Approach to the adult with metabolic acidosis
- Michael Emmett, MD
Michael Emmett, MD
- Editor-in-Chief — Nephrology
- Section Editor — Fluid and Electrolytes
- Chief of Internal Medicine
- Baylor University Medical Center
- Harold Szerlip, MD, FACP, FCCP, FASN, FNKF
Harold Szerlip, MD, FACP, FCCP, FASN, FNKF
- Director, Nephrology Division, Baylor University Medical Center, Dallas
- Program Director, Nephrology Training Program, Baylor University Medical Center
- Clinical Professor of Medicine, Texas A&M College of Medicine
- Adjunct Professor of Medicine, Texas College of Osteopathic Medicine
On a typical Western diet, approximately 15,000 mmol of carbon dioxide (which can generate carbonic acid as it combines with water) and 50 to 100 meq of nonvolatile acid (mostly sulfuric acid derived from the metabolism of sulfur-containing amino acids) are produced each day. Acid-base balance is maintained by pulmonary and renal excretion of carbon dioxide and nonvolatile acid, respectively.
Renal excretion of acid involves the combination of hydrogen ions with urinary titratable acids, particularly phosphate (HPO42- + H+ —> H2PO4-), and ammonia to form ammonium (NH3 + H+ —> NH4+) . The latter is the primary adaptive response since ammonia production from the metabolism of glutamine can be appropriately increased in response to an acid load .
Acid-base balance is usually assessed in terms of the bicarbonate-carbon dioxide buffer system:
Dissolved CO2 + H2O <—> H2CO3 <—> HCO3- + H+
The ratio between these reactants can be expressed by the Henderson-Hasselbalch equation. By convention, the pKa of 6.10 is used when the dominator is the concentration of dissolved CO2, and this is proportional to the pCO2 (the actual concentration of the acid H2CO3 is very low):
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- DEFINITION AND PATHOGENESIS
- - Increased acid generation
- - Loss of bicarbonate
- - Diminished renal acid excretion
- - Dilution acidosis
- DIAGNOSIS AND EVALUATION
- - Measurement of the arterial pH and pCO2
- - Determination of whether respiratory compensation is appropriate
- - Assessment of the serum anion gap
- Physiologic interpretation of the serum anion gap
- Causes of elevated anion gap metabolic acidosis
- Causes of hyperchloremic (normal anion gap) metabolic acidosis
- Combined elevated anion gap and hyperchloremic acidoses
- OVERVIEW OF THERAPY
- General approach and rationale
- Dosing of alkali therapy (when given)
- - Bicarbonate
- - Tromethamine
- - The virtual bicarbonate distribution space
- SUMMARY AND RECOMMENDATIONS