Morris C G, Low J
Intensive Care Medicine and Anaesthesia, Derby Hospitals Foundation Trust, Derby Royal Infirmary, London Road, Derby DE1 2QY, UK.
Anaesthesia. 2008 Mar;63(3):294-301. doi: 10.1111/j.1365-2044.2007.05370.x.
Metabolic acidaemia (pH < 7.35 not primarily related to hypoventilation) is common amongst the critically ill and it is essential that clinicians caring for such patients have an understanding of the common causes. The exclusive elimination routes of volatile (carbon dioxide), organic (lactic and ketone) and inorganic (phosphate and sulphate) acids mean compensation for a defect in any one is limited and requires separate provision during critical illness. We discuss the models available to diagnose metabolic acidosis including CO2/HCO3(-) and physical chemistry-derived (Stewart or Fencl-Stewart) approaches, but we propose that the base excess and anion gap, corrected for hypoalbuminaemia and iatrogenic hyperchloraemia, remain most appropriate for clinical usage. Finally we provide some tips for interpreting respiratory responses to metabolic acidosis and how to reach a working diagnosis, the consequences of which are considered in Part 2 of this review.
代谢性酸血症（pH < 7.35，并非主要由通气不足引起）在危重症患者中很常见，照顾此类患者的临床医生必须了解其常见病因。挥发性酸（二氧化碳）、有机酸（乳酸和酮酸）和无机酸（磷酸盐和硫酸盐）的唯一排泄途径意味着对任何一种酸排泄缺陷的代偿都是有限的，并且在危重症期间需要分别进行处理。我们讨论了可用于诊断代谢性酸中毒的模型，包括二氧化碳/碳酸氢根（CO2/HCO3(-)）以及基于物理化学原理的（Stewart或Fencl-Stewart）方法，但我们认为，校正低白蛋白血症和医源性高氯血症后的碱剩余和阴离子间隙仍最适用于临床。最后，我们提供了一些解读代谢性酸中毒呼吸反应及做出初步诊断的技巧，本综述的第2部分将讨论其后果。
