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Base excess (BE) was introduced by Siggaard-Andersen in 1960 as an answer to the forty-year-long quest for a reliable, stand-alone marker of metabolic acidosis/alka-losis, independent from co-existing respiratory derange-ments, and able to quantify the severity of the disorder [1]. Previously, several parameters had been examined.
Apr 11, 2018 · The low pH, the high Pa co2, and a standard base excess above 2 mmol per liter suggest a chronic respiratory acidosis ( Table 1 ). One thus expects the standard base excess, calculated as 0.4× ...
May 10, 2023 · Thus, base deficit and base excess are used interchangeably. Normal base excess values range from -3 to +3. Therefore, base excess of -5 indicates metabolic acidosis, whereas +5 indicates metabolic alkalosis. Base excess values are frequently used in critically ill patients to analyze acid-base disturbance (9).
We learn here that the concept of base excess was developed in 1958 by two Danish clinical biochemist pioneers of blood gas analysis, Poul Astrup and Ole Siggaard-Andersen, on the basis of in vitro human-blood-titration experiments. The aim of their experiments was to develop an index (they called it base excess) to quantify the (non ...
Furthermore, in fetal acid-base studies it is of interest to evaluate the correlation of clinical parameters (e.g. the APGAR score and the fetal heart frequency (FHF)) to the spectrum of these four metabolic acid-base variables, the "base excess family" (Table I). Therefore the question must arise: Which base excess should preferably be used?
Base excess (BE) is derived from the whole blood buffer curve developed by Siggaard-Anderson and is defined as the amount of acid or base necessary to titrate a 1 liter of blood to a pH of 7.4 if PCO 2 is held constant at 40 mmHg. 21,22 Because PCO 2 is held constant, the BE is reflective of the nonrespiratory component of the organism's buffer ...
May 31, 2022 · Understanding base excess (BE): merits and pitfalls. Base excess (BE) was introduced by Siggaard-Andersen in 1960 as an answer to the forty-year-long quest for a reliable, stand-alone marker of metabolic acidosis/alkalosis, independent from co-existing respiratory derangements, and able to quantify the severity of the disorder [ 1 ].
