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Key Points

  • Hyperkalemia is defined as the elevation of serum potassium levels above normal (usually greater than 5.5mEq/L); however, this definition may vary depending on institutional lab values.
  • Increases in potassium can be caused by increased intake, intracellular shifts of potassium, or impaired excretion.
  • Treatment of hyperkalemia centers around the stabilization of the cellular membrane to prevent excessive excitation, driving potassium intracellularly, and increasing potassium excretion.


  • Potassium is primarily an intracellular cation, with the cells containing approximately 98% of the total body potassium stores. The intracellular potassium concentration is approximately 140 mEq/L compared to the extracellular concentration of about 4-5 mEq/L.1
  • This contrasts with sodium which is primarily an extracellular cation. The difference in concentration between these cations is maintained by the Na-K-ATPase pump in the cell membrane.
  • Hyperkalemia is defined as the elevation of serum potassium levels above normal (usually greater than 5.5mEq/L); however, this definition may vary depending on institutional lab values.2


Pseudohyperkalemia is commonly encountered and results from potassium movement out of the cell during or after blood draws. Common causes of a hemolyzed blood sample include mechanical trauma during venipuncture or excessive fist-pumping during the blood draw.1

The etiology of true hyperkalemia can be divided into three categories:2,3

Increased Intake of Potassium

Increase potassium intake is an uncommon cause of hyperkalemia; however, this can be significant in patients with renal disease.

  • Foods such as dried fruits, nuts, avocados, seaweed, and lima beans are amongst the highest levels of total dietary potassium.1
  • Administration of drugs such as nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme (ACE) inhibitors, and cyclosporine can cause elevations in potassium levels.3 Succinylcholine can also cause an elevation in serum potassium of 0.5mEq/L, which is more problematic in patients with upregulation of extra junctional receptors, such as burn injuries, prolonged immobilization, and neuromuscular disease.2
  • Massive blood transfusions

Intracellular Shifts of Potassium

  • Extensive tissue damage (crushing injuries with rhabdomyolysis, hemolysis, internal bleeding)
  • Metabolic or respiratory acidosis
  • Sepsis or dehydration
  • Insulin resistance and diabetic ketoacidosis; the elevated potassium levels in ketoacidosis is due to a lack of insulin.3
  • Malignant hyperthermia
  • Tumor lysis syndrome in patients receiving chemotherapy
  • Acute release of potassium from transplanted organs

Impaired Excretion of Potassium

  • Usually seen in renal disease, elevations of potassium are not usually seen until the glomerular filtration rate (GFR) falls below 30 mL/min in acute renal failure.2
  • In chronic renal failure, patients can usually maintain normal potassium levels because potassium excretion is dependent on tubular secretion above a GFR of 8 mL/min.3

The causes of hyperkalemia in chronic renal failure patients include:

  • Decreased excretion: lowered GFR, potassium-sparing diuretics, ACE inhibitors, heparin (decreased aldosterone efficacy)
  • Intracellular release: metabolic acidosis, beta-blockers, insulin deficiency
  • Increased intake: blood transfusions, increased dietary intake

Typical Situations4

Common clinical scenarios where hyperkalemia is encountered include

  • Aortic cross-clamp release
  • Major trauma due to massive cell rupture and extravasation of intracellular potassium
  • Cardiac and transplant surgery
  • Paraplegic or burn injury patients after the administration of succinylcholine; increased extrajunctional receptors beyond normal levels can subsequently cause a significant release of potassium stores from the intracellular space.
  • Chronic renal insufficiency patients can tolerate chronic elevations in potassium much better than acute changes because the equilibration of serum and intracellular stores of potassium takes place over time, returning the resting membrane potential of excitable cells to nearly normal.5 Chronic renal insufficiency patients are no more susceptible to the hyperkalemic effects of succinylcholine than those with normal functioning kidneys.5


In the perioperative setting, it is crucial to optimize the patient’s potassium levels prior to surgery, as the cardiac effects of hyperkalemia can be difficult to manage.

  • A thorough history with careful consideration of renal and neuromuscular disease should be considered.
  • In patients with renal disease, hemodialysis can be considered prior to the operative setting.
  • Succinylcholine in patients with recent burn injuries or other neuromuscular disease processes that may have an abnormal increase in extra junctional receptors should be avoided.
  • Hyperkalemia can occur with high, low, or normal total body potassium stores. Hyperkalemic effects are primarily due to extracellular/intravascular increases in potassium, which may vary significantly from intracellular, and therefore, total body potassium stores.


Most patients are relatively asymptomatic with mild or moderate hyperkalemia. Hyperkalemia is usually diagnosed with ECG changes or by measuring potassium levels.1-3

ECG Changes

Classical ECG changes associated with hyperkalemia are well documented; however, ECG changes are insensitive and highly variable (Figures 1 and 2).

  • In mild hyperkalemia (5.5mEq/L-6.5mEq/L), peaked T waves with a prolonged PR segment are the earliest changes.
  • In moderate hyperkalemia (6.5mEq/L-8mEq/L), a loss of the P wave, prolonged QRS complex, ST segment elevations are seen with escape rhythms.
  • In severe hyperkalemia (greater than 8mEq/L), the classical sine wave can be seen in addition to ventricular fibrillation, bundle branch blocks, fascicular blocks, as well as asystole.2,3

Figure 1. ECG demonstrating tall, symmetrically peaked T waves. This patient had a serum K+ of 7.0. Source: Buttner R, Burns E. Hyperkalemia. Life in the Fastlane. CC-BY-NC-SA 4.0. Link.

Figure 2. ECG demonstrating peaked T waves, prolonged PR interval, and broad QRS complexes. This patient had a serum K+ of 9.3. Source: Buttner R, Burns E. Hyperkalemia. Life in the Fastlane. CC-BY-NC-SA 4.0. Link.


Patients who develop moderate to severe hyperkalemia (greater than 6.0mEq/L) should be treated rapidly to avoid myocardial instability. In patients with milder forms of hyperkalemia, potassium levels should be checked every 1-2 hours and aggressively treated, if necessary.4

  • The diagnosis should be confirmed by measuring a STAT serum potassium.
  • Pseudohyperkalemia should be ruled out.

Stop the administration of potassium-continuing solutions

  • Intravenous (IV) potassium replacement
  • IV fluids – lactated Ringer’s solution
  • Packed red blood cells

Membrane stabilization

  • Hyperventilate the patient
  • Calcium should be administered to depress the membrane threshold potential. Calcium can be given as either calcium chloride (500-1000 mg) or calcium gluconate (1000 mg). While calcium chloride has three times the amount of elemental calcium as calcium gluconate, calcium gluconate is usually preferred because it causes less irritation at the injection site and can be given through a peripheral intravenous catheter.6 Calcium chloride extravasation can cause tissue necrosis and ideally, should be given through a central venous catheter.
  • The effect of calcium for treating hyperkalemia is short-lived (30-60 minutes) and, therefore, should be combined with other therapies.
  • Calcium should not be administered with bicarbonate-containing solutions as it can lead to the precipitation of calcium carbonate.

Transfer of extracellular potassium into cells

  • Administration of 5-10 units of insulin along with 25-50g of glucose (to avoid accompanying hypoglycemia) drives the potassium intracellularly by increasing the activity of the Na-K-ATPase pump in skeletal muscle.
  • A common regimen is ten units of regular insulin with 50 mL of 50% dextrose solution (25 g of glucose).2 However, insulin should be given alone when the serum glucose is ≥ 250 mg/dL. Higher doses of insulin provide no additional effect of lowering potassium.
  • Administration of inhaled beta-agonists such as albuterol may drive potassium into the skeletal muscle, lowering the potassium an additional 0.5-1mEq/L.

Increase potassium excretion

  • Loop or thiazide diuretics may be used in patients with normal or mild to moderately impaired renal function to increase potassium loss in the urine. Furosemide in doses of 20-40 mg is commonly used to promote diuresis in non-oliguric patients without severe kidney function impairment. In hypovolemic patients with hyperkalemia and preserved renal function, isotonic saline is first administered to achieve euvolemia before diuretic administration.6
  • Gastrointestinal (GI) cation exchange resins bind potassium in the GI tract in exchange for other cations, such as sodium and calcium. Examples include patiromer, sodium zirconium cyclosilicate (SZC), and sodium polystyrene sulfonate (SPS)(Kayexalate). SZC is usually preferred over patiromer. The use of SPS has fallen out of favor, secondary to the risk of bowel necrosis.6
  • The most effective means of potassium excretion is hemodialysis, which is indicated in hyperkalemic patients with severely impaired kidney function.
  • The use of alkalinizing agents such as sodium bicarbonate will not decrease the potassium levels to a significant degree and does not protect against bradyarrhythmias commonly seen in hyperkalemia.

Table 1. Treatment of hyperkalemia.


  1. Mount DB. Causes and evaluation of hyperkalemia in adults. In: Post T, ed. UpToDate; 2023. Accessed February 5th, 2023.
  2. Simon LV, Hashmi MF, Farrell MW. Hyperkalemia. In: StatPearls (Internet). Treasure Island, FL: StatPearls Publishing. 2022. Accessed 18 January 2023. Link
  3. Prough DS, Funston JS, Saad AF, et al. Fluids, Electrolytes, and Acid Base Physiology. In: Barash PG, editor. Clinical Anesthesia, 8th Edition. Philadelphia, Pa; Wolters Kluwer Health; 2017: 1051-1056.
  4. Botz GH. Metabolic events. In: Gaba, DM, Burden AR, Howard SK, Fish KJ. Crisis Management in Anesthesiology. 2nd Edition. Philadelphia, PA. Elsevier/Saunders; 2015: 214-7.
  5. Brull SJ, Meistelman C. Pharmacology of neuromuscular blocking drugs. In: Miller RD, editor. Miller's Anesthesia. 9th edition. Philadelphia, PA; Elsevier/Saunders; 2019: 792-831.
  6. Mount DB. Treatment and prevention of hyperkalemia in adults. In: Post T, ed. UpToDate; 2023. Accessed February 5th, 2023.

Other References

  1. Buttner R, Burns E. Hyperkalemia. Life in the Fastlane. CC-BY-NC-SA 4.0. Link