Page 314 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice
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Mixed Acid-Base Disorders 305
each 1-mm Hg decrease in PCO 2 should be expected in is said to be inappropriate if a patient’s PCO 2 differs from
dogs. 16 Compensation to hyperventilation has only been expected PCO 2 by more than 2 mm Hg in a primary met-
studied in anesthetized cats. The [HCO 3 ] decreased abolic process or if a patient’s [HCO 3 ] differs from the
an average 0.26 mEq/L for each 1-mm Hg decrease expected [HCO 3 ] by more than 2 mEq/L in a respira-
in PCO 2 , a value similar to that obtained in dogs. 24 tory acid-base disorder. 2,16
In dogs with chronic respiratory alkalosis, a decrease An example illustrates how compensation can be
of 0.55 mEq/L in [HCO 3 ] is expected for each 1-mm estimated. Consider a dog with diarrhea caused by a par-
Hg decrease in PCO 2 . 2,16 It is interesting to note that even vovirus infection with the following arterial blood gas
in severe chronic respiratory alkalosis, the pH usually is results: pH ¼ 7.35, [HCO 3 ] ¼ 13 mEq/L, and PCO 2
normal. However, the normalization of pH in a clinical ¼ 24 mm Hg. The pH in the low normal range with
setting may take longer than 5 to 7 days. In humans with decreased [HCO 3 ] indicates that the primary process
sustained respiratory alkalosis, the pH may not return to is a metabolic acidosis. The expected compensation is
normal for 2 or more weeks. 40 Cats chronically exposed estimated assuming PCO 2 ¼ 36 mm Hg and [HCO 3 ]
to a hypoxic environment (FIO 2 ¼ 10%) for 28 days also ¼ 21 mEq/L as midpoint values. The change in
4
were able to maintain a normal arterial pH. Expected [HCO 3 ](△[HCO 3 ]) is:
compensation in cats cannot be inferred from this study,
but based on the ability to maintain a normal pH, it may D½HCO 3 ¼ midpoint ½HCO 3 patient ½HCO 3
be reasonable to assume that cats can compensate for ¼ 21 mEq=L 13 mEq=L ¼ 8 mEq=L
chronic respiratory alkalosis as well as dogs and humans.
In dogs with chronic respiratory acidosis, serum Knowing that for each mEq/L decrease in [HCO 3 ]in
[HCO 3 ] increases 0.35 mEq/L for each 1-mm Hg a metabolic acidosis, PCO 2 decreases 0.7 mm Hg
increase in PCO 2 . 16 Similar rules have been used in (see Table 12-2), the expected compensatory change
humans with chronic respiratory acidosis, but these rules in PCO 2 is estimated as:
have been shown to work well in unstable, but not in sta-
ble, patients with long-standing respiratory acidosis. 35 In
PCO 2expected ¼ midpoint PCO 2 DPCO 2
this latter group of patients, a 0.51-mEq/L increase in
[HCO 3 ] is expected for each 1-mm Hg increase in where
PCO 2 . 35 Thus arterial pH appears to remain near reference
ranges in human patients with long-standing respiratory DPCO 2 ¼ D½HCO 3 0:7 ¼ 5:6mmHg
3
acidosis. Similar results have been observed in dogs with
chronic respiratory acidosis and no other identifiable rea- Thus
son for increased [HCO 3 ] concentration other than
renal compensation. 22,25 Increases of 0.45 25 to 0.57 ¼ midpoint PCO 2 D½HCO 3 0:7
mEq/L 22 [HCO 3 ] for each 1-mm Hg increase in PCO 2expected
¼ 36 mm Hg 5:6 ¼ 30:4mmHg
PCO 2 have been observed in dogs with chronic respiratory
acidosis, suggesting that renal compensation in dogs with
long-standing respiratory acidosis may return arterial pH Because the expected compensation has an error margin
to normal in stable patients. of 2,
CLINICAL APPROACH PCO 2expected ¼ 30:4 2, or 28:4to32:4mmHg
The first step is a careful history to search for clues that This patient has a PCO 2 (24 mm Hg) that is more than
may lead the clinician to suspect the presence of acid-base 2 mm Hg lower than the minimal value for the expected
disorders, followed by a complete physical examination. PCO 2 (28.4 mm Hg), indicating the presence of respira-
Urinalysis, routine serum chemistries, and electrolyte tory alkalosis in addition to metabolic acidosis. A similar
concentrations are useful, but confirmation of a mixed line of thinking can be applied to calculate the expected
acid-base disorder requires blood gas analysis. After compensation in other primary acid-base disorders. Some
identifying the primary acid-base disorder (respiratory guidelines for adequate use of compensatory rules from
or metabolic), the expected compensation of the oppos- Table 12-2 are expressed in Box 12-3. Some useful
ing parameter [HCO 3 ] in a respiratory process; PCO 2 in guidelines for quickly detecting mixed acid-base
a metabolic process) should be calculated using the disorders in selected patients are shown in Box 12-4,
formulas in Table 12-2. A mixed acid-base disorder whereas potential technical problems that may lead to
should be suspected when inappropriate compensation misdiagnosing a mixed acid-base disorder are shown in
for the primary disorder is demonstrated. Compensation Box 12-5.