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Magill’s Medical Guide, 9th Edition

Hypokalemia

by Corie Richter

Category: Disorder

Anatomy or system affected: Cardiovascular system, urinary system

Specialties and related fields: Cardiology, hematology, internal medicine, nephrology

Definition: A condition that occurs when an individual’s serum potassium falls to 3.5 mEq/L or below.

Key terms:

acidosis: When the body fluids contain too much acid.

alkalosis: When the body fluids contain too little acid.

Bartter Syndrome: A rare, inherited kidney disease characterized by hypokalemia and alkalosis.

Cushing Syndrome: An endocrine disease caused by an excess of cortisol.

Gitelman Syndrome: An inherited kidney disorder that causes an imbalance of ions in the body, including potassium, magnesium, and calcium ions.

CAUSES AND SYMPTOMS

Hypokalemia is the deficiency of potassium in the bloodstream. It is not an illness, but rather a result of an underlying condition. 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.

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 normal range for the pH of arterial blood 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, increasing the hydrogen ion decreases the pH, and likewise 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 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 the most common electrolyte imbalance problems encountered in clinical medicine. However, it is very rare in healthy adult populations, with a statistical rate of 1 percent. Individuals taking diuretics have a 50 percent rate. Patients who take thiazide diuretics have a higher rate of hypokalemia than those on potassium-sparing diuretics. Hypokalemia 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.

Adequate potassium levels are vitalfor controlling 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.

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 common initial signs. Constipation, nausea, and bloating may be concomitant with palpitations, hypotension, and fainting.

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. 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. Two rare genetic disorders, Gitelman syndrome and Bartter syndrome, affect the kidney and cause inherited forms of hypokalemia. Gitelman syndrome is an autosomal recessive kidney disorder caused by mutations in the SLC12A3 or CLCNKB genes. Loss-of-function mutations in these genes impair the ability of the distal convoluted tubule to recapture salt, resulting in extensive ion losses, hypokalemia, low blood magnesium levels (hypomagnesemia), and low blood calcium levels (hypocalciuria). Bartter syndrome is due to mutations in one of five different genes: type I - SLC12A1, type II - KCNJ1, type III - CLCNKB, and type IV -BSND or a combination of mutations in the CLCNKA and CLCNKB genes. All these genes encode proteins involved in ion transport in the ascending limb of the Loop of Henle, and loss-of-function mutations in these genes prevent the Loop of Henle from reabsorbing salt and cause excess salt loss in the urine, leading to hypokalemia and alkalosis.

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.

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.

TREATMENT AND THERAPY

While not all causes may be identified, management of the condition is possible in most cases. Treatment of hypokalemia requires a four-pronged approach: 1) reduce potassium losses; 2) replenish potassium stores; 3) monitor for toxicity of hypokalemia; and 4) determine the cause of hypokalemia to prevent future episodes.

To decrease the loss of potassium ions, patients should discontinue all diuretics and laxatives, and begin using drugs that raise serum potassium levels, such as potassium-sparing diuretics, ACE inhibitors or angiotensin II-receptor blockers. If the patient is vomiting, suffering from diarrhea or hyperglycemia, these should be treated to ameliorate hypokalemia.

Replenishing potassium stores is best done with potassium chloride (K-dur) tablets because intravenous potassium solutions are poorly tolerated because they irritate veins. Oral potassium supplementation is much better tolerated.

Hypokalemia-induced toxicities are almost always heart-based, and a cardiologist should be consulted. All irregular heart rhythms should be aggressively treated.

Addressing the underlying conditions that cause hypokalemia includes seeing a renal specialist to address unexplained potassium loss due to kidney disorders, dietary considerations if hypokalemia is due to inadequate dietary intake, psychiatric help for hypokalemia that results from alcoholism or eating disorders, and endocrinology if the patient has an underlying condition that causes hypokalemia (e.g., Cushing syndrome, primary hyperaldosteronism, glucocorticoid-remediable hypertension, congenital adrenal hyperplasia). Surgical consultation if necessary as in the case of renal artery stenosis, adrenal cancers, intestinal obstructions that cause vomiting, or intestinal polyps that cause diarrhea.

For Further Information:

1 

Chen, Michael A. “Potassium in Diet: MedlinePlus Medical Encyclopedia.” NLM. 13 May 2014. Web. 6 January 2016. www.nlm.nih.gov/medlineplus/ency/article/002413.htm.

2 

Davis, Shanlee M, et al. “Profound Hypokalemia Associated with Severe Diabetic Ketoacidosis.” Pediatric Diabetes 17.1 (2016): 61-65. Academic Search Complete. Web. 12 Jan. 2016.

3 

Dimitrijevic, Zorica, Branka Mitic, and Vidojko Ðordevic. “Gitelman Syndrome as a Rare Cause of Hypokalemia—Case Report.” Acta Medica Medianae 53.3 (2014): 54-57. Academic Search Complete. Web. 12 Jan. 2016.

4 

Dugdale, David C. “Low Potassium Level: MedlinePlus Medical Encyclopedia.” NLM. 14 Apr. 2013. Web. 6 January 2016. www.nlm.nih.gov/medlineplus/ency/article/000479.htm.

5 

Halperin, M. L., Marc B. Goldstein, and Kamel S. Kamel. Fluid, Electrolyte, and Acid-base Physiology: A Problem-based Approach. Philadelphia: Saunders/Elsevier, 2010.

6 

Preston, Richard A. Acid-base, Fluids, and ElectrolytesMade Ridiculously Simple. Miami: MedMaster, 2011.

7 

Tejada, F., A. Cremades, M. Aviles, M. T. Castells, and R. Peñafiel. “Result Filters.” National Center for Biotechnology Information. NLM. n.d. Web. 6 January 2016. www.ncbi.nlm.nih.gov/pubmed/9843747.

8 

Traeger, Kelly Ann, and Sun Feng Wen. “Result Filters.” National Center for Biotechnology Information. NLM. n.d. Web. 6 January 2016. www.ncbi.nlm.nih.gov/pubmed/9843747.

Citation Types

Type
Format
MLA 9th
Richter, Corie. "Hypokalemia." Magill’s Medical Guide, 9th Edition, edited by Anubhav Agarwal,, Salem Press, 2022. Salem Online, online.salempress.com/articleDetails.do?articleName=MMG2022_0705.
APA 7th
Richter, C. (2022). Hypokalemia. In A. Agarwal, (Ed.), Magill’s Medical Guide, 9th Edition. Salem Press. online.salempress.com.
CMOS 17th
Richter, Corie. "Hypokalemia." Edited by Anubhav Agarwal,. Magill’s Medical Guide, 9th Edition. Hackensack: Salem Press, 2022. Accessed September 16, 2025. online.salempress.com.