Potassium homeostasis is mainly determined by the balance between absorption of potassium from the GI tract and subsequent excretion by the kidneys (all animals) and saliva (in adult ruminants). Transport of potassium is passive in the small intestine and active in the colon under the influence of aldosterone. The most important hormone affecting renal and salivary potassium excretion is aldosterone, which is released from the zona glomerulosa of the adrenal gland in response to hyperkalemia and other factors. One of aldosterone’s primary actions is to enhance the secretion of potassium ions in the distal renal tubules and collecting ducts.
At least 95% of whole body potassium is intracellular, with skeletal muscle containing 60%–75% of the intracellular potassium. Marked changes in serum or plasma potassium concentrations alter the resting membrane potential of cells, because the potassium gradient generated by Na+/K+-ATPase is the main cause for the negative electric potential across cell membranes. Therefore, hypokalemia or hyperkalemia alters the resting membrane potential, resulting in clinically important changes in cellular and organ function. Hypokalemia usually indicates whole body depletion of potassium, unless identified in animals with hyperinsulinemia due to hyperglycemia, in which case potassium may have translocated intracellularly. Whole-body potassium status in hyperkalemia cannot be inferred because many animals with hyperkalemia have concurrent acidemia and whole-body potassium depletion.
Hypokalemia can occur in any animal receiving large volumes of IV fluid or having a marked and sustained reduction in feed intake. Clinical signs in most animals with mild to moderate hypokalemia are mild and nonspecific. Severe hypokalemia is associated with ventroflexion of the head or recumbency due to generalized muscle weakness and cardiac arrhythmias, including both atrial and ventricular premature complexes that may lead to more complex cardiac arrhythmias. Prolonged and profound hypokalemia can result in a myopathy difficult to treat. Cats can be affected by a feline hypokalemic polymyopathy, and Burmese cats have an autosomal recessive disorder that leads to hypokalemic myopathy.
Hyperkalemia usually results from inadequate urinary excretion of ingested potassium and is common in monogastric animals with urinary tract obstruction and bladder rupture. Hyperkalemia in horses and ruminants can also result from exertional rhabdomyolysis, because skeletal muscle contains a large percentage of whole body potassium. Hyperkalemia also occurs in heavily muscled Quarter horses and related breeds as a genetic disorder (hyperkalemic periodic paralysis). Hyperkalemia frequently occurs in dogs with hypoadrenocorticism. Severe hyperkalemia is associated with generalized muscle weakness, depression, and cardiac conduction disturbances that may lead to lethal cardiac arrhythmias. Pseudohyperkalemia in serum can occur in animals with thrombocytosis as a result of the excessive release of intracellular potassium stores from platelets during clotting. Pseudohyperkalemia in serum and plasma occurs when extensive hemolysis is present because of the high potassium concentration in RBCs in most species, although some species have genetic differences in their erythrocytic potassium concentration.