Page 313 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

304 ACID-BASE DISORDERS

TABLE 12-2 Compensatory Response in Simple Acid-Base Disturbances in Dogs
and Cats*
Clinical Guide for Compensation
Disturbance Primary Change Dogs Cats {

Metabolic acidosis Each 1 mEq/L # HCO 3 PCO 2 # by 0.7 mm Hg PCO 2 does not change
Metabolic alkalosis Each 1 mEq/L " HCO 3 PCO 2 " by 0.7 mm Hg PCO 2 " by 0.7 mm Hg
Respiratory Acidosis

Acute Each 1 mm Hg " PCO 2 HCO 3 " by 0.15 mEq/L HCO 3 " by 0.15 mEq/L

Chronic Each 1 mm Hg " PCO 2 HCO 3 " by 0.35 mEq/L Unknown
{
Long-standing Each 1 mm Hg " PCO 2 HCO 3 " by 0.55 mEq/L Unknown

Respiratory Alkalosis

Acute Each 1 mm Hg # PCO 2 HCO 3 # by 0.25 mEq/L HCO 3 # by 0.25 mEq/L
}

Chronic Each 1 mm Hg # PCO 2 HCO 3 # by 0.55 mEq/L Similar to dogs
*Data in dogs from de Morais HSA, DiBartola SP. Ventilatory and metabolic compensation in dogs with acid-base disturbances. J Vet Emerg Crit Care
1991;1:39–49. 16 See text for references in cats.
{
Data from cats are derived from a very limited number of cats.
{
More than 30 days.
}
Exact degree of compensation has not been determined, but cats with chronic respiratory alkalosis maintain normal arterial pH.
not be interpreted as evidence of a mixed process until hypercapnia and is characterized by increased PCO 2 ,
þ
more data are available about respiratory compensation increased [H ], decreased pH, and a compensatory
in cats. increase in [HCO 3 ] in blood. Respiratory alkalosis is

Metabolic alkalosis is characterized by a decrease in that acid-base disorder resulting from a primary decrease
[H ], an increase in serum [HCO 3 ] and blood pH, in PCO 2 in the blood. It is synonymous with the term pri-
þ

and a secondary increase in PCO 2 as a result of compensa- mary hypocapnia and is characterized by decreased
tory hypoventilation. As a rule of thumb, a 1.0-mEq/L PCO 2 , decreased [H ], increased pH, and a compensatory
þ

increase in plasma [HCO 3 ] is expected to be associated decrease in [HCO 3 ] in blood.

with an adaptive 0.7-mm Hg increase in PCO 2 in dogs Adaptive changes in plasma [HCO 3 ] occur in two

with metabolic alkalosis. 16 Little is known about respira- phases. In respiratory acidosis, the first phase represents
tory compensation in cats with metabolic alkalosis. In one titration of nonbicarbonate buffers, whereas in respira-
study with 12- to 14-week-old kittens made alkalotic tory alkalosis, the first phase represents release of H þ
by selective dietary chloride depletion, a 1.0-mEq/L from nonbicarbonate buffers within cells. This response

increase in plasma [HCO 3 ] concentration was is completed within 15 minutes (see Chapter 11). The
associated with a 0.7-mm Hg increase in PCO 2 . 62 This second phase reflects renal adaptation and consists of
value is remarkably similar to that observed in humans increased net acid excretion and increased HCO 3

and dogs, but care should be exercised when reabsorption (decreased Cl reabsorption) in respiratory
extrapolating data from normal kittens to sick adult cats. acidosis and a decrease in net acid excretion in respiratory
Time is an important consideration when assessing alkalosis. Experimentally, renal adaptation requires 2 to 5
compensation. Even in the experimental setting in which days for a chronic steady state to be established. 21,46,51

sudden changes in [HCO 3 ] can be achieved, the respi- During acute respiratory acidosis, a compensatory
ratory response to acute metabolic acidosis in dogs occurs increase of 0.15 mEq/L in [HCO 3 ] for each 1-mm

slowly, and it often takes 17 to 24 hours for maximal Hg increase in PCO 2 should be expected in dogs. 16 There
respiratory compensation to develop. 16 Thus using the is a lack of data for compensation in cats with acute respi-
formulas within the first 24 hours of onset of metabolic ratory acid-base disorders, but values appear to be similar
acidosis may lead to an underestimation of the ventilatory to those observed in dogs. In anesthetized, artificially
response and the erroneous assumption that a mixed met- ventilated cats made hypercapnic by exposure to increas-
abolic and respiratory disorder is present. ing CO 2 levels, the average compensatory increase in

[HCO 3 ] was 0.07 to 0.1 mEq/L for each 1-mm Hg
METABOLIC COMPENSATION IN increase in PCO 2 . 24,54 In three awake cats exposed to an
RESPIRATORY PROCESSES FICO 2 of 4%, 53 [HCO 3 ] increased 0.16 mEq/L for each

Respiratory acidosis is that acid-base disorder resulting 1-mm Hg increase in PCO 2 , a value very similar to the one
from a primary increase in carbon dioxide tension (PCO 2 ) observed in dogs. During acute respiratory alkalosis, a

in the blood. It is synonymous with primary compensatory decrease of 0.25 mEq/L in [HCO 3 ] for