Báo cáo y học: Causes of metabolic acidosis in canine hemorrhagic shock: role of unmeasured io

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Báo cáo y học: "Causes of metabolic acidosis in canine hemorrhagic shock: role of unmeasured io" Available online http://ccforum.com/content/11/6/R130Research Open AccessVol 11 No 6Causes of metabolic acidosis in canine hemorrhagic shock: role ofunmeasured ionsDirk 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 andMarkus Rehm11Clinic of Anesthesiology, Ludwig-Maximilians-University, Marchioninistrasse 15, 81377 Munich, Germany2Department of Thoracic and Vascular Surgery, University of Ulm, Steinhövelstrasse 9, 89075 Ulm, Germany3Department of General, Visceral and Thoracic Surgery, Clinic of Nuremberg, Prof.-Ernst-Nathan-Strasse 1, 90419 Nuremberg, Germany4Sangart Inc., 6175 Lusk Blvd., San Diego, CA 92121, USA5Alliance Pharmaceutical Corp., 4660 La Jolla Village Drive, San Diego, CA 92122, USA6Clinic of Anesthesiology, Intensive Care Medicine and Pain Management, Krankenhaus Nordwest, Steinbacher Hohl 2-26, 60488 Frankfurt,Germany7Department of Physiology, Ludwig-Maximilians-University, Pettenkoferstrasse 12, 80336 Munich, GermanyCorresponding author: Dirk Bruegger, dirk.bruegger@med.uni-muenchen.deReceived: 14 Aug 2007 Revisions requested: 28 Sep 2007 Revisions received: 26 Nov 2007 Accepted: 14 Dec 2007 Published: 14 Dec 2007Critical Care 2007, 11:R130 (doi:10.1186/cc6200)This article is online at: http://ccforum.com/content/11/6/R130© 2007 Bruegger et al.; licensee BioMed Central Ltd.This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractIntroduction Metabolic acidosis during hemorrhagic shock is Results During induction of shock, pH decreased significantlycommon and conventionally considered to be due to from 7.41 to 7.19. The transient increase in lactatehyperlactatemia. There is increasing awareness, however, that concentration from 1.5 to 5.5 mEq/L during shock was notother nonlactate, unmeasured anions contribute to this type of sufficient to explain the transient increases in anion gap (+11.0acidosis. mEq/L) and strong ion gap (+7.1 mEq/L), suggesting that substantial amounts of unmeasured anions must have beenMethods Eleven anesthetized dogs were hemorrhaged to a generated. Capillary electrophoresis revealed increases inmean arterial pressure of 45 mm Hg and were kept at this level 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 (0.1until a metabolic oxygen debt of 120 mLO2/kg body weight had mEq/L), and urate (55.9 μEq/L) after shock induction.evolved. Blood pH, partial pressure of carbon dioxide, andconcentrations of sodium, potassium, magnesium, calcium,chloride, lactate, albumin, and phosphate were measured at Conclusion Large amounts of unmeasured anions werebaseline, in shock, and during 3 hours post-therapy. Strong ion generated after hemorrhage in this highly standardized model ofdifference and the amount of weak plasma acid were calculated. hemorrhagic shock. Capillary electrophoresis suggested thatTo detect the presence of unmeasured anions, anion gap and the hitherto unmeasured anions citrate and acetate, but notstrong ion gap were determined. Capillary electrophoresis was sulfate, contributed significantly to the changes in strong ionused to identify potential contributors to unmeasured anions. gap associated with induction of shock.Introduction tatemia. The increase in blood lactate generally originates fromDuring hemorrhagic shock, metabolic acidosis is common and both increased lactate production and reduced lactate metab-conventionally considered to be due essentially to hyperlac- olism. However, there is an increasing awareness that30 = 30 minutes post-therapy; 60 = 60 minutes post-therapy; 180 = 180 minutes post-therapy; A- = amount of weak plasma acid; AG = anion gap;Alb = serum concentration of albumin; B = baseline; Ca2+ = serum equivalents of calcium; Cl- = serum concentration of chloride; CPDA = citrate,phosphate, dextrose, and adenine; K+ = serum concentration of potassium; Lac- = serum concentration of lactate; Mg2+ = serum equivalents of mag-nesium; Na+ = serum concentration of sodium; pCO2 = partial pressure of carbon dioxide; Phos = serum concentration of phosphate; pT = post-treatment; PVA = polyvinyl alcohol; Sh = shock; SID = strong ion difference; SIDa = apparent strong ion difference; SIDe = effective strong ion differ-ence; SIG = strong ion gap. Page 1 of 14 (page number not for citation purposes)Critical Care Vol 11 No 6 Bruegger et al. ...