Hypokalemia

Hypokalemia is a potentially fatal condition in which the body fails to retain sufficient potassium to maintain health. The condition is also known as potassium deficiency. The prefix hypo- means low (contrast with hyper-, meaning high). The middle kal refers to kalium, which is Latin for potassium. The end portion of the word, -emia, means "in the blood" (note, however, that hypokalemia is usually indicative of a systemic potassium deficit).

Signs and symptoms

There may be no symptoms at all, but severe hypokalemia may cause:

Muscle weakness and myalgia
Increased risk of hyponatremia with resultant confusion and seizures
Disturbed heart rhythm (ranging from ectopy to arrhythmias)
Serious arrhythmias

EKG changes associated with hypokalemia^[1]:

Flattened (notched) T waves
U waves
ST depression
Prolonged QT interval

Causes

Hypokalemia can result from a variety of medical conditions:

Perhaps most obviously, insufficient consumption of potassium (that is, a low-potassium diet) can result in the condition. More commonly, however, hypokalemia occurs due to excessive loss of potassium, often associated with excess water loss, which "flushes" potassium out of the body. Typically, this is a consequence of vomiting and diarrhea, but may also occur with excessive sweating in athletes.

Certain medications can also accelerate the removal of potassium from the body, including thiazide diuretics, such as hydrochlorothiazide; loop diuretics, such as furosemide; as well as various laxatives. The antifungal amphotericin B is also associated with hypokalemia.

A special case of potassium loss occurs with diabetic ketoacidosis. In addition to urinary losses from polyuria and volume contraction, there is also the obligate loss of potassium from the kidney tubules as a cationic partner to the negatively charged ketone, β-hydroxybutyrate.

Hypomagnesemia can also cause hypokalemia, as magnesium is required for the adequate processing of potassium. This may come to light when hypokalemia persists despite potassium supplementation. Other electrolyte abnormalities may also be present.

Disease states that lead to abnormally high aldosterone levels will cause hypertension and excessive urinary losses of potassium. These include renal artery stenosis, Cushing's syndrome, or tumors (generally non-malignant) of the adrenal glands. Hypertension and hypokalemia can also be seen with a deficiency of the 11β-hydroxylase enzyme which allows cortisols to stimulate the aldosterone receptor. This deficiency can be congenital or can be caused by consumption of glycyrrhizin, which is contained in extract of licorice, sometimes found in Herbal supplements, candies and chewing tobacco.

Rare hereditary defects of renal salt transporters, such as Bartter syndrome or Gitelman syndrome can cause hypokalemia, in a manner similar to that of diuretics.

Rare hereditary defects of muscular ion channels and transporters that cause hypokalemic periodic paralysis can precipitate occasional attacks of severe hypokalemia and muscle weakness. The defects cause a heightened sensitivity to catechols and/or insulin and/or thyroid hormone that lead sudden influx of the potassium out of the extracellular fluid into the muscles.

Pathophysiology

Potassium is essential for many body functions, including muscle and nerve activity. Potassium is the principal intracellular cation, with a concentration of about 145 mEq/L, as compared with a normal value of about 4 mEq/L in extracellular fluid, including blood. More than 98% of the body's potassium is intracellular; measuring it from a blood sample is relatively insensitive, with small fluctuations in the blood corresponding to very large changes in the total bodily reservoir of potassium.

The electrochemical gradient of potassium between intracellular and extracellular space is essential for nerve function; in particular, potassium is needed to repolarize the cell membrane to a resting state after an action potential has passed. Decreased potassium levels in the extracellular space will cause hyperpolarization of the resting membrane potential. This hyperpolarization is caused by the effect of the altered potassium gradient on resting membrane potential as defined by the Goldman equation. As a result, a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential.

Pathophysiology of Hypokalemic Heart Arrythmias

Potassium is essential to the normal muscular function, in both voluntary (i.e skeletal muscle, e.g. the arms and hands) and involuntary muscle (i.e. smooth muscle in the intestines or cardiac muscle in the heart). Severe abnormalities in potassium levels can seriously disrupt cardiac function, even to the point of causing cardiac arrest and death. As explained above, hypokalemia makes the resting potential of potassium [E(K)] more negative. In certain conditions, this will make cells less excitable. However, in the heart, it causes myocytes to become hyperexcitable. This is due to two independent effects that may lead to aberrant cardiac conduction and subsequent arrhythmia: 1) there are more inactivated sodium (Na) channels available to fire, and 2) the overall potassium permeability of the ventricle is reduced (perhaps by the loss of a direct effect of extracellular potassium on some of the potassium channels), which can delay ventricular repolarization.

Treatment

The most important step in severe hypokalemia is removing the cause, such as treating diarrhea or stopping offending medication.

Mild hypokalemia (>3.0 mEq/L) may be treated with oral potassium chloride supplements (Sando-K®, Slow-K®). As this is often part of a poor nutritional intake, potassium-containing foods may be recommended, such as tomatoes, oranges or bananas. Both dietary and pharmaceutical supplements are used for people taking diuretic medications (see Causes, above).

Severe hypokalemia (<3.0 mEq/L) may require intravenous supplementation. Typically, saline is used, with 20-40 mEq KCl per liter over 3-4 hours. Giving intravenous potassium at faster rates may predispose to ventricular tachycardias and requires intensive monitoring.

Difficult or resistant cases of hypokalemia may be amenable to amiloride, a potassium-sparing diuretic, or spironolactone.

Hypokalemia in pets

Cats can develop hypokalemia in old age, but Burmese kittens may be genetically prone to the condition if both parents have a defective gene. Symptoms are: staggering, an inability to keep up head which droops alarmingly and animals have good appetite but fail to gain weight. Treatment is by adding ground potassium tablets to the animal's food.

References

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 836-887. ISBN 0-07-134682-1
Feline Hypokalemic Polymyopathy. in The Merck Veterinary Manual, 9th edition By Merck & Co. 2006. ISBN 0-911910-50-6

External link

Potassium in the human diet

Citations

[1] Verive M, Jaimovich D. Hypokalemia. eMedicine.com. URL: http://www.emedicine.com/ped/topic1121.htm. Accessed on: June 3, 2006.

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