Effects
     Characteristically causes metabolic acidosis mixed with a respiratory alkalosis
     Stimulates respiratory center -> Tachypnea -> RESPIRATORY ALKALOSIS
     Anion-gap METABOLIC ACIDOSIS by a threefold mechanism
          1. Uncoupling of oxidative phosphorylation thereby increasing the rate of oxygen consumption in the peripheral tissues
               Uncoupling of oxidative phosphorylation is also the cause of the hyperpyrexia seen in aspirin toxicity
          2. Salicylate toxicity inhibits enzymes involved with carbohydrate and lipid metabolism leading to ACCUMULATION OF ORGANIC ACIDS such as
               Pyruvic acid
               Lactic acid
               Acetoacetic acid
          3. Impair renal function causing accumulation of INORGANIC ACIDS such as
               Sulfuric acid
               Phosphoric acid
Sx (classic triad)
     Tinnitus
     Fever
     Tachypnea
Sx (other)
     Nausea
     Vomiting
Labs
     Near normal pH
     Primary decrease in PaCO2
     Concurrent decrease in HCO3-
     Blood gases one might expect to see could be: 
               pH 7.45, pCO2 21, pO2 124, HCO3 14
               pH 7.36, pCO2 22, HCO3 12

     It is necessary to use Winter's formula to calculate the expected compensatory PaCO2 that is a response to the primary metabolic acidosis
          In salicylate intoxication, the PaCO2 is lower than expected, indicating coexisting primary respiratory alkalosis

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The Compendium platform was created by David Kwinter, MD, CCFP(EM).