How to Cite This Chapter: Panju M, Srivaratharajah K, Merali Z, Mathew A, Kokot F, Franek E, Drabczyk R. Hypokalemia. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. https://empendium.com/mcmtextbook/chapter/B31.II. Accessed July 17, 2024.
Last Updated: December 15, 2021
Last Reviewed: December 15, 2021
Chapter Information

Definition, Etiology, PathogenesisTop

Hypokalemia is usually defined as a serum [K+] <3.5 mmol/L.


1) Inadequate potassium intake: Anorexia nervosa; protein-energy malnutrition; normal intake of potassium in patients losing potassium through the kidneys, gastrointestinal (GI) tract, or skin.

2) Increased influx of potassium into cells (transmineralization): Alkalosis, beta2-adrenergic receptor stimulation (beta2-agonists, increased sympathetic activity, thyrotoxicosis), phosphodiesterase inhibitors (theophylline, caffeine), insulin, aldosterone, refeeding syndrome, hypokalemic periodic paralysis.

3) Renal potassium loss (urinary potassium excretion >20 mmol/d in a patient with hypokalemia): Primary aldosteronism, secondary aldosteronism (renovascular hypertension, cancer, reninoma), glucocorticoid-remediable hyperaldosteronism, Bartter syndrome, Gitelman syndrome, apparent mineralocorticoid excess, Liddle syndrome, congenital adrenal hyperplasia (11-beta-hydroxylase or 17-alpha-hydroxylase deficiency), Cushing syndrome, hypokalemia-associated types of proximal or distal tubular acidosis, hypomagnesemia, drugs and toxins (loop and thiazide diuretics, acetazolamide, glucocorticoids, mineralocorticoids, amphotericin B, cisplatin, aminoglycosides, sirolimus, Chinese herbs, toluene).

4) Potassium loss via the GI tract: Vomiting, diarrhea, VIPoma (WDHA syndrome: watery diarrhea, hypokalemia, achlorhydria), fistulas, laxatives.

5) Loss of potassium via the skin: Excessive sweating, burns.

Common causes of hypokalemia include loop/thiazide diuretics, laxatives/diarrhea, and primary aldosteronism.

In some patients pseudohypokalemia is found; it is a laboratory artifact caused by storage of uncentrifuged blood samples with white blood cell counts >100×109/L (young granulocytes consume potassium), obtaining blood samples within 20 to 30 minutes of insulin administration, or prolonged storage of uncentrifuged blood samples at 25 to 28 degrees Celsius.

Clinical FeaturesTop

Clinical manifestations of hypokalemia result from its influence on the resting potential of myocytes and neurons (increased resting potential that may completely block action potentials), renal excretion of water (impaired urinary concentration leading to polyuria), and increased generation of ammonia (resulting in metabolic alkalosis). Manifestations depend on the severity of hypokalemia and rate at which it developed. Electrocardiographic (ECG) changes include U waves and prolonged QT intervals. Rapidly developing hypokalemia, even if moderate, may have a dramatic clinical course and manifest as dangerous arrhythmia (eg, torsades de pointes), muscle weakness, constipation up to adynamic ileus, urinary retention, and neurologic abnormalities (paresthesia, agitation, or apathy). Severe hypokalemia may be fatal due to arrhythmia or serious complications of rhabdomyolysis.


The diagnosis of hypokalemia is based on measurement of serum [K+] (<3.5 mmol/L). History may suggest the underlying condition. Because hypokalemia may be accompanied by other electrolyte or acid-base disturbances (most frequently by metabolic alkalosis), serum magnesium, calcium, and phosphate levels should be measured and blood gas analysis may be considered. Determining the cause of hypokalemia may require measurements of plasma renin activity, serum aldosterone and cortisone levels, and urinary potassium excretion. While previously in common use, the transtubular potassium gradient (TTKG) has been demonstrated to be invalid and should not be used for diagnosis of hypokalemia.Evidence 1Strong recommendation (downsides clearly outweigh benefits; right action for all or almost all patients). Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to indirectness (majority of evidence coming from animal studies). Kamel KS, Halperin ML. Intrarenal urea recycling leads to a higher rate of renal excretion of potassium: an hypothesis with clinical implications. Curr Opin Nephrol Hypertens. 2011 Sep;20(5):547-54. doi: 10.1097/MNH.0b013e328349b8f9. Review. PubMed PMID: 21788894.


1. Administer potassium (usually as KCl; in exceptional cases, in patients with metabolic acidosis, as potassium carbonate or citrate).

2. The method for potassium supplementation depends on the severity and symptoms of hypokalemia:

1) In asymptomatic patients with [K+] ≥2.5 mmol/L, administer 20 to 30 mmol of K+ (up to 40 mmol per dose) orally bid to qid.

2) In patients with [K+] <2.5 mmol/L or symptomatic hypokalemia, start from an IV infusion of up to 20 mmol K+/h (usually solutions containing ≥40 mmol K+/L should be administered via central venous access).

3. A decrease of 1 mmol/L in serum [K+] represents a potassium deficit of ~100 to 200 mmol. The existing potassium loss should be added to this deficit. Serum [K+] should be usually remeasured after supplementing 60 to 80 mmol.

4. Correct concomitant water and electrolyte disturbances.

5. In patients who are able to take oral medications, you may use an aldosterone receptor antagonist (spironolactone, eplerenone), or possibly an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker if there are other indications for using these drugs as well.

6. Patients with hypokalemia may fail to respond to treatment because of coexisting hypomagnesemia.

We would love to hear from you

Comments, mistakes, suggestions?

We use cookies to ensure you get the best browsing experience on our website. Refer to our Cookies Information and Privacy Policy for more details.