Morgan Thomas J, Venkatesh Balasubramanian, Hall Jonathan
Division of Anesthesiology and Intensive Care, Royal Brisbane Hospital, Queensland, Australia.
Crit Care Med. 2002 Jan;30(1):157-60. doi: 10.1097/00003246-200201000-00022.
To determine the relationship between the strong ion difference (SID) of a diluting crystalloid and its metabolic acid-base effects on in vitro blood dilution.
Prospective in vitro study.
University research laboratory.
Normal human blood.
Three solutions were prepared, each with [Na] 140 mmol/L. [Cl-] for solutions 1, 2, and 3 was 120, 110, and 100 mmol/L, respectively, the other anion being HCO3-. SID values were thus 20, 30, and 40 mEq/L, respectively. Serial dilutions of well-oxygenated fresh venous blood were performed anaerobically by using each of solutions 1-3 as well as 0.9% saline (SID = 0 mEq/L) and Hartmann's solution (SID = -4 mEq/L).
Blood gas and electrolyte analyses were performed before and after each dilution. Apart from dilutions with solution 3 (crystalloid SID 40 mEq/L) during which plasma SID did not change, plasma SID decreased during hemodilution. In contrast, base excess increased during hemodilution with solutions 3 and 2 (crystalloid SID 40 mEq/L and 30 mEq/L, respectively) and decreased only with the remaining three solutions. The relationships between hemoglobin concentrations and both plasma SID and whole blood base excess throughout dilution were linear, with slopes proportional to the SID of the diluent in each case. Linear regression revealed that the SID of crystalloid producing a zero base excess/hemoglobin concentration slope during blood dilution (i.e., no change in metabolic acid-base status) is 23.7 mEq/L.
On in vitro hemodilution, there is a simple linear relationship between diluent crystalloid SID and the rate and direction of change of plasma SID and whole blood base excess. Direct extrapolation to in vivo situations such as acute normovolemic hemodilution and large volume correction of extracellular fluid deficits requires experimental confirmation.
确定稀释性晶体液的强离子差（SID）与其对体外血液稀释的代谢性酸碱效应之间的关系。
前瞻性体外研究。
大学研究实验室。
正常人血液。
制备三种溶液，每种溶液的[Na]均为140 mmol/L。溶液1、2和3的[Cl⁻]分别为120、110和100 mmol/L，另一种阴离子为HCO₃⁻。因此，SID值分别为20、30和40 mEq/L。使用溶液1 - 3以及0.9%生理盐水（SID = 0 mEq/L）和哈特曼溶液（SID = -4 mEq/L）对充分氧合的新鲜静脉血进行厌氧连续稀释。
在每次稀释前后进行血气和电解质分析。除了用溶液3（晶体液SID 40 mEq/L）稀释期间血浆SID未变化外，血液稀释期间血浆SID降低。相比之下，用溶液3和2（晶体液SID分别为40 mEq/L和30 mEq/L）进行血液稀释期间碱剩余增加，而仅用其余三种溶液稀释时碱剩余降低。在整个稀释过程中，血红蛋白浓度与血浆SID和全血碱剩余之间的关系呈线性，斜率在每种情况下均与稀释剂的SID成比例。线性回归显示，在血液稀释期间产生零碱剩余/血红蛋白浓度斜率（即代谢性酸碱状态无变化）的晶体液SID为23.7 mEq/L。
在体外血液稀释中，稀释剂晶体液SID与血浆SID和全血碱剩余的变化速率及方向之间存在简单的线性关系。直接外推至体内情况，如急性等容性血液稀释和细胞外液 deficit 的大量纠正，需要实验证实。
