Page 118 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

108 ELECTROLYTE DISORDERS

nephropathy, the initial oral dosage of potassium gluco- specialized tissues and ventricular muscle, and the poten-
nate is 5 to 8 mEq/day divided in two or three doses, tial for reentry lead to axis deviations, widening of the
whereas the maintenance dosage can usually be reduced QRS complex, and ventricular asystole or ventricular
to 2 to 4 mEq/day. 60 It is difficult to estimate the amount fibrillation. Ventricular fibrillation in hyperkalemia is
of potassium required to reestablish normal balance from most likely the result of slow intraventricular conduction
the serum potassium concentration in a given patient and decreased duration of the refractory period. These
because potassium is an intracellular solute. Thus, the electrocardiographic changes have also been described
amount of potassium required for treatment must in cats with hyperkalemia secondary to urethral obstruc-
be determined by judicious supplementation and serial tion, and they represent the most life-threatening
measurement of serum potassium concentration during functional consequences of hyperkalemia. 146 Rarely,
treatment and recovery. wide-complex tachycardia without identifiable P waves
may occur in cats with hyperkalemia. 141 The causes of
HYPERKALEMIA hyperkalemia are listed in Box 5-2, and the clinical
approach to hyperkalemia is presented in Figure 5-13.
Hyperkalemia is uncommon if renal function and urine
output are normal. Soon after ingestion of a potassium SPECIFIC CAUSES OF HYPERKALEMIA
load, cellular uptake of potassium is mediated by insulin, IN DOGS AND CATS
epinephrine, and the resulting increase in ECF potassium Increased intake of potassium is unlikely to cause
concentration itself. Renal excretion of the potassium sustained hyperkalemia unless impaired renal excretion
load then follows. Sustained, chronic hyperkalemia is of potassium is present. Exceptions include iatrogenic
almost always associated with some impairment in urinary hyperkalemia resulting from calculation errors during
excretion of potassium. continuous infusion of potassium-containing fluids or
administration of drugs known to predispose to
CLINICAL AND LABORATORY hyperkalemia with concurrent potassium supplementa-
FEATURES tion. Examples of the latter situation include concurrent

Theclinicalmanifestationsofhyperkalemiareflectchanges use of nonspecific b-blockers (e.g., propranolol) or
in cell membrane excitability and reflect the magnitude angiotensin-converting enzyme inhibitors (e.g., enala-
and the rapidity of onset of hyperkalemia. Muscle weak- pril) with potassium supplementation (KCl used as a salt
ness develops with hyperkalemia, usually when serum substitute contains 13.4 mEq potassium/g) during treat-
potassium concentration exceeds 8.0 mEq/L. The elec- ment of heart failure (see Chapter 21).
trocardiographic findings caused by hyperkalemia are Translocation of potassium from ICF to ECF can
often characteristic, and the electrocardiogram may be cause hyperkalemia. Acute metabolic acidosis caused by
helpful in establishing a suspicion of hyperkalemia while mineral acids (e.g., NH 4 Cl and HCl) but not organic
awaiting results of the serum potassium concentration acids (e.g., lactic acid and ketoacids) causes potassium
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(Fig. 5-12). to shift out of cells in exchange for H ions that enter cells
The effects of hyperkalemia on the electrocardiogram to be buffered. The effect of acute inorganic metabolic
have been studied in dogs and cats. 41,43,186,187 Increased acidosis on serum potassium concentration in dogs is var-
amplitude and narrowing or “tenting” of the T waves iable and was characterized by a 0.16- to 1.67-mEq/L
may occur with mild increases in serum potassium con- increment in serum potassium concentration per 0.1-U
centration, but these changes are inconsistent in dogs decrement in pH in a review of previously published
and cats. Shortening of the QT–interval may also be studies. 4
observed. These changes reflect abnormally rapid repo- Induction of hypothyroidism in beagles led to a 41%
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larization. Moderate hyperkalemia may result in decrease in the Na ,K -ATPase content of skeletal mus-
prolongation of the PR–interval and widening of cle, which was associated with a decrease in the mean rest-
the QRS complex because of slowing of conduction ing plasma sodium concentration (from 148 to
through the atrioventricular system. With progression 142 mEq/L) and an increase in the mean resting plasma
of hyperkalemia, conduction through the atrial muscle potassium concentration (from 3.7 to 4.3 mEq/L). 171
is impaired, and decreases in the amplitude and widening Plasma potassium concentration also increased slightly
of the P wave are observed. In severe hyperkalemia, after exercise in the hypothyroid dogs (up to a mean of
atrial conduction ceases, the P waves disappear, and approximately 5.0 mEq/L) but not in the euthyroid dogs
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pronounced bradycardia with a sinoventricular rhythm presumably because decreased Na ,K -ATPase in the
may be observed. In extreme hyperkalemia, the QRS hypothyroid dogs resulted in slower reuptake of potas-
complex may merge with the T wave, creating a sine wave sium by muscle cells.
appearance, followed by ventricular fibrillation or Insulin deficiency and hyperosmolality contribute to
ventricular asystole. During progressive hyperkalemia, hyperkalemia in diabetic patients. Hyperosmolality may
atrial inexcitability, depressed conduction through the increase serum potassium concentration as water moves