Hyperkalemia (plasma potassium concentration >5.5 mmol/L) is common in animals with inadequate urine excretion, particularly when they are also acidemic (blood pH <7.2). Affected animals are depressed, with generalized muscle weakness, and may have electrocardiographic abnormalities. Treatment is to increase the rate of urine excretion and intravenously administer isotonic NaCl or NaHCO solutions.
Etiology of Hyperkalemia in Ruminants
Hyperkalemia is common in neonatal ruminants with diarrhea, dehydration, acidemia, and strong ion (metabolic) acidosis. Hyperkalemia often accompanies acidemia because low blood pH results in intracellular acidosis and leakage of potassium from the intracellular compartment to the extracellular space.
Hyperkalemia is exacerbated in calves with marked dehydration, because hypovolemia decreases renal blood flow and consequently the glomerular filtration rate, thereby minimizing the ability of the animal to excrete potassium.
Hyperkalemia is rare in steers, wethers, and bucks with obstructive urolithiasis and bladder or urethral rupture because excess potassium is secreted in adult ruminant saliva, and affected animals have a decrease in potassium intake because of illness. Hyperkalemia can be present in ruminants with exertional rhabdomyolysis due to damage to skeletal muscle cells.
Clinical Findings and Diagnosis of Hyperkalemia in Ruminants
Depression and generalized muscle weakness, possible electrocardiographic abnormalities
Serum or plasma potassium concentration >5.5 mmol/L
Severe hyperkalemia is usually associated with depression, weakness, lethargy, cardiac arrhythmias, and ECG abnormalities, particularly when the serum or plasma potassium concentration is >6.5 mmol/L. Severe cardiotoxic effects are almost always evident when the serum potassium concentration is 8–11 mmol/L.
Serum biochemical analysis is required to confirm a suspected diagnosis of hyperkalemia. In addition to measurement of serum potassium concentration, measurement of serum sodium, calcium, phosphorus, urea, creatinine concentrations, CK and AST activities and blood gas analysis can help guide treatment. An ECG may reveal bradyarrhythmias, although tachycardia is more common; a large study in neonatal calves with hyperkalemia identified suppression in P wave amplitude (plasma K>6.5 mmol/L) or loss of the P wave (plasma K >8.2 mmol/L), widened QRS complexes (plasma K >7.8 mmol/L), increased J point (plasma K >7.9 mmol/L), increased ST segment angle (plasma K >9.1 mmol/L), and symmetric T waves (narrowing of T wave duration and “tenting” of the T wave). The ECG effects of hyperkalemia are exacerbated by the presence of hyponatremia, acidemia, and hypocalcemia.
The ratio of plasma sodium to potassium concentration is important in development of cardiac arrhythmias; hyperkalemia in the presence of hyponatremia (plasma sodium:potassium ratio < 25:1) is commonly associated with the occurrence of cardiac arrhythmias and ECG abnormalities.
Treatment of Hyperkalemia in Ruminants
Intravenous administration of isotonic saline or isotonic sodium bicarbonate solutions (blood pH < 7.2) to restore urinary potassium excretion
Intravenous administration of hypertonic saline, hypertonic sodium bicarbonate, calcium, or glucose solutions (the latter with parenteral insulin) in select cases
Hyperkalemia should initially be treated by IV administration of 0.9% NaCl solution to increase the rate of urine production in dehydrated patients with a patent urinary system, and in select cases by IV administration of sodium bicarbonate, glucose, insulin, and sometimes calcium. Urine should be removed from the abdomen of animals with obstructive urolithiasis and ruptured bladder, and urethral patency should be established. Sodium bicarbonate is administered in order to correct systemic and intracellular acidosis and is the preferred intravenous solution to correct hyperkalemia in patients with acidemia (blood pH < 7.2).
The rationale for intravenous glucose and insulin administration is that insulin-mediated glucose entry into cells is accompanied by movement of potassium from the extracellular space to the intracellular compartment; however, serum potassium concentrations do not begin to decrease until at least 20 minutes after the start of intravenous glucose administration.
The rationale for calcium administration is that calcium counteracts many of the deleterious effects of hyperkalemia on arrhythmogenesis, and the intravenous administration of calcium may therefore improve cardiac output. However, hypertonic saline (2,400 mOsm/L) is just as effective as hypertonic sodium bicarbonate in decreasing hyperkalemia and hyperkalemia-associated bradyarrhythmias, likely because of hypernatremia-mediated intracellular movement of potassium, extracellular volume expansion, and increased rate of urine production. The focus of treatment in hyperkalemia should therefore be expanding plasma volume to assist in renal excretion of potassium, identifying and correcting acidemia, and increasing the serum sodium concentration. Contrary to previous understanding, routine provision of glucose and insulin seem unnecessary to correct hyperkalemia.
Prevention of Hyperkalemia in Ruminants
Hyperkalemia can be prevented via early diagnosis and treatment of its most common causes. Hyperkalemic periodic paralysis can be prevented in horses by feeding a low-potassium diet or the oral administration of acetazolamide.
Key Points
Hyperkalemia (plasma potassium concentration >5.5 mmol/L) is common in animals with inadequate urinary excretion, particularly when animals are also dehydrated and acidemic (blood pH < 7.2).
Hyperkalemia results in depression, generalized muscle weakness, and a variety of electrocardiographic abnormalities.
Treatment should focus on reestablishing urinary potassium excretion by intravenous administration of isotonic saline (normal blood pH) or isotonic sodium bicarbonate solutions (blood pH < 7.2).
