Hyperkalemia in cats is usually a secondary consequence of metabolic acidosis, where compensatory excretion of H+ ions occurs in the kidneys in an attempt to reduce blood acidity. Excretion of H+ ions leads to retention of K+ ions in the blood.
Potassium is the major intracellular cation in feline cells and is largely responsible for maintenance of intracellular volume. Serum potassium concentrations slightly exceed plasma concentrations because potassium is released from platelets during the clotting process. Potassium is responsible for maintaining resting cell membrane potential. Therefore, disorders of potassium concentration affect excitable membranes. Clinical signs are related to disturbances in skeletal (weakness) and cardiac (arrhythmia) muscles.
Chronic hyperkalemia almost always is associated with impairment in urinary potassium excretion. Clinical manifestations of hyperkalemia reflect changes in cell membrane excitability with muscle weakness and cardiac electrical conduction abnormalities. ECG changes in mild hyperkalemia include increased amplitude and narrowing of the T wave and shortening of the QT interval. Moderate hyperkalemia causes prolongation of the PR interval and widening of the QRS. As hyperkalemia progresses, P waves decrease in amplitude, become wide and eventually disappear. Bradycardia due to a sinoventricular rhythm may be observed, although is less pronounced in cats.
Translocation of potassium from ICF to ECF can occur in diabetes mellitus. Insulin deficiency and hyperosmolality contribute to the development of hyperkalemia in diabetic patients. Massive tissue breakdown may lead to transient hyperkalemia until released potassium is excreted by the kidneys. This may occur after reperfusion of aortic thromboembolism. Nonspecific beta-blockers (e.g. propranolol) decrease cellular uptake of potassium, and may cause hyperkalemia in the presence of a potassium load or decreased renal function.
Decreased urinary excretion of potassium is the most important cause of hyperkalemia in feline practice. It usually results from urethral obstruction, ruptured bladder, and anuric or oliguric renal failure. Oliguria or anuria with hyperkalemia are more likely to occur in acute renal failure, but they may be observed terminally in chronic renal failure. Patients with chronic renal disease have reduced ability to tolerate an acute potassium load and may require 1-3 days to reestablish external potassium balance when intake of potassium is abruptly increased (e.g., fluid therapy). Several drugs may reduce renal excretion of potassium. ACE inhibitors interfere with angiotensin II-mediated aldosterone secretion, whereas spironolactone competitively blocks aldosterone. Treatment of hyperkalemia will depend on the magnitude and rapidity of onset of the hyperkalemia. Patients with symptomatic hyperkalemia or ECG abnormalities should be treated. Mild chronic hyperkalemia (K < 6,5 mEq/L) may not require immediate therapy. Asymptomatic, non-oliguric patient: The underlying disease process should be treated and any source of potassium intake or drugs that cause potassium retention should be discontinued, if possible. Fluid therapy with potassium-free solutions ameliorates mild hyperkalemia by improving renal perfusion, enhancing urinary excretion of potassium, and by diluting the potassium in ECF.
Administration of glucose or NaHCO3 can be attempted in patients with mild hyperkalemia that did not respond to potassium discontinuation and fluid therapy. Administration of glucose (1-2 ml/kg of the 50% solution) will cause release of insulin and move potassium into the cells. The effects begin within an hour and last a few hours. Concurrent administration of insulin may improve the response but it increases the risk of hypoglycemia.
Adjunctive therapy: in selected cases of hyperkalemia, loop diuretics may be used to enhance the flow rate in the distal nephron and increase potassium excretion. Patients with renal failure are unlike to benefit from this maneuver.
Atropine may be attempted in patients that are bradycardic. During the hyperkalemia-induced bradycardia, the SA-node still works (the so-called sinoventricular rhythm) and is under vagal influence. Atropine injection may cause a mild increase of heart rate and temporarily reestablish cardiac output and blood pressure. Refractory cases may require hemodialysis or continuous renal replacement therapy.
- Cunha MG et al (2010) Renal and cardiorespiratory effects of treatment with lactated Ringer's solution or physiologic saline (0.9% NaCl) solution in cats with experimentally induced urethral obstruction. Am J Vet Res 71(7):840-846
- Kogika MM, de Morais HA (2008) Hyperkalemia: A quick reference. Vet Clin N Am Small Anim Pract 38:477-480
- Dow SW, Fettman MJ, Curtis CR, et al (1989) Hypokalemia in cats: 186 cases (1984-1987). J Am Vet Med Assoc 194:1604-1608