title: Acute acid-base disorders. 2. Specific disturbances.
abstract: Evaluation of the acid-base status of the body requires measurement of bicarbonate (total carbon dioxide) concentration, pH, and partial pressure of CO2 in arterial blood. Calculation of standard bicarbonate and base excess or deficit is not necessary. The normal concentration of free hydrogen ions (H+) is approximately 40 millimoles/liter, which is equivalent to a pH of 7.4. The normal load of fixed acids is 50 to 80 millimoles in 24 hours. A steady state is maintained by excretion of an equal amount of H+ by the kidneys, which at the same time regenerate bicarbonate to replenish buffer stores. Renal excretion of H+ is in the form of titratable acid and ammonium. Synthesis of ammonia can increase severalfold under the stimulus of acidosis. This is the chief mechanism of long-term compensation. Metabolic acidosis can be due to an excessive acid load (endogenous or exogenous), impaired renal excretion of H+, or bicarbonate loss. Determination of the "anion gap" (unmeasured anions) helps to establish the mechanism of acidosis. Acidosis with a normal anion gap is due to either bicarbonate loss or ingestion of certain chloride salts. A gap larger than normal indicates the presence in the body of acids other than acidfying chloride salts. Management of metabolic acidosis requires accurate diagnosis, clear understanding of the mechansim, and individualized treatment. Metabloic alkalosis is due to loss of H+ (usually from stomach or kidneys) or ingestion of alkali. Measurement of urinary chloride helps establish the mechanism of alkalosis. In saline-responsive alkalosis, the urinary chloride level is very low. This is usually due to gastric loss of H+, and the condition responds to administration of saline solution. When the urinary chloride level is only moderately low, the alkalosis is probably not due to gastric loss of H+. This form of alkalosis (saline-resistant) does not respond well to administration of saline solution and requires use of potassium in treatment. Apprpriate compensatory responses to acidosis or alkalosis are critical to survival. Compensation for metabloic acidosis consists of hyperventilation and enhanced renal excretion of H+, chiefly as ammonium. In metabolic alkalosis, compensation is mainly renal excretion of bicarbonate. Respiratory acidosis is due to alveolar hypoventilation. In chronic situations, a compensatory rise in serum bicarbonate concentration is expected. Management consists of treatment of the cause of hypoventilation. Respiratory alkalosis is due to hyperventilation. Treatment requires identification and correction of the cause of hyperventilation.
mesh_terms: D000137:Acid-Base Imbalance / Q000175:diagnosis / Q000209:etiology; D000138:Acidosis / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D000142:Acidosis, Respiratory / Q000503:physiopathology; D000208:Acute Disease; D000468:Alkalies / Q000627:therapeutic use; D000471:Alkalosis / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D000472:Alkalosis, Respiratory / Q000503:physiopathology; D000641:Ammonia / Q000378:metabolism; D000838:Anions; D001639:Bicarbonates / Q000627:therapeutic use; D002712:Chlorides / Q000652:urine; D006801:Humans; D007668:Kidney / Q000503:physiopathology
chemical_list: D000468:Alkalies; D000838:Anions; D001639:Bicarbonates; D002712:Chlorides; D000641:Ammonia