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Continuing Education Activity

Hyperkalemia is defined as a serum or plasma potassium level above the upper limits of normal, usually greater than 5.0 mEq/L to 5.5 mEq/L. While mild hyperkalemia is usually asymptomatic, high potassium levels may cause life-threatening cardiac arrhythmias, muscle weakness, or paralysis. Symptoms usually develop at higher levels, 6.5 mEq/L to 7 mEq/L, but the rate of change is more important than the numerical value. Patients with chronic hyperkalemia may be asymptomatic at increased levels, while patients with dramatic, acute potassium shifts may develop severe symptoms at lower ones. Infants have higher baseline levels than children and adults. This activity reviews the causes, pathophysiology, and presentation of hyperkalemia and highlights the role of the interprofessional team in its management.


  • Review the causes of hyperkalemia.
  • Describe the effects of hyperkalemia on the ECG.
  • Summarize the treatment options and order of treatment for hyperkalemia.
  • Outline the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by hyperkalemia.


Hyperkalemia is defined as a serum or plasma potassium level above the upper limits of normal, usually greater than 5.0 mEq/L to 5.5 mEq/L. While mild hyperkalemia is usually asymptomatic, high potassium levels may cause life-threatening cardiac arrhythmias, muscle weakness, or paralysis. Symptoms usually develop at higher levels, 6.5 mEq/L to 7 mEq/L, but the rate of change is more important than the numerical value. Patients with chronic hyperkalemia may be asymptomatic at increased levels, while patients with dramatic, acute potassium shifts may develop severe symptoms at lower ones. Infants have higher baseline levels than children and adults.

Pseudohyperkalemia is quite common and represents a false elevation in measured potassium due to specimen collection, handling, or other causes. Hyperkalemia should always be confirmed before aggressive treatment in cases where the serum potassium is elevated without explanation. True hyperkalemia may be caused by increased potassium intake, transcellular movement of intracellular potassium into the extracellular space, and decreased renal excretion. The urgency of therapy depends on symptoms, serum levels, and causes of hyperkalemia.[1][2]


The most common cause of hyperkalemia is pseudohyperkalemia, which is not reflective of the true serum potassium levels. Pseudohyperkalemia is most commonly due to hemolysis of the sample, causing intracellular potassium to be measured in the serum. Hemolysis is more common when a syringe is used than a vacuum device. Using tourniquets and excessive fist-pumping during the blood draw also increase the risk. Specimens drawn from patients with leukocytosis or thrombocytosis are also frequently associated with falsely elevated potassium concentrations.

Increased Potassium Intake

Increased potassium intake from food is a very uncommon cause of hyperkalemia in adult patients with normal renal function but can be an important cause in those with kidney disease. Foods with high potassium content include dried fruits, seaweed, nuts, molasses, avocados, and Lima beans. Many vegetables that are also high in potassium include spinach, potatoes, tomatoes, broccoli, beets, carrots, and squash. High-potassium-containing fruits include kiwis, mangoes, oranges, bananas, and cantaloupe. Red meats are also rich in potassium. While generally safe to consume even in large quantities by patients with normal potassium homeostasis, these foods should be avoided in patients with severe renal disease or other underlying conditions or medications predisposing them to hyperkalemia. Intravenous intake through high potassium-containing fluids, particularly total parenteral nutrition, medications with high potassium content, and massive blood transfusions can significantly elevate serum potassium levels.

Intracellular Potassium Shifts

Cellular injury can release large quantities of intracellular potassium into the extracellular space. This can be due to rhabdomyolysis from a crush injury, excessive exercise, or other hemolytic processes. Metabolic acidosis may cause intracellular potassium to shift into the extracellular space without red cell injury. Metabolic acidosis is most frequently caused by decreased, effective circulating arterial blood volume. Sepsis or dehydration may lead to hypotension and decreased tissue perfusion leading to metabolic acidosis with subsequent potassium elevation.

Insulin deficiency and diabetic ketoacidosis may cause dramatic extracellular shifts causing measured serum potassium to be elevated in the setting of whole-body potassium depletion. Certain medications, such as succinylcholine, may cause severe, acute potassium elevations in patients with up-regulation of receptors, particularly in subacute neuromuscular disease. Tumor lysis syndrome, particularly in patients receiving chemotherapy for hematogenous malignancy, may cause acute hyperkalemia due to massive cancer cell death.[3] Hyperkalemic periodic paralysis is a rare, autosomal dominant condition that causes potassium to shift into the extracellular space due to impaired sodium channel function in skeletal muscle.

Impaired Potassium Excretion

Acute or chronic kidney disease is a common cause of hyperkalemia. Hyperkalemia is usually not seen until the glomerular filtration rate falls below 30 ml/min. This is commonly due to primary renal dysfunction but may be due to acute volume depletion from dehydration or bleeding or decreased circulating blood volume due to congestive heart failure or cirrhosis. Tubular dysfunction due to aldosterone deficiency or insensitivity can also cause hyperkalemia.


Hyperkalemia is unusual in the general population, reported in less than 5% of the population worldwide, but may affect up to 10% of all hospitalized patients. Most cases in hospitalized patients are due to medications and renal insufficiency. Diabetes, malignancy, extremes of age, and acidosis are other important causes in inpatients. Hyperkalemia is rare in children but may occur in up to 50% of premature infants. Hyperkalemia is more commonly reported in men than women, perhaps due to increased muscle mass and higher rates of rhabdomyolysis, and increased prevalence of the neuromuscular disease. Other factors include non-Black patients and older age.[4]

Today there is a risk that empirical use of ACE inhibitors may cause hyperkalemia, which can be of concern in high-risk populations like people with diabetes, heart failure, and peripheral vascular disease.[5]


Potassium is usually an intracellular cation. Total body potassium stores are 50 to 75 mEq/kg body weight (approximately 3000 mEq).[6] The sodium-potassium pump is responsible for maintaining potassium within the cells, which pumps sodium out of and potassium into the cell in a 3:2 ratio. This results in approximately 140 mEq/L intracellular potassium concentration compared with 4 to 5 mEq/L in the extracellular fluid. Most potassium is excreted in urine through the kidneys, with about 10% in sweat and stool. Inside the kidney, potassium excretion occurs in the distal convoluted and cortical collecting ducts.

Elevated levels of the following influence renal potassium excretion:

  • Aldosterone
  • Diuretics (which deliver sodium to the distal tubule)
  • WNK1 and WNK4
  • High levels of serum potassium
  • A high flow of urine (osmotic diuresis)
  • Presence of negative ions in the distal tubule (bicarbonate)
Mechanism Causes
Increased potassium release from cells
  • Pseudohyperkalemia
  • Metabolic acidosis
  • Increased tissue catabolism
  • Beta blockers[7]
  • Insulin deficiency, hyperglycemia, and hyperosmolality
  • Exercise
  • Hyperkalemic periodic paralysis
  • Activators of ATP-dependent potassium channels (e.g., diazoxide, minoxidil, calcineurin inhibitors, and some volatile anesthetics)
  • Red cell transfusion
  • Succinylcholine
  • Red cell transfusion
  • Arginine hydrochloride
Reduced urinary potassium excretion
  • Reduced aldosterone secretion
  • Reduced distal sodium and water delivery
  • Selective impairment in potassium secretion
  • Ureterojejunostomy
  • Acute and chronic kidney disease
  • Gordon syndrome

Table 1. Causes and mechanism of hyperkalemia

History and Physical

Most patients are relatively asymptomatic with mild and even moderate hyperkalemia. Elevated potassium is often discovered on screening labs done in patients with nonspecific complaints or those with suspected electrolyte abnormalities due to infection, dehydration, or hypoperfusion. Causes include renal disease, diabetes, chemotherapy, major trauma, crush injury, or muscle pain suggestive of rhabdomyolysis. Medications that may predispose to the development of hyperkalemia include digoxin, potassium-sparing diuretics, non-steroidal anti-inflammatory drugs, ace-inhibitors or recent intravenous (IV) potassium, total parenteral nutrition, potassium penicillin, or succinylcholine. Patients may complain of weakness, fatigue, palpitations, or syncope.

Physical exam findings may include hypertension and edema in the setting of renal disease. There may also be signs of hypoperfusion. Muscle tenderness may be present in patients with rhabdomyolysis. Jaundice may be seen in patients with hemolytic conditions. Patients may have muscle weakness, flaccid paralysis, or depressed deep tendon reflexes.


The first test that should be ordered in a patient with suspected hyperkalemia is an ECG since the most lethal complication of hyperkalemia is cardiac condition abnormalities which can lead to dysrhythmias and death.

Elevated potassium causes ECG changes in a dose-dependent manner: 

  • K = 5.5 to 6.5 mEq/L ECG will show tall, peaked t-waves
  • K = 6.5 to 7.5 mEq/L ECG will show loss of p-waves
  • K = 7 to 8 ECG mEq/L will show widening of the QRS complex
  • K = 8 to 10 mEq/L will produce cardiac arrhythmias, sine wave pattern, and asystole

It should be noted that the rate of rising serum potassium is a greater factor than the level. Patients with chronic hyperkalemia may have relatively normal EGCs even at high levels, and significant ECG changes may be present at much lower levels in patients with sudden spikes in serum potassium.ECG features of hyperkalemia include:

  • Small or absent P wave
  • Prolonged PR interval
  • Augmented R wave
  • Wide QRS
  • Peaked T waves

Additional laboratory testing should include serum blood urea nitrogen and creatinine to assess renal function and urinalysis to screen for renal disease. Urine potassium, sodium, and osmolality may also help evaluate the cause. In patients with renal disease, the serum calcium level should also be checked because hypocalcemia may exacerbate the cardiac effects of hyperkalemia. A complete blood count to screen for leukocytosis or thrombocytosis may also be helpful. Serum glucose and blood gas analysis should be ordered in diabetics and patients with suspected acidosis. Lactate dehydrogenase should be ordered in patients with suspected hemolysis. Creatinine phosphokinases and urine myoglobin should be ordered in patients with suspected rhabdomyolysis. Uric acid and phosphorus should be ordered in patients with suspected tumor lysis syndrome. Digoxin toxicity may cause hyperkalemia, so serum levels should be checked in patients on digoxin. If no other cause is found, consider cortisol and aldosterone levels to assess for mineralocorticoid deficiency.

Since pseudohyperkalemia is so common, confirmation should be obtained in asymptomatic patients without typical ECG changes before initiating aggressive therapy.

Treatment / Management

The urgency with which hyperkalemia should be managed depends on how rapidly the condition develops, the absolute serum potassium level, the degree of symptoms, and the cause.[8][9][10]

Patients with neuromuscular weakness, paralysis, or ECG changes and elevated potassium of more than 5.5 mEq/L in patients at risk for ongoing hyperkalemia or confirmed hyperkalemia of 6.5 mEq/L should have aggressive treatment.

Treatment is usually prescribed in the following manner:

  1. Exogenous sources of potassium should be immediately discontinued.
  2. Treatment of the reversible cause should begin along with the management of hyperkalemia.
  3. Calcium therapy will stabilize the cardiac response to hyperkalemia and should be initiated first in the setting of cardiac toxicity. Calcium does not alter the serum concentration of potassium but is a first-line therapy in hyperkalemia-related arrhythmias and ECG changes. Calcium chloride contains three times more elemental calcium than calcium gluconate but is more irritating to peripheral vessels and more likely to cause tissue necrosis with extravasation, so it is usually only given through central venous lines or peripherally in cardiac arrest. Thus, calcium gluconate is the usual initial drug of choice in patients with evidence of cardiac toxicity.[11] As a precaution, calcium should never be given in bicarbonate-containing fluids, as it can cause the precipitation of calcium carbonate.
  4. Insulin and glucose, or insulin alone in hyperglycemic patients, will drive the potassium back into the cells, effectively lowering serum potassium.[12] A common regimen is ten units of regular insulin given with 50 ml of a 50% dextrose solution (D50). Patients should be monitored closely for the development of hypoglycemia. A 10% dextrose infusion at 50 to 75 ml/hour is associated with less hypoglycemia than bolus dosing with D50.
  5. Beta-2 adrenergic agents such as albuterol will also shift potassium intracellularly.[13] To be effective, beta-2 agonists are given in much higher doses than those commonly used for bronchodilation. Sodium bicarbonate infusion may be helpful in patients with metabolic acidosis. Bolus dosing of sodium bicarbonate is less effective. Intravenous epinephrine, however, should not be used to manage hyperkalemia due to an increased risk of causing angina.
  6. Loop or thiazide diuretics may help enhance potassium excretion. They may be used in non-oliguric, volume-overloaded patients but should not be used as monotherapy in symptomatic patients. In hypervolemic patients with preserved kidney function (e.g., patients with congestive cardiac failure), 40 mg of intravenous furosemide is administered every 12 hours or may be given as a continuous infusion. In euvolemic or hypovolemic patients with preserved kidney function, an isotonic saline infusion is given before as needed to the patient before administering 40 mg of intravenous furosemide every 12 hours or a continuous furosemide infusion.
  7. Gastrointestinal cation exchangers such as patiromer may be helpful, particularly in patients with renal insufficiency who cannot receive immediate dialysis. Sodium polystyrene sulfonate, though commonly used, is falling out of favor due to lack of effectiveness and adverse effects, particularly bowel necrosis in elderly patients. If used due to a lack of alternatives, it should not be given with sorbitol, which increases toxicity.[14]
  8. Hemodialysis should be performed in patients with end-stage renal disease or severe renal impairment.

Complications of treatment:

  • Hypokalemia
  • Inability to control hyperkalemia
  • Hypocalcemia as a result of bicarbonate infusion
  • Hypoglycemia due to insulin
  • Metabolic alkalosis from bicarbonate therapy
  • Volume depletion from diuresis

Differential Diagnosis

  • Acute tubular necrosis
  • Congenital adrenal hyperplasia
  • Digitalis toxicity
  • Electrical burn injuries
  • Head trauma
  • Hypocalcemia
  • Metabolic acidosis
  • Rhabdomyolysis
  • Thermal burns
  • Tumor lysis syndrome[3]


The prognosis is excellent for patients with mild transient hyperkalemia if the inciting cause is addressed and treated. Sudden onset, extreme hyperkalemia can cause cardiac arrhythmias that can be lethal in up to two-thirds of cases if not rapidly treated. Hyperkalemia is an independent risk factor for death in hospitalized patients.


  • Cardiac arrest
  • Weakness
  • Arrhythmias
  • Paralysis

Deterrence and Patient Education

Dietary restriction is not usually required, except in extreme cases. Patients with co-morbid conditions or those who take medications causing hyperkalemia should be counseled about urea and electrolytes monitoring as advised by the physician.

Enhancing Healthcare Team Outcomes

The management of hyperkalemia is done by an interprofessional team because of its potential to induce cardiac arrest and severe weakness. Once hyperkalemia is diagnosed, the primary condition must be treated. Patients with hyperkalemia need cardiac monitoring, and nurses should be familiar with ECG features of hyperkalemia, which are often the first to appear. The pharmacist has to ensure that all nephrotoxic medications and agents that raise potassium are discontinued and discuss their findings with the clinical team. Nursing will perform monitoring and follow-up, watching for signs of worsening hyperkalemia and alerting the clinical staff immediately for corrective action. All interprofessional team members must engage in open communication with the rest of the team, particularly when patient status changes necessitate intervention. Meticulous records are also crucial to proper patient care so that everyone involved operates from the same up-to-date patient data.

If hyperkalemia is severe, the nephrologist should be consulted. If ECG changes are present, a cardiology consult should be made. Treatment to lower the high potassium should be ongoing. These patients need cardiac monitoring 24/7 until hyperkalemia has resolved. The dietitian should educate the patient on a low potassium diet. For those with renal dysfunction, continued follow-up with a nephrologist is recommended. Only through open communication between members of the interprofessional team can the morbidity of hyperkalemia be avoided.


The majority of patients have an excellent prognosis. However, patients with chronic disorders like end-stage renal failure may require continual blood work to monitor potassium.[15][16] [Level 5]



9/4/2023 8:07:43 PM

Nursing Version:

Hyperkalemia (Nursing)



Lytvyn Y, Godoy LC, Scholtes RA, van Raalte DH, Cherney DZ. Mineralocorticoid Antagonism and Diabetic Kidney Disease. Current diabetes reports. 2019 Jan 23:19(1):4. doi: 10.1007/s11892-019-1123-8. Epub 2019 Jan 23     [PubMed PMID: 30673886]


Flury G. [The 'Dangerous' ECG]. Praxis. 2019 Jan:108(1):45-52. doi: 10.1024/1661-8157/a003155. Epub     [PubMed PMID: 30621532]


Williams SM, Killeen AA. Tumor Lysis Syndrome. Archives of pathology & laboratory medicine. 2019 Mar:143(3):386-393. doi: 10.5858/arpa.2017-0278-RS. Epub 2018 Nov 30     [PubMed PMID: 30499695]


Dunn JD, Benton WW, Orozco-Torrentera E, Adamson RT. The burden of hyperkalemia in patients with cardiovascular and renal disease. The American journal of managed care. 2015 Nov:21(15 Suppl):s307-15     [PubMed PMID: 26788745]


Ohkuma T, Harris K, Cooper M, Grobbee DE, Hamet P, Harrap S, Mancia G, Marre M, Patel A, Rodgers A, Williams B, Woodward M, Chalmers J, ADVANCE Collaborative Group. Short-Term Changes in Serum Potassium and the Risk of Subsequent Vascular Events and Mortality: Results from a Randomized Controlled Trial of ACE Inhibitors. Clinical journal of the American Society of Nephrology : CJASN. 2022 Aug:17(8):1139-1149. doi: 10.2215/CJN.00180122. Epub 2022 Jul 27     [PubMed PMID: 35896277]

Level 1 (high-level) evidence


Boddy K, King PC, Hume R, Weyers E. The relation of total body potassium to height, weight, and age in normal adults. Journal of clinical pathology. 1972 Jun:25(6):512-7     [PubMed PMID: 4625433]


Rosa RM, Silva P, Young JB, Landsberg L, Brown RS, Rowe JW, Epstein FH. Adrenergic modulation of extrarenal potassium disposal. The New England journal of medicine. 1980 Feb 21:302(8):431-4     [PubMed PMID: 6101508]


Campbell CA, Lam Q, Horvath AR. An evidence- and risk-based approach to a harmonized laboratory alert list in Australia and New Zealand. Clinical chemistry and laboratory medicine. 2018 Dec 19:57(1):89-94. doi: 10.1515/cclm-2017-1114. Epub     [PubMed PMID: 29672264]


Butler J, Vijayakumar S, Pitt B. Revisiting hyperkalaemia guidelines: rebuttal. European journal of heart failure. 2018 Sep:20(9):1255. doi: 10.1002/ejhf.1249. Epub     [PubMed PMID: 30182493]


Butler J, Vijayakumar S, Pitt B. Need to revisit heart failure treatment guidelines for hyperkalaemia management during the use of mineralocorticoid receptor antagonists. European journal of heart failure. 2018 Sep:20(9):1247-1251. doi: 10.1002/ejhf.1217. Epub 2018 Jun 8     [PubMed PMID: 29882618]


Long B, Warix JR, Koyfman A. Controversies in Management of Hyperkalemia. The Journal of emergency medicine. 2018 Aug:55(2):192-205. doi: 10.1016/j.jemermed.2018.04.004. Epub 2018 May 3     [PubMed PMID: 29731287]


Sterns RH, Grieff M, Bernstein PL. Treatment of hyperkalemia: something old, something new. Kidney international. 2016 Mar:89(3):546-54. doi: 10.1016/j.kint.2015.11.018. Epub 2016 Feb 2     [PubMed PMID: 26880451]


Gosmanov AR, Wong JA, Thomason DB. Duality of G protein-coupled mechanisms for beta-adrenergic activation of NKCC activity in skeletal muscle. American journal of physiology. Cell physiology. 2002 Oct:283(4):C1025-32     [PubMed PMID: 12225966]


Mistry M, Shea A, Giguère P, Nguyen ML. Evaluation of Sodium Polystyrene Sulfonate Dosing Strategies in the Inpatient Management of Hyperkalemia. The Annals of pharmacotherapy. 2016 Jun:50(6):455-62. doi: 10.1177/1060028016641427. Epub 2016 Apr 5     [PubMed PMID: 27048188]


Formiga F, Chivite D, Corbella X, Conde-Martel A, Arévalo-Lorido JC, Trullàs JC, Silvestre JP, García SC, Manzano L, Montero-Pérez-Barquero M, RICA investigators group. Influence of potassium levels on one-year outcomes in elderly patients with acute heart failure. European journal of internal medicine. 2019 Feb:60():24-30. doi: 10.1016/j.ejim.2018.10.016. Epub 2018 Oct 26     [PubMed PMID: 30722845]


Linde C, Qin L, Bakhai A, Furuland H, Evans M, Ayoubkhani D, Palaka E, Bennett H, McEwan P. Serum potassium and clinical outcomes in heart failure patients: results of risk calculations in 21 334 patients in the UK. ESC heart failure. 2019 Apr:6(2):280-290. doi: 10.1002/ehf2.12402. Epub 2019 Jan 10     [PubMed PMID: 30629342]

Level 2 (mid-level) evidence