eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic

Hyperkalemia

David Garth, MD, Attending Physician, Department of Emergency Medicine, Mary Washington Hospital

Updated: Aug 6, 2009

Introduction

Background

Hyperkalemia is a potentially life-threatening illness that can be difficult to diagnose because of a paucity of distinctive signs and symptoms. The physician must be quick to consider hyperkalemia in patients who are at risk for this disease process. Because hyperkalemia can lead to sudden death from cardiac arrhythmias, any suggestion of hyperkalemia requires an immediate ECG to ascertain whether electrocardiographic signs of electrolyte imbalance are present.

Pathophysiology

Potassium is a major ion of the body. Nearly 98% of potassium is intracellular, with the concentration gradient maintained by the sodium- and potassium-activated adenosine triphosphatase (Na⁺/K⁺ –ATPase) pump. The ratio of intracellular to extracellular potassium is important in determining the cellular membrane potential. Small changes in the extracellular potassium level can have profound effects on the function of the cardiovascular and neuromuscular systems. The normal potassium level is 3.5-5.0 mEq/L, and total body potassium stores are approximately 50 mEq/kg (3500 mEq in a 70-kg person).

Minute-to-minute levels of potassium are controlled by intracellular to extracellular exchange, mostly by the sodium-potassium pump that is controlled by insulin and beta2 receptors. A balance of GI intake and renal potassium excretion achieves long-term potassium balance.

Hyperkalemia is defined as a potassium level greater than 5.5 mEq/L.¹ Ranges are as follows:

• 5.5-6.0 mEq/L - Mild
• 6.1-7.0 mEq/L - Moderate
• 7.0 mEq/L and greater - Severe

Hyperkalemia results from the following:

• Decreased or impaired potassium excretion - As observed with acute or chronic renal failure² (most common), potassium-sparing diuretics, urinary obstruction, sickle cell disease, Addison disease, and systemic lupus erythematosus (SLE)
• Additions of potassium into extracellular space - As observed with potassium supplements (eg, PO/IV potassium, salt substitutes), rhabdomyolysis, and hemolysis (eg, blood transfusions, burns, tumor lysis)
• Transmembrane shifts (ie, shifting potassium from the intracellular to extracellular space) - As observed with acidosis and medication effects (eg, acute digitalis toxicity, beta-blockers, succinylcholine)
• Factitious or pseudohyperkalemia - As observed with improper blood collection (eg, ischemic blood draw from venipuncture technique), laboratory error, leukocytosis, and thrombocytosis

Frequency

United States

Hyperkalemia is diagnosed in up to 8% of hospitalized patients.

Mortality/Morbidity

• The primary cause of morbidity and death is potassium's effect on cardiac function.³
• The mortality rate can be as high as 67% if severe hyperkalemia is not treated rapidly.⁴

Sex

The male-to-female ratio is 1:1.

Clinical

History

• Hyperkalemia can be difficult to diagnose clinically because complaints may be vague. The history is most valuable in identifying conditions that may predispose to hyperkalemia.
• Hyperkalemia frequently is discovered as an incidental laboratory finding.
• Cardiac and neurologic symptoms predominate.
• Patients may be asymptomatic or report the following:
  • Generalized fatigue
  • Weakness
  • Paresthesias
  • Paralysis
  • Palpitations
• Hyperkalemia is suggested in any patient with a predisposition toward elevated potassium level. Potential potassium level elevation is observed in the following:
  • Acute or chronic renal failure, especially in patients who are on dialysis
  • Trauma, including crush injuries (rhabdomyolysis), or burns
  • Ingestion of foods high in potassium (eg, bananas, oranges, high-protein diets, tomatoes, salt substitutes). This alone is not likely to cause clinically significant hyperkalemia in most people; it is often a contributing factor to an acute potassium elevation.
  • Medications - Potassium supplements, potassium-sparing diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), beta-blockers, digoxin, succinylcholine, and digitalis glycoside
  • Medication combinations (ie, spironolactone, ACE inhibitors5
  • Redistribution - Metabolic acidosis (diabetic ketoacidosis [DKA]), catabolic states

Physical

• Evaluation of vital signs is essential to determine hemodynamic stability and presence of cardiac arrhythmias related to the hyperkalemia.¹
• Cardiac examination may reveal extrasystoles, pauses, or bradycardia.
• Neurologic examination may reveal diminished deep tendon reflexes or decreased motor strength.
• In rare cases, muscular paralysis and hypoventilation may be observed.
• Search for the stigmata of renal failure, such as edema, skin changes, and dialysis sites.
• Look for signs of trauma that could put the patient at risk for rhabdomyolysis.

Causes

• Pseudohyperkalemia
  • Hemolysis (in laboratory tube) most common
  • Thrombocytosis
  • Leukocytosis
  • Venipuncture technique (ie, ischemic blood draw from prolonged tourniquet application)
• Redistribution
  • Acidosis
  • Insulin deficiency
  • Beta-blocker drugs
  • Acute digoxin intoxication or overdose
  • Succinylcholine
  • Arginine hydrochloride
  • Hyperkalemic familial periodic paralysis
• Excessive endogenous potassium load
  • Hemolysis
  • Rhabdomyolysis
  • Internal hemorrhage
• Excessive exogenous potassium load
  • Parenteral administration
  • Excess in diet
  • Potassium supplements
  • Salt substitutes
• Diminished potassium excretion
  • Decreased glomerular filtration rate (eg, acute or end-stage chronic renal failure)
  • Decreased mineral corticoid activity
  • Defect in tubular secretion (eg, renal tubular acidosis II and IV)
  • Drugs (eg, NSAIDs, cyclosporine, potassium-sparing diuretics)
• Laboratory error⁶

Differential Diagnoses

Hypocalcemia

Other Problems to Be Considered

Cardiac arrhythmias

Workup

Laboratory Studies

• Potassium level - The relationship between the serum potassium level and symptoms is not consistent. For example, patients with a chronically elevated potassium level may be asymptomatic at much higher levels than other patients. The rapidity of change in the potassium level influences the symptoms observed at various potassium levels.
• BUN and creatinine level - For evaluation of renal status
• Calcium level - If patient has renal failure (because hypocalcemia can exacerbate cardiac rhythm disturbances)
• Glucose level - In patients with diabetes mellitus
• Digoxin level - If patient is on a digitalis medication
• Arterial or venous blood gas - If acidosis is suspected
• Urinalysis - If signs of renal insufficiency without an already known cause are present (to look for evidence of glomerulonephritis)

Other Tests

• Continuous cardiac monitoring - Indicated for evaluation of rhythm disturbances
• ECG is essential and may be instrumental in diagnosing hyperkalemia in the appropriate clinical setting. ECG changes have a sequential progression of effects, which roughly correlate with the potassium level.
• ECG findings may be observed as follows:
  • Early changes of hyperkalemia include peaked T waves, shortened QT interval, and ST-segment depression (see Media files 1-2). 
    
    

    

    Peaked T waves in hyperkalemia.

    
    
    
    

    

    Peaked T waves in hyperkalemia.

    
    
  • These changes are followed by bundle-branch blocks causing a widening of the QRS complex, increases in the PR interval, and decreased amplitude of the P wave (see Media files 3-4). 
    
    

    

    Widened QRS complexes in hyperkalemia.

    
    
    
    

    

    Widened QRS complexes in a patient whose serum potassium level was 7.8 mEq/L.

    
    
  • These changes reverse with appropriate treatment (see Media file 5). 
    
    

    

    ECG of a patient with pretreatment potassium level of 7.8 mEq/L and widened QRS complexes after receiving 1 ampule of calcium chloride. Notice narrowing of QRS complexes and reduction of T waves.

    
    
  • Without treatment, the P wave eventually disappears and the QRS morphology widens to resemble a sine wave. Ventricular fibrillation or asystole follows.
  • ECG findings generally correlate with the potassium level, but potentially life-threatening arrhythmias can occur without warning at almost any level of hyperkalemia.
• Cortisol and aldosterone levels - To check for mineralocorticoid deficiency when other causes are eliminated

Treatment

Prehospital Care

A patient with known hyperkalemia or a patient with renal failure with suspected hyperkalemia should have intravenous access established and should be placed on a cardiac monitor.⁷ In the presence of hypotension or marked QRS widening, intravenous bicarbonate, calcium, and insulin given together with 50% dextrose may be appropriate as discussed in Medication. Avoid calcium if digoxin toxicity is suspected. Magnesium sulfate (2 g over 5 min) may be used alternatively in the face of digoxin-toxic cardiac arrhythmias.

Emergency Department Care

• Perform continuous ECG monitoring with frequent vital sign checks when hyperkalemia is suspected or when laboratory values indicative of hyperkalemia are received.
• Initial management includes assessment of the ABCs and prompt evaluation of the patient's cardiac status with an ECG.
• Discontinue any potassium-sparing drugs or dietary potassium.
• If the hyperkalemia is severe (potassium >7.0 mEq/L) or if the patient is symptomatic, begin treatment before diagnostic investigation of the underlying cause.
  • Individualize treatment based upon the patient's presentation, potassium level, and ECG.
  • Not all patients should receive every medication listed in Medication. Patients with mild hyperkalemia, for example, may need only excretion enhancement.

Consultations

Consult a nephrologist or the dialysis team for patients with either severe symptomatic hyperkalemia or renal failure. Admit these patients to an ICU.

Medication

Direct treatment is aimed at stabilizing the myocardium, shifting potassium from the extracellular environment to the intracellular compartment, and promoting the renal excretion and GI loss of potassium.

Electrolyte supplements

These agents are used to treat hyperkalemia and to reduce the risk of ventricular fibrillation caused by hyperkalemia. They act quickly and can be lifesaving, thus they are the first-line treatment for severe hyperkalemia when the ECG shows significant abnormalities (eg, widening of QRS interval, loss of P wave, cardiac arrhythmias). Calcium usually is not indicated when the ECG shows only peaked T waves.

Calcium chloride or calcium gluconate (Kalcinate)

Calcium increases threshold potential, thus restoring normal gradient between threshold potential and resting membrane potential, which is elevated abnormally in hyperkalemia. One ampule of calcium chloride has approximately 3 times more calcium than calcium gluconate. Onset of action is <5 min and lasts about 30-60 min. Doses should be titrated with constant monitoring of ECG changes during administration; repeat dose if ECG changes do not normalize within 3-5 min.

Dosing

Adult

Calcium chloride: 5 mL of 10% sol IV over 2 min (stop infusion if bradycardia develops)
Calcium gluconate: 10 mL of 10% sol IV over 2 min (stop infusion if bradycardia develops)

Pediatric

Calcium chloride: 0.2 mL/kg/dose of 10% sol IV over 5 min; not to exceed 5 mL (stop infusion if bradycardia develops)
Calcium gluconate: 100 mg/kg (1 mL/kg) of 10% sol IV over 3-5 min; not to exceed 10 mL (stop infusion if bradycardia develops)

Interactions

May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; antagonizes effects of verapamil; large intakes of dietary fiber may decrease absorption and levels

Contraindications

Renal calculi; hypercalcemia; hypophosphatemia; renal or cardiac disease; digitalis toxicity

Precautions

Pregnancy

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

Precautions

Caution in digitalized patients, respiratory failure, acidosis, or severe hyperphosphatemia

Antidotes

Insulin is administered with glucose to facilitate the uptake of glucose into the cell, bringing potassium with it.

Dextrose (D-Glucose)

Glucose and insulin temporarily shift K⁺ into cells; effects occur within first 30 min of administration.

Dosing

Adult

1-2 amps D50W and 5-10 U regular insulin IV

Pediatric

0.5 g/kg (2 mL/kg) 25% dextrose solution with 0.1 U/kg regular insulin (1 U regular insulin/5 g glucose) IV over 30 min

Interactions

Caution when administering parenteral fluids to patients receiving corticosteroids or corticotropin, especially if solution contains Na⁺ ions

Contraindications

Diabetic coma if blood glucose levels extremely high
Avoid in severely dehydrated patients, especially those with delirium tremens, hepatic coma, or glucose-galactose malabsorption syndrome
Do not administer concentrated solution if intraspinal or intracranial hemorrhage is present

Precautions

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

May cause nausea, which also may occur with hypoglycemia; IV dextrose solutions may result in dilution of serum electrolyte concentrations or overhydration when patient is fluid overloaded; caution in patients suffering from congested states or pulmonary edema; hypertonic dextrose given peripherally may cause thrombosis (administer instead through central venous catheter); caution in subclinical diabetes mellitus or carbohydrate intolerance; increased risk of inducing significant hyperglycemia or hyperosmolar syndrome if solution administered rapidly, especially in patients with chronic uremia or carbohydrate intolerance; concentrated solutions should not be administered SC or IM; rates of dextrose infusion higher than 0.5 g/kg/h may produce glycosuria; at infusion rates of 0.8 g/kg/h, incidence of glycosuria is 5%; monitor fluid balance, electrolyte concentrations, and acid-base balance closely; dextrose administration may produce vitamin B complex deficiency

Insulin (Humulin, Humalog, Novolin)

Stimulates cellular uptake of K⁺ within 20-30 min; administer glucose along with insulin to prevent hypoglycemia (monitor blood glucose levels closely).

Dosing

Adult

5-10 U regular insulin and 1-2 amps D50W IV bolus

Pediatric

0.5 g/kg (2 mL/kg) 25% dextrose solution with 0.1 U/kg regular insulin (1 U regular insulin/5 g glucose) IV over 30 min

Interactions

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

Contraindications

Documented hypersensitivity; hypoglycemia

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

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

Alkalinizing agents

These agents increase the pH, which results in a temporary potassium shift from the extracellular to the intracellular environment. These agents enhance the effectiveness of insulin in patients with acidemia.

Sodium bicarbonate (Neut)

Bicarbonate ion neutralizes hydrogen ions and raises urinary and blood pH. Onset of action within minutes, lasts approximately 15-30 min. Only likely to be efficacious if underlying acidosis present. Monitor blood pH to avoid excess alkalosis.
Use 8.4% solution in adults and children, 4.2% solution in infants.

Dosing

Adult

1 mEq/kg slow IV push or continuous IV drip; not to exceed 50-100 mEq

Pediatric

Infants: 0.5 mEq/kg IV over 5-10 min; repeat in 10 min prn (only use 4.2% sol, not 8.4% sol used in older children and adults)
Children: 1-2 mEq/kg IV over 5-10 min; repeat in 10 min prn; monitor ABGs to avoid arterial pH >7.55

Interactions

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

Contraindications

Documented hypersensitivity; alkalosis; hypernatremia; hypocalcemia; severe pulmonary edema

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Use only 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 those seen in patients with CHF, cirrhosis, edema, corticosteroid use, or renal failure; avoid extravasation since can cause tissue necrosis

Beta2-adrenergic agonists

These agents promote cellular reuptake of potassium, possibly via the cyclic gAMP receptor cascade.

Albuterol (Ventolin, Proventil)

Adrenergic agonist that increases plasma insulin concentration, which may in turn help shift K⁺ into intracellular space. Lowers K⁺ level by 0.5-1.5 mEq/L. Can be very beneficial in patients with renal failure when fluid overload is concern. Onset of action is 30 min; duration of action is 2-3 h.

Dosing

Adult

5 mg mixed with 3 mL isotonic saline via high-flow nebulizer q20min as tolerated

Pediatric

<1 year: 0.05-0.15 mg/kg/dose with 3 mL isotonic saline nebulized
1-5 years: 1.25-2.5 mg/dose with 3 mL isotonic saline nebulized
5-12 years: 2.5 mg/dose with 3 mL isotonic saline nebulized
>12 years: 2.5-5 mg/dose with 3 mL isotonic saline nebulized

Interactions

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

Contraindications

Documented hypersensitivity

Precautions

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

Diuretics

These agents cause the loss of potassium through the kidney.

Furosemide (Lasix)

Effects are slow and frequently take an hour to begin. Lowers potassium level by inconsistent amount. Large doses may be needed in renal failure.

Dosing

Adult

20-40 mg IV push in patients not already on this drug
Double daily PO dose as IV slow push in patients already taking this drug

Pediatric

Neonates: 0.5-2 mg/kg/dose IV; not to exceed 2 mg/kg/dose
Infants and children: 0.5-2 mg/kg/dose IV; if response unsatisfactory, may increase by 1-2 mg/kg q6-8h; not to exceed 6 mg/kg/dose

Interactions

Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; may increase auditory toxicity of aminoglycosides, and hearing loss of varying degrees may occur; may enhance anticoagulant activity of warfarin; may increase plasma levels and toxicity of lithium

Contraindications

Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion

Precautions

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, CO₂, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter

Ethacrynic acid (Edecrin)

Increases excretion of water by interfering with chloride-binding cotransport system, which in turn inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.

Dosing

Adult

Oral: 25-400 mg qd or divided bid
Intravenous: 0.5-1 mg/kg/dose, may repeat q8-12h; not to exceed 100 mg/dose

Pediatric

Oral: 1 mg/kg qd, may increase gradually (q3d), not to exceed 3 mg/kg/d
Intravenous: 1 mg/kg/dose, may repeat q8-12h

Interactions

May cause additive ototoxicity with aminoglycosides or cisplatin; increases hypotensive effects of other diuretics or antihypertensives; may cause hypokalemia and increase toxicity of digoxin; may increase anticoagulant effect of warfarin; increases lithium serum levels

Contraindications

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

Precautions

Pregnancy

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

Precautions

Caution with blood dyscrasias, liver, or kidney; monitor electrolytes, calcium, glucose, uric acid, CO₂, creatinine, and BUN levels

Binding resins

These agents promote exchange of potassium for sodium in GI system.

Sodium polystyrene sulfonate (Kayexalate)

Exchanges Na⁺ for K⁺ and binds it in gut, primarily in large intestine, decreasing total body potassium. Onset of action after PO ranges from 2-12 h (longer when administered rectally). Lowers K⁺ over 1-2 h with duration of action of 4-6 h. Potassium level drops by approximately 0.5-1 mEq/L.
Multiple doses usually necessary.

Dosing

Adult

25-50 g mixed with 100 mL of 20% sorbitol PO/PR

Pediatric

1 g/kg/dose PO/PR

Interactions

Magnesium hydroxide, aluminum carbonate, or similar antacids or laxatives may cause systemic alkalosis

Contraindications

Documented hypersensitivity; hypernatremia

Precautions

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

Electrolytes

These agents have been successfully used in the treatment of acute SLOW released oral potassium overdose.

Magnesium sulfate

Nutritional supplement in hyperalimentation; cofactor in enzyme systems involved in neurochemical transmission and muscular excitability. In adults, 60-180 mEq of potassium, 10-30 mEq of magnesium, and 10-40 mmol of phosphate per day may be necessary for optimum metabolic response. Give IV for acute suppression of torsade. Repeat doses are dependent upon continuing presence of patellar reflex and adequate respiratory function.

Dosing

Adult

1-2 g IV over 30-60 s, repeat in 5-15 min if necessary; alternatively, 3-10 mg/min IV infusion

Pediatric

Not established

Interactions

Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade seen with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine

Contraindications

Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis

Precautions

Pregnancy

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

Precautions

Magnesium may alter cardiac conduction leading to heart block in digitalized patients; respiratory rate, deep tendon reflex, and renal function should be monitored when electrolyte is administered parenterally; caution when administering magnesium dose since may produce significant hypotension or asystole; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be given as antidote for clinically significant hypermagnesemia

Follow-up

Further Inpatient Care

• Order continuous cardiac monitoring for patients who are hyperkalemic.
• Definitive therapy is dialysis in patients with renal failure or when pharmacologic therapy is not sufficient. Any patient with significantly elevated potassium levels should undergo dialysis, as pharmacologic therapy alone is not likely to adequately bring down the potassium levels in a timely fashion.
• Monitor serial potassium levels.
• Resolve acid-base problems.
• Correct coexistent electrolyte disturbances.
• Treat digoxin toxicity, if present.

Further Outpatient Care

• Adjust diet to decrease potassium dietary load.
• Adjust medications that predispose to or exacerbate hyperkalemia.
• Repeat potassium level tests in 2-3 days.
• Reevaluate renal function if signs of renal insufficiency are present.

Transfer

• If unable to correct hyperkalemia with pharmacologic therapy and dialysis is unavailable, stabilize the patient and transfer to a center where dialysis can be performed.

Deterrence/Prevention

• Avoid foods high in potassium.
• Avoid medications that predispose to hyperkalemia.

Complications

• Life-threatening cardiac arrhythmias may ensue.
• Hypokalemia may result from the treatment of hyperkalemia.

Prognosis

• Expect full resolution with correction of the underlying etiology.
• Reduction of plasma potassium should begin within the first hour of initiation of treatment.

Patient Education

• Pursue diet modification.
• Discontinue use of medications that may worsen hyperkalemia.
• Encourage adherence to dialysis schedule if patient is noncompliant.

Miscellaneous

Medicolegal Pitfalls

• Ascertain whether the elevated potassium level is real or factitious. In a patient who does not have a predisposition to hyperkalemia, repeat the blood test before any actions are taken to bring down the potassium levels unless ECG changes are present.
• Continuous ECG monitoring is essential if the patient is found to be hyperkalemic.
• An ECG is essential to assess for cardiac conduction disturbances related to hyperkalemia.
• Liability is associated with failure to order the ECG quickly or failure to recognize and treat the condition based on the ECG. Severe hyperkalemia with ECG changes is a life-threatening emergency. Intravenous calcium is the initial treatment of choice to stabilize the cardiac membrane.
• Liability also can result from a delay in instituting definitive therapy after initial successful stabilization of the patient's condition. Medications, such as calcium, insulin, glucose, and sodium bicarbonate, are temporizing measures. Definitive loss of excess potassium can be achieved only with resin-binding agents, dialysis, or increased renal excretion. Begin administration of a resin-binding agent soon after the other drugs have been administered.
• Watch for overcorrection of potassium level.
• Liability may result from failure to adjust therapy for concurrent conditions. For example, in diabetic ketoacidosis (DKA) and in many other types of metabolic acidosis, the extracellular potassium level is elevated, yet the patient may have a total body deficit of potassium. Once the clinician initiates therapy for DKA, the extracellular potassium level decreases spontaneously.
• If the patient is taking digoxin, look for evidence of digitalis toxicity.

Multimedia

Media file 1: Peaked T waves in hyperkalemia.

Media file 2: Peaked T waves in hyperkalemia.

Media file 3: Widened QRS complexes in hyperkalemia.

Media file 4: Widened QRS complexes in a patient whose serum potassium level was 7.8 mEq/L.

Media file 5: ECG of a patient with pretreatment potassium level of 7.8 mEq/L and widened QRS complexes after receiving 1 ampule of calcium chloride. Notice narrowing of QRS complexes and reduction of T waves.

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Keywords

hyperkalemia, high potassium level, electrolyte imbalance, sodium-potassium pump, potassium level greater than 5.5 mEq/L, acute renal failure, chronic renal failure, potassium-sparing diuretics, urinary obstruction, sickle cell disease, Addison disease, systemic lupus erythematosus, SLE, rhabdomyolysis, hemolysis, acidosis, acute digitalis toxicity, beta-blockers toxicity, succinylcholine toxicity, pseudohyperkalemia

Contributor Information and Disclosures

Author

David Garth, MD, Attending Physician, Department of Emergency Medicine, Mary Washington Hospital
David Garth, MD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians
Disclosure: Nothing to disclose.

Medical Editor

Erik D Schraga, MD, Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Howard A Bessen, MD, Professor of Medicine, Department of Emergency Medicine, UCLA School of Medicine; Program Director, Harbor-UCLA Medical Center
Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD, Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of the previous chief editor, Rick Kulkarni, MD, to this article.

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