Hypokalemia

Hypokalemia is a condition that occurs when an individual’s serum potassium falls to 3.5 mEq/L or below. The condition has life-threatening potential due to the electrolytic imbalance of cells. A lack of sufficient potassium for even a short time can also result in heart damage and death. Causes can vary but a major etiology is excess fluid loss secondary to diuretics. Potassium is not retained with large volume fluid loss. The same results can occur with vomiting and diarrhea.

There are more than a few possible hypokalemia culprits, though most are related to the kidneys. The symptoms of low potassium vary from individual to individual, are often quite vague, and may initially go unrecognized. Symptoms generally manifest in the gastrointestinal track, muscles, kidneys, heart and nervous system. Weakness, fatigue and cramping of the muscles are fairly common initial signs. Constipation, nausea, and bloating may be concomitant with palpitations, hypotension, and fainting.

Overview

Slight drops in potassium levels do not necessarily signal an impending crisis. Often an adequate diet or oral administration of potassium is sufficient to resolve the issue. It should be noted that Hypokalemia itself is not an illness, but rather a result of an underlying condition.

Acid-base balance is an important mechanism that is adversely impacted by hypokalemia. Depleted potassium levels can quickly initiate the most common reaction: metabolic alkalosis. Understanding basic chemistry is essential to grasping the role of potassium.

The pH is measured from arterial blood. Normal is 7.35 to 7.45. Any value less than 7.35 is acidosis; greater than 7.45 is alkalosis. It is a measurement of hydrogen ion concentration. Therefore, by increasing the hydrogen ion decreases the pH, and likewise for decreasing the hydrogen ion increases the pH. Bicarbonate-carbonic acid, hemoglobin, proteins and phosphates act as buffering systems to stabilize hydrogen ion concentration changes. Acidosis and alkalosis occur when the buffering systems are inadequate.

Sodium is a player in this scenario, as well. The kidneys try to conserve sodium (and fluid) by swapping it for the excreted potassium or hydrogen ions. The hydrogen ions move from the extracellular to the intracellular fluid, but this cannot happen unless the potassium transfers into the extracellular fluid outside the cell.

Potassium is the most prevalent intercellular cation. Ions are molecules that have gained or lost valence electrons. Cations have net positive charges, while anions have net negative charges. This all leads to the electrical aspect of, in particular, muscle cells. The voltage across a cell membrane during the resting stage is the resting membrane potential. Cells in the heart, nerves, and skeletal muscle depend on the potassium concentration gradient across the membrane of the cell. Hypokalemia can quickly disturb the impulses, resulting in cellular inaction or delayed action.

The potassium deficit is one of clinical medicine’s most common electrolyte imbalance problems encountered. However, it is very rare in healthy adult populations, with a statistical rate of 1 percent. Individuals taking diuretics have a 50 percent rate. Thiazide patients have a higher rate of hypokalemia than those on potassium-sparing diuretics.

Impact

Adequate potassium levels are vital, aside from being an electrolyte that controls cardiac electrical activity as well as acid-base balance. Without them, the body would not be capable of building muscle or protein. It could not metabolize carbohydrates or maintain normal growth. Beyond the muscle dysfunction problems, acid-base disruption, and threat to mortality, there are some more subtle impacts.

Hypokalemia is very much a "which comes first" problem when involving diabetics. The excess glucose acts as a diuretic in the kidney, with the body excreting a high volume of potassium along with fluid. However, low potassium levels impede insulin release as well as desensitize end-organs. In essence, the cells starve because the glucose is not getting to them. An uncontrolled diabetic may well experience polyuria (frequent urination) and not replace lost fluids in sufficient quantities. The person becomes dehydrated, loses potassium, and all the major muscle groups rapidly lose the necessary ionization and deionization that contract them. The myocytes of the heart are exquisitely sensitive. Even slight shifts in the electrolytic balance can alter the heart rate and rhythm.

The pancreas is not the only endocrine organ to suffer from hypokalemia. Relationships between low potassium and various hormonal imbalances have been noted at least since the late 1990s. In a 1998 Journal of Physiology, Tejeda et al. demonstrated hypokalemia induced slightly increased estradiol levels and markedly decreased circulating progesterone in the estrous periods of mice. They described gonadotropin preovulatory surge as well as secondary follicle-stimulating hormone surge at estrus being decreased.

Kidney disease is a common factor in hypokalemia. It can be caused by lifestyle choices, illness, and genetics. Most people are unaware of the latter. While not a household term like end stage renal failure, there are two major genetic disorders: Gitelman syndrome and Bartter syndrome. Admittedly rare, both pose challenges when it comes to determining the etiology of hypokalemia. Gitelman syndrome is attributed to gene mutations. These affected genes prevent the re-absorption of salt, which also hastens the excretion of potassium and other ions. Bartter syndrome is also due to a defective gene that prevents transport in the ascending limb of the glomerus, with the same result of hypokalemia.

Hypokalemia is potentially fatal though the underlying cause may not be immediately evident. The first step in diagnosis is the standard metabolic profile to include a urine analysis. Clinicians can determine further necessary tests. Sometimes the condition is impacted by lifestyle choices such as smoking, drinking to excess, overmedication, use of illicit drugs, or toxic exposure. Patients may require imaging for Cushing syndrome, adenomas, renal artery stenosis, or enzyme assays. Thyroid function evaluation may be considered, also testing for various toxins.

While not all causes may be identified, management of the condition is possible in the majority of cases. Hypokalemia is not limited to any gender, race, or ethnic group. There are few statistics indicating its prevalence. One source indicated 15 percent of hospitalized patients have been admitted for the condition.

Bibliography

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