title: The aetiology and pathogenesis of cardiopulmonary bypass-associated metabolic acidosis using polygeline pump prime.
abstract: OBJECTIVE
  The pathogenesis of the metabolic acidosis of cardiopulmonary bypass (CPB) is not fully understood. New quantitative methods of acid-base balance now make it possible to describe it more clearly. Accordingly, we studied acid-base changes during CPB with polygeline pump prime and defined and quantified the factors which contribute to metabolic acidosis.
  
  
  METHODS
  Prospective cohort study.
  
  
  METHODS
  Tertiary institution.
  
  
  METHODS
  10 cardiac bypass graft surgery patients.
  
  
  METHODS
  Sampling of arterial blood at four time intervals: post-induction, on CPB during cooling and rewarming, and at skin closure. Measurement of serum Na+, K+, Mg++, Ca++, Cl-, bicarbonate, and phosphate concentrations, arterial blood gases, and serum albumin, lactate, and pyruvate concentrations at each collection point. Analysis of findings according to quantitative physicochemical principles, including calculation of the strong ion difference apparent, the strong ion difference effective, and the strong ion gap (SIG).
  
  
  RESULTS
  All patients developed a mild metabolic acidosis. The median serum standard bicarbonate concentration decreased from 25.0 mEq/l post-induction to 22.3 mEq/l at cooling and 22.2 mEq/l at rewarming (p < 0.05). The standard base excess decreased from a median of 1.55 mEq/l prior to CPB, to -2.50 mEq/l at cooling, -1.65 mEq/l at rewarming and, -0.85 mEq/l at skin closure (p < 0.001). This mild metabolic acidosis occurred despite a decrease in the median serum lactate concentration from 3.20 mEq/l post-induction to 1.83, 1.80, and 1.58 mEq/l at the three other time points. The increase in the median serum chloride concentration from 104.9 mEq/l post induction to 111.0, 111.1, and 110.0 mEq/l at the subsequent time points (p < 0.0001) was the main cause of the acidosis. There was also a significant increase in the SIG of 3.8 mEq/l at cooling and rewarming (p < 0.0001), suggesting a role for other unmeasured anions (polygeline) in the genesis of this acidosis.
  
  
  CONCLUSIONS
  Using quantitative biophysical methods, it can be demonstrated that, in patients receiving a pump prime rich in chloride and polygeline, the metabolic acidosis of CPB is mostly due to iatrogenic increases in serum chloride concentration and unmeasured strong anions (SIG). Its development is partially attenuated by iatrogenic hypoalbuminaemia. Changes in lactate concentrations did not play a role in the development of metabolic acidosis in our patients.
authors.affiliation: Department of Intensive Care Medicine, Austin and Repatriation Medical Centre, Heidelberg, Australia.
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: 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* / Q000503:physiopathology; D000368:Aged; D001784:Blood Gas Analysis; D002712:Chlorides / Q000097:blood*; D015331:Cohort Studies; D001026:Coronary Artery Bypass / Q000009:adverse effects; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010952:Plasma Substitutes / Q000009:adverse effects*; D011097:Polygeline / Q000009:adverse effects*; D011446:Prospective Studies
chemical_list: D002712:Chlorides; D010952:Plasma Substitutes; D011097:Polygeline