AUTHOR INFORMATION

Section 1 of 12

Authored by David Garth, MD, Consulting Staff, Department of Emergency Medicine, Mary Washington Hospital

David Garth, MD, is a member of the following medical societies: American Academy of Emergency Medicine

Edited by Erik D Schraga, MD, Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Howard A Bessen, MD, Professor of Medicine, UCLA School of Medicine; Program Director, Department of Emergency Medicine, Harbor-UCLA Medical Center; John Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess Medical Center; Assistant Professor of Medicine, Harvard Medical School; and Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital

Author's Email:	David Garth, MD
Editor's Email:	Erik D Schraga, MD

eMedicine Journal, February 20 2007, VOLUME 8, Number 2

INTRODUCTION

Section 2 of 12

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. Ranges are as follows:

• 5.5-6.0 mEq/L - Mild condition

• 6.1-7.0 mEq/L - Moderate condition

• 7.0 mEq/L and greater - Severe condition

Hyperkalemia results from the following:

• Decreased or impaired potassium excretion - As observed with acute or chronic renal failure (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, venipuncture, 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:

• In the US: 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.

• The mortality rate can be as high as 67% if severe hyperkalemia is not treated rapidly.

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

CLINICAL

Section 3 of 12

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)

• Medications - Potassium supplements, potassium-sparing diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), beta-blockers, digoxin, succinylcholine, and digitalis glycoside

• 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.

• 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 error

DIFFERENTIALS

Section 4 of 12

Hypocalcemia

Other Problems to be Considered:

Cardiac arrhythmias

WORKUP

Section 5 of 12

Lab Studies:

• Potassium level: The relationship between 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. Rapidity of change in 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 patient with diabetes mellitus

• Digoxin level - If patient is on a digitalis medication

• ABG level - If acidosis is suspected

• Urinalysis - If signs of renal insufficiency 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 Images 1-2).

• 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 Images 3-4).

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

• 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

Section 6 of 12

Prehospital Care: A patient with known hyperkalemia or renal failure with suspected hyperkalemia should have intravenous access established and should be placed on a cardiac monitor. 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 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 the Medication section. 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

Section 7 of 12

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

Drug Category: 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.

Drug Name	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.
Adult Dose	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 Dose	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)
Contraindications	Renal calculi; hypercalcemia; hypophosphatemia; renal or cardiac disease; digitalis toxicity
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
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Caution in digitalized patients, respiratory failure, acidosis, or severe hyperphosphatemia

Drug Category: Antidotes -- Insulin is administered with glucose to facilitate the uptake of glucose into the cell, bringing potassium with it.

Drug Name	Dextrose (D-Glucose) -- Glucose and insulin temporarily shift K+ into cells; effects occur within first 30 min of administration.
Adult Dose	1-2 amps D50W and 5-10 U regular insulin IV
Pediatric Dose	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
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
Interactions	Caution when administering parenteral fluids to patients receiving corticosteroids or corticotropin, especially if solution contains Na+ ions
Pregnancy	C - Safety for use during pregnancy has not been established.
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

Drug Name	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).
Adult Dose	5-10 U regular insulin and 1-2 amps D50W IV bolus
Pediatric Dose	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
Contraindications	Documented hypersensitivity; hypoglycemia
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
Pregnancy	A - Safe in pregnancy
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

Drug Category: 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.

Drug Name	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.
Adult Dose	1 mEq/kg slow IV push or continuous IV drip; not to exceed 50-100 mEq
Pediatric Dose	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
Contraindications	Documented hypersensitivity; alkalosis; hypernatremia; hypocalcemia; severe pulmonary edema
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
Pregnancy	A - Safe in pregnancy
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

Drug Category: Beta2-adrenergic agonists -- These agents promote cellular reuptake of potassium, possibly via the cyclic gAMP receptor cascade.

Drug Name	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.
Adult Dose	5 mg mixed with 3 mL isotonic saline via high-flow nebulizer q20min as tolerated
Pediatric Dose	<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
Contraindications	Documented hypersensitivity
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
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in hyperthyroidism, diabetes mellitus, and cardiovascular disorders

Drug Category: Diuretics -- These agents cause the loss of potassium through the kidney.

Drug Name	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.
Adult Dose	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 Dose	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
Contraindications	Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion
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
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Perform frequent serum electrolyte, CO2, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter

Drug Category: Binding resins -- These agents promote exchange of potassium for sodium in GI system.

Drug Name	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.
Adult Dose	25-50 g mixed with 100 mL of 20% sorbitol PO/PR
Pediatric Dose	1 g/kg/dose PO/PR
Contraindications	Documented hypersensitivity; hypernatremia
Interactions	Magnesium hydroxide, aluminum carbonate, or similar antacids or laxatives may cause systemic alkalosis
Pregnancy	C - Safety for use during pregnancy has not been established.
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

Drug Category: Loop diuretics -- Some diuretics can promote the loss of calcium through the kidney.

Drug Name	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.
Adult Dose	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 Dose	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
Contraindications	Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion
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
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Caution with blood dyscrasias, liver, or kidney; monitor electrolytes, calcium, glucose, uric acid, CO2, creatinine, and BUN levels

Drug Category: Electrolytes -- These agents have been successfully used in the treatment of acute SLOW released oral potassium overdose.

Drug Name	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.
Adult Dose	1-2 g IV over 30-60 s, repeat in 5-15 min if necessary; alternatively, 3-10 mg/min IV infusion
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis
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
Pregnancy	B - Usually safe but benefits must outweigh the risks.
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

Section 8 of 12

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 working.

• 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

Section 9 of 12

Medical/Legal Pitfalls:

• Assess and treat the patient, not the potassium level. Ascertain whether the elevated potassium level is real or factitious.

• 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. Calcium chloride 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.

TEST QUESTIONS

Section 10 of 12

CME Question 1: Which of the following drugs should be administered first to the patient with hyperkalemia and a widened QRS complex on ECG?

A: Calcium chloride
B: Kayexalate
C: Digoxin
D: Furosemide
E: Sodium bicarbonate

The correct answer is A: Calcium (administered as gluconate or chloride) helps to stabilize the cardiac myocyte resting membrane potential. This effect is rapid and may be lifesaving, but it is short-lived; more definitive therapy should be instituted as soon as possible.

CME Question 2: Which of the following scenarios puts the patient at highest risk for complications of hyperkalemia?

A: Acute myocardial infarction with a potassium level of 6.1 mEq/L
B: Renal failure with potassium level of 6.8 mEq/L
C: A patient receiving an intravenous infusion of D5 1/2NS with 40 mEq/L of added KCl who is discovered to have a potassium level of 6.2 mEq/L
D: A patient with diabetic ketoacidosis who has a potassium level of 6.1 mEq/L
E: None of the above

The correct answer is C: The acuity of the rise in extracellular potassium levels affects the likelihood of complications. Patients who are receiving intravenous potassium and are discovered to be hyperkalemic are at especially high risk for complications because they may have experienced an abrupt rise in extracellular potassium.

Pearl Question 1 (T/F): Flattened T waves are the earliest ECG finding in a patient with hyperkalemia.

The correct answer is False: Peaked T waves are one of the earliest ECG manifestations of hyperkalemia. Other early signs of hyperkalemia are a shortened QT interval and ST-segment depression.

Pearl Question 2 (T/F): When the laboratory reports a potassium value of 6.9 mEq/L for a patient with hyperkalemia, the clinician should immediately order therapy following an algorithm based on the absolute level of potassium.

The correct answer is False: In patients with hyperkalemia, the clinician should immediately obtain an ECG to evaluate the underlying cardiac rhythm. The ECG findings help to determine appropriate medical management.

Pearl Question 3 (T/F): Life-threatening arrhythmias almost never are observed until the serum potassium level is greater than 8.0 mEq/L.

The correct answer is False: ECG findings follow a progression that correlates with the potassium level and that invariably leads to fatal arrhythmia at high levels, but potentially life-threatening arrhythmias can occur without warning at almost any level of hyperkalemia.

Pearl Question 4 (T/F): Insulin and glucose cause an absolute loss of potassium from the body.

The correct answer is False: Insulin and glucose temporarily cause potassium to shift from the extracellular environment into the intracellular space.

PICTURES

Section 11 of 12

Caption: Picture 1. Peaked T waves in hyperkalemia.
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Caption: Picture 2. Peaked T waves in hyperkalemia.
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Caption: Picture 3. Widened QRS complexes in hyperkalemia.
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Caption: Picture 4. Widened QRS complexes in a patient whose serum potassium level was 7.8 mEq/L.
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Caption: Picture 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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BIBLIOGRAPHY

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• AHA/ILCOR Guidelines: American Heart Association in Collaboration with the International Liaison Committee on Resuscitation: Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: an international consensus on science. Circulation 2000; 102: I1-I384.
• Allon M, Dunlay R, Copkney C: Nebulized albuterol for acute hyperkalemia in patients on hemodialysis. Ann Intern Med 1989 Mar 15; 110(6): 426-9[Medline].
• Charytan D, Goldfarb DS: Indications for hospitalization of patients with hyperkalemia. Arch Intern Med 2000 Jun 12; 160(11): 1605-11[Medline].
• Commerford PJ, Lloyd EA: Arrhythmias in patients with drug toxicity, electrolyte, and endocrine disturbances. Med Clin North Am 1984 Sep; 68(5): 1051-78[Medline].
• Davey M: Calcium for hyperkalaemia in digoxin toxicity. Emerg Med J 2002 Mar; 19(2): 183[Medline].
• Gennari FJ: Disorders of potassium homeostasis. Hypokalemia and hyperkalemia. Crit Care Clin 2002 Apr; 18(2): 273-88, vi[Medline].
• Hawkins RC: Poor knowledge and faulty thinking regarding hemolysis and potassium elevation. Clin Chem Lab Med 2005; 43(2): 216-20[Medline].
• Kao KC, Huang CC, Tsai YH, et al: Hyperkalemic cardiac arrest successfully reversed by hemodialysis during cardiopulmonary resuscitation: case report. Chang Gung Med J 2000 Sep; 23(9): 555-9[Medline].
• Mandal AK: Hypokalemia and hyperkalemia. Med Clin North Am 1997 May; 81(3): 611-39[Medline].
• Martinez-Vea A, Bardaji A, Garcia C, Oliver JA: Severe hyperkalemia with minimal electrocardiographic manifestations: a report of seven cases. J Electrocardiol 1999 Jan; 32(1): 45-9[Medline].
• Mattu A, Brady WJ, Robinson DA: Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med 2000 Oct; 18(6): 721-9[Medline].
• Mitch WE, Wilcox CS: Disorders of body fluids, sodium and potassium in chronic renal failure. Am J Med 1982 Mar; 72(3): 536-50[Medline].
• Moore ML, Bailey RR: Hyperkalaemia in patients in hospital. N Z Med J 1989 Oct 25; 102(878): 557-8[Medline].
• Nijsten MW, de Smet BJ, Dofferhoff AS: Pseudohyperkalemia and platelet counts. N Engl J Med 1991 Oct 10; 325(15): 1107[Medline].
• Oster JR, Perez GO, Vaamonde CA: Relationship between blood pH and potassium and phosphorus during acute metabolic acidosis. Am J Physiol 1978 Oct; 235(4): F345-51[Medline].
• Perazella MA: Drug-induced hyperkalemia: old culprits and new offenders. Am J Med 2000 Sep; 109(4): 307-14[Medline].
• Pruitt BA, Goodwin CW, Vaughan GM: The metabolic problems of the burn patient. Acta Chir Scand Suppl 1985; 522: 119-39[Medline].
• Ranjit S, Kissoon N, Jayakumar I: Aggressive management of dengue shock syndrome may decrease mortality rate: a suggested protocol. Pediatr Crit Care Med 2005 Jul; 6(4): 412-9[Medline].
• Sacchetti A, Stuccio N, Panebianco P, Torres M: ED hemodialysis for treatment of renal failure emergencies. Am J Emerg Med 1999 May; 17(3): 305-7[Medline].
• Tran HA: Extreme hyperkalemia. South Med J 2005 Jul; 98(7): 729-32[Medline].
• Williams ME: Endocrine crises. Hyperkalemia. Crit Care Clin 1991 Jan; 7(1): 155-74[Medline].
• Wong SL, Maltz HC: Albuterol for the treatment of hyperkalemia. Ann Pharmacother 1999 Jan; 33(1): 103-6[Medline].
• Zull DN: Disorders of potassium metabolism. Emerg Med Clin North Am 1989 Nov; 7(4): 771-94[Medline].

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