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Strong Ion Approach to Acid-Base Disorders 325
normal. However, it should be pointed out that Siggaard- less than 5 mmol/L are suggestive of an increase in
Andersen studied human blood with a constant protein unmeasured strong anions. 15 Formulas to estimate
concentration. A BE nomogram has been developed for changes in BE resulting from changes in SID and A tot
dogs 21 using Siggaard-Andersen’s approach. However, are presented in Box 13-4. A complete description of
the canine nomogram has rarely been used because blood thederivationoftheseformulas,aswellastheirlimitations,
7
gas analyzers use the van Slyke equation to calculate BE can be found elsewhere. The BE algorithm isa useful clin-
from measured values for pH, PCO 2 , and hemoglobin con- ical tool despite a few shortcomings. These formulas were
7
centration. Because blood gas analyzers were developed helpful in understanding complex acid-base disorders in
for the human medical market, the van Slyke equation uses dogsandcats. 18,32,52 Unfortunately,nocontrolledclinical
values that assume human blood is being analyzed. studies have been performed in dogs and cats with acid-
The BE has been used clinically for more than a decade base disturbances to assess the accuracy of these formulas,
to assess the metabolic acid-base status in human and there are theoretical limitations in extrapolating tradi-
patients 54 and has been adapted for use in dogs and tional BE calculations for use in dogs and cats. 17 In addi-
cats. 15,18 This approach attempts to take into account tion, the influence of protein on BE is estimated based on
the effect that changes in sodium (i.e., dilutional acidosis data for human albumin, which behaves differently than
andconcentrationalkalosis),chloride(i.e.,hypochloremic canine and feline albumin.
alkalosis and hyperchloremic acidosis), phosphate (i.e.,
hyperphosphatemic acidosis), and plasma protein (i.e., SIMPLIFIED STRONG ION EQUATION
hypoproteinemic alkalosis and hyperproteinemic acidosis) Constable’s simplified strong ion equation assumes that
concentrations exert on plasma pH, purportedly plasma ions act as strong ions, volatile buffer ions
5
facilitating identification and quantification of unmea- (HCO 3 ), or nonvolatile buffer ions (A ). Therefore
sured strong ions (i.e., organic acidosis) in plasma. Values plasma contains three types of charged entities: SID,
BOX 13-4 Estimation of Change in Base Excess Caused by Changes in
[SID] and [A tot ]
Changes in Base Excess Caused By Changes Contribution from Changes in Free Water in
in [A tot ] mEq/L
Albumin Contribution (D Albumin in mEq/L)
þ þ
D Free Water ¼ 0:25ð½Na ð½Na Þ
patient normal
D Albumin ¼ 3:7 alb normal alb patient
½
½
Chloride Contribution in (D Chloride in mEq/L)
Phosphate Contribution (D Phosphate in mEq/L)
½
½
If phosphate concentration is in mmol/L: D Chloride ¼ Cl normal Cl corrected
½
D Phosphate ¼ 1:8 Phosphate patient Contribution from Unidentified Strong Anions
-
(D [XA ] in mEq/L)
If phosphate concentration is in mg/dL:
½
D Phosphate ¼ 0:58 Phosphate
patient
DAlbumin þ DPhosphate
½
Changes in Base Excess Caused By Changes D XA ¼ BE patient ð
½
in [SID] þ D Free water þ D ChlorideÞ
SID, Strong ion difference; [A tot ], total plasma concentration of nonvolatile weak buffers; [alb] normal , normal albumin concentration (midpoint)
in g/dL; [alb] patient , patient’s albumin concentration in g/dL; [Phosphate] patient , patient’s inorganic phosphorus concentration in mmol/L or
mg/dL; [Na ] patient , patient’s sodium concentration in mEq/L; [Na ] normal , normal sodium concentration (midpoint) in mEq/L; [Cl ] normal ,
þ
þ
normal chloride concentration (midpoint) in mEq/L; [Cl ] corrected , patient’s corrected chloride concentration in mEq/L; [BE] patient , patient’s
base excess in mEq/L. Reference values for the author’s laboratory: [alb] normal ¼ 3.1 g/dL; [Na ] normal ¼ 156 mEq/L for cats and 146 mEq/L
þ
for dogs; [Cl ] normal , ¼ 120 mEq/L for cats and 110 mEq/L for dogs.
Adapted from de Morais HSA, Muir WW. Strong ions and acid-base disorders. In: Bonagura JD, editor. Kirk’s current veterinary therapy XII,
12th ed. Philadelphia: WB Saunders, 1995: 121–127.
