Hypokalemia refers to the condition in which the concentration of potassium in the blood is low. The prefix hypo- means low (contrast with hyper-, meaning high). Kal refers to kalium, the Neo-Latin for potassium, and -emia means "in the blood." Normal serum potassium levels are between 3.5 to 5.0 mEq; at least 95% of the body's potassium is found inside cells, with the remainder in the blood. This concentration gradient is maintained principally by the Na+/K+-ATPase pump
Mild hypokalemia is often without symptoms, although it may cause a small elevation of blood pressure, and can occasionally provoke cardiac arrhythmias. Moderate hypokalemia, with serum potassium concentrations of 2.5-3 mEq/L, may cause muscular weakness, myalgia, and muscle cramps (owing to disturbed function of the skeletal muscles), and constipation (from disturbed function of smooth muscles). With more severe hypokalemia, flaccid paralysis, hyporeflexia, and tetany may result. There are reports of rhabdomyolysis occurring with profound hypokalemia with serum potassium levels less than 2 mEq/L. Respiratory depression from severe impairment of skeletal muscle function is not uncommon. Some electrocardiographic (ECG) findings associated with hypokalemia are flattened T waves, increased U waves, ST segment depression, and prolongation of the QT interval. The prolonged QT interval may lead to arrhythmias
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 heavy fluid losses that "flush" potassium out of the body. Typically, this is a consequence of vomiting, diarrhea, excessive perspiration, or losses associated with surgical procedures 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, β-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. Alkalosis can cause transient hypokalemia by two mechanisms. First, the alkalosis causes a shift of potassium from the plasma and interstitial fluids; perhaps mediated by stimulation of Na+-H+ exchange and a subsequent activation of Na+/K+-ATPase activity. Second, an acute rise of plasma HCO3- concentration (caused by vomiting, for example) will exceed the capacity of the renal proximal tubule to reabsorb this anion, and potassium will be excreted as an obligate cation partner to the bicarbonate. It should be noted that metabolic alkalosis is often present in states of volume depletion, and thus alkalosis is typically not the main cause of hypokalemia seen in in volume-depleted states. 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 11β-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.
Hypokalemia can be measured by acquiring a sample of blood, preparing blood serum, and using a potassium sensitive electrode for measuring the concentration of potassium ions. Atomic absorption spectroscopy can also be used to measure the potassium ions. Since hypokalemia results in abnormalities in heart behavior, the electrocardiogram is usually used in the diagnosis of hypokalemia. The diagnosis of the cause of hypokalemia can be helped by measuring the potassium content of the urine. Where urinary potassium is under 25 mmoles per day, it means that the patient has experienced excessive losses of potassium due to diarrhea. The urinary potassium test is useful in cases where the patient is denying the practice of laxative or enema abuse. In contrast, where hypokalemia is due to the use of diuretic drugs, the content of potassium in the urine will be high-over 40 mmoles per day.
The prognosis for correcting hypokalemia is excellent. However, in emergency situations, where potassium is administered intravenously, the physician must be careful not to give too much potassium. The administration of potassium at high levels, or at a high rate, can lead to abnormally high levels of serum potassium.
The most important treatment in severe hypokalemia is addressing the cause, such as improving the diet, treating diarrhea or stopping an offending medication. Patients without a significant source of potassium loss and who show no symptoms of hypokalemia may not require treatment. Mild hypokalemia (>3.0 mEq/L) may be treated with oral potassium chloride supplements (Klor-Con, Sando-K, Slow-K). As this is often part of a poor nutritional intake, potassium-containing foods may be recommended, such as leafy green vegetables, tomatoes, citrus fruits, oranges or bananas. Both dietary and pharmaceutical supplements are used for people taking diuretic medications (see Causes, above). Severe hypokalemia (