Page 589 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice
P. 589

576        FLUID THERAPY

            to the tissues. 56  This may be of particular benefit to the   a heart rate of 180 bpm, weak femoral pulses, and the feet
            animal in shock. These contradictory findings in acidosis   are cold. The respiratory rate is 60 breaths/minute. On
            make it difficult to determine if restoring a normal pH is   auscultation no murmurs or arrhythmias are heard and
            beneficial. In addition there is concern that bicarbonate   no abnormal breath sounds are evident.
            therapy is itself associated with adverse effects. The few   On  presentation,  flow  by  oxygen  is  provided  and  a
            clinical  trials  of  bicarbonate  therapy  for  the  treatment   cephalic venous catheter is placed. Blood work collected
            of acidemia in human medicine have had disappointing   at the time of catheter placement reveals the following:
            results. 19,92,93,144
               Bicarbonate combines with hydrogen ions in the extra­
                                                                                     Measured        Reference
            cellular  fluid  to  form  carbonic  acid,  which  rapidly  is
                                                                 Parameter              Value          Range
            convertedinto carbon dioxide and water in the presence
            of carbonic anhydrase. Hydrogen ions and bicarbonate
                                                                 pH                     6.911         7.34-7.38
            cannot readily cross the cell membrane so they are some­  PvCO 2  mm Hg     45.6          40-46
            what trapped in the extracellular fluid space. In contrast   PvO 2  mm Hg   32.7          49-67
            the carbon dioxide formed as a result of bicarbonate ther­  HCO 3  mEq/L    9.5           22-24
            apy rapidly diffuses into cells and causes intracellular aci­  SBE mEq/L    21.2          2to0
            dosis. 12   To avoid this the patient must increase alveolar   Glucose mg/dL   133        65-112
            ventilation  substantially  to  prevent  elevations  in  blood   Lactate mmol/L   19     <2.5
            PCO 2 . This is challenging for the compromised patient,   Packed cell volume %   70      37-55
            such as one in circulatory shock, and paradoxical intracel­  Total protein g/dL   3.5     5.4-7.1
            lular acidosis following bicarbonate therapy can occur. 128
               In addition the drop in ionized calcium associated with   A   severe   lactic   acidosis   without   respiratory
            alkalinization and the hypertonicity of sodium bicarbon­  compensation  is  evident  with  hemoconcentration  and
            ate can also have adverse effects. There are only two small,   hypoproteinemia.
            prospective, randomized clinical trials in human medicine   Rapid administration of 2000 mL of lactated Ringer’s
            evaluating the role of sodium bicarbonate in the therapy   solution via a pressure bag and 300 mL of 6% hetastarch is
            of lactic acidosis. 19,92  No difference in cardiovascular per­  provided. Following this the perfusion parameters have
            formance could be identified in these studies following   improved; the mucous membranes are still pale, capillary
            therapy  and  there  was  a  significant  drop  in  ionized   refill time is approximately 2 seconds, heart rate is 150
            calcium  associated  with  therapy.  Although  the  role  of   bpm, and the femoral pulses are assessed as being stron­
            sodium  bicarbonate  therapy  in  lactic  acidosis  remains   ger. Another 1000 mL of lactated Ringer’s solution and
            somewhat controversial, there is unanimous  agreement   another 200 mL of hetastarch is given rapidly. The perfu­
            that identification and treatment of the underlying cause   sion  parameters  at  this  time  are  greatly  improved
            for  lactic  acidosis  is  the  first  and  foremost  important   although the heart rate remains elevated.
            step. 6,12  Only after aggressive resuscitation efforts have   Following initial resuscitation, a full physical examina­
            been  made  should  bicarbonate  therapy  be  considered.   tion reveals abdominal pain. There is hemorrhagic gelati­
            The 2008  Surviving  Sepsis  guidelines  recommend  that   nous diarrhea evident on rectal examination. A dose of
            sodium  bicarbonate  should  not  be  administered  to   hydromorphone IV is given at this time, following which
            patients with a lactic acidosis unless the pH is less than   the heart rate drops to 120 bpm. A second venous blood
            7.15. 26  The role of sodium bicarbonate in patients with   sample is evaluated, which reveals a resolution of the lactic
            a pH less than 7.15 is uncertain because of the lack of   acidosis, PCV of 58%, and a total protein of 3.2 g/dL. An
            studies  evaluating  this  question.  Some  authors  in  the   ongoing fluid plan of 1 mL/kg/hr of 6% hetastarch and
            human  literature  advise  against  bicarbonate  therapy  at   200 mL/hr of lactated Ringer’s with appropriate potas­
            any  pH. 6,48   Sodium  bicarbonate  is  contraindicated  in   sium chloride supplementation is instituted.
            patients with volume overload such as congestive heart
            failure or in patients with ventilatory compromise.   CASE 1 - Case Notes
                                                                 This dog presented in severe circulatory shock with signs
                                                                 suggestive of vasoconstriction. Given the signalment, the
             CASE EXAMPLES                                       absence of any previous history of heart disease, and no
                                                                 murmur or arrhythmia detected, cardiogenic shock was
            CASE 1: Hypovolemic Shock
                                                                 considered  unlikely  and  the  diagnosis  of  hypovolemic
            A 2-year-old male neutered Labrador weighing 30 kg is   shock was made. The severe lactic acidosis supports the
            presented collapsed. There is no history of trauma, toxin   physical examination findings of severe shock. The lack
            ingestion, or previous medical problems. On presentation   of respiratory compensation is likely secondary to central
            the dog is found to be severely obtunded, has very pale   nervous system depression as a result of poor brain perfu­
            mucous membranes, a capillary refill time of 4 seconds,   sion. The very high PCV  in combination with the low
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