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Medical condition with insufficient potassium

Mild hypokalemia is often without symptoms, although it may cause elevation of blood pressure, and can provoke the development of an abnormal heart rhythm. Severe hypokalemia, with serum potassium concentrations of 2.5–3 meq/L (Nl: 3.5–5.0 meq/L), may cause muscle weakness, myalgia, tremor, and muscle cramps (owing to disturbed function of skeletal muscle), and constipation (from disturbed function of smooth muscle). With more severe hypokalemia, flaccid paralysis and hyporeflexia may result. Reports exist 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 some people. Psychological symptoms associated with severe hypokalemia can include delirium, hallucinations, depression, or psychosis.

Not eating a diet with enough potassium containing foods or fasting can cause the gradual onset of hypokalemia. This is a rare cause and may occur in those with anorexia nervosa or those on a ketogenic diet.

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 diarrhea, excessive perspiration, losses associated with crush injury, or surgical procedures. Vomiting can also cause hypokalemia, although not much potassium is lost from the vomitus. Rather, heavy urinary losses of K+ in the setting of post emetic bicarbonaturia force urinary potassium excretion. (See discussion of alkalosis below.) Other gastrointestinal causes include pancreatic fistulae and the presence of adenoma.

Certain medications can cause excess potassium loss in the urine. Blood pressure medications such as loop diuretics (e. g. furosemide) and thiazide diuretics (e. g. hydrochlorothiazide) commonly cause hypokalemia. Other medications such as the antifungal amphotericin B or the cancer drug cisplatin can also cause long term hypokalemia. Diuretic abuse among athletes and people with eating disorders may present with hypokalemia due to urinary potassium loss. A special case of potassium loss occurs with diabetic ketoacidosis. Hypokalemia is observed with low total body potassium and a low intracellular concentration of potassium. In addition to urinary losses from polyuria and volume contraction, also an obligate loss of potassium from kidney tubules occurs as a cationic partner to the negatively charged ketone, β hydroxybutyrate. A low level of magnesium in the blood can also 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. An increase in the pH of the blood (alkalosis) can cause temporary hypokalemia by causing a shift of potassium out of the plasma and interstitial fluids into the urine via a number of interrelated mechanisms.1) Type B intercalated cells in the collecting duct reabsorb H+ and secrete HCO3, while in type A intercalated cells protons are secreted via both H+ K+ATPases and H+ ATP ases on the apical/luminal surface of the cell. By definition, the H+ K+ATPase reabsorbs one potassium ion into the cell for every proton it secretes into the lumen of the collecting duct of a nephron. In addition, when H+ is expelled from the cell (by H+ATP ase), cations—in this case potassium—are taken up by the cell in order to maintain electroneutrality (but not through direct exchange as with the H+ K+ATPase). In order to correct the pH during alkalosis, these cells will use these mechanisms to reabsorb great amounts of H+, which will concomitantly increase their intracellular concentrations of potassium. This concentration gradient drives potassium to be secreted across the apical surface of the cell into the tubular lumen through potassium channels (this facilitated diffusion occurs in both Type B intercalated cells and Principal cells in the collecting duct).2) Metabolic alkalosis is often present in states of volume depletion, such as vomiting, so potassium is also lost via aldosterone mediated mechanisms.3) During metabolic alkalosis, the 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. 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 nonmalignant) of the adrenal glands, e. g., Conn's syndrome (primary hyperaldosteronism). Cushing's syndrome can also lead to hypokalemia due to excess cortisol binding the Na+/K+ pump and acting like aldosterone. Hypertension and hypokalemia can also be seen with a deficiency of the 11 beta hydroxysteroid dehydrogenase type 2 enzyme which allows cortisols to stimulate aldosterone receptors. This deficiency—known as apparent mineralocorticoid excess syndrome—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. As opposed to disease states of primary excesses of aldosterone, blood pressure is either normal or low in Bartter's or Gitelman's.

In addition to alkalosis, other factors can cause transient shifting of potassium into cells, presumably by stimulation of the Na+/K+ pump. These hormones and medications include insulin, epinephrine, and other beta agonists (e. g. salbutamol or salmeterol), and xanthines (e. g. theophylline). Stimulants (amphetamines, methylphenidate, cocaine) can also cause hypokalemia by stimulating beta 2 receptors. 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 the normal changes in potassium produced by catecholamines and/or insulin and/or thyroid hormone, which lead to movement of potassium from the extracellular fluid into the muscle cells.

A handful of published reports describe individuals with severe hypokalemia related to chronic extreme consumption (4–10 L/day) of cola. The hypokalemia is thought to be from the combination of the diuretic effect of caffeine and copious fluid intake, although it may also be related to diarrhea caused by heavy fructose ingestion.

Pseudohypokalemia is a decrease in the amount of potassium that occurs due to excessive uptake of potassium by metabolically active cells in a blood sample after it has been drawn. It is a laboratory artifact that may occur when blood samples remain in warm conditions for several hours before processing.

About 98% of the body's potassium is found inside cells, with the remainder in the extracellular fluid including the blood. This concentration gradient is maintained principally by the Na+/K+ pump. 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 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 to initiate an action potential. In the heart, hypokalemia causes arrhythmias because of less than complete recovery from sodium channel inactivation, making the triggering of an action potential less 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.

Hypokalemia leads to characteristic ECG changes (PR prolongation, ST segment and T wave depression, U wave formation).

Treatment includes addressing the cause, such as improving the diet, treating diarrhea, or stopping an offending medication. People without a significant source of potassium loss and who show no symptoms of hypokalemia may not require treatment. Acutely, repletion with 10 mEq of potassium is typically expected to raise serum potassium by 0.1 mEq/L immediately after administration. However, for those with chronic hypokalemia, repletion takes time due to tissue redistribution. For example, correction by 1 mEq/L can take more than 1000 mEq of potassium over many days. Potassium chloride supplements by mouth have the advantage of containing precise quantities of potassium, but the disadvantages of a taste which may be unpleasant, and the potential for side effects including nausea and abdominal discomfort. Potassium bicarbonate is preferred when correcting hypokalemia associated with metabolic acidosis. Giving IV potassium at faster rates (20–25 meq/hr) may inadvertently expose the heart to a sudden increase in potassium, potentially causing dangerous abnormal heart rhythms such as heart block or asystole. Faster infusion rates are therefore generally only performed in locations in which the heart rhythm can be continuously monitored such as a critical care unit. When peripheral infusions are necessary, the burning can be reduced by diluting the potassium in larger amounts of fluid, or adding a small dose of lidocaine to the intravenous fluid, Even in severe hypokalemia, oral supplementation is preferred given its safety profile. Sustained release formulations should be avoided in acute settings.

Hypokalemia which is recurrent or resistant to treatment may be amenable to a potassium sparing diuretic, such as amiloride, triamterene, spironolactone, or eplerenone. Concomitant hypomagnesemia will inhibit potassium replacement, as magnesium is a cofactor for potassium uptake.