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Potassium Chloride

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Last Update: May 8, 2023.

Continuing Education Activity

Potassium chloride is a medication used in the management and treatment of hypokalemia. It is in the electrolyte supplement class of medications. This activity outlines the indications, action, and contraindications for potassium chloride as a valuable agent in the management and treatment of hypokalemia. This activity will highlight the mechanism of action, adverse event profile, and other key factors (e.g., off-label uses, dosing, pharmacodynamics, pharmacokinetics, monitoring, relevant interactions) pertinent for members of the healthcare team in the management and treatment of patients with hypokalemia and related conditions.


  • Describe the treatment considerations for patients with hypokalemia.
  • Review the common clinical scenarios in which potassium chloride is used.
  • Identify the typical complications of both oral and intravenous potassium chloride use.
  • Explain the importance of collaboration and communication amongst the interprofessional team to improve outcomes for patients receiving potassium chloride.
Access free multiple choice questions on this topic.


Potassium is the predominant cation of intracellular fluid. As a component of extracellular fluid, potassium has a normal range of approximately 3.5 to 5.0 mEq/L. Potassium levels below this range, or hypokalemia, broadly result from increased excretion, decreased intake, and increased movement into cells. Regardless of the cause, hypokalemia is a significant clinical derangement to address due to the increased risk of life-threatening cardiac arrhythmias. Potassium chloride (KCl) is the preferred agent for correcting most presentations of hypokalemia.[1][2]

Specific instances that may warrant KCl use include:

Diabetic ketoacidosis (DKA): DKA usually presents with hyperkalemia due to the associated hyperosmolality and underlying insulin deficiency. This finding is deceptive; in DKA, total body potassium actually decreases. When administering insulin to move excess glucose from the bloodstream into the intracellular compartment, potassium moves intracellularly as well. As hypokalemia can result from insulin treatment, the clinician can administer KCl to maintain an adequate serum potassium level.[3]

Kidney disease: Renal potassium handling plays a significant role in determining the serum potassium level. Most potassium reabsorption occurs at the proximal convoluted tubule and loop of Henle. Potassium secretion begins at the distal convoluted tubule. The collecting duct may secrete or reabsorb potassium based on input from chemical messengers (e.g., aldosterone), tubular delivery of water and sodium, and serum potassium status. Pathology at any of these segments can influence how much potassium is retained or excreted. Examples of tubular pathologies that result in hypokalemia include genetic channelopathies (e.g., Bartter syndrome) and type I renal tubular acidosis.[4][5]

Hyperaldosteronism: Aldosterone is a mineralocorticoid that signals renal collecting duct cells to both retain sodium and water and secrete potassium and hydrogen ions. Conditions that promote excessive aldosterone activity can lead to excessive potassium secretion, leading to hypokalemia. Hyperaldosteronism can result from conditions that either produce excessive aldosterone (e.g., aldosterone-producing adrenal adenoma) or aberrantly stimulate the renin-angiotensin-aldosterone system (e.g., renal artery stenosis). Excessive mineralocorticoid activity can also occur in aldosterone-independent manners, as well. For example, consumption of glycyrrhizin in licorice can lead to apparent mineralocorticoid excess due to inhibition of 11β-hydroxysteroid dehydrogenase type 2. Inhibition of this enzyme prevents cortisol from being metabolized, allowing it to exert mineralocorticoid effects.[6][7][8]

Medications: Medication-induced hypokalemia occurs primarily via renal potassium loss or intracellular shift. Diuretics (excluding potassium-sparing diuretics), corticosteroids, and certain antimicrobials promote urinary potassium excretion. Examples of medications that promote the intracellular movement of potassium include β2-receptor agonists and xanthines.[9]

Gastrointestinal (GI) disease: GI-related potassium losses primarily occur due to vomiting and diarrhea. In vomiting, there is renal wasting of potassium induced primarily by metabolic alkalosis. Metabolic alkalosis results due to the loss of hydrogen and chloride ions. To replace the lost gastric acid, reactions involving carbonic anhydrase occur within parietal cells to yield hydrogen and hydroxyl ions. The hydrogen ions are secreted into the gastric lumen while the hydroxyl ions react with carbon dioxide to form bicarbonate. Bicarbonate then enters the bloodstream, resulting in hypochloremic metabolic alkalosis. In diarrhea, potassium is excreted with sodium, bicarbonate, and water, resulting in a hyperchloremic (i.e., normal anion gap) metabolic acidosis. In the setting of diarrhea, potassium bicarbonate is preferable to KCl.[10][11][12][2]

Other: During cardiac surgery, KCl serves to induce cardioplegia by interfering with phase 0 of the cardiac action potential. Cardioplegia allows surgeons to operate directly on the heart while maintaining tissue perfusion with extracorporeal life support.[13][14]

Mechanism of Action

Regardless of the administration route, KCl is used to increase the potassium content of the body. Approximately 98% of all potassium in the body exists within cells, particularly skeletal muscle cells. This intracellular predominance is utilized by all cells for tonicity homeostasis and membrane potential dynamics. In cardiomyocytes and neurons, repolarization occurs through the movement of potassium ions out of cells through channel proteins. Both hypokalemia and hyperkalemia can interfere with normal cardiac electrophysiology, potentially leading to life-threatening arrhythmias. Notably, potassium abnormalities rarely manifest as central nervous system pathologies (e.g., seizures).[15][16][17][18][19]


The Food and Drug Administration (FDA) currently approves KCl use in the following formulations: extended-release tablet, extended-release capsule, injectable, oral solution, and powder for oral solution. Each formulation is available only by prescription. For every 20 mEq of intravenous KCl administered, serum potassium increases by approximately 0.25 mEq/L. More information is available in the FDA’s database for current drug labels.[20]

It is preferable to treat mild (3.0 to 3.4 mEq/L) hypokalemia with approximately 75 mEq of oral KCl per day. For moderate (2.5 to 2.9 mEq/L) hypokalemia, the total oral KCl per day is about 100 mEq. Intravenous KCl may be used as an alternative in these cases if the patient cannot tolerate oral KCl. Severe (less than 2.5 mEq/L) or symptomatic hypokalemia necessitates intravenous administration of KCl. If the necessary infusion rate for such cases is greater than 10 mEq/hour, the KCl should be administered through a central line with cardiac monitoring.[21][9]

Adverse Effects

Adverse effects from normal use of KCl are typically related to the administration route. The FDA notes particular adverse effects for each administration route. In general, oral formulations most commonly correlate with GI irritation, including vomiting and diarrhea. Tablet and capsule forms may cause ulcerative/stenotic lesions with prolonged exposure to GI surfaces. Injectable KCl formulations have the potential to cause injection site complications (e.g., phlebitis, erythema, thrombosis, etc.). Also, rapid injection of KCl can precipitate mild hyperkalemia. This review discusses the symptoms of hyperkalemia in the Toxicity section.[2][20]


As KCl is used to increase body potassium content, its use with other drugs that achieve this outcome is contraindicated. Examples of such medications include potassium-sparing diuretics, non-steroidal anti-inflammatory drugs, and angiotensin-converting enzyme inhibitors.[22]

Certain medical conditions involve hyperkalemia as part of their pathophysiologies. As such, KCl use in these cases is contraindicated. Examples of notable conditions that involve hyperkalemia include type IV renal tubular acidosis, chronic kidney disease, and leakage from cell breakdown (e.g., rhabdomyolysis, tumor lysis syndrome, etc.).[23][24]


Given the narrow normal range of serum potassium, careful monitoring is a requirement when utilizing KCl. For hospitalized patients receiving oral KCl, serum potassium checks should occur at least daily to determine treatment effectiveness. Patients treated with intravenous KCl may require more frequent checking, especially if the serum potassium level addressed is below 2.5 mEq/L. The use of continuous cardiac monitoring can aid in correlating symptoms with telling electrocardiogram (ECG) changes (e.g., peaked T waves in hyperkalemia, flattened T waves in hypokalemia, etc.).[21][25]


KCl toxicity is primarily a discussion of hyperkalemia. Like hypokalemia, the potentially fatal complication of hyperkalemia is cardiac arrhythmia. The risk for cardiac arrhythmia is significant at serum potassium levels greater than 6.0 to 6.5 mEq/L. Other manifestations of symptomatic hyperkalemia include ascending muscle weakness and GI disturbance (e.g., nausea, local mucosal necrosis, etc.).[18][26]

Enhancing Healthcare Team Outcomes

When making decisions regarding KCl use, input from the entire interprofessional healthcare team can prove valuable. The ordering/prescribing clinician needs to determine whether oral or IV administration is warranted for the patient's condition. Pharmacists can assist with dosing, particularly at times when intravenous KCl infusion rates merit careful consideration. Nurses can monitor minute-to-minute vital signs and correlate them with symptom development. With these contributions, decisions regarding using KCl are possible, with higher chances for positive outcomes. These types of interprofessional efforts across disciplinary lines will drive better patient outcomes and minimize adverse events when using potassium chloride. [Level 5]

Review Questions


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Cohn JN, Kowey PR, Whelton PK, Prisant LM. New guidelines for potassium replacement in clinical practice: a contemporary review by the National Council on Potassium in Clinical Practice. Arch Intern Med. 2000 Sep 11;160(16):2429-36. [PubMed: 10979053]
Nyenwe EA, Kitabchi AE. The evolution of diabetic ketoacidosis: An update of its etiology, pathogenesis and management. Metabolism. 2016 Apr;65(4):507-21. [PubMed: 26975543]
Palmer BF. Regulation of Potassium Homeostasis. Clin J Am Soc Nephrol. 2015 Jun 05;10(6):1050-60. [PMC free article: PMC4455213] [PubMed: 24721891]
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Lee FT, Elaraj D. Evaluation and Management of Primary Hyperaldosteronism. Surg Clin North Am. 2019 Aug;99(4):731-745. [PubMed: 31255203]
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Ferrari P. The role of 11β-hydroxysteroid dehydrogenase type 2 in human hypertension. Biochim Biophys Acta. 2010 Dec;1802(12):1178-87. [PubMed: 19909806]
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Kraut JA, Kurtz I. Treatment of acute non-anion gap metabolic acidosis. Clin Kidney J. 2015 Feb;8(1):93-9. [PMC free article: PMC4377741] [PubMed: 25852932]
Dobson GP, Faggian G, Onorati F, Vinten-Johansen J. Hyperkalemic cardioplegia for adult and pediatric surgery: end of an era? Front Physiol. 2013;4:228. [PMC free article: PMC3755226] [PubMed: 24009586]
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Roumelioti ME, Glew RH, Khitan ZJ, Rondon-Berrios H, Argyropoulos CP, Malhotra D, Raj DS, Agaba EI, Rohrscheib M, Murata GH, Shapiro JI, Tzamaloukas AH. Fluid balance concepts in medicine: Principles and practice. World J Nephrol. 2018 Jan 06;7(1):1-28. [PMC free article: PMC5760509] [PubMed: 29359117]
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Disclosure: Robert McMahon declares no relevant financial relationships with ineligible companies.

Disclosure: Khalid Bashir declares no relevant financial relationships with ineligible companies.

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