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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
- Flattened (notched) T waves
- U waves
- ST depression
- Prolonged QT interval
Hypokalemia can result from one or more of the following medical conditions:
- Perhaps the most obvious cause is insufficient consumption of potassium (that is, a low-potassium diet). However, without excessive potassium loss from the body, this is a rare cause of hypokalemia.
- A more common cause is excessive loss of potassium, often associated with excess water loss, which "flushes" potassium out of the body. Typically, this is a consequence of vomiting, diarrhea, or excessive perspiration.
- Certain medications can 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 has also been 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 obligate loss of potassium from kidney tubules as a cationic partner to the negatively charged ketone, ß-hydroxybutyrate.
- Hypomagnesemia can cause hypokalemia. Magnesium is required for adequate processing of potassium. This may become evident when hypokalemia persists despite potassium supplementation. Other electrolyte abnormalities may also be present.
- Disease states that lead to abnormally high aldosterone levels can cause hypertension and excessive urinary losses of potassium. These include renal artery stenosis and tumors (generally non-malignant) of the adrenal glands. Hypertension and hypokalemia can also be seen with a deficiency of the 11ß-hydroxylase enzyme which allows cortisols to stimulate aldosterone receptors. This deficiency can either be congenital or 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. These defects cause a heightened sensitivity to catechols and/or insulin and/or thyroid hormone that lead to sudden influx of potassium from the extracellular fluid into the muscle cells.
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 3.5 - 5.0 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.
- 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>
- Difficult or resistant cases of hypokalemia may be amenable to amiloride, a potassium-sparing diuretic, or spironolactone.
When replacing potassium intravenously, infusion via central line is encouraged to avoid the frequent occurence of a burning sensation at the site of a peripheral iv, or the rare occurence of damage to the vein. When peripheral infusions are necessary, the burning can be reduced by diluting the potassium in larger amounts of IV fluid, or mixing 3 ml of 1% lidocaine to each 10 meq of kcl per 50 ml of IV fluid. The practice of adding lidocaine, however, raises the likelihood of serious medical errors .
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