Base Excess: the basics

October 2017

Chris Higgins
Little Acre, Main Road
Shurdington
Nr Cheltenham
Gloucester
GL51 4XF, UK
E-mail: [email protected]

Blood gas analysis, which allows assessment of patient between actual base excess (ABE) and standard base
acid-base status, involves measurement of the pH and excess (SBE). Since an understanding of the clinical utility
partial pressure (p) of oxygen (pO2(a)) and carbon dioxide of base excess depends on appreciating the difference
(pCO2(a)) in arterial blood. These measurements allow between respiratory and metabolic acid-base disorders
calculation of further parameters that are generated and the compensation they invoke, the article begins
during blood gas analysis, including concentration of with a very brief and necessarily simplistic overview of
plasma bicarbonate [HCO-3] and base excess (BE), the the traditional approach to acid-base pathophysiology
subject of this article. BE helps in the assessment of and interpretation of blood gas analysis reports.
acid-base status because it is a quantitative measure
of the non-respiratory (metabolic) component of acid- Health demands that hydrogen ion concentration [H+],
base balance. Abnormal BE is thus a feature of both i.e. pH of extracellular fluid is maintained within narrow
metabolic acidosis and metabolic alkalosis; and the limits (pH 7.35-7.45) despite normal metabolism being
extent to which BE deviates from normal is indicative associated with continuous production of volatile acid
of the severity of these two acid-base disturbances. (carbon dioxide, CO2) and non-volatile acids (lactic acid,
BE is by definition unaffected by changes in pCO2(a) phosphoric acid, acetoacetic acid, ß-hydroxybutyric
(the respiratory component of acid-base balance) and acid, etc.). Three main physiological processes are
therefore remains within normal limits in respiratory acid- involved in the maintenance of normal blood pH
base disturbances unless they have provoked metabolic (termed acid-base balance or acid-base homeostasis).
compensation. This article will include discussion of the They are respiratory elimination of CO2 in expired air;
concept of base excess, its derivation, and the distinction blood buffering of hydrogen ions by bicarbonate (and

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 other chemical buffers, including hemoglobin; and renal in bicarbonate concentration [HCO-3]. The compensatory
regulation of bicarbonate and hydrogen-ion excretion response is increased respiratory ventilation and thereby
in urine. Acid-base homeostasis is thus dependent reduction in pCO2(a). Although both [HCO-3] and pCO2(a)
on adequate bicarbonate buffer in blood as well as are abnormally reduced, the ratio that determines that
normally functioning lungs and kidneys. pH is normal or at least closer to normal was the case
prior to compensation. Compensation of acid-base
The so-called “traditional” approach to acid-base disorders underlines the prime physiological importance
pathophysiology that underlies the application of blood of maintaining ECF pH within normal limits.
gas analysis in assessment of patient acid-base status
developed from the pioneering work of two clinician- Metabolic disturbances provoke a respiratory
physiologists, Henderson and Hasselbalch, a little over compensatory response, and respiratory disturbances
a century ago. The familiar modified version of their provoke a compensatory metabolic response via
Henderson-Hasselbalch equation reveals the relationship renal regulation of bicarbonate and hydrogen-ion
between blood pH and two other parameters generated excretion. The renal mechanisms involved in metabolic
during blood gas analysis: pCO2(a) and plasma compensation for respiratory acid-base disturbances are
bicarbonate concentration [HCO-3] [1], viz.: slower than those involved in respiratory compensation
for metabolic disturbances (days compared to hours).
pH = pK + log([HCO-3] / pCO2(a) × 0.03) Eqtn. 1 [1] Compensation may be complete (pH restored to normal
limits) but more often is partial (pH returns towards
Removing constants from this equation we can state normal but remains just outside normal range).

pH ∞ [HCO-3] / pCO2(a) Eqtn. 2 Although each of the four acid-base disturbances can
occur in isolation, some patients with multiple medical
or in words: pH is proportional to, or determined by, the conditions may be suffering more than one, or even
ratio of bicarbonate concentration [HCO-3] to pCO2(a). more than two types of acid-base disturbance So for
So long as the ratio remains within normal limits, pH example, a diabetic patient in ketoacidosis who also has
remains within normal limits. Equation 2 also allows a history of chronic lung disease may well present with
that acidemia (reduced blood pH) can result from either a mixed acid-base disorder (compensated metabolic
a decrease in bicarbonate concentration [HCO-3] or acidosis due to diabetes, and compensated respiratory
increase in pCO2(a); whilst alkalemia (increased blood acidosis due to chronic lung disease).
pH) can result from either an increase in bicarbonate
concentration [HCO-3] or decrease in pCO2(a). Base excess – a measure of the metabolic
component of acid-base disorders
Since pCO2(a) is determined by the rate of respiratory
ventilation, it is referred to as the respiratory component In accordance with the traditional approach to acid-base
of acid-base balance, and bicarbonate is referred to as physiology, we have seen that blood pH is determined
the non-respiratory or metabolic component of acid- by the respiratory component (pCO2(a)) and the non-
base balance. This nomenclature is used to identify respiratory (metabolic) component ([HCO-3]). Elucidation
the four main classes of primary acid-base disturbance of acid-base disorders, particularly mixed disorders,
listed in Table I below. The third column in this table is helped by quantitating the individual contribution
highlights the quite normal compensatory response to that each of these two components is making to the
primary acid-base disturbance, which aims to restore patient’s pH. pCO2(a) is a reliable defining index of the
normal pH by restoring the ratio described in equation respiratory component, but [HCO-3] is an unsatisfactory
2 above. For example, the reduced pH that occurs in index of the metabolic component, not least because it
metabolic acidosis is a consequence of primary reduction can be affected by change in pCO2(a) [1].

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 Initial (uncompensated) Type of compensation –
Acid-base disturbance
blood gas values resulting blood gas values
Respiratory increased ventilation
pH reduced (<7.35)
pH now closer to normal, may be
Metabolic acidosis [HCO-3] reduced (<23 mmol/L)
low normal
(primary decrease in [HCO-3]) pCO2(a) normal (4.7-6.0 kPa)
[HCO-3] unchanged – still reduced
(35-45 mmHg)
pCO2(a) now reduced
pH increased (>7.45) Respiratory decreased ventilation
Metabolic alkalosis [HCO-3] increased (>28 mmol/L) pH now closer to normal
(primary increase in [HCO-3]) pCO2(a) normal (4.7-6.0 kPa) [HCO-3] unchanged – still increased
(35-45 mmHg) pCO2(a) now increased
Metabolic – renal adjustments
pH reduced (<7.35)
pH now closer to normal, may be
Respiratory acidosis [HCO-3] normal (23-28 mmol/L)
low normal
(primary increase in pCO2(a)) pCO2(a) increased (>6.0 kPa)
[HCO-3] now increased
(>45 mmHg)
pCO2(a) unchanged, still increased
Respiratory alkalosis Metabolic – renal adjustments
pH increased (>7.45)
(primary decrease in pCO2(a)) pH now closer to normal, may be
[HCO-3] normal (23-28 mmol/L)
high normal
pCO2(a) decreased (<4.7kPa)
[HCO-3] now decreased
(<35 mm Hg)
pCO2(a) unchanged, still decreased
TABLE I: The four acid-base disturbances (with metabolic component [HCO-3] highlighted)

An alternative to bicarbonate as an index of the Normal base excess, i.e. 0 mmol/L (range –3 mmol/L to
metabolic component is base excess (BE), a parameter +3 mmol/L), indicates that any deviation from normal
devised from experimentation and traditional acid-base pH (i.e. <7.35 or >7.45) is due solely to deviation from
theory by Siggaard-Andersen in 1960 [2]. normal of the respiratory component, pCO2(a).

BE can be defined as the concentration of strong Returning to the definition above: “BE is the
acid or strong base (expressed in mmol/L) required to concentration of acid or base required to ….. etc. etc.”
return the pH of an in vitro sample of whole blood to explains why BE could have a positive or negative value.
pH 7.40, whilst pCO2(a) of the sample is maintained at If the in vitro sample was >7.40 (relatively alkalotic), then
5.32 kPa (40 mmHg) and temperature of the sample is acid would be needed to return pH to 7.40, whereas
maintained at 37 °C [3]. (Note that the pH and pCO2(a) if the sample was <7.40 (relatively acidotic), then base
values in this definition are at the midpoint of their would be needed to return the pH to 7.40. In the first
respective reference range.) case BE would have a positive value (i.e. the sample
has relatively too much base), and in the second case,
By artificially maintaining the pCO2(a) of an in vitro BE would have negative value (i.e. the sample has not
blood sample within normal limits, any deviation from enough base). Thus, an abnormally negative base excess
normal pH 7.40 must be due to the total effect of the (e.g. BE –8 mmol/L) indicates metabolic acidosis and an
non-respiratory metabolic component (which includes abnormally positive base excess (e.g. BE +8 mmol/L)
the bicarbonate contribution). If there is no deviation, indicates metabolic alkalosis. The higher the number
i.e. the in vitro sample with pCO2(a) 5.32 kPa already (integer), the more severe is the metabolic disturbance.
has a pH of 7.40, no added strong acid or base is A negative BE is sometimes referred to as a base deficit
required and base excess is therefore zero. (BD).

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 Calculation of BE – distinction between or 150 g/L) is used (i.e. 5 g/dL or 50 g/L). All other

Actual BE (ABE) and Standard (SBE) elements of the Van Slyke equation (Eqtn. 3 above)
remain unchanged. The simple expedient of using a

From his original in vitro titration work on whole-blood standardized low hemoglobin concentration (5 g/dL) or,

samples Siggaard-Andersen developed a complex as in some algorithms, (3 g/dL) rather than the patient’s

equation which he named the Van Slyke equation in actual hemoglobin concentration renders a base excess

honor of the US luminary of acid-base physiology, Donald value that is CO2–invariant, i.e. not affected by change

Van Slyke [4]. This equation allows calculation of whole- in pCO2(a).

blood base excess from plasma pH, plasma bicarbonate

[HCO-3] and blood hemoglobin concentration [Hb] in The base excess derived from this modified equation is,

mmol/L: confusingly, variously described in the literature as:

BE = {[HCO-3] – 24.4 + (2.3 × [Hb] + 7.7) × (pH – 7.4)} • base excess (BE)

× (1 – 0.23 × [Hb]) (Eqtn. 3) • standard base excess (SBE),

• base excess of extracellular fluid (BEecf), or

The base excess derived from this equation is, • concentration of base in extracellular fluid (ECF),

confusingly, variously described in the literature as: cBase(ECF).

• base excess (BE) To illustrate the practical significance of the difference

• actual base excess (ABE), between the two expressions of base excess, consider

• whole-blood base excess (BEblood) or the blood gas results from a patient with Type 2

• concentration of base in blood(B), cBase(B). respiratory failure and fluctuating pCO2(a) (Table II
below) reported by Morgan [8]. If base excess is a truly

Although the in vitro accuracy of this expression of base CO2-invariant parameter, then this patient’s base excess

excess has been confirmed [5], it is less satisfactory than should not have been affected by the 2 hour decrease

this implies because it has been shown to be affected by in pCO2(a) from 172 mmHg to 124 mmHg since his

extreme in vivo change in pCO2(a) [6, 7] – it is apparently metabolic acid-base status ([HCO-3]) was unchanged.

not a truly CO2-invariant parameter, as it ideally needs In fact, actual base excess increased significantly (>4

to be. mmol) but standard base excess increased very little (1.6
mmol/L).

The CO2 invariance of this expression of base excess

in vitro but not in vivo is attributed to the fact that Because standard base excess is less affected by in vivo

in vivo buffering occurs throughout the total ECF change in pCO2(a) than actual base excess, it is widely

(i.e. intravascular plus interstitial) and not just the considered to be the preferable index of the metabolic

intravascular ECF as reflected in isolated (in vitro) blood component [7, 9, 10, 11]. Results of a 2009 study [12],

samples. This whole-blood base excess effectively however, suggest that in critically ill patients, standard

overestimates the buffering effect of hemoglobin in base excess may not be as independent of pCO2(a) as

vivo. was once supposed.

To overcome this problem a modified version of the Van Base excess, compensation and mixed
Slyke equation was devised [7] which better simulates acid-base disorders
the buffering effect of hemoglobin throughout the
whole ECF. Rather than input the patients actual blood By definition base excess remains normal (in the range of

hemoglobin concentration, a standardized hemoglobin –3 to +3) in the two acute (uncompensated) respiratory

concentration of a third of normal value (15 g/dL acid-base disorders: acute respiratory acidosis and

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 Reference range Patient’s initial Results 2 hours
results later
pH 7.35-7.45 7.16 7.30
pCO2(a) (mmHg) 35-45 172 124
[HCO- 3] (mmol/L) 22-28 59 59
Actual Base Excess (mmol/L) –3 to +3 19.1 23.5
Standard Base Excess (mmol/L) –3 to +3 29.1 30.7
TABLE II: Blood gas results from a patient with Type 2 respiratory failure [adapted from ref 8]

Acid-base disturbance Initial (uncompensated) Type of compensation – re-

blood gas values sulting blood gas values
Respiratory increased ventilation
pH reduced (<7.35)
Metabolic acidosis pH now closer to normal, may be low
BE abnormal (<-3 mmol/L)
(primary decrease in [HCO-3]) normal
pCO2(a) normal (4.7-6.0 kPa)
BE remains unchanged and abnormal
(35-45 mmHg)
pCO2(a) now reduced
pH increased (>7.45) Respiratory decreased ventilation
Metabolic alkalosis BE abnormal (>+3 mmol/L) pH now closer to normal
(primary increase in [HCO-3]) pCO2(a) normal (4.7-6.0 kPa) BE remains unchanged and abnormal
(35-45 mmHg) pCO2(a) now increased
Respiratory acidosis pH reduced (<7.35) Metabolic – renal adjustments
(primary increase in PaCO2) BE normal (–3 to +3 mmol/L) pH now closer to normal, may be low
pCO2(a) increased (>6.0 kPa) normal
(>45 mmHg) BE abnormal (>+3 mmol/L)
pCO2(a) unchanged, still increased
Respiratory alkalosis pH increased (>7.45) Metabolic – renal adjustments
(primary decrease in pCO2(a)) BE normal (–3 to + 3 mmol/L) pH now closer to normal, may be high
pCO2(a) decreased (<4.7kPa) normal
(<35 mmHg) BE abnormal (<-3 mmol/L)
pCO2(a) unchanged, still decreased

TABLE III: The four acid-base disturbances (with metabolic index, base excess (BE) highlighted)

acute respiratory alkalosis. Base excess is abnormal (<- complex, mixed acid-base disorders are contributing to
3) in primary metabolic acidosis and abnormal (>+3) in the patient’s acid-base status.
primary metabolic alkalosis. Base excess is also abnormal
during metabolic compensation for primary respiratory These derived equation rules allow calculation of the
disorders. Table III is a summary of this information approximate expected compensatory response to
with BE values (highlighted). primary acid-base disorders.

The four equation rules in Table IV below, developed Thus, for example, supposing we have a patient whose
from a 1998 study [13], help in predicting appropriate clinical history (chronic obstructive pulmonary disease
compensation for primary acid-base disturbance. (COPD)), and blood gas results (pH 7.34, pCO2(a) 60
If these rules are not reflected in patient results, it mmHg (7.98 kPa), SBE +7.6 mmol/L) indicate chronic
suggests either incomplete compensation or that more (compensated) respiratory acidosis. We can use the

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 Acid-base disturbance Equation rule
1. Acute respiratory acidosis/alkalosis ∆SBE = 0 × ∆PaCO2
2. Chronic respiratory acidosis/alkalosis ∆SBE = 0.4 × ∆PaCO2
3. Metabolic acidosis ∆pCO2(a) = ∆BE
4. Metabolic Alkalosis ∆pCO2(a) = 0.6 × ∆BE

TABLE IV: The four pCO2(a)/SBE rules [13]

Note: ∆SBE = amount that patient’s standard base excess (SBE) deviates from normal (0 mmol/L);
∆pCO2(a) = amount that patient’s pCO2(a) deviates from normal (40 mmHg).

above rule 2 to confirm that the abnormal SBE is due Summary

to metabolic compensation alone. In this case (0.4
× ∆pCO2(a)) = 0.4 × 20 = 8, which is, more or less, • Base excess is a calculated parameter generated
equal to the patient’s SBE. We can therefore conclude during blood gas analysis.
that the metabolic compensation reflected in the SBE • The clinical utility of base excess is as an index of
is appropriate, and that these blood gas results are the metabolic (non-respiratory) component of acid-
internally consistent with a single acid-base disorder, base balance; it is therefore helpful in assessing
namely chronic (i.e. compensated) respiratory acidosis. patient acid-base status.
If the SBE were in fact significantly less or more than • There are two expressions of base excess: actual
+7.6 mmol/L, then consideration should be given to base excess (ABE) and standard base excess (SBE)
the possibility that the acid-base status of this patient that differ very slightly in the way they are calculated.
is more complex than previously thought, and might • SBE (alternative nomenclature: BEecf and
reflect a mixed disturbance (e.g. chronic respiratory cBase(ECF)) is widely considered to be preferable to
acidosis and metabolic acidosis or chronic respiratory ABE because it is less affected by change in pCO2(a).
acidosis and chronic respiratory alkalosis). • In health, base excess (SBE and ABE) is maintained
within the approximate reference range of minus
Rule 3 states that in metabolic acidosis, the compensatory (–)3 mmol/L to plus (+)3 mmol/L.
change in pCO2(a) (measured in mmHg) is approximately • Base excess (SBE and ABE) is abnormal in metabolic
identical to the change in SBE that induced it. Thus, acidosis and metabolic alkalosis – abnormally
consider a case of metabolic acidosis in which SBE is negative value in metabolic acidosis and abnormally
–15 mmol/L, i.e. ∆SBE is 15. Respiratory compensation positive value in metabolic alkalosis.
for this degree of metabolic acidosis should, according • The magnitude of the deviation from normal
to the rule, result in a ∆pCO2(a) of 15. This represents a (reference) range of base excess (SBE and ABE) is
measured pCO2(a) of (40 – 15) 25 mmHg. Thus, a single indicative of the severity of metabolic acidosis and
acid-base disorder (namely, compensated metabolic metabolic alkalosis.
acidosis) is confirmed in a patient with SBE –15 mmol/L, if • Base excess (ABE and SBE) is unaffected by
pCO2(a) is approximately equal to 25 mmHg (3.32 kPa). respiratory acid-base disturbances unless they
provoke metabolic compensation.
Rule 1 reminds that acute (as opposed to chronic) • Compensation for respiratory acidosis is associated with
respiratory acid-base disorders are not associated with abnormally positive base excess value (ABE and SBE).
significant metabolic compensation (because the renal Compensation for respiratory alkalosis is associated with
mechanism involved is relatively slow), and in such abnormally negative base excess value (ABE and SBE).
cases BE remains within normal limits, i.e. ∆SBE = 0, • Base excess (SBE) results are used in “rule of
irrespective of the pCO2(a). thumb” calculations to assess compensation for
acid-base disturbances.

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Data subject to change without notice.

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