Acid-base and Electrolyte Disorders

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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