Hayhoe M, Bellomo R, Liu G, McNicol L, Buxton B
Department of Intensive Care Medicine, Austin and Repatriation Medical Centre, Heidelberg, Australia.
Intensive Care Med. 1999 Jul;25(7):680-5. doi: 10.1007/s001340050930.
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.
Prospective cohort study.
Tertiary institution.
10 cardiac bypass graft surgery patients.
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).
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.
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.
体外循环（CPB）代谢性酸中毒的发病机制尚未完全明确。酸碱平衡的新定量方法现在使更清晰地描述它成为可能。因此，我们研究了使用聚明胶肽预充液进行CPB期间的酸碱变化，并确定和量化了导致代谢性酸中毒的因素。
前瞻性队列研究。
三级医疗机构。
10例心脏搭桥手术患者。
在四个时间点采集动脉血：诱导后、CPB期间降温及复温时、皮肤缝合时。在每个采集点测量血清Na⁺、K⁺、Mg²⁺、Ca²⁺、Cl⁻、碳酸氢盐和磷酸盐浓度、动脉血气以及血清白蛋白、乳酸和丙酮酸浓度。根据定量物理化学原理分析结果，包括计算表观强离子差、有效强离子差和强离子间隙（SIG）。
所有患者均发生轻度代谢性酸中毒。血清标准碳酸氢盐浓度中位数从诱导后25.0 mEq/L降至降温时的22.3 mEq/L和复温时的22.2 mEq/L（p<0.05）。标准碱剩余从中位数CPB前的1.55 mEq/L降至降温时的 -2.50 mEq/L、复温时的 -1.65 mEq/L和皮肤缝合时的 -0.85 mEq/L（p<0.001）。尽管血清乳酸浓度中位数从诱导后3.20 mEq/L降至其他三个时间点的1.83、1.80和1.58 mEq/L，但仍发生了这种轻度代谢性酸中毒。血清氯浓度中位数从诱导后的104.9 mEq/L升至随后时间点的111.0、111.1和110.0 mEq/L（p<0.0001）是酸中毒的主要原因。降温及复温时SIG也显著升高3.8 mEq/L（p<0.0001），提示其他未测定阴离子（聚明胶肽）在这种酸中毒发生中起作用。
使用定量生物物理方法可以证明，在接受富含氯和聚明胶肽预充液的患者中，CPB的代谢性酸中毒主要归因于血清氯浓度和未测定强阴离子（SIG）的医源性增加。医源性低白蛋白血症部分减轻了其发展。乳酸浓度变化在我们患者的代谢性酸中毒发生中未起作用。
