Research

Causes of metabolic acidosis in canine hemorrhagic shock: role of unmeasured ions

Dirk Bruegger¹ , Gregor I Kemming¹ , Matthias Jacob¹ , Franz G Meisner² , Christoph J Wojtczyk³ , Kristian B Packert¹ , Peter E Keipert⁴ , N Simon Faithfull⁵ , Oliver P Habler⁶ , Bernhard F Becker⁷ and Markus Rehm¹

¹Clinic of Anesthesiology, Ludwig-Maximilians-University, Marchioninistrasse 15, 81377 Munich, Germany

²Department of Thoracic and Vascular Surgery, University of Ulm, Steinhövelstrasse 9, 89075 Ulm, Germany

³Department of General, Visceral and Thoracic Surgery, Clinic of Nuremberg, Prof.-Ernst-Nathan-Strasse 1, 90419 Nuremberg, Germany

⁴Sangart Inc., 6175 Lusk Blvd., San Diego, CA 92121, USA

⁵Alliance Pharmaceutical Corp., 4660 La Jolla Village Drive, San Diego, CA 92122, USA

⁶Clinic of Anesthesiology, Intensive Care Medicine and Pain Management, Krankenhaus Nordwest, Steinbacher Hohl 2-26, 60488 Frankfurt, Germany

⁷Department of Physiology, Ludwig-Maximilians-University, Pettenkoferstrasse 12, 80336 Munich, Germany

author email corresponding author email

Critical Care 2007, 11:R130doi:10.1186/cc6200

Published:	14 December 2007

See related commentary by Venkatesh and Morgan, http://ccforum.com/content/12/1/113

Abstract

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.