Hyperkalemia Hyperkalemia decreases the resting membrane potential, predisposing the cell to excitability. This results in cardiac arrythmias. Causes of hyperkalemia Hyperkalemia is usually due to decreased renal excretion of potassium, due to renal failure, urinary tract obstruction or rupture, or hypoaldosteronism. Pseudohyperkalemia 1) Serum: Serum K+ is higher than plasma K+ due to release of K+ from platelets during clotting. The difference between serum and plasma K+ in dogs with normal platelet counts can be as high as 0.6 mEq/L. This difference is greater with higher platelet counts. 2) Hemolysis: This will increase K+ in animals with high K+ in their erythrocytes, including horses, pigs, cattle and cats. Remember that certain dog breeds have high K+ in their mature red blood cells, such as Akitas and other Japanese breeds. All dogs have high K+ in their reticulocytes, so K+ can be artefactually elevated in hemolysed samples (or samples with delayed separation from cells) with high reticulocyte counts from any dog breed. 3) Leukocytosis: Very high leukocyte counts (> 100,000/uL) can result in hyperkalemia due to leakage of intracellular K+ from cells. 4) Age: Potassium is higher in foals < 5 months of age than adult horses. Foals < 1 week old have higher K+ than foals > 1 week old. 5) K+ EDTA: Contamination of serum/plasma sample with K+ EDTA will result in very high (non-physiologic) K+ values (>20 mEq/L) as well as marked hypocalcemia and hypomagnesiumia (due to chelation). Increased intake: This is usually iatrogenic and does not usually result in hyperkalemia if kidney function is normal, e.g. KCl administration. Transcellular shifts: Shifting of K+ from ICF to ECF occurs with tissue necrosis, exercise (this occurs especially in horses and is due to release of K+ from muscles - K+ is a local vasodilator for muscle cells), uroperitoneum (especially in foals), hypertonicity (e.g. diabetes mellitus - occurs due to solvent drag) and hyperchloremic metabolic acidosis. A high anion gap metabolic acidosis (titration acidosis) does not usually result in hyperkalemia as the organic anion moves into the cell with H+. Hyperkalemia in animals with a titration acidosis is not due to translocation, but due to decreased renal excretion of K+. Decreased renal excretion: Hyperkalemia is a feature of anuric or oliguric acute renal failure (e.g. bladder obstruction), chronic renal failure (horses), third space losses (uroabdomen), and Addison's disease. Addison's disease (hypoaldesteronemia) causes a low sodium and high potassium with a sodium:potassium ratio of < 27:1. Electrolyte changes (high K+, low Na+) mimicking Addison's disease can be seen with repeated drainage of thoracic effusions, severe diarrhea due to Salmonella or whipworm infection, and lymphangiosarcoma, although the precise mechanism is unclear. Inherited causes Hyperkalemic polymyopathy of horses: This is due to a genetic defect in the alpha subunit of the sodium channel of muscle cells (the sodium channels remain perpetually open) observed in Quarterhorses and other heavily muscled breeds like Appaloosas and Paints. It is a familial condition in the Quarterhorse and appears to be inherited as an autosomal dominant condition. The condition appears to be clinically worse in males. It is characterized by intermittent episodes of msucle fasciculation and weakness concurrent with increases in serum K+ values. Normokalemic variants have been described. Drug-induced hyperkalemia: Trimethoprim induces hyperkalemia by inhibiting sodium resorption in the cortical collecting ducts of the kidney.

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