1.abnormally low level of potassium in the circulating blood leading to weakness and heart abnormalities; associated with adrenal tumors or starvation or taking diuretics
1.(MeSH)Abnormally low potassium concentration in the blood. It may result from potassium loss by renal secretion or by the gastrointestinal route, as by vomiting or diarrhea. It may be manifested clinically by neuromuscular disorders ranging from weakness to paralysis, by electrocardiographic abnormalities (depression of the T wave and elevation of the U wave), by renal disease, and by gastrointestinal disorders. (Dorland, 27th ed)
definition of Wikipedia
Hypokalemia (n.) [MeSH]
|Classification and external resources|
An ECG in a person with a potassium level of 1.1 showing the classical ECG changes of ST segment depression, inverted T waves, large U waves, and a slightly prolonged PR interval.
Hypokalemia (American English) or hypokalaemia (British English), also hypopotassemia or hypopotassaemia (ICD-9), refers to the condition in which the concentration of potassium (K+) in the blood is low. The prefix hypo- means "under" (contrast with hyper-, meaning "over"); kal- refers to kalium, the Neo-Latin for potassium, and -emia means "condition of the blood."
Normal plasma potassium levels are between 3.5 to 5.0 mEq/L; 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+ 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 (Nl: 3.5-5.0 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 and hyporeflexia 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 found in many patients.
Some electrocardiographic (ECG) findings associated with hypokalemia include flattened or inverted T waves, a U wave, ST depression and a wide PR interval. Due to prolonged repolarization of ventricular Purkinje fibers, a prominent U wave occurs, that is frequently superimposed upon the T wave and therefore produces the appearance of a prolonged QT interval.
Hypokalemia can result from one or more of the following medical conditions:
Potassium is essential for many body functions, including muscle and nerve activity. The electrochemical gradient of potassium between the 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. Lower 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.
In the heart, hypokalemia causes hyperpolarization in the myocytes' resting membrane potential. The more negative membrane potentials in the atrium may cause arrhythmias because of more complete recovery from sodium-channel inactivation, making the triggering of an action potential more likely. In addition, the reduced extracellular potassium (paradoxically) inhibits the activity of the IKr potassium current and delays ventricular repolarization. This delayed repolarization may promote reentrant arrhythmias.
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 (<3.0 mEq/L) may require intravenous (IV) supplementation. Typically, a saline solution is used, with 20-40 mEq KCl per liter over 3–4 hours. Giving IV potassium at faster rates (20-25 mEq/hr) may predispose to ventricular tachycardias and requires intensive monitoring. A generally safe rate is 10 mEq/hr. Even in severe hypokalemia, oral supplementation is preferred given its safety profile. Sustained release formulations should be avoided in acute settings.
Difficult or resistant cases of hypokalemia may be amenable to a potassium-sparing diuretic, such as amiloride, triamterene, or spironolactone or eplerenone. Concomittant hypomagnesiumemia will inhibit potassium replacement as magnesium is a cofactor for potassium uptake.
When replacing potassium intravenously, infusion via a central line is encouraged to avoid the frequent occurrence of a burning sensation at the site of a peripheral IV, or the rare occurrence 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.
Burmese hypokalaemia (Familial Episodic Hypokalaemic Polymyopathy) is characterised by episodes of low serum potassium levels and high CPK (an enzyme that indicates muscle damage). Clinical signs include skeletal muscle weakness, which is episodic in nature and can affect the whole animal or may be localised to certain muscles. This is most obvious in the neck muscles, but sometimes occurs in just the limbs. As a result affected cats tend to have problems walking and holding their head correctly.
A research team consisting of veterinarians and geneticists from the University of Bristol (Langford), UC Davis, University of Sydney, Massey University and Justus Liebig University have recently identified the genetic mutation responsible for Burmese hypokalaemia, allowing a genetic test to be developed (see here). This is an autosomal recessive disease, meaning that two copies of the mutated gene are required for disease.
Affected cats can usually be managed effectively by giving potassium supplements to their diet . This will reduce the signs of disease or minimise their frequency and severity. In some affected cats signs seem to disappear when they get to 1-2 years of age without the need for further treatment.
A feline form of hypokalemic periodic paralysis has been described in Burmese kittens, which appears to be related to an autosomal recessive mutation. Although these kittens are not hypokalemic between episodes, regular supplementation of [KCl] seems effective.
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