The aetiology and pathogenesis of cardiopulmonary bypass-associated metabolic acidosis using polygeline pump prime
The aetiology and pathogenesis of cardiopulmonary bypass-associated metabolic acidosis using polygeline pump prime
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DOI：
10.1007/s001340050930
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发表时间：
1999-07-01
影响因子：
38.9
通讯作者：
Buxton, B
中科院分区：
文献类型：
--
作者：
Hayhoe, M;Bellomo, R;Buxton, B
目的：体外循环（CPB）中代谢性酸中毒的发病机制尚未完全清楚。新的酸碱平衡定量方法使我们有可能更清楚地描述它。因此，我们研究了酸碱变化，在CPB与聚明胶肽泵总理和定义和量化的因素，有助于代谢性acidosis.Design：前瞻性队列研究。设置：三级机构。参与者：10心脏搭桥移植手术patients.Interventions：采样动脉血在四个时间间隔：诱导后，在CPB期间冷却和复温，并在皮肤闭合。在每个采集点测量血清Na+、K+、Mg++、Ca++、Cl-、碳酸氢盐和磷酸盐浓度、动脉血气以及血清白蛋白、乳酸盐和丙酮酸盐浓度，根据定量理化原理分析结果？包括计算强离子差表观值、强离子差有效值和强离子间隙（SIG）。测量和主要结果：所有患者均发生轻度代谢性酸中毒。中位血清标准碳酸氢盐浓度从害虫诱导时的25.0 mEq/l降至冷却时的22.3 mEq/l和复温时的22.2 mEq/l（p < 0.05）。标准碱过量从CPB前的中位数1.55 mEq/l降低至冷却时的-2.50 mEq/l，复温时的-1.65 mEq/l和皮肤闭合时的-0.85 mEq/l（p < 0.001）。尽管中位血清乳酸浓度从诱导后的3.20 mEq/l降至其他三个时间点的1.83、1.80和1.58 mEq/l，但仍发生了轻度代谢性酸中毒。中位血清氯化物浓度从诱导后的104.9 mEq/l增加至111.01、111.1和随后时间点的110.0 mEq/l（p < 0.0001）是酸中毒的主要原因。冷却和复温时SIG也显著增加，为3.8 mEq/l（p < 0.0001），表明其他未测量阴离子的作用（聚明胶肽）在这种酸中毒的成因。结论：使用定量生物物理方法，可以证明，在接受富含氯化物和聚明胶肽的泵预充的患者中，CPB的代谢性酸中毒主要是由于血清氯化物浓度和未测量的强阴离子（SIG）的医源性增加。医源性低白蛋白血症部分减弱了其发展。在我们的患者中，乳酸浓度的变化在代谢性酸中毒的发生中没有发挥作用。
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.Design: Prospective cohort study.Setting: Tertiary institution.Participants: 10 cardiac bypass graft surgery patients.Interventions: 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).Measurements and main results: All patients developed a mild metabolic acidosis. 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 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 111.01 111.1, and 110.0 mEq/l at the subsequent time points (p < 0.0001) was the main cause of the acidosis. There was also a 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.