Research
Causes of metabolic acidosis in canine hemorrhagic shock: role of unmeasured ions
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* Corresponding author: Dirk Bruegger dirk.bruegger@med.uni-muenchen.de
1 Clinic of Anesthesiology, Ludwig-Maximilians-University, Marchioninistrasse 15, 81377 Munich, Germany
2 Department of Thoracic and Vascular Surgery, University of Ulm, Steinhövelstrasse 9, 89075 Ulm, Germany
3 Department of General, Visceral and Thoracic Surgery, Clinic of Nuremberg, Prof.-Ernst-Nathan-Strasse 1, 90419 Nuremberg, Germany
4 Sangart Inc., 6175 Lusk Blvd., San Diego, CA 92121, USA
5 Alliance Pharmaceutical Corp., 4660 La Jolla Village Drive, San Diego, CA 92122, USA
6 Clinic of Anesthesiology, Intensive Care Medicine and Pain Management, Krankenhaus Nordwest, Steinbacher Hohl 2-26, 60488 Frankfurt, Germany
7 Department of Physiology, Ludwig-Maximilians-University, Pettenkoferstrasse 12, 80336 Munich, Germany
Critical Care 2007, 11:R130 doi:10.1186/cc6200
Published: 14 December 2007Abstract
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 mLO2/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), α-ketoglutarate (35.3 μEq/L), fumarate (6.2 μEq/L), sulfate (0.1 mEq/L), and urate (55.9 μEq/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.