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Changes of serum chloride and metabolic acid‐base state in critical illness
Author(s) -
Funk G.C.,
Doberer D.,
Heinze G.,
Madl C.,
Holzinger U.,
Schneeweiss B.
Publication year - 2004
Publication title -
anaesthesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.839
H-Index - 117
eISSN - 1365-2044
pISSN - 0003-2409
DOI - 10.1111/j.1365-2044.2004.03901.x
Subject(s) - metabolic alkalosis , acid–base reaction , acid–base imbalance , medicine , albumin , acid–base homeostasis , chloride , serum chloride , sodium , base (topology) , critical illness , alkalosis , metabolic acidosis , metabolic disorder , critically ill , metabolic pathway , biochemistry , metabolism , chemistry , acidosis , organic chemistry , mathematical analysis , mathematics
Summary Alterations of electrolytes and albumin cause metabolic acid‐base disorders. It is unclear, however, to what degree these plasma components affect the overall metabolic acid‐base state in the course of critical illness. We performed serial analyses of the metabolic acid‐base state in 30 critically ill patients over the course of 1 week. We applied a physical–chemical acid‐base model and used a linear regression model to determine the influence of sodium, chloride, unmeasured anions and albumin on the net metabolic acid‐base state. Progressive hypochloraemia was identified as the main cause of developing metabolic alkalosis. Changes in serum chloride and unmeasured anions were responsible for changes of 41% and 22% in the metabolic acid‐base state, respectively. Sodium and albumin played a minor role. In conclusion, chloride is the major determinant of metabolic acid‐base state in critical illness.