Understanding Stewart's Approach

UNDERSTANDING STEWART’S
APPROACH
Dr. Dipankar Dutta
• Peter Stewart entered the arena in the early
1980s
• By that time most practitioners were tracking
pH
• In 1960, there had been a landmark
development - the introduction of ‘base
excess’ (BE) by Siggaard-Andersen and Engel
• BE is usually defined as the concentration of
titratable hydrogen ion required to return the
pH of in vitro whole blood to 7.4 at 37 °C, with
PCO2 held at 40 mm Hg
• BE = {[HCO3]−24.4 + (2.3 × [Hb] + 7.7) × (pH −
7.4)} ×(1 − 0.023 × [Hb])
GENERAL PRINCIPLES OF STEWART’S APPROACH
• Electroneutrality
• Conservation of mass---- the amount of a

substance remains constant unless it is added,
removed, generated or destroyed. The relevance is
that the total concentration of an incompletely
dissociated substance is the sum of concentrations
of its dissociated and undissociated forms.
• It is too easy to believe that the concentrations of the hydrogen and
bicarbonate ions, [H+] and [HCO3-], are at the heart of the problem.
• In plasma,  virtually no hydrogen ions present; so  the only thing

that cannot be responsible is [H+]
• And, clinically, both respiratory and metabolic changes affect the

[HCO3-]
So, what is responsible for [H+] and [HCO3-]

• Assuming electroneutrality, the Gamblegram demonstrates
that the ions that fill the SID between the strong cations and
anions are primarily bicarbonate (a factor thus dependent on
the SID) and the total amount of weak acids, including
albumin, which is the most important weak acid.
• The standard (or plasma) base excess allows for altered
buffering in extravascular extracellular fluid and is routinely
calculated by blood gas machines using the Van Slyke
equation
• The reference normal value for standard base excess is 0

mmol/L, and the normal range is −3 to 3 mmol/L, with
increasingly negative values indicating metabolic acidosis and
positive values indicating metabolic alkalosis.
Applying at Bedside
• Weak acids  opposite to the SID in determining
the metabolic side of acid-base disorders.
Acidosis is caused by a decrease in the SID but an
increase in the total weak acid concentration,
whereas the converse is true for alkalosis.
• Albumin in plasma has an overall negative charge

due to the dissociation of hydrogen ions from the
histidine residues
• A 71-year-old female with chronic obstructive
pulmonary disease was admitted to the general
medical ward with pneumonia.
• Physical examination showed rapid shallow
breathing, tachycardia, and expiratory crackles
over the right lung base.
• She was treated with controlled oxygen by face
mask, inhaled β-agonists, steroids and
intravenous antibiotics.
• As congestive cardiac failure was suspected, a loop
diuretic (furosemide) was also prescribed
• (pH =7.32, PaCO2 = [60 mmHg], PaO2 = [52 mmHg]
and SBic 28 mmol/L on room air)
• DAY 4 -- she developed vague abdominal pain,

accompanied by severe tachycardia, tachypnea,
hypotension (blood pressure 86/45 mmHg) and
oliguria. Fluid resuscitation with Hartmann’s solution
was started and the patient was transferred for
urgent surgery.
• Laparotomy confirmed perforated diverticular
disease and severe peritonitis resulting in
sepsis and septic shock. Repeated ABG
evaluations, performed during the 4 days
preceding surgery had shown a steadily
increasing BE without any discernible effect on
pH.
Immediately before OT
• hypercapnic respiratory failure with
concomitant metabolic alkalosis
• “overcompensation” is certainly present
• “primary” metabolic alkalosis with
“compensatory” respiratory acidosis
• septic, hypotensive, and oliguric  surprising
to observe metabolic alkalosis and not ???
acidosis
• The AG (22.6–28.6, depending on calculation
method) had not been calculated because
metabolic acidosis was not detected by
traditional methods of interpretation
• When both the SID effect and ATOT effect on apparent
metabolic alkalosis were calculated, a hidden
metabolic acidosis was revealed (a true BE of −16.4)
due to unmeasured anions, which was well in keeping
with her clinical condition (sepsis and septic shock).
• This acidosis was masked by widened SID (due to

hypochloremia, almost certainly diuretic induced) and
lowered ATOT (due to hypoalbuminemia)
• Stewart’s criticism of the importance of HCO3− and
H+, classifying them as “dependent” variables, is felt
a sacrilege by many physiologists as well as
clinicians.
• HCO3− should be forgotten and “parked” in the back

of the mind and practitioners should be more open-
minded toward adapting the Stewart approach.
Conclusion
• Traditional approaches may adequately detect

simple acid–base disorders in stable patients
but fail to unravel complex disturbances. A
combined Stewart and BE approach may solve
this problem.
Thank you

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UNDERSTANDING STEWART’S

• Conservation of mass---- the amount of a

• In plasma,  virtually no hydrogen ions present; so  the only thing

• And, clinically, both respiratory and metabolic changes affect the

So, what is responsible for [H+] and [HCO3-]

• The reference normal value for standard base excess is 0

• Albumin in plasma has an overall negative charge

• DAY 4 -- she developed vague abdominal pain,

• This acidosis was masked by widened SID (due to

• HCO3− should be forgotten and “parked” in the back

• Traditional approaches may adequately detect

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