Quintard H, Hubert S, Ichai C
Service de réanimation médicochirugicale, département d'anesthesie-réanimation Est, hôpital Saint-Roch, 5, rue Pierre-Dévoluy, CHU de Nice, 06006 Nice cedex 01, France.
Ann Fr Anesth Reanim. 2007 May;26(5):423-33. doi: 10.1016/j.annfar.2007.02.012. Epub 2007 Apr 25.
To explain the different approaches for interpreting acid-base disorders; to develop the Stewart model which offers some advantages for the pathophysiological understanding and the clinical interpretation of acid-base imbalances.
Record of french and english references from Medline data base. The keywords were: acid-base balance, hyperchloremic acidosis, metabolic acidosis, strong ion difference, strong ion gap.
Data were selected including prospective and retrospective studies, reviews, and case reports.
Acid-base disorders are commonly analysed by using the traditional Henderson-Hasselbalch approach which attributes the variations in plasma pH to the modifications in plasma bicarbonates or PaCO2. However, this approach seems to be inadequate because bicarbonates and PaCO2 are completely dependent. Moreover, it does not consider the role of weak acids such as albuminate, in the determination of plasma pH value. According to the Stewart concept, plasma pH results from the degree of plasma water dissociation which is determined by 3 independent variables: 1) strong ion difference (SID) which is the difference between all the strong plasma cations and anions; 2) quantity of plasma weak acids; 3) PaCO2. Thus, metabolic acid-base disorders are always induced by a variation in SID (decreased in acidosis) or in weak acids (increased in acidosis), whereas respiratory disorders remains the consequence of a change in PaCO2. These pathophysiological considerations are important to analyse complex acid-base imbalances in critically ill patients. For example, due to a decrease in weak acids, hypoalbuminemia increases SID which may counter-balance a decrease in pH and an elevated anion gap. Thus if using only traditional tools, hypoalbuminemia may mask a metabolic acidosis, because of a normal pH and a normal anion gap. In this case, the association of metabolic acidosis and alkalosis is only expressed by respectively a decreased SID and a decreased weak acids concentration. This concept allows to establish the relationship between hyperchloremic acidosis and infusion of solutes which contain large concentration of chloride such as NaCl 0.9%. Finally, the Stewart concept permits to understand that sodium bicarbonate as well as sodium lactate induces plasma alkalinization. In fact, sodium remains in plasma, whereas anion (lactate or bicarbonate) are metabolized leading to an increase in plasma SID.
Due to its simplicity, the traditional Henderson-Hasselbalch approach of acid-base disorders, remains commonly used. However, it gives an inadequate pathophysiological analysis which may conduct to a false diagnosis, especially with complex acid-base imbalances. Despite its apparent complexity, the Stewart concept permits to understand precisely the mechanisms of acid-base disorders. It has to become the most appropriate approach to analyse complex acid-base abnormalities.
解释解释酸碱紊乱的不同方法；建立斯图尔特模型，该模型在酸碱失衡的病理生理理解和临床解释方面具有一些优势。
来自医学文献数据库的法语和英语参考文献记录。关键词为：酸碱平衡、高氯性酸中毒、代谢性酸中毒、强离子差、强离子间隙。
选择的数据包括前瞻性和回顾性研究、综述及病例报告。
酸碱紊乱通常采用传统的亨德森 - 哈塞尔巴尔赫方法进行分析，该方法将血浆pH值的变化归因于血浆碳酸氢盐或动脉血二氧化碳分压（PaCO2）的改变。然而，这种方法似乎并不充分，因为碳酸氢盐和PaCO2是完全相互依赖的。此外，它没有考虑弱酸如白蛋白在血浆pH值测定中的作用。根据斯图尔特概念，血浆pH值取决于血浆水的解离程度，这由3个独立变量决定：1）强离子差（SID），即血浆中所有强阳离子和阴离子之间的差值；2）血浆弱酸的量；3）PaCO2。因此，代谢性酸碱紊乱总是由SID的变化（酸中毒时降低）或弱酸的变化（酸中毒时增加）引起，而呼吸性紊乱仍然是PaCO2变化的结果。这些病理生理因素对于分析危重症患者复杂的酸碱失衡很重要。例如，由于弱酸减少，低白蛋白血症会增加SID，这可能抵消pH值的降低和阴离子间隙的升高。因此，如果仅使用传统方法，低白蛋白血症可能会掩盖代谢性酸中毒，因为pH值正常且阴离子间隙正常。在这种情况下，代谢性酸中毒和碱中毒的关联仅分别表现为SID降低和弱酸浓度降低。这个概念有助于建立高氯性酸中毒与输注含高浓度氯离子的溶质（如0.9%氯化钠）之间的关系。最后，斯图尔特概念有助于理解碳酸氢钠以及乳酸钠会导致血浆碱化。事实上，钠离子留在血浆中，而阴离子（乳酸根或碳酸氢根）被代谢，导致血浆SID增加。
由于其简单性，传统的酸碱紊乱亨德森 - 哈塞尔巴尔赫方法仍然常用。然而，它提供的病理生理分析不充分，可能导致误诊。尽管斯图尔特概念看似复杂，但它能精确理解酸碱紊乱的机制。它必须成为分析复杂酸碱异常的最合适方法。
