Introduction Metabolic acidosis during hemorrhagic shock is common
and conventionally considered to be due to hyperlactatemia. There
is increasing awareness, however, that other nonlactate, unmeasured
anions contribute to this type of acidosis. Methods Eleven
anesthetized dogs were hemorrhaged to a mean arterial pressure of
45 mm Hg and were kept at this level until a metabolic oxygen debt
of 120 mLO(2)/kg body weight had evolved. Blood pH, partial
pressure of carbon dioxide, and concentrations of sodium,
potassium, magnesium, calcium, chloride, lactate, albumin, and
phosphate were measured at baseline, in shock, and during 3 hours
post-therapy. Strong ion difference and the amount of weak plasma
acid were calculated. To detect the presence of unmeasured anions,
anion gap and strong ion gap were determined. Capillary
electrophoresis was used to identify potential contributors to
unmeasured anions. Results During induction of shock, pH decreased
significantly from 7.41 to 7.19. The transient increase in lactate
concentration from 1.5 to 5.5 mEq/L during shock was not sufficient
to explain the transient increases in anion gap (+ 11.0 mEq/L) and
strong ion gap (+ 7.1 mEq/L), suggesting that substantial amounts
of unmeasured anions must have been generated. Capillary
electrophoresis revealed increases in serum concentration of
acetate (2.2 mEq/L), citrate (2.2 mEq/L), alpha-ketoglutarate (35.3
mu Eq/L), fumarate (6.2 mu Eq/L), sulfate (0.1 mEq/L), and urate
(55.9 mu Eq/L) after shock induction. Conclusion Large amounts of
unmeasured anions were generated after hemorrhage in this highly
standardized model of hemorrhagic shock. Capillary electrophoresis
suggested that the hitherto unmeasured anions citrate and acetate,
but not sulfate, contributed significantly to the changes in strong
ion gap associated with induction of shock.
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