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Hyperkalemia in Wikipedia

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This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Hyperkalemia". (Source - Retrieved 2006-09-07 14:14:40 from


Hyperkalemia (hyper is high, kalium is the Latin name for potassium) is an elevated blood level (above 5.0 mmol/L) of the electrolyte potassium. Extreme degrees of hyperkalemia are considered a medical emergency due to the risk of potentially fatal arrhythmias.

Signs and symptoms

Symptoms are fairly nonspecific, and generally include malaise, palpitations and muscle weakness; mild breathlessness may indicate metabolic acidosis, one of the settings in which hyperkalemia may occur. Often, however, the problem is detected during screening blood tests for a medical disorder, or it only comes to medical attention after complications have developed, such as cardiac arrhythmia or sudden death.

During the medical history taking, a doctor will dwell on kidney disease and medication use (see below), as these are the main causes. The combination of abdominal pain, hypoglycemia and hyperpigmentation, often in the context of a history of other autoimmune disorders, may be signs of Addison's disease, itself a medical emergency.


In order to gather enough information for diagnosis, the measurement of potassium needs to be repeated, as the elevation can be due to hemolysis of the material in the first sample. Generally, blood tests for renal function (creatinine, blood urea nitrogen), glucose and occasionally creatine kinase and cortisol will be performed. Calculating the trans-tubular potassium gradient can sometimes help in distinguishing the cause of the hyperkalemia.

Electrocardiography (ECG) is generally done early to identify any influences on the heart. High, tent-shaped T-waves, a small P wave and a wide QRS complex (that becomes sinusoidal) all identify the influence of excess potassium on the heart. This finding alone is an important reason for treatment, as it may forewarn ventricular fibrillation.

Often arterial blood gas measurements and renal ultrasound will be performed.

Differential diagnosis

Causes include:

Ineffective elimination from the body

Excessive release from cells

Excessive intake

  • Intoxication with salt-substitute, potassium-containing dietary supplements, or potassium-chloride (KCl) infusion. Note that for a person with normal kidney function and nothing interfering with normal elimination (see above), hyperkalemia by potassium intoxication would be seen only with large infusions of KCl or massive doses of oral KCl supplements.

Lethal injection

Hyperkalemia is intentionally brought about in an execution by lethal injection, potassium chloride being the third and last of the three drugs generally administered to cause death, after sodium thiopental has rendered the subject unconscious, then pancuronium bromide has been added to cause respiratory collapse.


Potassium is the most important intracellular cation and participates in many cellular processes, including transmission of action potentials in nerve cells. Its main dietary sources are vegetables (tomato and potato), fruits (orange and banana) and meat. Elimination is through the gastrointestinal tract and the kidney.

The renal elimination of potassium is passive (through the glomeruli), and resorption is active in the proximal tubule and the ascending limb of the loop of Henle. In the distal tubule, there is active excretion of potassium in the distal tubule and the collecting duct; both are controlled by aldosterone.

Hyperkalemia develops when there is excessive production (oral intake, tissue breakdown) or ineffective elimination of potassium. Ineffective elimination can be hormonal (in aldosterone deficiency) or due to causes in the renal parenchyma that impair excretion.

Increased extracellular potassium levels result in depolarization of the membrane potentials of cells. This depolarization opens some voltage-gated sodium channels, but not enough to generate an action potential. After a short while, the open sodium channels inactivate and become refractory, increasing the threshold to generate an action potential. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillation or asystole.


When arrhythmias occur, or when potassium levels exceed 6.5 mmol/l, emergency lowering of potassium levels is mandated. Several agents are used to lower K levels. Choice depends on the degree and cause of the hyperkalemia, and other aspects of the patient's condition.

  • Calcium supplementation (calcium gluconate 10%, preferably through a central venous catheter as the calcium may cause phlebitis) does not lower potassium but decreases myocardial excitability, protecting against life threatening arrhythmias.
  • Insulin (e.g. intravenous injection of 10u of insulin {along with 50ml of 50% dextrose to prevent hypoglycemia}) will lead to a shift of potassium ions into cells, secondary to increased activity of the sodium-potassium ATPase.
  • Bicarbonate therapy (e.g. 1 ampule (45mEq) infused over 5 minutes) is effective in cases of metabolic acidosis. The bicarbonate ion will stimulate an exchange of cellular H+ for Na+, thus leading to stimulation of the sodium-potassium ATPase.
  • Salbutamol (albuterol, Ventolin®) is a β2-selective catacholamine that is administered by nebuliser (e.g. 10-20 mg). This drug promotes movement of K into cells, lowering the blood levels.
  • Polystyrene sulfonate (Calcium Resonium, Kayexalate) is a binding resin that binds K within the gut and removes it from the body by defecation. Calcium Resonium (15g three times a day in water) can be given by mouth. Kayexelate can be given by mouth or as an enema. In both cases, the resin adsorbs K within the gut and carries it out of the body by defecation. This medication may cause diarrhea.
  • Refractory or very severe cases may need dialysis to remove the potassium from the circulation.
  • Chronic management of hyperkalemia may include diuretics such as furosemide (Lasix®) or hydrochlorothiazide.
  • When mineralocorticoid deficiency is contributing, high dose hydrocortisone and intravenous saline solution may be all that is necessary.

See also


  • Kasper DL et al (Eds). Harrison's Principles of Internal Medicine, 16th ed, chapter 41, pages 258-61. ISBN 0-07-140235-7.
  • Rose, B.D. and T.W. Post, Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed. 2001, pages 888-930. ISBN 0-07-134682-1
  • Schaefer TJ, Wolford RW (2005). Disorders of potassium. Emerg Med Clin North Am, 23(3), 723-47.

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