Page 278 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Metabolic Acid-Base Disorders 269

mEq/kg1MNaCl. 92,93 Animals treated withbicarbonate 2.5 mEq/kg NaHCO 3 . 21 Arterial pH increased after

showed a greater decrease in pH and HCO 3 concentra- administration of Carbicarb but decreased after
tion and higher lactate concentration than the other NaHCO 3 . Mixed venous P CO 2 was unchanged after
groups. Gut lactate production was greater in dogs that Carbicarb administration but increased after NaHCO 3 .
received NaHCO 3 than in dogs that received NaCl, and Arterial lactate concentration increased after administra-
was higher in the group that received tion of NaHCO 3 but stabilized after Carbicarb, whereas
portal vein P CO 2
NaHCO 3 . Arterial blood pressure and cardiac output lactate use by the gut, muscle, and liver improved with
declined in the untreated group and the group that Carbicarb but decreased after NaHCO 3 . Hepatocyte
received NaHCO 3 but were higher in the group that pH i increased after Carbicarb and decreased after
and hepatic NaHCO 3 . Arterial blood pressure decreased to a lesser
received NaCl. Increased portal vein P CO 2
accumulation of lactate presumably caused hepatocyte extent and cardiac output stabilized with Carbicarb,
pH i to decrease. The ability of the liver to extract lactate whereas cardiac output decreased with NaHCO 3 .It
dependsonadequatehepaticbloodflowandnormalhepa- was concluded that Carbicarb had a beneficial effect on
tocyte pH i , both of which are decreased in this model. myocardial contractility. Myocardial contractility may
During hypoxia (PO 2 <30 mm Hg), the liver is unable decrease after NaHCO 3 administration as a result of
to increase its lactate extraction, despite an increased load increased venous P CO 2 and decreased myocardial pH i .
delivered from the ischemic gut. The investigators Decreased cardiac output follows and leads to decreased
concluded that use of NaHCO 3 during lactic acidosis blood flow and decreased O 2 delivery to gut, muscle, and
might not be effective and might even be detrimental. liver, resulting in decreased lactate use and increased pro-
Dichloroacetate (DCA) stimulates the enzyme pyruvate duction. Carbicarb improved arterial pH without
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dehydrogenase, which converts pyruvate to acetyl CoA. impairing myocardial contractility, presumably because
In the canine model of hypoxic lactic acidosis described it did not increase venous P CO 2 . This study suggests that
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91
before, DCA was compared with NaCl. DCA increased Carbicarb is superior to NaHCO 3 in the treatment of lac-

pH and HCO 3 concentration and maintained a constant tic acidosis in dogs.
lactate concentration, whereas NaCl treatment was In another study, Carbicarb was compared with

associatedwithadecreaseinpHandHCO 3 concentration sodium bicarbonate and hypertonic saline in a canine
and an increase in lactate concentration. Hepatic lactate model of hemorrhagic shock. 19 All dogs received identi-
extraction increased with DCA, whereas liver and muscle cal sodium loads. Groups that received Carbicarb and
accumulation of lactate decreased. Muscle pH i increased sodium bicarbonate experienced similar increases in
with DCA, but neither treatment changed arterial blood serum bicarbonate, but arterial P CO 2 increased more in
pressure or cardiac output. DCA was also studied in a car- bicarbonate-treated dogs than in those treated with
diac arrest model in dogs. 216 This study compared DCA, Carbicarb. Hemodynamics, oxygen delivery, and oxygen
DCA and NaHCO 3 ,NaHCO 3 , and no treatment. Bicar- consumption improved in all three groups, and these
bonate treatment increased arterial pH, but DCA did effects were attributed to the sodium load. Carbicarb,
not.DCAdidnotdecreaselactateconcentrationorincrease NaHCO 3 , and NaCl were compared in a model of hyp-
pH in either the peripheral circulation or CNS. In a canine oxic lactic acidosis in anesthetized, mechanically
model of hemorrhagic shock, DCA administration ventilated dogs. 193 Carbicarb increased arterial pH, base
decreased arterial lactate concentrations but was associated excess, and cardiac index without an increase in lactate.
withdecreasedcardiacstrokevolume,decreasedmyocardial Bicarbonate increased P CO 2 , but no adverse effects of
efficiency, and reduced myocardial lactate consumption. 15 NaHCO 3 on hemodynamics or pH i were detected.
Thus, there are conflicting results regarding the usefulness A sodium-free 0.3 N solution of tromethamine
of DCA in canine models of lactic acidosis. (THAM) is another CO 2 -consuming alkalinizing agent
þ
Carbicarb is an equimolar mixture of Na 2 CO 3 and that is capable of buffering both nonvolatile (H ) and
NaHCO 3 that limits the generation of CO 2 during the volatile (H 2 CO 3 derived from CO 2 ) acid. THAM and
buffering process: sodium bicarbonate had similar buffering ability when
evaluated in dogs with experimentally induced metabolic
Na 2 CO 3 þ H 2 O þ CO 2 ! 2HCO 3 þ 2Na þ acidosis. 163 Dogs treated with THAM did not experience

the transient hypernatremia and hypercapnia that were
However, some of the HCO 3 generated from this reac- observed in bicarbonate-treated dogs.

tion can buffer H released from nonbicarbonate buffers TREATMENT OF METABOLIC
þ
and generate CO 2 in the presence of carbonic anhydrase:
ACIDOSIS
þ The main goal in the treatment of metabolic acidosis is
2HCO 3 þ 2H ! 2H 2 CO 3 ! 2H 2 O þ 2CO 2
prompt diagnosis and specific treatment of the underly-
In the canine model of hypoxic lactic acidosis described ing cause of the acid-base disorder. Correction of the
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earlier, 2.5 mEq/kg Carbicarb was compared with underlying disease that is responsible for the patient’s