Method of analyzing acidbase

disorders

Traditional
(bicarbonate-centered)
model

The Stewart
(strong ion) model

Traditional Approach
(Bicarbonate centered)
The traditional model use easily
measured concentrations of blood
carbon
dioxide
[CO2]
and
bicarbonate [HCO3-]. As in any
chemical reaction in equilibrium, a
change in the concentration of the
reactant or product will move the
reaction in the direction that would
reestablish
equilibrium
(Le
Chateliers principle).

Cause the
equilibrium
shift:

Retention of CO2
Production nonvolatile acid from protein and
organic molecule metabolism
Losses bicarbonate pass through feces and urine
Intake acid or acid precursor

Cause of
acid
deficiency :

Consumption of hydrogen in several organic

anion metabolism
Depletion acid from vomiting and urine
Losses of ions due to diarrhea
Depletion CO2 from hyperventilation

Compensation:
Acid-base equilibrium is regulated by buffering
agent that linked with Hydrogen to regulation pH
alteration

Extracellular buffer

Intracellular buffer

Bicarbonate and
ammonia

Protein and
phosphate

CO2 can move

through H2CO3 to
hydrogen and
bicarbonate

Bicarbonate
buffering system is
the primary keys

Anion Gap
Is the different between (positive charged ion) and
(negative charged ion) in serum, plasma, or urine and the
large of different assumed as Gap
If Gap higher than the normal
value indicated as high anion
gap metabolic acidosis

Measured cation : Na, K, Ca, Mg

Unmeasured cation : protein, H, paraprotein di myeloma
Measured anion : Cl, HCO3, PO43Unmeasured anion : sulfat dan protein

 Anion Gap
The anion gap, consisting of the sum total of all
unmeasured charged specie (predominantly
albumin) in plasma, is calculated below as :

Normal value < 11mEq/L

Anion Gap Classification

High
Anion Gap
Normal
Anion Gap
Low Anion
Gap

The Stewart (or strong ion) model

The method to estimate acid-base balance with mathematics
models it is relevant because it is a powerful construct that can
shed light on an important biologic system

variables:
a. Dependent : H, OH, HCO3, CO3, HA, A
b. Independent : PCO2, A tot, SID
All the variable will construct a complex mathematics model

SID (strong ion difference) : the difference between total

concentration of strong cation and strong anion

Metabolic
disturbance

Intravenous
Fluids and
Content

Compensation
for respiratory
disorder and
Urinary

& STRONG
ION

Gastrointestinal
Losses

Urinary Charge
Gap

Metabolic disturbance & STRONG ION

Gastrointestinal Losses & STRONG ION

Losses of ions due to diarrhea are associated with
the development of metabolic acidosis or metabolic
alkalosis.
Diarrhea is the cause of metabolic alkalosis, rather than
acidosis. Large losses of chloride may occur in patients who
have villous adenomas or other secretory diarrheas that cause
depletion of chloride. Na, K, and Cl concentration would be less
than the normal plasma bicarbonate concentration.

High losses of chloride from vomiting or after the

use of loop diuretics, cause hypocloremic alkalosis

Urinary Charge Gap& STRONG ION

Measurements of urinary electrolyte concentrations and flow rate
indicate renal acidbase function even without measurement of
urinary bicarbonate.

. Negative
Urinary Charge
Gap

A negative value for the urinary net

charge gap indicates the presence of the
unmeasured cation, ammonium (excretion
of ammonium chloride).

. Positive Urinary
Charge Gap

A positive value for the urinary net charge

gap indicates excretion of an unmeasured
anion.

Compensation for respiratory disorder and Urinary &

STRONG ION

Respiratory alkalosis : The

hyperchloremic
renal
compensation for respiratory
alkalosis is the excretion of
filtered sodium and potassium
with bicarbonate, because low
PaCO2 decreases proximal and
distal hydrogen secretion.

Respiratory acidosis : high PaCO2

increases production of ammonia
by
the
kidney,
results
in
hypochloremia. The elevated PaCO2
increases the renal reabsorption of
sodium and bicarbonate, so the
compensation is maintained.

Intravenous Fluids and Content &

STRONG ION
Saline-induced
acidosis,
which
develops because the infusion of
aproportionately
high
sodium
chloridecontaining solution, one
with a sodium-to-chloride ratio of
less than 140:100, will decrease the
plasma strong ion difference and the
bicarbonate concentration.
The insufficient urinary excretion of the extra chloride as
ammonium chloride leads to metabolic acidosis.

Figure 1 (facing page). Renal Tubular Cells with Transporters That Are Targets
of Hormones, Diuretics, and Mutations Affecting AcidBase Balance.

Conclusion
Clinical evidence can be interpreted with the use of
both the strong ion theory and the traditional
bicarbonate centered approach to provide an optimal
understanding of acidbase disorders.

An understanding of the consequences of these

disturbances helps in the diagnosis and treatment of
the associated acid base disorders.

References

Julian L. Seifter, M.D. 2014. Disorders of Fluids and

Electrolytes : Integration of Acid-Base and Electrolyte
Disorders. Review. N Engl J Med. 371: 1821-31

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