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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 Š  ¼ midpoint ½HCO 3 Š  patient ½HCO 3 Š
            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 Š  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 Š  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.
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