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Metabolic acidosis developing during cardiopulmonary bypass is related to a decrease in strong ion difference

Department of Anaesthesia, Critical Care and Pain Medicine, Royal Infirmary of Edinburgh, Edinburgh, UK, peter.alston{at}ed.ac.uk

Laura Cormack

Department of Anaesthesia, Critical Care and Pain Medicine, Royal Infirmary of Edinburgh, Edinburgh, UK, Department of Cardiothoracic Surgery, Royal Infirmary of Edinburgh, Edinburgh, UK, Department of Anaesthesia, Golden Jubilee Hospital, Clydebank, UK

Catherine Collinson

Department of Anaesthesia, Critical Care and Pain Medicine, Royal Infirmary of Edinburgh, Edinburgh, UK, Department of Cardiothoracic Surgery, Royal Infirmary of Edinburgh, Edinburgh, UK, Department of Anaesthesia, Golden Jubilee Hospital, Clydebank, UK

Metabolic acidosis is a frequent complication of cardio-pulmonary bypass (CPB). Commonly, its cause is ascribed to hypoperfusion; however, iatrogenic causes, related to the composition and volume of intravascular fluids that are administered, are increasingly being recognized. The aim of this study was to determine if metabolic acidosis during CPB was associated with hypoperfusion, change in strong ion difference (SID) or haemodilution. Forty-nine patients undergoing cardiac surgery using CPB in the Royal Infirmary of Edinburgh (RIE) or the HCI, Clydebank were included in the study. Arterial blood samples were aspirated before induction of anaesthesia and the end of CPB. Samples were subjected to blood gas analysis and measurement of electrolytes and lactate. Changes in concentrations were then calculated. Change variables that were found to be significant (p B-0.1) univariate correlates of the change in hydrogen ion concentration were identified and entered into a multivariate regression model with hydrogen ion concentra tion at the end of CPB as the outcome variable (r²=0.65, p<0.001). Change variance in hydrogen ion concentration was created by first entering the baseline hydrogen ion concentration into the model. Next, any variance resulting from the respiratory component of acidosis was removed by entering the change in arterial carbon dioxide tension (regression coefficient (ß)=0.67, p<0.01). Change in SID (ß=-0.34, p<0.01) and surgical institution (ß=-0.40, p<0.01) were then found to be predictors of the remaining variance whilst change in concentration of lactate (ß in=0.16, p=0.07) and volume of intravascular fluid that was administered (ß=-0.07, p=0.52) were rejected from the model. These findings suggest that the metabolic acidosis developing during CPB is partially the result of iatrogenic decrease in SID rather than hypoperfusion, as estimated by lactate concentration, or haemodilution.

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