Hypokalemia- Hipopotasemia - نقص بوتاسيوم الدم - 低血鉀症 -
Hypokaliämie - 低カリウム血症 - гипокалиемия - hipokaliemia - υποκαλιαιμία - hạ kali máu - хипокалемија - ipokaliemia - хипокалиемия - هیپوکالمی - היפּאָקאַלעמיאַ
The purpose of this blog is to collate all the key information regarding Hypokalemic Periodic Paralys, its symptoms, side effects and treatment. Information in English and Spanish. *****
K is the most abundant intracellular cation, but only about 2% of total body K is extracellular. Because most intracellular K is contained within muscle cells, total body K is roughly proportional to lean body mass. An average 70-kg adult has about 3500 mEq of K.
K is a major determinant of intracellular osmolality. The ratio between K concentration in the ICF and ECF strongly influences cell membrane polarization, which in turn influences important cell processes, such as the conduction of nerve impulses and muscle (including myocardial) cell contraction. Thus, relatively small alterations in serum K concentration can have significant clinical manifestations.
In the absence of factors that shift K in or out of cells (see K shifts), the serum K concentration correlates closely with total body K content. Once intracellular and extracellular concentrations are stable, a decrease in serum K concentration of about 1 mEq/L indicates a total K deficit of about 200 to 400 mEq. Patients with K < 3 mEq/L typically have a significant K deficit.
Pearls & Pitfalls
A decrease in serum K concentration of about 1 mEq/L indicates a total K deficit of about 200 to 400 mEq.
Factors that shift K in or out of cells include the following:
Insulin moves K into cells; high concentrations of insulin thus lower serum K concentration. Low concentrations of insulin, as in diabetic ketoacidosis, cause K to move out of cells, thus raising serum K, sometimes even in the presence of total body K deficiency.
β-Adrenergic agonists, especially selective β2-agonists, move K into cells, whereas β-blockade and α-agonists promote movement of K out of cells.
Acute metabolic acidosis causes K to move out of cells, whereas acute metabolic alkalosis causes K to move into cells. However, changes in serum HCO3 concentration may be more important than changes in pH; acidosis caused by accumulation of mineral acids (nonanion gap, hyperchloremic acidosis) is more likely to elevate serum K. In contrast, metabolic acidosis due to accumulation of organic acids (increased anion gap acidosis) does not cause hyperkalemia. Thus, the hyperkalemia common in diabetic ketoacidosis results more from insulin deficiency than from acidosis. Acute respiratory acidosis and alkalosis affect serum K concentration less than metabolic acidosis and alkalosis. Nonetheless, serum K concentration should always be interpreted in the context of the serum pH (and HCO3 concentration).
Dietary K intake normally varies between 40 and 150 mEq/day. In the steady state, fecal losses are usually close to 10% of intake. The remaining 90% is excreted in the urine so alternations in renal K secretion greatly affect K balance.
When K intake is > 150 mEq/day, about 50% of the excess K appears in the urine over the next several hours. Most of the remainder is transferred into the intracellular compartment, thus minimizing the rise in serum K. When elevated K intake continues, aldosterone secretion is stimulated and thus renal K excretion rises. In addition, K absorption from stool appears to be under some regulation and may fall by 50% in chronic K excess.
When K intake falls, intracellular K again serves to buffer wide swings in serum K concentration. Renal K conservation develops relatively slowly in response to decreases in dietary K and is far less efficient than the kidneys' ability to conserve Na. Thus, K depletion is a frequent clinical problem. Urinary K excretion of 10 mEq/day represents near-maximal renal K conservation and implies significant K depletion.
Acute acidosis impairs K excretion, whereas chronic acidosis and acute alkalosis can promote K excretion. Increased delivery of Na to the distal nephrons, as occurs with high Na intake or loop diuretic therapy, promotes K excretion.
False K concentrations:
Pseudohypokalemia, or falsely low serum K, occasionally is found when blood specimens from patients with chronic myelocytic leukemia and a WBC count > 105/μL remain at room temperature before being processed because of uptake of serum K by abnormal leukocytes in the sample. It is prevented by prompt separation of plasma or serum in blood samples.
Pseudohyperkalemia, or falsely elevated serum K, is more common, typically occurring due to hemolysis and release of intracellular K. To prevent false results, phlebotomy personnel should not rapidly aspirate blood through a narrow-gauge needle or excessively agitate blood samples. Pseudohyperkalemia can also result from platelet count > 400,000/μL due to release of K from platelets during clotting. In cases of pseudohyperkalemia, the plasma K (unclotted blood), as opposed to serum K, is normal.