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

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Chapter | 17 Fluid, Electrolyte, and Acid-Base Balance
the acidosis in calves associated with diarrhea was largely
due to the loss of bicarbonate into the bowel. This view
has been challenged in an elegant paper utilizing a quantitative
strong ion approach to assess the mechanism of the
acid-base abnormality ( Constable et al. , 2005 ). A profound
metabolic acidosis without dehydration leading to depression,
recumbency, and death has been described in goat
kids ( Tremblay et al ., 1991 ), which appears to be similar
to reports in calves ( Kasari and Naylor, 1984, 1986 ). The
cause was undetermined, but the acidosis was usually
associated with an increased anion gap. Sodium bicarbonate
therapy, if initiated early in the course of the disease,
was often curative. The acidosis observed in these calves
may have been associated with increases in both D and L
isomers of lactate generated by bacterial fermentation as
described in several recent clinical and research studies
of calves with indigestion associated with milk ingestion
(Ewaschuk et al ., 2003, 2004 ; Lopez et al ., 2004 ; Lorenz
et al ., 2005 ; Omole et al ., 2001 ; Stampfli, 2005 ). Additional
causes of a metabolic acidosis include ingestion of certain
medications or toxic compounds such as salicylate, methanol,
ethylene glycol, or paraldehyde, which result in the
accumulation of exogenous anions ( DiBartola, 1992b ).
b . Compensation
A metabolic acidosis is recognized quickly, and the compensating
respiratory response of increased ventilation will
begin reduction of the p CO 2 within minutes. In dogs, the
anticipated respiratory response is a reduction of p CO 2
by 0.7 mmHg for each mEq/l decrease in bicarbonate ( de
Morais, 1992a, 1992b ). This minimizes the fall in pH, but
the protective effects of the respiratory response are relatively
short lived, lasting only a few days. Long-term correction
of a metabolic acidosis requires renal bicarbonate
retention and enhanced renal acid excretion, primarily as
ammonium ion because there is little ability to increase the
titratable acidity, which consists primarily of phosphate
buffers ( Rose, 1984 ). Complete correction of a metabolic
acidosis may be difficult in patients with intrinsic renal
disease or diseases that would impair the kidney’s ability
to excrete acid or retain bicarbonate such as renal tubular
acidosis.
2 . Respiratory
A respiratory acidosis is characterized by a decrease in
pH and an increase in p CO 2 . Respiratory acidosis develops
because of decreased effective alveolar ventilation or
breathing an atmosphere with elevated CO 2 . The initial
buffering of the acid load produced by a respiratory acidosis
is almost exclusively by the intracellular buffers. The
principal ECF buffer, the bicarbonate-carbonic acid buffer
pair, cannot buffer a respiratory acidosis. Carbon dioxide
diffuses through the lung much more readily than O 2 ;
thus, diseases that compromise ventilation normally result
in decreases in p O 2 before significant increases in p CO 2
develop. The respiratory center is extremely sensitive to
minor changes in p CO 2 , and increased p CO 2 normally provides
the major stimulus to ventilation ( Rose, 1984 ). In
contrast, hypoxemia does not begin to promote enhanced
ventilation until the arterial p O 2 is substantially decreased.
If, however, the arterial p CO 2 is held at normal values or is
elevated because of intrinsic lung disease, then ventilation
begins to be enhanced as the arterial p O 2 falls below 70 to
80 mmHg ( Rose, 1984 ).
a . Causes of Respiratory Acidosis
Any disorder that interferes with normal effective ventilation
may produce a respiratory acidosis. The most common
causes are primary pulmonary diseases ranging from acute
upper respiratory obstruction, to pneumonia, to pneumothorax,
and chronic obstructive lung disease. Diseases or drugs
that affect the central nervous system may inhibit the medullary
respiratory center and can produce a profound respiratory
acidosis. An additional cause of special importance
in veterinary medicine is general anesthesia with volatile
agents using a closed system. Under these conditions, ventilation
may be seriously reduced without producing hypoxia.
The high oxygen content of the gas mixture maintains high
pO 2 in the blood, but depression of the respiratory center
may result in insufficient alveolar ventilation so that CO 2
accumulates. This problem can be overcome through the use
of a positive pressure ventilatory apparatus and careful monitoring
of arterial blood gases during general anesthesia.
b . Compensation
The compensating response for a respiratory acidosis is
renal retention of bicarbonate and increased excretion of
hydrogen ion. This response requires several days, and thus
the response is seen only in a chronic respiratory acidosis.
In dogs with chronic respiratory acidosis, a compensating
increase of 0.35 mEq/l of bicarbonate is anticipated for each
mmHg increase in pCO 2 ( de Morais, 1992a, 1992b ). The
extent of the rise in the plasma bicarbonate concentration
in chronic respiratory acidosis is determined by increased
renal hydrogen secretion ( Rose, 1984 ). Exogenous bicarbonate
is unnecessary, and should bicarbonate be administered
to patients with a respiratory acidosis, it would be excreted
without affecting the final plasma bicarbonate concentration.
D . Alkalosis
1 . Metabolic Alkalosis
Metabolic alkalosis is characterized by an increase in pH and
bicarbonate. Metabolic alkalosis occurs with some frequency
in domestic animals and is commonly observed in association
with digestive disturbances in ruminants. The development
of a metabolic alkalosis requires an initiating process
capable of generating an alkalosis and the additional factors
that are necessary for maintaining the alkalosis ( Rose, 1984 ).
Generation of a metabolic alkalosis can be due to excessive