Page 123 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Disorders of Potassium: Hypokalemia and Hyperkalemia 113

blocking b 2 -adrenergic stimulation of cell membrane Thus, if compatible electrocardiographic changes are
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Na ,K -ATPase. Similar to digoxin, cardiac glycoside observed, hyperkalemia should be treated regardless of
toxins found in the plant oleander (e.g., oleandrin, digi- its magnitude. An acute increase in serum potassium con-
þ
toxigenin, and Nerium) inhibit Na ,K -ATPase and can centration to more than 6.5 mEq/L should be treated
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cause hyperkalemia and arrhythmias. The deleterious promptly. Asymptomatic animals with normal urine out-
effects of oleandrin are blocked by infusion of fructose- put and chronic hyperkalemia in the range of 5.5 to
1,6-diphosphate. 126 Angiotensin-converting enzyme 6.5 mEq/L may not require immediate treatment, but
inhibitors (e.g., enalapril) and angiotensin II receptor a search for the underlying cause should be initiated.
blockers (e.g., losartan) contribute to hyperkalemia by Underlying diseases should be treated promptly (e.g.,
decreasing production of aldosterone by the adrenal relief of urethral obstruction, establishment of urine out-
glands and blunting glomerular efferent arteriolar con- put in patients with oliguria or anuria, and 0.9% NaCl and
striction, which potentially can decrease delivery of mineralocorticoids in patients with hypoadreno-
sodium and water to the distal nephron and impair renal corticism). Fluid therapy with lactated Ringer’s solution
potassium excretion. Prostaglandins stimulate renin (potassium concentration, 4 mEq/L) also ameliorates
release, and use of nonsteroidal anti-inflammatory drugs hyperkalemia by improving renal perfusion and enhanc-
may contribute to development of hyperkalemia. These ing urinary excretion of potassium. However, use of a
drugs also may impair the stimulatory effect of potassium-free solution (e.g., 0.9% NaCl and 0.45%
prostaglandins on potassium channels in the luminal NaCl) has a greater dilutional effect on the ECF potas-
membranes of renal tubular cells. Heparin impairs aldos- sium concentration.
terone production by decreasing the number and affinity Hyperkalemia may be treated by antagonizing the
of angiotensin II receptors in the zona glomerulosa of the effects of potassium on cell membranes using calcium
adrenal glands and may contribute to hyperkalemia in the gluconate, by driving potassium from ECF to ICF with
presence of other predisposing factors. 144 Potassium- sodium bicarbonate or glucose (with or without concur-
sparing diuretics (e.g., spironolactone, amiloride, and rent insulin administration), or by removing potassium
triamterene) reduce urinary excretion of potassium and from the body with a cation exchange resin or dialysis.
can cause hyperkalemia. Spironolactone competitively First, any source of intake must be discontinued (e.g.,
inhibits binding of aldosterone to its cytoplasmic receptor potassium-containing fluids and potassium penicillin).
in the principal cells of the collecting duct. Amiloride and The clinician also should review the history to verify that
triamterene block sodium channels in the luminal the patient is not currently being treated with any drug
membranes of the principal cells. Trimethoprim is similar known to contribute to hyperkalemia (e.g., nonsteroidal
in structure to amiloride and also inhibits sodium anti-inflammatory drugs, b-blockers, angiotensin-
channels in the luminal membranes of the principal cells. converting enzyme inhibitors, and potassium-sparing
Trimethoprim is most likely to cause hyperkalemia at high diuretics).
dosages, when urine pH is low (<6.0), and when used in Hyperkalemia decreases the resting potential of cells.
patients with renal insufficiency. 148 The immunosuppres- By administering calcium gluconate, the ECF concentra-
sive drugs cyclosporin A and tacrolimus contribute to tion of calcium is increased and the threshold potential is
hyperkalemia in renal transplant patients by several decreased, thus normalizing the difference between the
mechanisms, including decreased aldosterone produc- resting and threshold potential and restoring normal
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tion, inhibition of Na ,K -ATPase, and interference membrane excitability (see Fig. 5-2). Administered cal-
with luminal potassium channels in renal tubular cells. cium begins to work within minutes, but its effect lasts
Infusions of total parenteral nutrition solutions less than 1 hour. The dosage of calcium gluconate is
containing lysine and arginine may contribute to 2 to 10 mL of a 10% solution to be administered slowly
hyperkalemia because these amino acids may enter cells with electrocardiographic monitoring.
in exchange for potassium. In many hospitalized animals, Glucose works by increasing endogenous insulin
however, the cause of mild hyperkalemia cannot be deter- release and moving potassium into cells. Its effects begin
mined. In these instances, hyperkalemia often resolves within 1 hour and last a few hours. Glucose-containing
with appropriate fluid therapy and treatment of the fluids (5% or 10% dextrose) or 50% dextrose (1 to
primary disease. 2 mL/kg) can be used for this purpose. The combination
of insulin with glucose may result in greater reduction in
TREATMENT serum potassium concentration, but there is a risk of
8
Appropriate treatment is dependent on the magnitude hypoglycemia. Insulin (0.55 to 1.1 U/kg regular insulin
and rapidity of onset of the hyperkalemia, as well as the added to parenteral fluids) and dextrose (2 g dextrose per
underlying cause. Abnormalities of serum ionized cal- unit of insulin added) have been recommended to treat
cium concentration and acid-base balance may aggravate hyperkalemia in cats with urethral obstruction. 172
the functional consequences of hyperkalemia as reflected Sodium bicarbonate also works by moving K þ ions
þ
by muscular weakness and electrocardiographic changes. into cells as H ions leave cells to titrate administered