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

V. Physiology of Acid-Base Balance
539
do appear to be significant differences in the normal range
of the anion gap of different species as indicated in Table
17-4 (Adrogue et al ., 1978 ; Bristol, 1982 ; Feldman and
Rosenberg, 1981 ; Gossett and French, 1983 ; Polzin et al .,
1982 ; Shull, 1978, 1981 ). Age-related changes in anion gap
have been reported in horses ( Gossett and French, 1983 ),
with young foals having a significantly larger anion gap
than adults. Further experimental data will be necessary to
more clearly establish the normal range for the anion gap of
animals under varying conditions.
The simple calculation of anion gap can be employed
in the categorization of acid-base disorders with regard
to potential causal factors and may serve as a prognostic
guide in a variety of circumstances ( Bristol, 1982 ; Garry
and Rings, 1987 ; Shull, 1978 ). Decreases in anion gap can
be seen with increases in cationic proteins associated with
polyclonal gammopathy or multiple myeloma. Decreases in
anion gap resulting from decreases in unmeasured anions
occur most commonly with hypoalbuminemia and hyperchloremic
metabolic acidosis, but they also may be noted
with overhydration. The causal factors associated with a
hyperchloremic metabolic acidosis with a normal to low
anion gap can often be differentiated based on the serum
potassium concentration. Hyperchloremic metabolic acidosis
associated with gastrointestinal fluid losses from diarrhea
or renal causes such as renal tubular acidosis most
often manifests a hypokalemia ( Saxton and Seldin, 1986 ;
Ziemer et al ., 1987a, 1987b ). Hyperchloremic metabolic
acidosis associated with decreased mineralocorticoid secretion
or activity such as seen in Addison’s disease or renal
failure generally presents with a hyperkalemia ( Saxton and
Seldin, 1986 ). There are indications that changes in hydrogen
ion concentration may alter protein equivalency and
thus alter the anion gap in either an acidosis or alkalosis
( Adrogue et al ., 1978 ; Madias et al ., 1979 ).
Dehydration and alkalosis are potential, but minor, causes
of increased anion gap. Most commonly, elevations of anion
gap are associated with the development of a metabolic acidosis
in which there is an increase in anions, which are not
routinely measured in the clinical laboratory. This is called a
high anion gap acidosis and may be associated with an accumulation
of metabolizable acids as in a lactic acidosis associated
with anaerobic exercise, grain overload, or hypovolemic
shock or ketoacidosis resulting from diabetes or ketosis or
with the accumulation of nonmetabolizable acids as in uremic
acidosis or various intoxications (see Table 17-3 ). The
presence of a metabolic acidosis with a high anion gap thus
provides grounds to undertake a thorough investigation of
disease processes capable of producing an accumulation of
these unmeasured anions. The anion gap also may be useful
in the identification of mixed acid-base imbalances. When the
change in the anion gap does not approximate the change in
bicarbonate, a mixed metabolic acid-base imbalance should
be suspected. In cases of grain overload in herbivores, a large
ion gap may be due to increased ECF levels of D-lactic acid,
which is not detected by the usual assays for lactic acid
because they detect only the L-isomer produced in mammalian
metabolism. Either a special assay for D-lactate
must be performed, or an increased level of D-lactate may
be assumed based on history and other clinical data.
G . Bicarbonate and Total CO 2
If respiratory disturbances can be eliminated, the metabolic
component of acid-base balance is indicated by the
bicarbonate concentration. Bicarbonate is usually estimated
by determination of the “ CO 2 content ” or “ total
CO 2 ” of plasma or serum samples.
Bicarbonate actually accounts for approximately 95%
of the measured total CO 2 , and thus the total CO 2 provides
a measure of metabolic changes in acid-base balance. The
bicarbonate determined in this fashion will be decreased
in a metabolic acidosis and increased in a metabolic
alkalosis. Estimates of bicarbonate are often provided in
automated chemistry profiles. These determinations may
indicate the metabolic acid-base status. However, if acidbase
abnormalities are suspected, a proper blood gas evaluation
should be undertaken.
H . Buffer Base, Standard Bicarbonate,
and Base Excess or Base Deficit
These values are mathematically derived from the measurements
of blood pH and p CO 2 and provide an indication
of the metabolic component of acid-base balance.
It should be noted that the metabolic changes indicated
by these parameters do not always reflect the primary
acid-base imbalances but may represent compensating
responses for primary respiratory disorders.
The buffer base indicates the sum of all the buffer
anions in blood under standardized conditions. The standard
bicarbonate is the plasma bicarbonate concentration
that would be found under specific conditions, which
eliminate respiratory influences on the values obtained.
The base excess, which is sometimes considered as the
base deficit when the value is negative, indicates the deviation
of the buffer base from normal. This derived value
is often supplied in routine assessment of acid-base balance
and is generally taken as an indication of the deviation
of bicarbonate from normal. In an animal with a
metabolic acidosis, the calculated base deficit provides a
means of estimating the amount of bicarbonate required
to correct acid-base balance to normal. This estimate is
calculated by multiplying the base deficit by the probable
bicarbonate space (which is variably estimated from 0.25
to 0.55 l/kg body weight). In newborn animals, the bicarbonate
may be even higher, 0.40 to 0.65 l/kg body weight.
The usual figure used is 0.3 to 0.4 l/kg. For a 20-kg