Quantitative physico-chemical analysis of the acidosis of cardiac arrest 英文参考文献.docVIP

Quantitative physico-chemical analysis of the acidosis of cardiac arrest 英文参考文献.doc

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Quantitative physico-chemical analysis of the acidosis of cardiac arrest 英文参考文献

Available online /content/9/4/347 Commentary Quantitative physico-chemical analysis of the acidosis of cardiac arrest Heatherlee Bailey Associate Program Director of Emergency Medicine, Assistant Professor of Emergency Medicine, Drexel University College of Medicine, Philadelphia, PA, USA Corresponding author: Heatherlee Bailey, HBaileyMD@ Published online: 22 July 2005 Critical Care 2005, 9:347-348 (DOI 10.1186/cc3770) This article is online at /content/9/4/347 ? 2005 BioMed Central Ltd See related research by Makino et al. in this issue [/content/9/4/R357] Abstract The study Makino and colleagues performed their prospective obser- vational study in Japan. In that country there is no pre-hospital administration of medication. Blood samples were drawn on arrival before any iatrogenic manipulation. This allows a relatively rare opportunity to collect and study unaltered human cardiac arrest data. The authors comment that some intravenous fluid might have been started immediately before blood draw. Saline-based intravenous fluids are well known to create an acid–base disturbance, in particular a nongap hyperchloremic metabolic acidosis [6–8]. The fluid used during resuscitation was Ringer-based, which has a much smaller effect on the acid–base balance. Metabolic acidosis is a common finding after cardiac arrest. Until recently this acidosis was mainly attributed to lactate. The physico- chemical approach to acid–base balance permits the detection of previously unmeasured ions. These ions have been shown to affect the acid–base status of patients. Introduction The acid–base disturbance in patients suffering cardiac arrest is more complex than previously thought. Makino and colleagues have presented a quantitative assessment of the components that create the disturbance [1]. As previously reported, hyperlactatemia is not the sole cause of metabolic

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