Page 331 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice
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322        ACID-BASE DISORDERS


            can be associated with sodium gain in animals with   Theadministrationofsubstancescontainingmoresodium
            hyperadrenocorticism or in those treated with isotonic  than chloride (e.g., NaHCO 3 ) also increases SID, causing
            or hypertonic NaHCO 3 because the effective SID of   metabolic alkalosis.
            NaHCO 3 solutions is high, whereas animals treated with  A particular type of hypochloremic alkalosis that does
            isotonic or hypertonic NaCl will have hypernatremia and  not respond to chloride administration alone (as NaCl) is
            decreased SID because the effective SID of NaCl      called chloride-resistant metabolic alkalosis and usually is
            solutions is 0 mEq/L. 11  Hypernatremia is further   caused by hyperadrenocorticism or hyperaldosteronism.
            discussed in Chapter 3. Therapy for concentration alkalo-  Increased concentrations of cortisol or aldosterone cause
            sis should be directed at treating the underlying cause  sodium retention by activating the type I renal mineralo-
                                             þ
            responsible for the change in [Na ]. If necessary,   corticoid receptors. 53  Experimentally, administration of
                þ
            [Na ] and osmolality should be corrected (see        desoxycorticosterone acetate (DOCA) twice daily in
            Chapter 3).                                          sodium-supplemented dogs caused a significant increase


                                                                 in [Na ] and [HCO 3 ] with no change in [Cl ]. 35  When
                                                                      þ
            Hypochloremic Alkalosis                              NaHCO 3 was added to the diet instead of NaCl, [Na ]
                                                                                                               þ

            If thereis no changein the watercontent ofplasma, plasma  and  [HCO 3 ]  increased  significantly,  but  [Cl ]

                þ
            [Na ] will be normal. Other strong cations (e.g., Mg 2þ ,  decreased. 35  Approximately 30% of dogs with hyperadre-
                   þ
            Ca 2þ ,K ) are regulated for purposes other than acid-base  nocorticism have mild hypernatremia. 34,38  In a study of
            balance,andtheirconcentrationsneverchangesufficiently  117 dogs with hyperadrenocorticism, 34  only 12 had

            to substantially affect SID. Consequently, when water  [Cl ] less than 105 mEq/L. However, 25 of these dogs

            content is normal, SID changes only as a result of changes  had hypernatremia, and the [Cl ], although within the
                                þ
            in strong anions. If [Na ] remains constant, decreases in  normal range, could have been low relative to the

                                                                    þ
            [Cl ] can increase SID (so-called hypochloremic alkalosis;  [Na ] (i.e., corrected hypochloremia). The mean

                                                                    þ

            Figure 13-6). Primary decreases in [Cl ] unrelated to  [Na ] was 150 mEq/L; the mean [Cl ] was 108

            increases in plasma water content are recognized by the  mEq/L; and the mean [Cl ] after correcting for changes
            presence of a low corrected chloride concentration (see  in free water  was 105 mEq/L. The corrected
            Chapter 4). Hypochloremic alkalosis may be caused by  hypochloremia that occurs in the presence of high miner-
            an excessive loss of chloride relative to sodium or by  alocorticoid or glucocorticoid concentrations likely is
            administration of substances containing more sodium  responsible for the mild metabolic alkalosis observed in
            than chloride as compared with normal ECF composition.  these patients. The lack of response to NaCl can be
            Excessive loss of chloride relative to sodium as compared  explained by a resetting of the regulatory mechanism
            with normal ECF composition can occur in the urine after  and associated increased urinary loss of chloride. 29  Thus
            administration of diuretics that cause chloride wasting  in so-called chloride-resistant metabolic alkalosis, some-
            (e.g., furosemide) or when the fluid lost has a low or nega-  thing (e.g., excessive mineralocorticoid activity) prevents
            tive SID as in the case of vomiting of stomach contents.  chloride retention, and consequently SID cannot be
                                                                 lowered by chloride administration.
               180                                                 Therapy of chloride-responsive hypochloremic alkalo-
                                                                 sis is directed at correcting the SID with a solution
               160
                      SC        HCO 3    SID  AG  HCO 3    SID  HCO 3    SID  containing chloride (e.g., 0.9% NaCl, lactated Ringer’s
               140
              Ionic strength (mEq/L)  120  Na    AG  SA      Cl    AG  SA    expansion of extracellular volume is desired, intravenous
                                            A

                                                                 solution, K Cl supplemented fluids). In cases in which
                                           SA
                                 A
                                                      A
               100
                                                                 infusion of 0.9% NaCl is the treatment of choice.
                                                                 Corrected hypochloremia and hypochloremic alkalosis
                80

                                                                 are discussed more in Chapters 4 and 10.
                                 Cl
                                                      Cl
                60
                40
                20                                               SID ACIDOSIS
                                                                 Three general mechanisms can cause SID to decrease,
                0                                                resulting in SID (metabolic) acidosis: (1) a decrease in
                     Cations    Anions  Hyperchloremic Hypochloremic  þ
                               (normal)   acidosis  alkalosis    [Na ]; (2) an increase in [Cl ]; and (3) an increased con-
            Figure 13-6 Gamblegram of normal plasma and change in ionic  centration of other strong anions (e.g., L-lactate in lactic
            strength of anions secondary to increases (hyperchloremic acidosis)  acidosis, ß-hydroxybutyrate in diabetic ketoacidosis, sul-
            or decrease (hypochloremic alkalosis) in chloride (Cl ) content in  fate in uremic acidosis). Common causes of SID acidosis

            plasma. SID is decreased in hyperchloremic acidosis and increased in  are presented in Box 13-3.
            hypochloremic alkalosis, whereas anion gap (AG) remains constant
            during primary chloride changes. Na , Sodium; SC , other strong  Dilutional Acidosis
                                      þ
                                                þ
            cations; SA , other strong anions; A , net charge of nonvolatile  Dilutional acidosis occurs whenever there is an excess of


            buffers; HCO 3 , bicarbonate.                        water in plasma and is recognized clinically by the
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