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  • Meeting abstract
  • Open Access

Metabolic acidosis and cardiopulmonary bypass: hypoperfusion or iatrogenic?

  • 1,
  • 1 and
  • 1
Critical Care20026 (Suppl 2) :2

  • Published:


  • Plasma Protein
  • Cardiopulmonary Bypass
  • Body Surface Area
  • Sodium Bicarbonate
  • Metabolic Acidosis


Many patients develop, to a varying extent, a metabolic acidosis during cardiopulmonary bypass (CPB). Often this acidosis is assumed to be the result of tissue hypoperfusion. However, fluids administered to patients before and during CPB, through their effects upon the strong ion difference (SID), may cause metabolic acidosis [1,2]. These fluids may also produce acidosis by haemodilution because of the decrease in plasma protein concentration [2]. The aim of this study was to determine whether metabolic acidosis occurring during CPB is the result of hypoperfusion or is iatrogenic.


Forty-nine adult patients undergoing cardiac surgery with CPB were studied. Arterial blood was sampled before the induction of anaesthesia during the re-warming phase of CPB (35°C). Blood gas analysis and concentrations of electrolytes, plasma proteins and lactate were measured. The volumes and compositions of fluids administered were recorded.


Factors that were found to correlate significantly (P < 0.05) with the change in hydrogen ion concentration between the two time points were identified. Change in arterial carbon dioxide concentration was used to remove the respiratory component of acidosis. These predictor factors were then entered after change in arterial carbon dioxide tension, to first remove the respiratory component of acidosis, into a multivariate linear regression model (P < 0.001, r2 = 0.65) so as to examine their influence on the change variance in hydrogen ion concentration. Only the amount of sodium bicarbonate administered (β = -0.404, P < 0.001) and the change in SID (β =-0.339, P = 0.004) were found to predict the change in hydrogen ion concentration. Change in lactate concentration (P = 0.072) and the total volume of fluid administered moderated by body surface area (P = 0.523) were excluded from the model.


Our sample size is underpowered to detect factors that might have a small effect size. Also, the regression model only explained 65% of the variance so factors other than those that we have identified influence the change in hydrogen ion concentration. However, our findings suggest that metabolic acidosis arising during CPB is largely induced by change in the SID and the type of fluids administered, whilst haemodilution and hypoperfusion do not appear to have important roles in its genesis. Whether this metabolic acidosis or its correction has any influence on outcome from cardiac surgery merits further research.

Authors’ Affiliations

Department of Anaesthesia, Critical Care and Pain Medicine, Royal Infirmary of Edinburgh, Edinburgh, EH3 9YW, UK
Department of Anaesthesia, HCI, Clydebank, UK


  1. Liskaser FJ, Bellomo R, Hayhoe M, et al.: Role of pump prime in the etiology and pathogenesis of cardiopulmonary bypass-associated acidosis. Anesthesiology 2000, 93: 1170-1173. 10.1097/00000542-200011000-00006View ArticlePubMedGoogle Scholar
  2. Sirker AA, Rhodes A, Grounds RM, Bennett ED: Acid-base physiology: the 'traditional' and the 'modern' approaches. Anaesthesia 2002, 57: 348-356. 10.1046/j.0003-2409.2001.02447.xView ArticlePubMedGoogle Scholar


© BioMed Central Ltd 2002