Page 277 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

268 ACID-BASE DISORDERS

hypocapnia and venous hypercapnia. 8,20,154,237 The ven- increased amounts of lactate as a result of excessive anaer-
tilation-to-perfusion ratio is increased because of obic metabolism and possibly as a result of less than nor-
decreased pulmonary blood flow, accounting for the mal hepatic extraction of lactate. Induction of remission
observed arterial hypocapnia. Venous hypercapnia results with doxorubicin chemotherapy did not improve
from anaerobic metabolism and a greater than normal hyperlactatemia in dogs with lymphosarcoma. 176
addition of CO 2 to venous blood from hypoperfused
tissues and diminished CO 2 excretion in the lungs Treatment
because of pulmonary hypoperfusion. These increases The outcome of lactic acidosis depends on the severity
gradients occur only if and reversibility of the underlying disease process respon-
in arteriovenous pH and P CO 2
pulmonary ventilation continues. Respiratory arrest sible for the acid-base disturbance. If treatment of lactic
8
gradients. In sum- acidosis is to be successful, prompt diagnosis and correc-
abolishes arteriovenous pH and P CO 2
tion of the underlying disease state are crucial. Tissue per-
is not an accurate reflection of CO 2
mary, arterial P CO 2
removal from tissues during CPR, and analysis of mixed fusion and oxygen delivery should be improved by
is recommended. 8,20,152,154,237 aggressive fluid therapy to expand ECFV. Ventilation
venous P CO 2
During CPR and ventilation with 100% O 2 , arterial with O 2 should be considered if the patient’s spontaneous
PO 2 may be normal, but tissue perfusion is low (20% ventilation is inadequate. Infections should be treated
to 25% of normal). 112 After NaHCO 3 administration, with appropriate antimicrobial agents, and cardiac output
additional CO 2 is produced, and venous hypercapnia should be improved, if necessary, by administration of
persists if ventilation is inadequate. Improving tissue per- inotropic agents. If the underlying disease cannot be
fusion is much more important during CPR than is corrected, the prognosis for patients with lactic acidosis
NaHCO 3 administration. Effective cardiac compression is very poor. If the underlying disease can be corrected,
and adequate perfusion allow delivery of O 2 to and the accumulated lactate is metabolized, yielding an equiv-

removal of CO 2 from tissues. Conversely, tissue acidosis alent amount of HCO 3 , and the acidosis is reversed.
is aggravated and pH i is decreased by NaHCO 3 adminis- When the pH of the patient’s blood decreases to
tration if the CO 2 generated cannot be removed from the below 7.1 to 7.2, administration of alkali is justified to
tissues by the lungs. The increase in tissue CO 2 decreases prevent the detrimental effects of severe acidosis on
pH i because CO 2 diffuses more rapidly into cells than the cardiovascular system (e.g., impaired myocardial

does the charged HCO 3 , thereby lowering the intracel- contractility, impaired cardiovascular responsiveness to
ratio. Intracellular acidosis of the catecholamines, increased susceptibility to ventricular
lular HCO 3 /P CO 2
myocardium leads to impaired cardiac contractility, arrhythmias). Small doses of NaHCO 3 should be
decreased cardiac output, and aggravation of lactic acido- administered to increase the patient’s pH to 7.2. 4,112,144
sis. Thus, the main goals of CPR are to provide adequate Approximately 10% to 15% of administered NaHCO 3
tissue perfusion by effective cardiac compression and to is converted immediately to CO 2 . 112 It is essential that
ventilate the patient with 100% O 2 . In one study of short ventilation increase to allow removal of accumulated
(5 minutes) and prolonged (15 minutes) cardiac arrest in CO 2 from the body. It is probably safe to administer
dogs, NaHCO 3 administration improved acidosis with- NaHCO 3 if the patient can reasonably be expected to
. 234 The authors increase ventilation spontaneously. If not, administration
out a significant increase in P CO 2
concluded that NaHCO 3 might be useful to reverse the of NaHCO 3 may be detrimental. In any case, NaHCO 3
acidosis of cardiac arrest if ventilation is adequate and should be administered slowly to minimize the increase
NaHCO 3 is administered in a reasonable therapeutic in mixed venous P CO 2 .
window. The volume of distribution (V d ) of administered

HCO 3 is variable, depending on the severity of the aci-
3
Lymphosarcoma in Dogs dosis. Thus, there is no simple way to calculate the dos-
Dogs with lymphosarcoma had higher lactate age of NaHCO 3 required to increase the pH to 7.2.
concentrations than control animals, and their lactate Volumes of distribution of 0.21 and 0.5 have been
concentrations increased significantly 30 minutes after recommended for calculation of the bicarbonate
administration of 500 mg/kg dextrose. 231 Blood lactate space. 4,112 Sodium bicarbonate should be used cautiously
concentrations were higher before and 1 hour after infu- and only in amounts necessary to increase the pH to 7.2.
sion of lactated Ringer’s solution in dogs with lymphosar- It should be administered slowly over several minutes to a
coma as compared with control animals. 230 Blood lactate few hours, and at least 30 minutes should be allowed to
concentration returned to baseline during the second elapse after the infusion before judging its effect. 4
hour of the 6-hour infusion. The authors concluded that The use of NaHCO 3 in lactic acidosis is controver-
dogs with stage III or IV lymphosarcoma might have sial. 170,220 Using the canine model of hypoxic lactic acido-
abnormal carbohydrate metabolism and a transient sis described above, 11 affected dogs were left untreated,
inability to handle lactate loads. Tumors may produce treated with 2.5 mEq/kg NaHCO 3 , or treated with 2.5