eMedicine Specialties > Nephrology > Acid-Base, Fluid, and Electrolyte Disorders

Hyperkalemia: Treatment & Medication

Author: Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
Coauthor(s): Rosemary Ouseph, MD, Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine; Vibha Nayak, MD, Assistant Professor of Nephrology, Director of Home Dialysis, Kidney Disease Program, University of Louisville; Son Dinh, MD, Nephrologist, Southland Renal Medical Group, Inc
Contributor Information and Disclosures

Updated: Apr 7, 2009

Treatment

Medical Care

Orient the medical care of patients with hyperkalemia toward 5 different aims.

  • Evaluation for potential toxicities
  • Decreasing potassium intake
  • Increasing potassium uptake into cells
  • Increasing potassium excretion
  • Determining the cause to prevent future episodes

Although explicated below in a step-by-step format, these different aspects of hyperkalemia treatment generally are addressed simultaneously. The aggressiveness of therapy is directly related to the rapidity with which hyperkalemia has developed, the absolute level of hyperkalemia, and the evidence of toxicity. The faster the rise of potassium, the higher the level, and the greater the evidence of cardiotoxicity, the more aggressive therapy should be.

  • The first step is to determine whether the hyperkalemia is producing life-threatening toxicity.
    • Perform an ECG to look for cardiotoxicity.
    • Administer intravenous calcium to ameliorate cardiac toxicity, if present.
  • The second step is to identify and remove sources of potassium intake.
    • Discontinue oral and parenteral potassium supplements.
    • Remove potassium-containing salt substitutes.
    • Examine the patient's diet. Change the diet to a low-potassium tube feed or a 2-g potassium ad-lib diet.
  • The third step is to enhance potassium uptake by cells to decrease the serum concentration.
    • Parenteral glucose and insulin infusions are very effective in enhancing potassium uptake. Although glucose stimulates insulin secretion, administration of glucose alone often is not as effective in this clinical situation. The onset of action is within 20-30 minutes, and the duration is variable, from 2-6 hours. Continuous infusions of insulin and glucose-containing intravenous fluids can be used for prolonged effect. Measure glucose and potassium every 2 hours.
    • Correct metabolic acidosis with sodium bicarbonate. This therapeutic modality is less effective and less predictable in producing a hypokalemic response, due to the variable effect of different forms of metabolic acidosis on the serum potassium level. This particularly is true in patients with chronic renal failure. Nonetheless, if the acidosis is severe, then a trial of parenteral sodium bicarbonate therapy is warranted.
    • Beta-adrenergic agonists also are quite effective but are perhaps somewhat more controversial and more likely to produce side effects. In the United States, the most commonly used preparation is nebulized albuterol. The dose for treating hyperkalemia, 10 mg, is substantially higher than the usual dose for the treatment of bronchospasm and requires the assistance of a respiratory therapist. This therapy is highly effective and preferred over alkali therapy in patients with renal failure. Parenteral isoproterenol or albuterol also decrease potassium. However, isoproterenol is not used commonly, and parenteral albuterol is not available in the United States. Some investigators have reported tachycardia and chest discomfort using beta-agonist therapy for hyperkalemia. Discontinue beta-adrenergic antagonists.
  • The fourth step is to increase potassium excretion from the body.
    • Renal excretion is enhanced easily in the individual with normal kidney function by the administration of parenteral saline accompanied by a loop diuretic, such as furosemide.
      • Discontinue potassium-sparing diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and other drugs that inhibit renal potassium excretion.
      • Monitor volume status and aim to maintain euvolemia.
    • Renal excretion can be enhanced by administration of an aldosterone analogue, such as 9-alpha fluorohydrocortisone acetate (Florinef). Florinef especially is helpful in patients with hyporeninemia or hypoaldosteronism.
  • Gastrointestinal excretion can be increased by the use of cation exchange resins, such as Kayexalate. Kayexalate can be administered orally or rectally (as a retention enema). Because the major site of action for this drug is the colon, rectal administration is preferred for hyperkalemic emergencies.
    • The effectiveness of this drug is enhanced if the enema can be retained for an hour.
    • Repeated enemas can be used but occasionally cause colon perforation.
    • The onset of action occurs within 2 hours and is long lasting. The serum potassium level can be decreased by 2 mEq/L with a single enema. Kayexalate administered orally also is quite effective if it is suspended in 70% sorbitol.
  • Emergency dialysis is a final recourse for patients who are experiencing potentially lethal hyperkalemia that is unresponsive to more conservative measures or for patients who have complete renal failure. Initiation of dialysis often can take several hours; therefore, even if dialysis is contemplated, initiate the other modalities of therapy first.
  • The final step in the medical management of hyperkalemia is to determine the cause of hyperkalemia in order to prevent future episodes. This should include examination of the following:
    • Sources of potassium intake
    • Causes of decreased renal excretion
    • Causes for impaired cellular uptake

Surgical Care

Surgery generally is not needed for the care of a patient with hyperkalemia.

  • Patients with metabolic acidosis and consequent hyperkalemia due to ischemic gut obviously require exploration.
  • Patients with hyperkalemia due to rhabdomyolysis may need surgical decompression of swollen ischemic muscle compartments.
  • Patients without end-stage renal disease who require hemodialysis for control of hyperkalemia need placement of a hemodialysis catheter for emergent dialysis.

Consultations

  • For severe hyperkalemia, early consultation with a nephrologist for aid in efficient therapy and plans for dialysis is highly recommended.
  • For emergency pacemaker placement, the aid of a cardiologist may be required for patients with refractory heart block.

Diet

A low-potassium diet with 2 g of potassium is recommended to minimize potassium intake.

Activity

No restrictions on activity are necessary unless continuous monitoring for cardiotoxicity is required.

Medication

The goals of pharmacotherapy are to reduce potassium levels and morbidity and to prevent complications.

Beta-adrenergic agonists

Through an activation of cyclic adenosine monophosphate (AMP), these agonists stimulate the adenosine triphosphatase (ATPase) pump, thereby shifting potassium into the intracellular compartment.


Isoproterenol (Dey-Dose, Isuprel, Arm-a-Med)

Has beta1-adrenergic and beta2-adrenergic receptor activity.

Adult

5 mcg/min IV initial, titrate to response; not to exceed 20 mcg/min

Pediatric

0.1 mcg/kg/min IV, titrate to response; not to exceed 2 mcg/min

Bretylium increases action of vasopressors on adrenergic receptors, which may, in turn, result in arrhythmias; guanethidine may increase effect of direct-acting vasopressors, possibly resulting in severe hypertension; tricyclic antidepressants may potentiate pressor response of direct-acting vasopressors

Documented hypersensitivity; tachyarrhythmias, tachycardia, or heart block caused by digitalis intoxication; ventricular arrhythmias that require inotropic therapy; angina pectoris

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

By increasing myocardial oxygen requirements while decreasing effective coronary perfusion, isoproterenol may have a deleterious effect on the injured or failing heart; in some patients presumably with organic disease of the AV node and its branches, isoproterenol paradoxically may worsen heart blocks or precipitate Adams-Stokes attacks; caution in coronary artery disease, coronary insufficiency, diabetes, or hyperthyroidism; if heart rate >110 beats per min, decreasing infusion rate or temporarily discontinuing infusion may be advisable


Albuterol (Proventil, Ventolin)

Adrenergic agonist that increases plasma insulin concentrations. Increase in insulin may shift potassium into intracellular space.

Adult

10-20 mg nebulized or 0.5 mg IV over 15 min

Pediatric

2.5 mg IV and repeat in 2 h prn

Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation by albuterol; cardiovascular effects may increase with MAOIs, inhaled anesthetics, tricyclic antidepressants, and sympathomimetic agents

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hyperthyroidism, diabetes mellitus, and cardiovascular disorders

Calcium salts

Calcium antagonizes cardiotoxicity of hyperkalemia by stabilizing cardiac cell membrane against undesirable depolarization. Has no effect on serum level of potassium. Onset of effect is rapid, within 15 min, but relatively short lived.


Calcium gluconate (Kalcinate)

Moderates nerve and muscle performance and facilitates normal cardiac function.

Adult

100-300 mg elemental calcium IV diluted in 150 mL D5W over 10 min; initial rate of infusion should be 0.3-2 mg of elemental calcium per kg/h

Pediatric

2 mg/kg of elemental calcium IV (about 20 mg/kg of calcium gluconate 10%)

May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; antagonizes effects of verapamil

Documented hypersensitivity; renal calculi; hypercalcemia; hypophosphatemia; renal or cardiac disease; digitalis toxicity

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients who are digitalized; respiratory failure; acidosis; severe hyperphosphatemia


Calcium chloride

Prevents deleterious effects caused by severe hyperkalemia as measured by ECG, pending correction of increased potassium in extracellular fluid. Generally, second choice to calcium gluconate due to irritating effects when administered parenterally.

Adult

Known or suspected hyperkalemia (K+ >6 mEq/L): 2-4 mg/kg IV (10% solution)

Pediatric

0.2 mL (20 mg)/kg of IV (10% solution)

Coadministration with digoxin may cause arrhythmias; may antagonize effects of calcium channel blockers, atenolol, and sodium polystyrene sulfonate

Ventricular fibrillation not associated with hyperkalemia; digitalis toxicity; hypercalcemia; renal insufficiency; cardiac disease

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure

Hormones

Insulin stimulates cellular uptake of potassium, lowering serum potassium level.


Insulin (Novolin, Humulin)

Stimulates cellular uptake of potassium within 20-30 min. Administer glucose along with insulin to prevent hypoglycemia. Monitor blood sugar levels frequently.

Adult

10 U IV and either 50 mL D50W bolus or 500 mL D10W over 1 h

Pediatric

0.5-1 g/kg IV followed by 1 U of regular insulin per 3 g glucose

Medications that may decrease hypoglycemic effects of insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid estrogens, ethacrynic acid, calcitonin, oral contraceptives, diazoxide, dobutamine, phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin; medications that may increase hypoglycemic effects of insulin include calcium, ACE inhibitors, alcohol, tetracyclines, beta-blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone

Documented hypersensitivity; hypoglycemia

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hyperthyroidism may increase renal clearance of insulin and may need more insulin to treat hyperkalemia; hypothyroidism may delay insulin turnover, requiring less insulin to treat hyperkalemia; monitor glucose carefully; dose adjustments of insulin may be necessary in patients diagnosed with renal and hepatic dysfunction

Diuretics

Loop diuretics markedly enhance renal potassium excretion, consequently lowering serum levels. Parenterally administered drug has a more rapid onset of action and is preferable in emergent situations. Simultaneous administration of saline can prevent severe volume depletion.


Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in ascending loop of Henle and distal renal tubule. Individualize dose to patient. Depending on the response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until desired diuresis occurs. When treating infants, titrate with increments of 1 mg/kg per dose until a satisfactory effect is achieved. Oral absorption of furosemide is variable from person to person. If rapid and effective therapy is mandated, then IV route is preferred. Occasionally, a continuous infusion of furosemide, as high as 40 mg/h, is used for severe edema but rarely is required for the treatment of hyperkalemia.

Adult

20-80 mg/d PO/IV/IM; titrate as high as 600 mg/d

Pediatric

1-2 mg/kg per dose PO; not to exceed 6 mg/kg per dose; not to administer >q6h
1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg

Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently

Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter; profound diuresis may occur with fluid and electrolyte loss; caution in hepatic failure


Bumetanide (Bumex)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in ascending loop of Henle and distal renal tubule. Individualize dose to patient. Start at 1-2 mg IV; titrate to as high as 10 mg/d. Rarely, doses as high as 24 mg/d are used for edema but generally are not required for treatment of hyperkalemia.

Adult

0.5-2 mg/dose PO qd/bid; not to exceed 10 mg/d
Alternatively, 0.5-1 mg/dose IV/IM; not to exceed 10 mg/d

Pediatric

Not established

Decreases effects of indomethacin and probenecid; may increase lithium toxicity

Documented hypersensitivity; anuria; increasing azotemia

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Profound diuresis may occur with fluid and electrolyte loss; caution in hepatic failure; monitor serum sodium, bicarbonate, calcium, magnesium, phosphate, and potassium

Cation exchange resins

Stimulate the exchange of sodium for potassium in the colon, thus increasing intestinal excretion of potassium.


Sodium polystyrene sulfonate (Kayexalate)

Exchanges sodium for potassium and binds it in the gut, primarily in the large intestine, and decreases total body potassium. Onset of action after oral administration ranges from 2-12 h and is longer when administered rectally.

Adult

25-50 g PO in 25-50 mL sorbitol q6h
25-50 g PR in 25-50 mL sorbitol as retention enema q6h

Pediatric

1 g/kg PO in sorbitol q6h
2 g/kg PR in sorbitol as retention enema q6h

Systemic alkalosis may occur if administered concurrently with magnesium hydroxide, aluminum carbonate or similar antacids, and laxatives

Documented hypersensitivity; hypernatremia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution when administering to patients who can be affected adversely by a small increase in sodium loads, such as severe hypertension, severe congestive heart failure, and marked edema; constipation, with the possibility of fecal impaction, may occur; treat constipation with 10-20 mL of 70% sorbitol every 2 h or as necessary to produce at least 1-2 watery stools daily

Electrolytes

Used to correct metabolic acidosis if acidosis is severe.


Sodium bicarbonate (Neut)

Used only when patient is diagnosed with bicarbonate-responsive acidosis, hyperkalemia, tricyclic antidepressant overdose, or phenobarbital overdose. Routine use is not recommended.
To estimate the dose that should be administered may use the following formula: HCO3- (mEq) = 0.5 X weight in kg X (24 - serum HCO3- in mEq/L)
This formula has many limitations; however, the practitioner can determine roughly the amount of bicarbonate required and subsequently titrate against the pH and anion gap.

Adult

Generally for parenteral use, 1-2 amps of sodium bicarbonate containing a total of 50-100 mEq is adequate
650-1300 mg PO bid or tid
If the patient has a relatively normal serum bicarbonate level but severe ECG changes of hyperkalemia, then 1 ampule or 50 mEq may be infused q15min, monitoring serum bicarbonate and serum sodium to avoid severe alkalosis and hypernatremia
Alternatively, 2 ampules of sodium bicarbonate (100 mEq) may be added to 1 L 10% dextrose in water and infused at 250-500 mL/h if tolerated

Pediatric

Not established

Urinary alkalinization induced by increased sodium bicarbonate concentrations may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; increases levels of amphetamines pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine

Documented hypersensitivity; alkalosis; hypernatremia; hypocalcemia; severe pulmonary edema; unknown abdominal pain

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Only use sodium bicarbonate to treat documented metabolic acidosis and hyperkalemia-induced cardiac arrest; can cause alkalosis, decreased plasma potassium, hypocalcemia, and hypernatremia; caution in electrolyte imbalances, such as in patients with CHF, cirrhosis, edema, corticosteroid use, or renal failure; when administering, avoid extravasation because can cause tissue necrosis

More on Hyperkalemia

Overview: Hyperkalemia
Differential Diagnoses & Workup: Hyperkalemia
Treatment & Medication: Hyperkalemia
Follow-up: Hyperkalemia
Multimedia: Hyperkalemia
References
Further Reading
[ CLOSE WINDOW ]

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Further Reading

Clinical guidelines:
Potassium in pre-dialysis patients. Caring for Australasians with Renal Impairment - Disease Specific Society. 2005 Dec. 6 pages. NGC:006168

The pharmacologic management of chronic heart failure. Department of Veterans Affairs - Federal Government Agency [U.S.]
Veterans Health Administration - Federal Government Agency [U.S.]. 2001 Feb (revised 2003 Aug). 45 pages. NGC:003566

Clinical trials:
Genetic Determinants of the Hypokalemic and Hyperglycemic Effect of Albuterol Inhalation
Inhibition of Aldosterone in Patients With Chronic Renal Disease

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Keywords

hyperkalemia, potassium, high potassium, congestive heart failure, chronic renal failure, potassium foods, potassium health, aldosterone, foods high in potassium, potassium rich foods, potassium levels, potassium food, blood potassium, ACE inhibitor, potassium heart, potassium supplement, ACEI, elevated potassium, potassium effects, symptoms of potassium, high potassium levels, high potassium level, serum potassium, aldosterone renin, Kayexalate, potassium mEq, blood potassium levels, aldosterone renin angiotensin, high potassium causes, hyperkalemia causes, high levels of potassium, high potassium diet, symptoms of high potassium, hypoaldosteronism

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Contributor Information and Disclosures

Author

Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Rosemary Ouseph, MD, Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine
Rosemary Ouseph, MD is a member of the following medical societies: American Society for Bone and Mineral Research, American Society of Nephrology, and American Society of Transplant Surgeons
Disclosure: Nothing to disclose.

Vibha Nayak, MD, Assistant Professor of Nephrology, Director of Home Dialysis, Kidney Disease Program, University of Louisville
Vibha Nayak, MD is a member of the following medical societies: American Society of Nephrology
Disclosure: Nothing to disclose.

Son Dinh, MD, Nephrologist, Southland Renal Medical Group, Inc
Son Dinh, MD is a member of the following medical societies: American Society of Nephrology and National Kidney Foundation
Disclosure: Nothing to disclose.

Medical Editor

Anil Kumar Mandal, MD, Clinical Professor, Department of Internal Medicine, Division of Nephrology, University of Florida School of Medicine
Anil Kumar Mandal, MD is a member of the following medical societies: American College of Clinical Pharmacology, American College of Physicians, American Society of Nephrology, and Central Society for Clinical Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Christie P Thomas, MBBS, FRCP, FASN, FAHA, Professor, Department of Internal Medicine, Division of Nephrology; Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics
Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Nephrology, American Society of Transplantation, American Thoracic Society, International Society of Nephrology, and Royal College of Physicians
Disclosure: Genzyme Grant/research funds Other

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

 
 
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