Printed from acutecaretesting.org
Journal Scan
December 2018
Understanding base excess – a review article
Summarized from Berend K. Diagnostic use of base excess in acid-base disorders. New Eng J Med 2018; 378: 1419-28.
Arterial blood gas analysis has two clinical utilities: assessment of blood oxygenation status and assessment of acid-base status. Assessment of acid-base status depends on measurement of pH and partial pressure of carbon dioxide (pCO2) in a sample of arterial blood using electrodes housed in the blood gas analyzer, and two further calculated parameters, bicarbonate (HCO3-) concentration and base excess (BE), that are derived by calculation from measured pH and pCO2 values.
Knowledge of patient pH, pCO2 and HCO3- is sufficient to determine if acid-base status is normal (all three parameters within their respective normal range) and if it is not, will indicate which of four uncompensated acid-base disturbances (respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic alkalosis) is present. Each of these uncompensated acid-base disturbances is characterized by a particular pattern of pH, pCO2 and HCO3- results, and depends on the notion that pCO2 is the respiratory component of acid-base balance and HCO3- is the (non-respiratory) metabolic component of acid-base balance.
So how does base excess contribute to assessment of patient acid-base status and what is base excess anyway? Answers to these questions are contained in this recently published review article on base excess that helps to demystify aspects of this somewhat controversial blood gas parameter that students of acid-base pathophysiology often struggle to understand.
The article begins with a useful brief historical overview of the application of blood gas analysis in assessing acid-base status, from inception of blood gas analysis in the early 1950s. 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-respiratory) metabolic component of acid-base balance. They defined base excess as the amount of strong acid (in mmol/L) that needs to be added in vitro to 1 liter of fully oxygenated blood in order to return the sample to standard (normal) conditions (pH 7.40, pCO2 40 mmHg and temperature 37 °C.) Of course, as the author points out, if blood already has a pH of 7.40, a pCO2 of 40 mmHg and a temperature of 37 °C, then base excess is by definition 0 mmol/L.
The notion that base excess was, as Astrup and Siggaard-Andersen claimed, an accurate index of the non-respiratory component of acid-base balance was challenged by US experts in the field, precipitating the so-called “great trans-atlantic acid-base debate” which the author outlines. In response to US criticism of the assumptions made in developing the equation used to calculate base excess, Siggaard-Andersen made a slight change (detailed by the author of this review) to the equation and called the changed index: standard base excess (SBE).
Following this historical perspective, the author focuses on the confusing nomenclature surrounding the concept of base excess and defines some terms including: actual base excess (ABE), standard base excess (SBE) and base deficit (BD). He also details the equations used in blood gas analyzer algorithms to calculate ABE and SBE.
There follows a section devoted to discussion of how SBE can be used to fully elucidate acid-base disturbances, including compensated acid-base disturbances and mixed acid-base disturbances. In particular, the author provides two algorithms that incorporate SBE (and albumin-corrected anion gap): one for investigation of acidemia (pH <7.38) and the other for investigation of alkalemia (pH >7.42). Three case histories are included to illustrate the use of these algorithms.
The final section of this article is a review and discussion of the accumulated evidence in the literature that SBE is a useful predictor of severity of critical illness associated with hypovolemic shock and consequent metabolic acidosis.
Knowledge of patient pH, pCO2 and HCO3- is sufficient to determine if acid-base status is normal (all three parameters within their respective normal range) and if it is not, will indicate which of four uncompensated acid-base disturbances (respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic alkalosis) is present. Each of these uncompensated acid-base disturbances is characterized by a particular pattern of pH, pCO2 and HCO3- results, and depends on the notion that pCO2 is the respiratory component of acid-base balance and HCO3- is the (non-respiratory) metabolic component of acid-base balance.
So how does base excess contribute to assessment of patient acid-base status and what is base excess anyway? Answers to these questions are contained in this recently published review article on base excess that helps to demystify aspects of this somewhat controversial blood gas parameter that students of acid-base pathophysiology often struggle to understand.
The article begins with a useful brief historical overview of the application of blood gas analysis in assessing acid-base status, from inception of blood gas analysis in the early 1950s. 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-respiratory) metabolic component of acid-base balance. They defined base excess as the amount of strong acid (in mmol/L) that needs to be added in vitro to 1 liter of fully oxygenated blood in order to return the sample to standard (normal) conditions (pH 7.40, pCO2 40 mmHg and temperature 37 °C.) Of course, as the author points out, if blood already has a pH of 7.40, a pCO2 of 40 mmHg and a temperature of 37 °C, then base excess is by definition 0 mmol/L.
The notion that base excess was, as Astrup and Siggaard-Andersen claimed, an accurate index of the non-respiratory component of acid-base balance was challenged by US experts in the field, precipitating the so-called “great trans-atlantic acid-base debate” which the author outlines. In response to US criticism of the assumptions made in developing the equation used to calculate base excess, Siggaard-Andersen made a slight change (detailed by the author of this review) to the equation and called the changed index: standard base excess (SBE).
Following this historical perspective, the author focuses on the confusing nomenclature surrounding the concept of base excess and defines some terms including: actual base excess (ABE), standard base excess (SBE) and base deficit (BD). He also details the equations used in blood gas analyzer algorithms to calculate ABE and SBE.
There follows a section devoted to discussion of how SBE can be used to fully elucidate acid-base disturbances, including compensated acid-base disturbances and mixed acid-base disturbances. In particular, the author provides two algorithms that incorporate SBE (and albumin-corrected anion gap): one for investigation of acidemia (pH <7.38) and the other for investigation of alkalemia (pH >7.42). Three case histories are included to illustrate the use of these algorithms.
The final section of this article is a review and discussion of the accumulated evidence in the literature that SBE is a useful predictor of severity of critical illness associated with hypovolemic shock and consequent metabolic acidosis.
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