Last updated: September 11, 2023

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Summarytoggle arrow icon

Hypokalemia (low serum potassium) is a common electrolyte disorder that is typically caused by potassium loss (e.g., due to diarrhea, vomiting, or diuretic medication). Mild hypokalemia may be asymptomatic or cause mild nonspecific symptoms such as nausea, muscle weakness, and fatigue. Severe deficiency can cause cardiac arrhythmias and death. Treatment consists of oral or IV supplementation in conjunction with treatment of the underlying cause. In concurrent hypomagnesemia, which may lead to refractory hypokalemia, the simultaneous repletion of magnesium and potassium is necessary.

See also “Hyperkalemia.”

Definitiontoggle arrow icon

  • Serum potassium (K+) level < 3.5 mEq/L [2]
  • Severe hypokalemia: K+ level < 2.5 mEq/L

Etiologytoggle arrow icon

Hypokalemia is most often caused by renal or gastrointestinal potassium loss. Other electrolyte imbalances (e.g., hypomagnesemia), alkalosis, and several medications can also have an impact on potassium homeostasis.

Etiology of hypokalemia [2][3]
Gastrointestinal loss
Renal loss
Intracellular shift
Insufficient intake

Pathophysiologytoggle arrow icon

K+ acts like H+: Hypokalemia leads to alkalosis and vice versa!

Particularly acute extracellular changes in concentration influence excitability! Chronic changes lead to intracellular compensation!

Hypomagnesemia can lead to refractory hypokalemia!

Clinical featurestoggle arrow icon

Patients may be asymptomatic, particularly if the deficiency is mild. Symptoms usually occur if serum K+ levels are < 3.0 mEq/L and/or decrease rapidly. [3]

Hypokalemia (and hyperkalemia) can cause cardiac arrhythmia and may lead to ventricular fibrillation!

Diagnosticstoggle arrow icon

All patients require an ECG and laboratory studies to confirm the diagnosis and rule out concurrent electrolyte abnormalities. Further diagnostic tests depend on the suspected underlying etiology.

Initial evaluation

Laboratory studies [2]

Consider confirming abnormal serum potassium levels with a repeat blood draw.

ECG findings in hypokalemia [3][14]

To remember that low potassium may result in a flattened T wave, think of: "No pot, no tea (T)!"

Identification of underlying etiology

  • Review the patient's history and medication list to help identify potential causes of hypokalemia.
  • If the etiology is still unclear, further testing can help determine the underlying etiology.
  • Imaging is not routinely required but may be necessary if certain underlying etiologies are suspected. [2]
Evaluation of underlying etiology in hypokalemia [2][15]
Type of potassium loss Clinical features Recommended tests Findings and interpretation
Extrarenal losses
  • TSH
  • T3 and T4
  • TSH
  • ↑ T3 and T4
Renal loss

Treatmenttoggle arrow icon


Most patients require potassium chloride (KCl) repletion, management of concurrent electrolyte abnormalities (see “Electrolyte repletion”), and treatment of the underlying cause. See “Potassium replacement” for further details on repletion regimens for hypokalemia, treatment goals, warnings, and adverse effects.

  • Severe hypokalemia (< 2.5 mEq/L) and/or high risk of recurrent severe hypokalemia
  • Moderate hypokalemia (2.5–2.9 mEq/L)
    • KCl: Oral repletion is preferred unless the patient is unable to tolerate PO, has severe symptoms, or has ECG changes in hypokalemia. [17]
    • Disposition is usually determined by treatment of the underlying disorder.
  • Mild hypokalemia (3.0–3.5 mEq/L) with easily reversible cause
    • Prioritize treatment of the underlying condition (e.g., GI fluid losses).
    • Consider oral supplementation, e.g., KCl
    • Consider increasing dietary potassium intake. [19]
    • Patients can usually be discharged after stabilization.

High concentrations of IV potassium can cause local venous irritation and potentially lead to cardiac arrhythmias. Limit the rate of infusion according to the type of IV access and place patients on a continuous cardiac monitor.

Correction of hypokalemia is a common cause of hyperkalemia in hospitalized patients; monitor K+ levels frequently in patients receiving potassium repletion. [17][18]

In patients with hypokalemia, avoid solutions containing dextrose, which can increase insulin secretion and worsen hypokalemia. [16]

Treatment of underlying condition

See “Etiology of hypokalemia.”

Potassium supplementation will be ineffective if concurrent hypomagnesemia is left untreated (see “Magnesium repletion”).

Patients with a continued source of potassium loss (e.g., those on diuretics) may require long-term potassium supplementation. [16]

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Referencestoggle arrow icon

  1. Kardalas E, Paschou SA, Anagnostis P, Muscogiuri G, Siasos G, Vryonidou A. Hypokalemia: a clinical update. Endocrine Connections. 2018; 7 (4): p.R135-R146.doi: 10.1530/ec-18-0109 . | Open in Read by QxMD
  2. Domino FJ. The 5-Minute Clinical Consult 2011. Lippincott Williams & Wilkins ; 2010
  3. Marini JJ, Wheeler AP. Critical Care Medicine. Lippincott Williams & Wilkins ; 2010
  4. Ronco C, Bellomo R, Kellum JA. Critical Care Nephrology. Elsevier Health Sciences ; 2009
  5. Greenberg A. Primer on Kidney Diseases E-Book. Elsevier Health Sciences ; 2009
  6. Levis JT. ECG diagnosis: hypokalemia.. Perm J. 2012; 16 (2): p.57.doi: 10.7812/tpp/12-015 . | Open in Read by QxMD
  7. Gleadle J, Li J, Yong T. Clinical Investigations at a Glance. John Wiley & Sons ; 2017
  8. Viera AJ, Wouk N. Potassium disorders: Hypokalemia and hyperkalemia. Am Fam Physician. 2015; 92 (6): p.487-495.
  9. Asmar A, Mohandas R, Wingo CS. A Physiologic-Based Approach to the Treatment of a Patient With Hypokalemia. Am J Kidney Dis. 2012; 60 (3): p.492-497.doi: 10.1053/j.ajkd.2012.01.031 . | Open in Read by QxMD
  10. Gennari FJ. Hypokalemia. N Engl J Med. 1998; 339 (7): p.451-458.doi: 10.1056/nejm199808133390707 . | Open in Read by QxMD
  11. Magee CC, Tucker JK, Singh AK. Core Concepts in Dialysis and Continuous Therapies. Springer ; 2016
  12. Mehta M, Mathews A. The Hospitalist Manual. PMPH-USA ; 2010
  13. Liamis G. Diabetes mellitus and electrolyte disorders. World J Clin Cases. 2014; 2 (10): p.488.doi: 10.12998/wjcc.v2.i10.488 . | Open in Read by QxMD
  14. Lote CJ. Principles of Renal Physiology. Springer Science & Business Media ; 2000
  15. Bryson PD. Comprehensive Reviews in Toxicology. CRC Press ; 1996
  16. Porth C. Essentials of Pathophysiology. Lippincott Williams & Wilkins ; 2011
  17. Aronson PS, Giebisch G. Effects of pH on Potassium: New Explanations for Old Observations. Journal of the American Society of Nephrology. 2011; 22 (11): p.1981-1989.doi: 10.1681/asn.2011040414 . | Open in Read by QxMD
  18. Unwin RJ, Luft FC, Shirley DG. Pathophysiology and management of hypokalemia: a clinical perspective. Nature Reviews Nephrology. 2011; 7 (2): p.75-84.doi: 10.1038/nrneph.2010.175 . | Open in Read by QxMD
  19. $Contributor Disclosures - Hypokalemia. All of the relevant financial relationships listed for the following individuals have been mitigated: Jan Schlebes (medical editor, is a shareholder in Fresenius SE & Co KGaA). None of the other individuals in control of the content for this article reported relevant financial relationships with ineligible companies. For details, please review our full conflict of interest (COI) policy.
  20. Agabegi SS, Agabegi ED. Step-Up To Medicine. Lippincott Williams & Wilkins ; 2013
  21. Lederer E. Hypokalemia. In: Batuman V, Hypokalemia. New York, NY: WebMD. Updated: December 29, 2016. Accessed: February 9, 2017.
  22. Mount DB. Clinical manifestations and treatment of hypokalemia in adults. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. Last updated: January 7, 2016. Accessed: February 9, 2017.

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