Page 259 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

250 ACID-BASE DISORDERS

an increase in serum potassium concentration does
not occur in acute metabolic acidosis caused by organic
0.10
acids (e.g., lactic acid, ketoacids).* Acute infusion of
Urinary excretion of NH 4 + plus NH 3 (mmoles/min) 0.05 Normal Acidosis sion of HCl led to hyperkalemia and increased portal
Dog
b-hydroxybutyrate in normal dogs caused an increase in
insulin in portal venous blood and hypokalemia, presum-
2
ably as a result of potassium uptake by cells. Acute infu-
2
vein glucagon concentration. These acute changes in
serum potassium concentration are not the result of
2,49
changes in renal excretion of potassium.
The hyperkalemia associated with acute metabolic aci-
dosis caused by mineral acids is transient. In a study of
acute and chronic metabolic acidosis induced in dogs
by administration of HCl or NH 4 Cl, hyperkalemia was
observed after acute infusion of HCl, but hypokalemia
41
developed after 3 to 5 days of NH 4 Cl administration.
The observed hypokalemia was associated with inappro-
priately high urinary excretion of potassium and increased
plasma aldosterone concentration. 41 Similar findings in
0 rats with chronic metabolic acidosis induced by NH 4 Cl
5.0 6.0 7.0 8.0 53
have been reported. Acute metabolic acidosis induced
Urinary pH
Figure 9-11 Effect of acidosis on urinary ammonium by administration of mineral acid decreases renal proximal
excretion. (From Pitts RF: Fed Proc 7:418, 1948.) tubular reabsorption of sodium, leading to volume con-
traction and increased distal delivery of sodium. Increased
þ
þ
þ
Na -H and Na -K exchange then occurs in the distal
þ
nephron, mediated by increased distal tubular fluid flow
or nonvolatile acid produced each day is excreted in urine and hyperaldosteronism. These findings suggest that
as ammonium, either as the chloride salt or in exchange mild hypokalemia and potassium depletion are likely to
for sodium. The more acidic the urine, the greater the develop during chronic metabolic acidosis caused by
proportion of ammonium that exists as NH 4 . The administration of a mineral acid. The observation of
þ
kidneys can also increase their production of ammonium hyperkalemia during chronic metabolic acidosis should
from glutamine during acidosis. At any given urine pH, prompt consideration of impaired renal potassium excre-
the rate of ammonium salt excretion is higher in the pres- tion or some other cause of hyperkalemia (see Chapter 5).
ence of acidosis, 68 and renal ammonium excretion can
increase fivefold to tenfold (from basal ammonium excre-
tion of 30 to 60 mEq to as much as 300 mEq per day) in REFERENCES
response to chronic metabolic acidosis (Fig. 9-11).
1. Adrogue HJ, Brensilver J, Madias NE. Changes in the
POTASSIUM AND ACID-BASE plasma anion gap during chronic metabolic acid-base
disturbances. Am J Physiol 1978;235:F291.
BALANCE 2. Adrogue HJ, Chap Z, Ishida T, et al. Role of the endocrine
pancreas in the kalemic response to acute metabolic acidosis
The distribution of potassium ions between intracellular in conscious dogs. J Clin Invest 1985;75:798.
fluid and ECF may be affected by acid-base disorders. 3. Adrogue HJ, Madias NE. Changes in plasma potassium
concentration during acute acid base disturbances. J Clin
When HCl was infused acutely into nephrectomized
Invest 1981;71:456.
dogs, approximately 50% of the H load was buffered 4. Aguilera-Tejero E, Fernandez H, Estepa JC, et al. Arterial
þ
intracellularly. 55,65 Intracellular sodium and potassium blood gases and acid-base balance in geriatric dogs. Res
þ
ions entered ECF in exchange for the H entering cells, Vet Sci 1997;63:253.
and serum potassium concentration increased. These 5. Astrup P. New approach to acid-base metabolism. Clin
Chem 1961;7:1.
early animal studies and observations in a small number 6. Astrup P, Jorgensen K, Siggaard-Andersen O, et al. Acid-
of human patients 10 led to the prediction that metabolic
base metabolism: new approach. Lancet 1960;1:1035.
acidosis would be associated with a 0.6-mEq/L increase 7. Atkins CE, Tyler R, Greenlee P. Clinical, biochemical, acid-
in serum potassium concentration for each 0.1-U base, and electrolyte abnormalities in cats after hypertonic
decrease in pH. A review of animal studies demonstrated sodium phosphate enema administration. Am J Vet Res
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observed during acute metabolic acidosis caused by min-
3
eral acids (e.g., HCl, NH 4 Cl) was variable. Furthermore, *References 2, 3, 28, 48, 49, 66.