Metabolic acidosis.
Metabolic acidosis occurs in a number of diseases and even certain normal activities such as heavy exercise. It arises from increased endogenous acid production, exogenous acid (or acid-precursor) administration, base losses, and depression of renal acid secretion. Although the magnitude of acidosis is important, the ultimate pathophysiological impact of any metabolic acidosis is defined by the rate of change and the specific cause of the acidosis. This review discusses whole body, organ, and cellular effects of metabolic acidosis, its diagnosis by pathophysiologic categories, and treatment. The diagnosis is made by a synthesis of the clinical history, physical examination, other hematological values, serum and urinary chemistries, and arterial blood gases and electrolytes. Calculation of the anion and osmolal gaps can be effectively used to further narrow the diagnostic possibilities. Supportive care and therapy directed at the cause of the metabolic acidosis are the mainstays of treatment, since most acidotic states will spontaneously correct once the initiating cause is removed or reversed. Theoretical and clinical evidence are discussed for alkalinizing agents, whose use remains controversial except in the treatment of metabolic acidosis associated with hyperkalemia and certain drug or toxin ingestions.
Swenson
E R
ER
School of Medicine, University of Washington, Seattle, USA. eswenson@u.washington.edu
D000138:Acidosis / Q000175:diagnosis / Q000503:physiopathology* / Q000628:therapy; D000141:Acidosis, Renal Tubular / Q000503:physiopathology; D001639:Bicarbonates / Q000008:administration & dosage / Q000378:metabolism / Q000627:therapeutic use; D002021:Buffers; D002712:Chlorides / Q000378:metabolism; D006801:Humans; D006985:Hyperventilation; D012720:Severity of Illness Index; D013217:Starvation / Q000503:physiopathology
D001639:Bicarbonates; D002021:Buffers; D002712:Chlorides