In many circumstances, more than a single acid-base disturbance exists. Examples include combined metabolic and respiratory acidosis with cardiogenic shock; metabolic alkalosis and anion-gap acidosis in pts with vomiting and diabetic ketoacidosis; and anion-gap metabolic acidosis with respiratory alkalosis in pts with salicylate toxicity. The diagnosis may be clinically evident and/or suggested by relationships between the PCO2 and [HCO3−] that diverge from those found in simple disorders. For example, the PCO2 in a pt with metabolic acidosis and respiratory alkalosis will be considerably less than that predicted from the [HCO3−] and Winter’s formula [PaCO2 = (1.5 × [HCO3−]) + 8 + 2].
In “simple” anion-gap acidosis, the anion gap increases in proportion to the fall in [HCO3−]. A lesser drop in serum [HCO3−] than in the anion gap suggests a coexisting metabolic alkalosis. Conversely, a proportionately larger drop in [HCO3−] than in the anion gap suggests the presence of a mixed anion-gap and non-anion-gap metabolic acidosis. Notably, however, these interpretations assume 1:1 relationships between unmeasured anions and the fall in [HCO3−], which are not uniformly present in individual pts or as acidoses evolve. For example, volume resuscitation of pts with DKA will typically increase glomerular filtration and the urinary excretion of ketones, resulting in a decrease in the anion gap in the absence of a supervening non-anion-gap acidosis.
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