title: Role of the splanchnic circulation in acid-base balance during cardiopulmonary bypass.
abstract: OBJECTIVE
  The role of the splanchnic circulation in the development of the metabolic acidosis of cardiopulmonary bypass (CPB) is not fully understood. New quantitative methods of acid-base balance now offer the ability to define this phenomenon more accurately. Accordingly, we studied acid-base changes across the splanchnic circulation during CPB and defined and quantified the factors that contributed to acid-base balance.
  
  
  METHODS
  Prospective cohort study.
  
  
  METHODS
  Tertiary institution.
  
  
  METHODS
  Ten patients undergoing CPB for coronary artery bypass surgery.
  
  
  METHODS
  Sampling of arterial and hepatic venous blood at four time intervals: postinduction, on CPB during cooling and rewarming, and at skin closure.
  
  
  METHODS
  Measurement of serum Na+, K+, Mg++, Ca++, Cl-, HCO3-, and phosphate concentrations, arterial and hepatic venous blood gases and serum albumin, and lactate and pyruvate concentrations at each collection point. Analysis of findings according to quantitative physicochemical principles.
  
  
  RESULTS
  All patients developed a mild metabolic acidosis with a decrease in median serum bicarbonate concentration from 24.97 mEq/L after induction to 22.29 mEq/L at cooling and 22.23 mEq/L at rewarming (p < .05). Before CPB, the pH decreased by 0.0275 (p < .05) across the splanchnic circulation, representing an increase of 2.26 nmol/L of hydrogen ions. Nevertheless, the splanchnic circulation induced a metabolic alkalosis, with a median transsplanchnic increase in the base excess of 1.50 mEq/L (p < .05). This change was largely due to a decrease in serum chloride and lactate concentration across the splanchnic circulation (p < .05). The acidifying effect of the splanchnic circulation was therefore the result of cell respiration with a median increase in carbon dioxide tension of 5.75 mm Hg (p < .05), causing the strong ion difference effective to increase by 1.94 mEq/L (p < .05). There were no other anions or acids added to the circulation by splanchnic organs (no change in strong ion gap). During and after CPB the splanchnic metabolic alkalinizing effect continued and the respiratory acidifying effect was reduced. This caused the splanchnic circulation to be pH neutral at these times.
  
  
  CONCLUSIONS
  Using quantitative biophysical methods it can be demonstrated that the splanchnic circulation does not contribute to the metabolic acidosis of CPB, and that it continues to have a metabolic alkalinizing effect involving significant lactate extraction. However, its respiratory acidifying effect continues, although at a reduced rate.
authors.affiliation: Department of Intensive Care Medicine, Austin and Repatriation Medical Centre, Heidelberg, Austria.
authors.forename: M
authors.initials: M
authors.lastname: Hayhoe
authors.forename: R
authors.initials: R
authors.lastname: Bellomo
authors.forename: G
authors.initials: G
authors.lastname: Liu
authors.forename: J A
authors.initials: JA
authors.lastname: Kellum
authors.forename: L
authors.initials: L
authors.lastname: McNicol
authors.forename: B
authors.initials: B
authors.lastname: Buxton
mesh_terms: D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000209:etiology / Q000378:metabolism*; D000368:Aged; D001639:Bicarbonates / Q000097:blood; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D002712:Chlorides / Q000097:blood; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008670:Metals / Q000097:blood; D008875:Middle Aged; D011446:Prospective Studies; D013152:Splanchnic Circulation
chemical_list: D001639:Bicarbonates; D002712:Chlorides; D008670:Metals