Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

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Chapter | 17 Fluid, Electrolyte, and Acid-Base Balance
animal with a base deficit of 10 mEq/l (10 mmol/l), the
bicarbonate required would be calculated as follows:
bicarbonate required 20 kg 0 .
3 l/kg
10
mEq/l
60
mEq
(17-12)
This calculation provides only a crude guide to bicarbonate
requirements, but it can be a useful step in the quantitative
approach for correcting a serious primary metabolic
acidosis.
I . Nontraditional or Strong Ion Approach to
Acid-Base Balance
Peter Stewart ( Stewart 1981, 1983 ) was the first to describe a
quantitative physiochemical approach to acid-base balance.
In this approach, the acid-base status of the aqueous solutions
of the body is determined not only by the Henderson-
Hasselbalch equation but also by a series of seven other
relationships, all of which could be represented by equations
which must be satisfied simultaneously. Acid-base balance
is determined by three independent variables: (1) strong ion
difference [SID], (2) the partial pressure of CO 2 , and (3) the
total concentration of nonvolatile weak acids [Atot], the
principal component of which is the plasma proteins but also
includes inorganic phosphate. Bicarbonate and hydrogen ion
concentration, and thus pH, are dependent variables determined
by the independent variables listed here. The appeal
of Stewart’s approach is the focus on factors that are causally
related to acid-base balance, the independent variables.
The interested reader is referred to Stewart’s original work.
A number of authors have attempted to adapt Stewart’s
approach for practical application in human and veterinary
medicine ( de Morais, 1992b ; Fencl and Leith, 1993 ; Fencl
and Rossing, 1989 ; Frischmeyer and Moon 1994 ; Gilfix
et al. , 1993 ; Jones, 1990 ; Kowalchuck and Scheuermann,
1994; Whitehair et al. , 1995 ). Many of these early papers
directed to animal species used the human values for Atot
and K a, which may not be appropriate. Species-specific data
are now available.
In a landmark paper, Peter Constable (1997) refined
Stewart’s model and developed an approach that he called
the simplified strong ion model of acid-base equilibrium.
The simplified strong ion model was developed from the
assumption that plasma ions act as strong ions, volatile
buffer ions (HCO 3
), or nonvolatile buffer ions. Plasma
pH is determined by five independent variables: p CO 2 ,
strong ion difference, concentration of individual nonvolatile
plasma buffers (albumin, globulin, and phosphate),
ionic strength, and temperature. The simplified strong ion
model conveys, on a fundamental level, the mechanism for
change in acid-base status, explains many of the anomalies
when the Henderson-Hasselbalch equation is applied to
plasma, and is conceptually and algebraically simpler than
Stewart’s strong ion model. The model has provided an in
vitro method for determination of species-specific values
for [Atot] and K a, which has been applied to the plasma
of horses, dogs, cattle, pigeons, and humans ( Constable,
1997 ; Constable and Stampfli, 2005 ; Stampfli et al. , 1999,
2006 ; Stampfli and Constable, 2003 ).
Strong electrolytes are completely dissociated in aqueous
solution and chemically nonreactive. The [SID] is simply
the difference between the total concentration of strong
cations (sodium, potassium, and magnesium) and the total
concentration of strong anions (chloride, sulfate, lactate,
acetoacetate, and 3-OH-hydroxybutyrate). Because they are
present in higher concentrations in the body fluids, sodium,
potassium, and chloride are normally the principal determinants
of [SID]. The [SID] is synonymous with buffer base as
described by Singer and Hastings (1948) and, as such, can
be considered as roughly equivalent to the metabolic component
of the traditional approach to acid-base balance. In
fluids such as the CSF, which are normally devoid of protein,
bicarbonate concentration is the same as the [SID].
Abnormalities in pCO 2 are viewed in essentially the same
manner in both the traditional and nontraditional approach
to acid-base balance as described earlier. The contribution
of plasma proteins to acid-base balance is not considered
in the traditional approach to acid-base balance. The
plasma proteins, or, perhaps more correctly, plasma albumin,
make up the majority of [Atot], whereas inorganic
phosphate normally accounts for less than 5% of [Atot].
The [Atot] in body fluids exists in both dissociated [A ] and
undissociated [HA] forms. A decrease in [Atot] because of
hypoalbuminemia causes an alkalosis with an increase in
bicarbonate, whereas hyperalbuminemia has the opposite
effect. Hypoalbuminemia is one of the most common causes
of alkalosis in older human patients ( McAuliffe et al. , 1986 ).
Changes in A associated with changes in albumin concentration
also have a direct and frequently overlooked effect
on anion gap. Increases in A result in an increase in anion
gap, whereas decreases in A cause a decrease in anion
gap ( McAuliffe et al. , 1986 ). Change in protein concentration
may potentiate or ameliorate the effects of alterations
in SID on acid-base balance. As an example, in a vomiting
dog, the elevated plasma protein associated with dehydration
may reduce the bicarbonate increase anticipated for a given
change in chloride concentration and SID.
Protein and inorganic phosphate remain within the normal
range in many clinical situations, and acid-base balance
is then largely controlled by changes in pCO 2 mediated by
the respiratory system, whereas changes in [SID] are largely
under the control of the kidneys. Renal compensation for
primary respiratory disorders and respiratory compensation
for primary metabolic acid-base disturbances are thought
to be similar in both the traditional and nontraditional
approach. Precise quantification of the anticipated compensating
responses to primary acid-base disturbances based on
change in SID has not yet been determined .