The aetiology and pathogenesis of cardiopulmonary bypass-associated metabolic acidosis using polygeline pump prime

Objective: The pathogenesis of the metabolic acidosis of cardiopulmonary by pass (CPB) is not fully understood. New quantitative methods of acid-base b alance now make it possible to describe it more clearly. Accordingly, we st udied acid-base changes during CPB with polygeline pump prime and defined a nd quantified the factors which contribute to metabolic acidosis. Design: Prospective cohort study. Setting: Tertiary institution. Participants: 10 cardiac bypass graft surgery patients. Interventions: Sampling of arterial blood at four time intervals: post-indu ction, on CPB during cooling and rewarming, and at skin closure. Measuremen t of serum Na+, K+, Mg++, Ca++, Cl-, bicarbonate, and phosphate concentrati ons, arterial blood gases, and serum albumin, lactate, and pyruvate concent rations at each collection point, Analysis of findings according to quantit ative physicochemical principles? including calculation of the strong ion d ifference apparent, the strong ion difference effective, and the strong ion gap (SIG). Measurements and main results: All patients developed a mild metabolic acid osis. The median serum standard bicarbonate concentration decreased from 25 .0 mEq/l pest-induction to 22.3 mEq/l at cooling and 22.2 mEq/l at rewarmin g (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 occurre d despite a decrease in the median serum lactate concentration from 3.20 mE q/l post-induction to 1.83, 1.80, and 1.58 mEq/l at the three other time po ints. The increase in the median serum chloride concentration from 104.9 mE q/l post induction to 111.01 111.1, and 110.0 mEq/l at the subsequent time points (p < 0.0001) was the main cause of the acidosis. There was also a si gnificant 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 ge nesis 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 seru m chloride concentration and unmeasured strong anions (SIG). Its developmen t is partially attenuated by iatrogenic hypoalbuminaemia. Changes in lactat e concentrations did not play a role in the development of metabolic acidos is in our patients.