Casting the Light on "Lytes"--Hypokalemia
World Small Animal Veterinary Association World Congress Proceedings, 2008
Michael Schaer, DVM, DACVIM, DACVECC
University of Florida, College of Veterinary Medicine
Gainesville, FL, USA

This condition occurs when the serum potassium concentration is less than 3.5 mmol/L (normal range is 3.5-5.5 mmol/L).


The causes of hypokalemia can be classified into 4 major categories:

1.  Dilutional Hypokalemia and Decreased Intake: This situation is usually acquired iatrogenically where the animal is given intravenous or subcutaneous fluids which are devoid of potassium or contain too little potassium to meet the daily requirements and to replace any excessive losses occurring through the gastrointestinal tract or kidney. It is important to note that the 4 mmol/L of potassium in lactated Ringer's solution is inadequate for maintenance needs and that practically all maintenance doses of parenteral solutions require potassium supplementation.

2.  Transcellular Maldistribution: A common cause for this is metabolic alkalosis which allows for the transfer of potassium from the extracellular fluid (ECF) to the intracellular fluid (ICF) during the body's attempt to mobilize hydrogen ions into the ECF. Certain hormones such as insulin, epinephrine and aldosterone can lower serum potassium levels by this mechanism.

3.  Loss of Potassium via the Gastrointestinal Tract: This condition often occurs with excessive vomiting and diarrhea while the appetite is impaired.

4.  Loss of Potassium through Urine: Can occur under various clinical situations:

a.  Urinary loss of potassium is aggravated by a high sodium intake.

b.  Alkalosis.

c.  Renal tubular dysfunction as seen in renal tubular acidosis and chronic renal insufficiency.

d.  Severe malnourishment wherein there is a very low intake but continued excretion of potassium.

e.  Use of diuretics concomitant to inadequate intake as commonly seen with the potent kaliuretic agent furosemide.

f.  Hyperaldosteronism in which the mineralocorticoid promotes excessive renal excretion of potassium.

Clinical Findings

The clinical signs of hypokalemia occur from a disturbance in neuromuscular function due to impaired electrical conduction at the cell membrane level. Neuromuscular signs are seldom present until serum potassium has decreased to 2.5 mmol/L or less. Muscle weakness and cardiac conduction abnormalities eventually occur as a result of a hyperpolarization block at the neuromuscular junction. Other signs that can accompany severe or chronic hypokalemia include paralysis, muscle cramps, paresthesia, respiratory muscle impairment, lethargy and confusion, inability to concentrate urine, carbohydrate intolerance, anorexia, vomiting, and depressed bowel motility.

Hypokalemia can sustain a metabolic alkalosis because of its tendency to promote renal proximal tubular HCO3- reabsorption. This acid-base disorder can, in turn, worsen the potassium imbalance because the alkalosis drives potassium intracellularly. The use of intravenous 0.9% saline solution supplemented with potassium chloride while correcting the cause are essential for treating metabolic alkalosis-associated hypokalemia.

Electrocardiographic changes first appear when the serum potassium level is less than 2.5 mmol/L; however, their occurrence is not as reliable as those accompanying hyperkalemia. The abnormalities include: depressed ST segment; lowering, flattening, or inversion of the T wave; presence of an elevated U wave (in humans); increased P wave amplitude; prolonged PR interval, and prolonged QRS interval. Certain cardiac arrhythmias can also occur and include: sinus bradycardia, primary heart block, paroxysmal atrial tachycardia, and AV dissociation. Life-threatening arrhythmias are not commonly associated with hypokalemia.

Differential Diagnosis

Several conditions can affect myoneural function including polyradiculoneuropathy, myasthenia gravis, organophosphate intoxication, diabetic neuropathy and hypercalcemia, hypocalcemia, and hyperkalemia.


The treatment of chronic mild hypokalemia (3.0-3.5 mmol/ L) can be accomplished with dietary measures which include the addition of high potassium-containing foods such as oranges, bananas, grapes or nuts to the diet. Commercial oral potassium supplement tablets and elixirs are also available. Elixirs may induce emesis; to avoid this, they should be diluted with water. The daily dose of these oral preparations is 0.5-1.0 mmol/kg mixed in food once or twice daily. A veterinary powdered supplement is commercially available (Tumil-K®--Vibrac, Ft Worth, Texas) and given at a recommended dose of ¼ teaspoonful (2 mmol) per 4.5 kg body weight PO in food twice daily. Adjust dose as necessary.

Parenteral Treatment of Severe Hypokalemia

The treatment of severe or acute hypokalemia with or without metabolic alkalosis requires the administration of diluted intravenous potassium chloride solution. Unfortunately, no accurate formulas exist for calculating the exact amount of potassium chloride needed to restore normal serum potassium levels. The excessive amounts of potassium lost through polyuria, from the gastrointestinal tract, and the commonly marked decreases accompanying the use of fluids and insulin in the treatment of diabetic ketoacidosis make the dependability of any formula unreliable. An important fact to remember is: when potassium chloride is given intravenously, the rate is more critical than the total amount administered. Under most circumstances the rate should not exceed 0.5 mmol/kg/hr. However, under the most dire circumstances, the rate can be increased to 1.5 mmol/kg/hr along with close ECG monitoring. Small animals should not receive more than 10 mmol/hr for fear of fatal consequences because of the effects of a more concentrated solution on the wall of the right ventricle, if the solution is given through a central intravenous line.

When administered over a 24-hour period via intravenous infusion in lactated Ringer's or isotonic saline, the following mmols of potassium chloride can be safely administered:


Measured serum
(K+ mmol/L)

Amount KCl per kg
body weight
given over 24 hours



2-3 mmol



3-5 mmol


< 2.5

5-10 mmol

An alternative and time tested guideline for potassium supplementation is provided in Table 1.

Table 1. Recommended amount of potassium chloride and rate of infusion.

Serum potassium

mmol KCl to
add to
250 ml Fluid

mmol KCl to
add to 1 L Fluid

Maximal fluid
infusion rate*

< 2.0




















*So as not to exceed 0.5 mmol/kg/hr.
Source: from Greene RW, Scott RC. Lower urinary tract disease. In Ettinger SJ (ed): Textbook of Veterinary Internal Medicine, Philadelphia, WB Saunders Co, p 1572, 1975.

It is important remember that the preceding amounts are only ranges that must be adjusted to the specific needs of each patient. For instance, a 5 kg ketoacidotic diabetic cat with a serum potassium measuring 2.0 mmol/L can require as much as 30 mmol KCl over the first 24 hours. Potassium supplementation is a clinical exercise in titration, thereby requiring repeated monitoring of serum potassium levels.

Under life-threatening conditions when the serum potassium is < 1.8 mmol/L, potassium chloride solution might require an expedient delivery. This can be accomplished using KCl solution (2 mmol/ml) and administering it via an automatic syringe at a rate of 0.004 to 0.008 ml/kg/min. Hourly serum potassium determinations are advised. Regular maintenance treatment can begin when the serum potassium level reaches 3.5 mmol/L. This technique should only be reserved for the most critically hypokalemic patient.

Anticipated Response

The increase in serum potassium concentration will occur slowly and gradually over a few days, particularly if there are continued ongoing losses. It is important to correct any coexisting magnesium deficits because hypomagnesemia causes further renal potassium losses.

For uncomplicated maintenance, potassium chloride can be supplemented at a dosage of 7-8 mmol per 250 ml or 20-30 mmol per 1000 ml. The serum potassium level should be measured once every 2-3 days under routine circumstances.

Speaker Information
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Michael Schaer, DVM, DACVIM, DACVECC
University of Florida
College of Veterinary Medicine
Gainesville, Florida, USA

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