Page 273 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

264 ACID-BASE DISORDERS

described. 84 The particular protocol of insulin adminis- insulin and fluid therapy also lead to correction of the aci-
tration is probably less crucial to the ultimate outcome dosis and should have a similar effect on the oxygen-
than the individualized care provided by the veterinarian hemoglobin dissociation curve.
during management of the diabetic animal. Overzealous therapy with NaHCO 3 may contribute to
Several factors may contribute to a delay in the repair late development of metabolic alkalosis because insulin

of the HCO 3 deficit in patients with diabetic promotes metabolism of retained ketoacid anions to

ketoacidosis. 100 Ketoacid anions that have been excreted HCO 3 . This excess HCO 3 should be readily excreted

in the urine are lost to the body and cannot be in the urine if renal function is adequate. Other poten-

metabolized to HCO 3 . After treatment with fluids tially detrimental effects of NaHCO 3 therapy include
and insulin, recovery may be faster in patients with a high aggravation of hyperosmolality as a consequence of the
anion gap because the retained ketoanions are obligatory sodium load, tetany resulting from a sudden
7,9
metabolized, yielding HCO 3 . Thus, withholding decrease in ionized serum calcium concentration, and
alkali may be more rational for diabetic patients with high precipitation of severe hypokalemia as extracellular potas-
anion gap metabolic acidosis than for those with sium ions move into cells during administration of insulin
hyperchloremic metabolic acidosis. Dilutional acidosis and correction of acidosis. For all these reasons, NaHCO 3
may occur if ECF volume (ECFV) is expanded with is not used unless severe acidosis (pH <7.1 to 7.2) is pres-
alkali-free solutions such as 0.9% saline. If hyperventila- ent and then only in small amounts (see the Treatment of

tion persists, it may impair renal reabsorption of HCO 3 , Metabolic Acidosis section).
and renal acid excretion may require several days to
become fully augmented. Uremic Acidosis
The use of NaHCO 3 to treat diabetic ketoacidosis is Pathophysiology
highly controversial, and clear benefits of its use have The metabolic acidosis of chronic renal failure is usually

not been demonstrated in human patients. For example, mild to moderate in severity (plasma HCO 3 concentra-
there was no difference in recovery (based on rate of tion, 12 to 15 mEq/L) and may be hyperchloremic early
decrease of blood glucose and ketone concentrations in the course of the disease process. 239 Later in the course
and rate of increase of blood or cerebrospinal fluid of the disease, the anion gap increases because of reten-

[CSF] pH or HCO 3 concentration) when NaHCO 3 tion of phosphates, sulfates, and organic anions. Acid-
was or was not administered to human patients with dia- base status is usually well preserved in chronic renal failure
betic ketoacidosis who presented with blood pH values in until GFR decreases to 10% to 20% of normal. In retro-
the range of 6.90 to 7.14. 166 In another study, treatment spective studies of small animal patients with chronic
with NaHCO 3 delayed resolution of ketosis in diabetic renal failure, plasma HCO 3 concentrations were less
ketoacidosis. 178 than 16 mEq/L in 40% of dogs with chronic renal failure
There are several theoretical arguments against the use caused by amyloidosis 72 and less than 15 mEq/L in 63%
of NaHCO 3 in diabetic ketoacidosis. Acidosis in the CNS of cats with chronic renal failure of various causes. 71 A
may develop after NaHCO 3 administration. The blood- high anion gap was observed in 43% of affected dogs
brain barrier is permeable to CO 2 but less permeable to (>25 mEq/L) and in 19% of affected cats (>35 mEq/

the charged HCO 3 ion. If NaHCO 3 is administered, L) in these studies. In acute renal failure, there has been

ratio increases, insufficient time for the kidneys to adapt to the disease
pH increases in ECF as the HCO 3 /P CO 2
and compensatory hyperventilation decreases somewhat. state, and the metabolic acidosis of acute renal failure is
increases and CO 2 diffuses into the CNS. usually more severe than that observed in chronic renal
As a result, P CO 2
However, bicarbonate diffusion into CNS lags behind failure. Complications such as sepsis and marked tissue

ratio catabolism may contribute to the severity of metabolic
that of CO 2 . During this time, the HCO 3 P CO 2
and pH in the CNS may decrease. This has been referred acidosis in acute renal failure.
192
to as paradoxical CNS acidosis. The frequency of Delivery of HCO 3 from the proximal tubules to the
occurrence of this complication and its clinical signifi- distal nephron is increased in chronic renal failure. 235 In
cance are uncertain. 135 dogs with experimentally induced unilateral renal disease,
The pathophysiology of diabetic ketoacidosis also renal HCO 3 reabsorption was not different in the dis-

affects oxygen delivery to tissues. Chronic acidosis shifts eased and control kidneys, but bicarbonaturia developed
the oxygen-hemoglobin dissociation curve to the right, when the normal kidney was removed, and the contralat-
thus enhancing delivery of oxygen to the tissues. Con- eral diseased kidney was forced to function in a uremic
versely, phosphorus deficiency in diabetes decreases red environment. 165 The osmotic diuresis characteristic of
cell 2,3-diphosphoglycerate concentration and causes a uremia may thus contribute to the increased delivery of

shift of the oxygen-hemoglobin dissociation curve back HCO 3 to the distal tubules. Increased parathyroid hor-
to the left. Correction of acidosis with NaHCO 3 shifts mone concentration as a result of renal secondary hyper-
the curve farther to the left and potentially decreases oxy- parathyroidism does not seem to have important adverse
gen delivery to tissues. However, administration of effects on HCO 3 reabsorption inexperimentallyinduced