Liskaser F J, Bellomo R, Hayhoe M, Story D, Poustie S, Smith B, Letis A, Bennett M
Departments of Anaesthesia and Intensive Care, Austin and Repatriation Medical Centre, Melbourne, Australia.
Anesthesiology. 2000 Nov;93(5):1170-3. doi: 10.1097/00000542-200011000-00006.
The development of metabolic acidosis during cardiopulmonary bypass (CPB) is well recognized but poorly understood. The authors hypothesized that the delivery of pump prime fluids is primarily responsible for its development. Accordingly, acid-base changes induced by the establishment of CPB were studied using two types of priming fluid (Haemaccel, a polygeline solution, and Ringer's Injection vs. Plasmalyte 148) using quantitative biophysical methods.
A prospective, double-blind, randomized trial was conducted at a tertiary institution with 22 patients undergoing CPB for coronary artery bypass surgery. Sampling of arterial blood was performed at three time intervals: before CPB (t1), 2 min after initiation of CPB at full flows (t2), and at the end of the case (t3). Measurements of Na+, K+, Mg2+, Cl-, HCO3-, phosphate, Ca2+, albumin, lactate, and arterial blood gases at each collection point were performed. Results were analyzed in a quantitative manner.
Immediately on delivery of pump prime fluids, all patients developed a metabolic acidosis (base excess: 0. 95 mEq/l (t1) to -3.65 mEq/l (t2) (P < 0.001) for Haemaccel-Ringer's and 1.17 mEq/l (t1) to -3.20 mEq/l (t2). The decrease in base excess was the same for both primes (-4.60 vs. -4.37; not significant). However, the mechanism of metabolic acidosis was different. With the Haemaccel-Ringer's prime, the metabolic acidosis was hyperchloremic (Delta Cl-, +9.50 mEq/l; confidence interval, 7.00-11.50). With Plasmalyte 148, the acidosis was induced by an increase in unmeasured anions, most probably acetate and gluconate. The resolution of these two processes was different because the excretion of chloride was slower than that of the unmeasured anions (Delta base excess from t1 to t3 = -1.60 for Haemaccel-Ringer's vs. +1.15 for Plasmalyte 148; P = 0.0062).
Cardiopulmonary bypass-induced metabolic acidosis appears to be iatrogenic in nature and derived from the effect of pump prime fluid on acid-base balance. The extent of such acidosis and its duration varies according to the type of pump prime.
体外循环（CPB）期间代谢性酸中毒的发生已得到充分认识，但了解甚少。作者推测灌注液的输注是其发生的主要原因。因此，使用两种灌注液（贺斯，一种聚明胶肽溶液，与林格注射液对比血浆代用品148），采用定量生物物理方法研究了CPB建立过程中引起的酸碱变化。
在一家三级医疗机构对22例行冠状动脉搭桥手术并接受CPB的患者进行了一项前瞻性、双盲、随机试验。在三个时间点采集动脉血样本：CPB前（t1）、CPB全流量启动后2分钟（t2）和手术结束时（t3）。对每个采集点的Na +、K +、Mg2 +、Cl -、HCO3 -、磷酸盐、Ca2 +、白蛋白、乳酸和动脉血气进行测量。对结果进行定量分析。
在输注灌注液后，所有患者立即出现代谢性酸中毒（碱剩余：贺斯-林格组从0.95 mEq/l（t1）降至-3.65 mEq/l（t2）（P < 0.001），血浆代用品148组从1.17 mEq/l（t1）降至-3.20 mEq/l（t2）。两种灌注液的碱剩余下降幅度相同（-4.60对-4.37；无显著性差异）。然而，代谢性酸中毒的机制不同。使用贺斯-林格灌注液时，代谢性酸中毒为高氯性（ΔCl -，+9.50 mEq/l；置信区间，7.00 - 11.50）。使用血浆代用品148时，酸中毒是由未测定阴离子增加引起的，最可能是乙酸盐和葡萄糖酸盐。这两个过程的缓解情况不同，因为氯的排泄比未测定阴离子慢（从t1到t3的碱剩余变化：贺斯-林格组为-1.60，血浆代用品148组为+1.15；P = 0.0062）。
体外循环引起的代谢性酸中毒本质上似乎是医源性的，源于灌注液对酸碱平衡的影响。这种酸中毒的程度及其持续时间因灌注液类型而异。
