in this article are several case vignettes that show the explanatory power of the strong ion approach in clinical practice. Some of these examples have been presented in a companion article on the physiological approach to acid–base balance by Berend et al.7 Other cases that are interpreted with a strong ion approach are included in the Supplementary Appendix, available with the full text of this article at NEJM.org. The more complex chemistry of the hydrogen-ion concentration in intracellular and extracellular fluid compartments is beyond the scope of this article.

[1]  A. D. de Vries,et al.  Physiological approach to assessment of acid-base disturbances. , 2015, The New England journal of medicine.

[2]  R. Luke,et al.  It is chloride depletion alkalosis, not contraction alkalosis. , 2012, Journal of the American Society of Nephrology : JASN.

[3]  F. Gennari Pathophysiology of metabolic alkalosis: a new classification based on the centrality of stimulated collecting duct ion transport. , 2011, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[4]  R. Rodby,et al.  Unexpectedly Severe Metabolic Acidosis Associated with Sodium Thiosulfate Therapy in a Patient with Calcific Uremic Arteriolopathy , 2011, Seminars in dialysis.

[5]  R. Omron,et al.  A Physicochemical Model of Crystalloid Infusion on Acid-Base Status , 2010, Journal of intensive care medicine.

[6]  N. Madias,et al.  Assessing acid-base disorders. , 2009, Kidney international.

[7]  B. Koeppen The kidney and acid-base regulation. , 2009, Advances in physiology education.

[8]  V. Chadha,et al.  Hereditary renal tubular disorders. , 2009, Seminars in nephrology.

[9]  J. Kraut,et al.  Acid-base analysis: a critique of the Stewart and bicarbonate-centered approaches. , 2008, American journal of physiology. Renal physiology.

[10]  G. Perez,et al.  Acid-base disturbances in gastrointestinal disease , 1987, Digestive Diseases and Sciences.

[11]  H. Corey Stewart and beyond: new models of acid-base balance. , 2003, Kidney international.

[12]  J. I. Logan,et al.  Milk alkali syndrome. , 2002, The Ulster medical journal.

[13]  J. Waters,et al.  Normal Saline Versus Lactated Ringer’s Solution for Intraoperative Fluid Management in Patients Undergoing Abdominal Aortic Aneurysm Repair: An Outcome Study , 2001, Anesthesia and analgesia.

[14]  S. Nielsen,et al.  The renal thiazide-sensitive Na-Cl cotransporter as mediator of the aldosterone-escape phenomenon. , 2001, The Journal of clinical investigation.

[15]  P. Constable,et al.  A simplified strong ion model for acid-base equilibria: application to horse plasma. , 1997, Journal of applied physiology.

[16]  M. Halperin,et al.  Glue-sniffing and distal renal tubular acidosis: sticking to the facts. , 1991, Journal of the American Society of Nephrology : JASN.

[17]  V. Fencl,et al.  Acid-base disorders in critical care medicine. , 1989, Annual review of medicine.

[18]  D. Batlle,et al.  The use of the urinary anion gap in the diagnosis of hyperchloremic metabolic acidosis. , 1988, The New England journal of medicine.

[19]  E. Weinman,et al.  Parathyroid hormone and dibutyryl cAMP inhibit Na+/H+ exchange in renal brush border vesicles. , 1985, The American journal of physiology.

[20]  R. Narins,et al.  The role of the anion gap in detecting and managing mixed metabolic acid-base disorders. , 1984, Clinics in endocrinology and metabolism.

[21]  N. Madias,et al.  Hypochloremia as a consequence of anion gap metabolic acidosis. , 1984, The Journal of laboratory and clinical medicine.

[22]  P A Stewart,et al.  Modern quantitative acid-base chemistry. , 1983, Canadian journal of physiology and pharmacology.

[23]  M. Oh,et al.  The anion gap. , 1977, The New England journal of medicine.

[24]  R. Narins,et al.  Clinical use of the anion gap. , 1977, Medicine.

[25]  F. Rector,et al.  Symposium on acid-base homeostasis. The generation and maintenance of metabolic alkalosis. , 1972, Kidney international.

[26]  J. Fordtran Organic anions in fecal contents. , 1971, The New England journal of medicine.

[27]  J. Gamble Sodium and chloride and acid-base physiology. , 1960, Bulletin of the Johns Hopkins Hospital.

[28]  William B. Schwartz,et al.  The Effect of DOCA on Electrolyte Balance in Normal Man and its Relation to Sodium Chloride Intake * , 1952, The Yale journal of biology and medicine.