Rhodes, Andrew and Cusack, Rebecca J. (2000) Arterial blood gas analysis and lactate. Current Opinion in Critical Care, 6 (3), 227-231. (doi:10.1097/00075198-200006000-00015).
Abstract
It has long been recognized that a disturbance of the homeostatic mechanisms controlling the body's acid-base balance is associated with an increased risk of organ dysfunction and death in the critically ill patient. Despite acid-base imbalance being an integral aspect of ongoing pathologic processes in a large number critically ill patients, the importance of understanding the fundamental principals behind the physiology has been largely ignored. Measurement of the standard bicarbonate and base excess have been used for decades as indicators of metabolic acid-base disturbances. These techniques, however, are dependent upon normal electrolyte, water, and albumin content in the patients. Needless to say, these conditions are rarely met in the critically ill patient, and estimations of the degree of metabolic disturbance may be, therefore, inaccurate. The anion gap has been proposed to give a better indication as to the origin of the metabolic upset. However, this measurement is still reliant upon normal albumin and PCO2 levels. Serum lactate levels have been used as a prognostic marker in the critically ill with some degree of success, but the metabolism of lactate is complex and incompletely understood. The belief that lactates can be accurately used as a stand-alone marker of outcome and mortality is thus naive. More recently, quantitative studies on acid-base imbalance have shown that three independent variables determine the hydrogen and bicarbonate ion concentrations in complex solutions such as plasma. These principles have been developed such that estimates of metabolic derangement can be made in the critically ill without making incorrect assumptions about albumin and free water concentrations. These newer techniques may give improved insights as to the origins to the acid-base disturbances seen in the critically ill and thus aid therapy. (C) 2000 Lippincott Williams and Wilkins, Inc.
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