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Method of analyzing acidbase
disorders
Traditional
(bicarbonate-centered)model
The Stewart
(strong ion) model
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Traditional Approach
(Bicarbonate centered)
The traditional model use easily
measured concentrations of blood
carbon dioxide [CO2] andbicarbonate [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
Chateliersprinciple).
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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 the
equilibriumshift:
Consumption of hydrogen in several organic
anion metabolism Depletion acid from vomiting and urine
Losses of ions due to diarrhea
Depletion CO2 from hyperventilation
Cause ofacid
deficiency :
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Compensation:Acid-base equilibrium is regulated by buffering
agent that linked with Hydrogen to regulation pHalteration
Extracellular buffer
Bicarbonate andammonia
Intracellular buffer
Protein andphosphate
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Bicarbonatebuffering system isthe primary keys
CO2 can movethrough H2CO3 tohydrogen and
bicarbonate
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Anion Gap
Is the different between (positive charged ion) and(negative charged ion) in serum, plasma, or urine and thelarge of different assumed as Gap
Measured cation : Na, K, Ca, Mg
Unmeasured cation: protein, H, paraprotein di myeloma
Measured anion : Cl, HCO3, PO43-
Unmeasured anion : sulfat dan protein
If Gap higher than the normalvalue indicated as high anion
gap metabolic acidosis
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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
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Anion Gap Classification
High
Anion Gap
Normal
Anion Gap
Low Anion
Gap
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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
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& STRONGION
Metabolic
disturbance
Gastrointestinal
Losses
Urinary Charge
Gap
Compensation
for respiratory
disorder and
Urinary
Intravenous
Fluids and
Content
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Metabolic disturbance & STRONG ION
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Gastrointestinal Losses & STRONG ION
Losses of ions due to diarrhea are associated withthe development of metabolic acidosis or metabolicalkalosis.
Diarrhea is the cause of metabolic alkalosis, rather thanacidosis. Large losses of chloride may occur in patients whohave villous adenomas or other secretory diarrheas that causedepletion of chloride. Na, K, and Cl concentration would be lessthan the normal plasma bicarbonate concentration.
High losses of chloride from vomiting or after theuse of loop diuretics, cause hypocloremic alkalosis
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Urinary Charge Gap& STRONG ION
Measurements of urinary electrolyte concentrations and flow rate
indicate renal acidbase function even without measurement of
urinary bicarbonate.
A negative value for the urinary netcharge gap indicates the presence of theunmeasured cation, ammonium (excretionof ammonium chloride).
. NegativeUrinary ChargeGap
A positive value for the urinary net chargegap indicates excretion of an unmeasuredanion.
. Positive UrinaryCharge Gap
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Compensation for respiratory disorder and Urinary &STRONG ION
Respiratory alkalosis : The
hyperchloremic renalcompensation for respiratoryalkalosis is the excretion offiltered sodium and potassiumwith bicarbonate, because lowPaCO2 decreases proximal and
distal hydrogen secretion.
Respiratory acidosis : high PaCO2increases production of ammoniaby the kidney, results inhypochloremia. The elevated PaCO2increases the renal reabsorption ofsodium and bicarbonate, so thecompensation is maintained.
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Intravenous Fluids and Content &STRONG ION
The insufficient urinary excretion of the extra chloride as
ammonium chloride leads to metabolic acidosis.
Saline-induced acidosis, which
develops because the infusion of
aproportionately high sodium
chloridecontaining solution, onewith a sodium-to-chloride ratio of
less than 140:100, will decrease the
plasma strong ion difference and the
bicarbonate concentration.
Figure 1 (facing page) Renal Tubular Cells with Transporters That Are Targets
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Figure 1 (facing page). Renal Tubular Cells with Transporters That Are Targetsof Hormones, Diuretics, and Mutations Affecting AcidBase Balance.
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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 thesedisturbances helps in the diagnosis and treatment of
the associated acidbase disorders.
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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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THANK YOU