Role of pump prime in the etiology and pathogenesis of cardiopulmonary bypass-associated acidosis

Citation
Fj. Liskaser et al., Role of pump prime in the etiology and pathogenesis of cardiopulmonary bypass-associated acidosis, ANESTHESIOL, 93(5), 2000, pp. 1170-1173
Citations number
9
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
ANESTHESIOLOGY
ISSN journal
00033022 → ACNP
Volume
93
Issue
5
Year of publication
2000
Pages
1170 - 1173
Database
ISI
SICI code
0003-3022(200011)93:5<1170:ROPPIT>2.0.ZU;2-A
Abstract
Background: The development of metabolic acidosis during cardiopulmonary by pass (CPB) is well recognized but poorly understood. The authors hypothesiz ed that the delivery of pump prime fluids is primarily responsible for its development. Accordingly, acid-base changes induced by the establishment of CPB mere studied using two types of priming fluid (Haemaccel, a polygeline solution, and Ringer's Injection is. Plasmalyte 148) using quantitative bi ophysical methods. Methods: A prospective, double-blind, randomized trial was conducted at a t ertiary institution with 22 patients undergoing CPB for coronary artery byp ass surgery. Sampling of arterial blood was performed at three time interva ls: before CPB (t(1)), 2 min after initiation of CPB at full flows (t(2)), and at the end of the case (t(3)) Measurements of Na+, K+, Mg2+, Cl-, HCO3- , phosphate, Ca2+, albumin, lactate, and arterial blood gases at each colle ction point were performed. Results were analyzed in a quantitative manner. Results: Immediately on delivery of pump prime fluids, all patients develop ed a metabolic acidosis (base excess: 0.95 mEq/1 (t(1)) to -3.65 mEq/1 (t(2 )) (P < 0.001) for Haemaccel-Ringer's and 1.17 mEq/1 (t(1)) to -3.20 mEq/1 (t(2)). 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 hy perchloremic (<Delta> Cl-, +9.50 mEq/1; confidence interval, 7.00-11.50). W ith Plasmalyte 148, the acidosis was induced by an increase in unmeasured a nions, most probably acetate and gluconate, The resolution of these two pro cesses was different because the excretion of chloride was slower than that of the unmeasured anions (Delta base excess from t(1) to t(3) = -1.60 for Haemaccel-Ringer's vs. +1.15 for Plasmalyte 148; P = 0.0062), Conclusions: Cardiopulmonary bypass-induced metabolic acidosis appears to b e iatrogenic in nature and derived from the effect of pump prime fluid on a cid-base balance. The extent of such acidosis and its duration varies accor ding to the type of pump prime.