Fluid and Electrolyte DisorderFluid and Electrolyte DisorderDisorders of PotassiumDisorders of Potassium

施雲娥施雲娥2006.06.142006.06.14Docu

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Potassium is the primary intracellularPotassium is the primary intracellularion in theion in the humunhumun bodybody

Approximately 45~55mEq/kgApproximately 45~55mEq/kg 98% in intracellular98% in intracellular 2% in2% in extracellularextracellular

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Disproportionate distribution of Potassium isDisproportionate distribution of Potassium ismaintained by Namaintained by Na+ -- KK+ - ATPase pump.

Move KK+ into and NaNa+ out of cell Intracellular KK+ concentration：140mEq/L Extracellular KK+ concentration：3.5~5.0mEq/L

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Intracellular PotassiumPotassium：：70% in skeletal muscle.70% in skeletal muscle.30% in liver and red30% in liver and redblood cells.blood cells.

Extracellular PotassiumPotassium：：serum.serum.interstitalinterstital space.space.

Potassium is dynamic. constantly movingPotassium is dynamic. constantly movingaccording bodyaccording body’’s needs.s needs.

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K has many physiologic functions within cells.K has many physiologic functions within cells. IntraIntra-- andand extracellularextracellular fluid K concentrationsfluid K concentrations

influences cell membrane polarization.influences cell membrane polarization. Influences cell processes, such as the conductionInfluences cell processes, such as the conduction

of nerve impulses and muscle (includingof nerve impulses and muscle (includingmyocardial) cell contraction.myocardial) cell contraction.

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Control of Potassium HomeostasisControl of Potassium Homeostasis

Dietary intake and gastrointestinalDietary intake and gastrointestinalexcretionexcretion

Urinary excretionUrinary excretion HormonesHormones AcidAcid--base balancebase balance Body fluid tonicityBody fluid tonicity

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Dietary intake and Gastrointestinal excretionDietary intake and Gastrointestinal excretion

Potassium is abundance in fruits, vegetable, andPotassium is abundance in fruits, vegetable, andmeats.meats.

Dietary intake of K normally varies between 40Dietary intake of K normally varies between 40and 150and 150 mEqmEq/day./day.

Fecal losses are relatively constant and smallFecal losses are relatively constant and small(roughly 10% of intake).(roughly 10% of intake).

Eliminated in feces increases with diarrhea orEliminated in feces increases with diarrhea orunderingundering chronic kidney disease.chronic kidney disease.Docu

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Urinary excretionUrinary excretion

Kidney is the primary route of potassiumKidney is the primary route of potassiumelimination.elimination.

Determined by distal tubular potassiumDetermined by distal tubular potassiumsecretion in the principal cells of corticalsecretion in the principal cells of corticalcollecting duct.collecting duct.

Normal daily potassium excreted 40 to 90Normal daily potassium excreted 40 to 90mEqmEq/L in urine./L in urine.

Vary based onVary based on dietydiety intake,potassiumintake,potassium conc.,andconc.,andaldosteronealdosterone activity.activity.Docu

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HormonesHormones

The most important is insulinThe most important is insulin：：stimulates Nastimulates Na+ --KK+ - ATPase pump to increase cellularpotassium uptake in the liver,muscle, andadipose tissue.

Catecholamines ：：stimulatesstimulates ß--receptorreceptoractivates Naactivates Na+ -- KK+ - ATPase pump and stimulateglycogenolysis.

Aldosterone ：：promotes potassium excretionpromotes potassium excretionthrough kidney.through kidney.Docu

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AcidAcid--base balancebase balance

Acute metabolic acidosis promotes theAcute metabolic acidosis promotes themovement of K out of cells into the ECF.movement of K out of cells into the ECF.

metabolic acidosis due to accumulation ofmetabolic acidosis due to accumulation oforganic acids does not causeorganic acids does not cause hyperkalemiahyperkalemia

Acute metabolic alkalosis promotes the transferAcute metabolic alkalosis promotes the transferof K in the opposite direction.of K in the opposite direction.

Acute respiratory acidosis and alkalosis appearAcute respiratory acidosis and alkalosis appearto have less of an effect on plasma Kto have less of an effect on plasma Kconcentration .concentration .Docu

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AcidAcid--base balancebase balance

In inorganicIn inorganic acidosis.plasmaacidosis.plasma potassiumpotassiumconcentration increase by 0.6 to 0.8concentration increase by 0.6 to 0.8mEqmEq/L per 0.1 U decrease in PH./L per 0.1 U decrease in PH.

In metabolic alkalosis decreases plasmaIn metabolic alkalosis decreases plasmapotassium concentration 0.6potassium concentration 0.6 mEqmEq/L for/L foreach 0.1 U PH increment.each 0.1 U PH increment.

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Body fluid tonicityBody fluid tonicity

HyperosmolalityHyperosmolality enhanced movement ofenhanced movement ofpotassium from cell intopotassium from cell into extracellularextracellular fluid.fluid.

Most commonly in diabeticMost commonly in diabetic ketoacidosisketoacidosis.. HypoHypo--osmolalityosmolality does not affect potassiumdoes not affect potassium

distribution.distribution.

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HypokalemiaHypokalemia

HypokalemiaHypokalemia is defined as a potassiumis defined as a potassiumlevel less than 3.5level less than 3.5 mEqmEq/L./L.

MildMild hypokalemiahypokalemia is a serum level of 3is a serum level of 3--3.53.5mEqmEq/L./L.

ModerateModerate hypokalemiahypokalemia is serum level ofis serum level of2.52.5--33 mEqmEq/L./L.

SevereSevere hypokalemiahypokalemia is defined as a levelis defined as a levelless than 2.5less than 2.5 mEqmEq/L./L.Docu

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Etiology and PathogenesisEtiology and Pathogenesis

Decreased intake of K .Decreased intake of K . Excessive losses of K in the urine ,fromExcessive losses of K in the urine ,from

the GI tract or skin.the GI tract or skin. TranscellularTranscellular shift of K into cells .shift of K into cells .

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GI lossesGI losses1.Vomiting or1.Vomiting or nasogastricnasogastric suctioningsuctioning2.Diarrhea2.Diarrhea3.Enemas or laxative use3.Enemas or laxative use

Renal lossesRenal losses1.Thiazide and loop diuretics1.Thiazide and loop diuretics2.Renal tubular acidosis2.Renal tubular acidosis3.Hyperaldosteronism3.Hyperaldosteronism4.Magnesium depletion4.Magnesium depletionDocu

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TranscellularTranscellular shift of K into cellsshift of K into cells

GlycogenesisGlycogenesis during TPN or afterduring TPN or afteradministration of insulin.administration of insulin.

Stress-induced Catecholamine release andadministration ß22--agonistsagonists

Metabolic alkalosisMetabolic alkalosis Anabolic stateAnabolic state

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Mechanism of DrugMechanism of Drug--inducedinduced hypokalemiahypokalemia

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SYMPTOMSSYMPTOMS

Symptoms are highly dependent on theSymptoms are highly dependent on thedegree ofdegree of hypokalemiahypokalemia and rapidity ofand rapidity ofonset.onset.

MildMild hypokalemiahypokalemia is often asymptomatic.is often asymptomatic. ModerateModerate hypokalemiahypokalemia isis assciatedassciated withwith

cramping, weakness, malaise, andcramping, weakness, malaise, and myalgiasmyalgias.. SevereSevere hypokalemiahypokalemia is associated withis associated with

cardiac arrhythmias.cardiac arrhythmias.DocuCom

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SIGNSSIGNS

CardiovascularCardiovascular：：Essential hypertensionEssential hypertensionand ECGand ECG changes.(STchanges.(ST--segment depressionsegment depressionoror flattening,Tflattening,T--wave inversion, and Uwave inversion, and U--wavewaveelevation). arrhythmias .elevation). arrhythmias .

MusculoskeletalMusculoskeletal：：Cramping and impairedCramping and impairedmuscle contraction.muscle contraction.

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GENERAL APPROACH TO THERAPYGENERAL APPROACH TO THERAPY

Serum potassium 3.5Serum potassium 3.5--44 mEqmEq/L are sign of early/L are sign of earlypotassiumpotassium depletion.Nodepletion.No pharmacologicpharmacologictherapy.increasetherapy.increase dietary of potassiumdietary of potassium--rich foods.rich foods.

Serum potassium 3Serum potassium 3--3.53.5 mEqmEq/L are still/L are still debabledebablewhether pharmacologicwhether pharmacologic therapy.buttherapy.but oral Koral Ksupplementation is indicated in ptsupplementation is indicated in pt’’withwith underingunderingcardiac conditions or concomitantcardiac conditions or concomitant digoxindigoxin therapy.therapy.

Serum potassium below 3Serum potassium below 3 mEqmEq/L should be treated to/L should be treated toachieve values>4achieve values>4 mEqmEq/L./L.Docu

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NONPHARMACOLOGIC THERAPYNONPHARMACOLOGIC THERAPY

Best and most abundant source ofBest and most abundant source ofpotassium comes from dietarypotassium comes from dietary sources.insources.inparticular fresh fruits and vegetables, fruitparticular fresh fruits and vegetables, fruitjuices, and meats.juices, and meats.

Salt substitutes are another effective,Salt substitutes are another effective,inexpensive source of potassium.inexpensive source of potassium.

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Foods That Are High in PotassiumFoods That Are High in Potassium

Highest content(>1000 mg/100g)Highest content(>1000 mg/100g)Dried figsDried figsMolassesMolasses

Very high content(>500 mg/100g)Very high content(>500 mg/100g)Dried fruits (Dried fruits (dates,prunesdates,prunes))NutsNutsAvocadosAvocadosBran cerealsBran cerealsLima beansLima beans

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Foods That Are High in PotassiumFoods That Are High in Potassium

high content(>250 mg/100g)high content(>250 mg/100g)VegetablesVegetables：：Spinach, Tomatoes, Broccoli,Spinach, Tomatoes, Broccoli,

Squash, Beets, Cauliflower,Squash, Beets, Cauliflower,Carrots, PotatoesCarrots, Potatoes

FruitsFruits：：BabanasBabanas, Cantaloupe, Kiwi, Oranges,, Cantaloupe, Kiwi, Oranges,MangosMangos

MeatsMeats：：Ground beef, Steak, pork, Lamb, VealGround beef, Steak, pork, Lamb, VealDocuCom

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PHARMACOLOGIC THERAPYPHARMACOLOGIC THERAPY

Five factors must be consideredFive factors must be considered：：(1)the patient(1)the patient’’s normal baseline potassium conc.s normal baseline potassium conc.(2)underlying medical conditions that may affect(2)underlying medical conditions that may affect

potassium balance.potassium balance.(3)concomitant medications that may affect(3)concomitant medications that may affect

potassium balance.potassium balance.(4)the patient(4)the patient’’s dietary and salt intake.s dietary and salt intake.(5)the patient(5)the patient’’s ability to comply with thes ability to comply with the

therapeutic regimen.therapeutic regimen.DocuCom

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General rule for potassium replacementGeneral rule for potassium replacement

11 mEqmEq/L fall in serum potassium from 4 to 3/L fall in serum potassium from 4 to 3mEqmEq/L represents a total body deficit of/L represents a total body deficit ofapproximately 200approximately 200 mEqmEq..

When the serum potassium fallsWhen the serum potassium falls belowsbelows 33mEq/L,themEq/L,the total body deficit increases by 200 tototal body deficit increases by 200 to400400 mEqmEq for each 1for each 1 mEqmEq/L reduction in serum/L reduction in serumconcentration.concentration.

Total daily dose should be divided into3Total daily dose should be divided into3--4 doses.4 doses.DocuCom

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Intravenous potassium use should be limitedIntravenous potassium use should be limited

Severe cases ofSevere cases of hypokalemiahypokalemia ( serum conc.( serum conc.< 2.5mEq/L)< 2.5mEq/L)

Patients exhibiting signs and symptoms ofPatients exhibiting signs and symptoms ofhypokalemiahypokalemia such as ECG changes orsuch as ECG changes ormuscle spasms.muscle spasms.

Patients unable to tolerate oral therapy.Patients unable to tolerate oral therapy.

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PrecautionsPrecautions

Do not infuse rapidly.Do not infuse rapidly. High plasma concentrations of potassium mayHigh plasma concentrations of potassium may

cause death due to cardiac depression,cause death due to cardiac depression,arrhythmias, or arrest.arrhythmias, or arrest.

Monitor potassium replacement therapyMonitor potassium replacement therapywhenever possible by continuous or serial ECGwhenever possible by continuous or serial ECG

When concentration >40When concentration >40 mEqmEq/L infused, local/L infused, localpain and phlebitis may occur.pain and phlebitis may occur.Docu

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Potassium should be mixed in salinePotassium should be mixed in saline--containing solutions(e.g.,0.9% or0.45%containing solutions(e.g.,0.9% or0.45%NACL).NACL).

Glucose solutions are not ideal choices forGlucose solutions are not ideal choices foradministeringadministering KClKCl, because subsequent, because subsequentelevation in the patient's plasma insulinelevation in the patient's plasma insulinlevel could result intracellular shifting oflevel could result intracellular shifting ofpotassium.potassium.Docu

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Guidelines for potassium IVGuidelines for potassium IV

1010 to 20to 20 mEqmEq of potassium is diluted in 100 mlof potassium is diluted in 100 ml0.9% NACL for IV0.9% NACL for IV administration.Throughadministration.Through aaperipheral vein over 1 hour.peripheral vein over 1 hour.

In severe case dilute 40 to 60In severe case dilute 40 to 60 mEqmEq in 1000 mlin 1000 ml0.45% NACL and infuse not exceed 400.45% NACL and infuse not exceed 40 mEq/hmEq/hthrough a central intravenous line.through a central intravenous line.

Serum potassium conc. should be monitored.Serum potassium conc. should be monitored. ECG monitoring should mandatory to identifyECG monitoring should mandatory to identify

lifelife--threateningthreatening hyperkalemiahyperkalemia..DocuCom

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ALTERNATIVE THERAPIESALTERNATIVE THERAPIES

SpironolactoneSpironolactone：：initial dose 25initial dose 25--50mg50mg daily.max.dosedaily.max.dose400mg/day.Side effects400mg/day.Side effects：：hyperkalemiahyperkalemia ,,hgynecomastiahgynecomastia , breast tenderness , and impotence in, breast tenderness , and impotence inmen.men.

TriamtereneTriamterene：：starting dose 50 mg twicestarting dose 50 mg twice daily.titrateddaily.titrated toto100mg twice daily. Side effects100mg twice daily. Side effects：：hyperkalemia,sodiumhyperkalemia,sodiumdepletion, and metabolic acidosis.depletion, and metabolic acidosis.

AmilorideAmiloride：： starting dose 5 mg daily.10mg in severestarting dose 5 mg daily.10mg in severehypokalemiahypokalemia. Side effects. Side effects：：hyperkalemiahyperkalemia, and, andmetabolic acidosis.metabolic acidosis.Docu

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HyperkalemiaHyperkalemia

Defined as a potassium level greater thanDefined as a potassium level greater than5.55.5 mEqmEq/L./L.

5.55.5 -- 6.06.0 mEqmEq/L/L -- Mild conditionMild condition 6.16.1 –– 6.96.9 mEqmEq/L/L -- Moderate conditionModerate condition 7.07.0 mEqmEq/L and greater/L and greater -- Severe conditionSevere condition

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EPIDEMIOLOGYEPIDEMIOLOGY

HyperkalemiaHyperkalemia less common thanless common than hypokalemiahypokalemia.. In hospitalized patients has estimated 1.4% toIn hospitalized patients has estimated 1.4% to

10%.10%. MostMost hyperkalemiahyperkalemia are result of overcorrectionare result of overcorrection

ofof hypokalemiahypokalemia with potassiumwith potassium supplimentssuppliments.. SevereSevere hyperkalemiahyperkalemia occurs more commonly inoccurs more commonly in

elderly patients with renal insufficiency whoelderly patients with renal insufficiency whoreceive potassiumreceive potassium supplimentssuppliments..Docu

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Etiology and PathogenesisEtiology and Pathogenesis

IncreasedIncreased potsssiumpotsssium intake.intake. Decreased potassium excretion.Decreased potassium excretion. Tubular unresponsiveness toTubular unresponsiveness to aldosteronealdosterone.. Redistribution of potassium into theRedistribution of potassium into the

extracellularextracellular space.space.

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Excessive endogenous potassium loadExcessive endogenous potassium load

HemolysisHemolysisRhabdomyolysisRhabdomyolysis Internal hemorrhageInternal hemorrhageTumorTumor lysislysis syndromesyndrome

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Excessive exogenous potassium loadExcessive exogenous potassium load

Excess in dietExcess in dietPotassium supplementsPotassium supplements Salt substitutesSalt substitutesOTC herbal productsOTC herbal products

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Diminished potassium excretionDiminished potassium excretion

Renal insufficiency Medication that interferes with urinary excretion:

1.ACE inhibitors and angiotensin receptor blockers2.Potassium-sparing diuretics (e.g. amiloride and

spironolactone)3.NSAIDs such as ibuprofen, naproxen, or celecoxib4.The calcineurin inhibitor immunosuppressants

cyclosporin5.The antibiotic trimethoprim6.The antiparasitic drug pentamidine

Mineralocorticoid deficiency or resistance.DocuCom

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RedistributionRedistribution

Metabolic acidosisMetabolic acidosis Insulin deficiency andInsulin deficiency and hypertonicityhypertonicityBetaBeta--blocker drugsblocker drugsDepolarizing muscle relaxants :Depolarizing muscle relaxants :egeg..

SuccinylcholineSuccinylcholineHyperkalemicHyperkalemic periodic paralysisperiodic paralysis

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Tubular unresponsiveness toTubular unresponsiveness to aldosteronealdosterone

AlterationAlteration aldactonealdactone--binding sitebinding siteSickle cell anemiaSickle cell anemiaSystemic lupusSystemic lupus erythematosuserythematosusAmyloidosisAmyloidosis

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PseudohyperkalemiaPseudohyperkalemia

HemolysisHemolysis (in lab tube) most common(in lab tube) most commonThrombocytosisThrombocytosisLeukocytosisLeukocytosisVenipunctureVenipuncture technique (technique (ieie, ischemic, ischemic

blood draw from prolonged tourniquetblood draw from prolonged tourniquetapplication)application)

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SYMPTOMSSYMPTOMS

Patients may be asymptomatic or reportPatients may be asymptomatic or reportthe following:the following:1.Generalized fatigue1.Generalized fatigue2.Weakness2.Weakness3.Paresthesias3.Paresthesias4.Paralysis4.Paralysis5.Palpitations5.PalpitationsDocu

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SIGNSSIGNS

HyperkalemiaHyperkalemia is usually asymptomatic until cardiacis usually asymptomatic until cardiactoxicity supervenes .ECG changes include :toxicity supervenes .ECG changes include :

Plasma K > 5.5Plasma K > 5.5 mEqmEq/L are shortening of the QT/L are shortening of the QTinterval and tall, symmetric, peaked T wavesinterval and tall, symmetric, peaked T waves

Plasma K > 6.5Plasma K > 6.5 mEqmEq/L widening of the QRS complex,/L widening of the QRS complex,PR interval prolongation, and disappearance of the PPR interval prolongation, and disappearance of the Pwave.wave.

Finally, the QRS complex degenerates into a sine waveFinally, the QRS complex degenerates into a sine wavepattern and ventricularpattern and ventricular asystoleasystole or fibrillation ensues.or fibrillation ensues.Docu

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ElectrocardiographicElectrocardiographic manifestation ofmanifestation of hyperkalemiahyperkalemia

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ECG patterns inECG patterns in hypokalemiahypokalemia and inand in hyperkalemiahyperkalemia

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Therapeutic modalities ofTherapeutic modalities of hyperkalemiahyperkalemia

Agents that antagonize the cardiac effectsAgents that antagonize the cardiac effectsofof hyperkalemiahyperkalemia..

Agents that shift potassium from theAgents that shift potassium from theextracellularextracellular into the intracellular space.into the intracellular space.

Agents that enhance potassium elimination.Agents that enhance potassium elimination.

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Treatment algorithm forTreatment algorithm for hyperkalemiahyperkalemia

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Treatment ofTreatment of hyperkalemiahyperkalemia

MildMild hyperkalemiahyperkalemia (plasma K < 6(plasma K < 6 mEqmEq/L) may/L) maydiminished K intake or discontinuance of drugsdiminished K intake or discontinuance of drugssuch as Ksuch as K--sparing diuretics,sparing diuretics, ß22-- --blockers,blockers,NSAIDsNSAIDs, or ACE inhibitors. Addition of a loop, or ACE inhibitors. Addition of a loopdiuretic can also enhance renal K excretion.diuretic can also enhance renal K excretion.

SeverSever hyperkalemiahyperkalemia or moderateor moderate hyperkalemiahyperkalemiawith clinical symptoms or ECG changes requireswith clinical symptoms or ECG changes requiresimmediate treatment.immediate treatment.Docu

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Treatment ofTreatment of hyperkalemiahyperkalemia

No ECG abnormalities and the plasma K < 6No ECG abnormalities and the plasma K < 6mEqmEq/L . sodium polystyrene/L . sodium polystyrene sulfonatesulfonate ininsorbitolsorbitol can be given orally or rectally by enema.can be given orally or rectally by enema.

About 1About 1 mEqmEq of K is removed per gram of resinof K is removed per gram of resingiven.given.

Onset within 1 hour. can repeated every 4 hours.Onset within 1 hour. can repeated every 4 hours. Oral dose 15 to 60 g SPS in 70%Oral dose 15 to 60 g SPS in 70% sorbitolsorbitol..

retention enema 60 to 100 g SPS in 100 to 200retention enema 60 to 100 g SPS in 100 to 200ml 30%ml 30% sorbitolsorbitol or 10% dextrose.or 10% dextrose.Docu

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Emergency care inEmergency care in hyperkalemiahyperkalemia

IV bolus of 10IV bolus of 10 mLmL 10% calcium10% calcium gluconategluconate overover5 to 10 min.5 to 10 min.

Does not lower potassium but reverseDoes not lower potassium but reversecardiotoxicitycardiotoxicity caused by K+, protecting againstcaused by K+, protecting againstlife threateninglife threatening arrhythmiasarrhythmias..

Reverses ECG changes within minutes.Reverses ECG changes within minutes. Duration 30 to 60 minutes.Duration 30 to 60 minutes. Be repeated as needed based on ECG finding.Be repeated as needed based on ECG finding.Docu

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55 to 10 U regular insulin can be given withto 10 U regular insulin can be given with50 ml of 50% glucose as IV boluses.50 ml of 50% glucose as IV boluses.

Followed by 10% D/W at 50Followed by 10% D/W at 50 mL/hmL/h totoprevent hypoglycemia.prevent hypoglycemia.

InsulinInsulin will lead to a shift of potassiumwill lead to a shift of potassiumions into cells, secondary to increasedions into cells, secondary to increasedactivity of theactivity of the sodiumsodium--potassiumpotassium ATPaseATPasepump.pump.Docu

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SodiumSodium bicarbonatebicarbonate therapy bolus ortherapy bolus orinfusion of 50 to 100infusion of 50 to 100 mEqmEq over 2over 2--5 min.5 min.

Effective in cases of metabolic acidosis.Effective in cases of metabolic acidosis. The sodium bicarbonate raisingThe sodium bicarbonate raising

extracellularextracellular PH.PH. Causing rapid intracellular potassium shift.Causing rapid intracellular potassium shift.

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Inhalation of a highInhalation of a high--dosedose ß --agonist such asagonist such asalbuterolalbuterol (10 to 20 mg) over 10 min (5 mg/(10 to 20 mg) over 10 min (5 mg/mLmLconcentration).orconcentration).or IV (0.5 mg over 15 min)IV (0.5 mg over 15 min)

Onset of action is within 30 min. Duration ofOnset of action is within 30 min. Duration ofeffect is 2 to 4 h.effect is 2 to 4 h.

Stimulates NaStimulates Na+ -- KK+ - ATPase pump andandstimulatesstimulates ß receptors.

Cardiac side effects such as tachycardia. Reserved as adjunctive therapy.Docu

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The definitive treatment ofThe definitive treatment of hyperkalemiahyperkalemia isisremove K from the bodyremove K from the body

Removal of K can be accomplished via the GIRemoval of K can be accomplished via the GItract by administration of sodium polystyrenetract by administration of sodium polystyrenesulfonatesulfonate or byor by hemodialysishemodialysis..

HemodialysisHemodialysis should be instituted promptlyshould be instituted promptlyafter emergency measures in patients with renalafter emergency measures in patients with renalfailure or if emergency treatment is ineffective.failure or if emergency treatment is ineffective.Docu

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LONGLONG--TERM TREATMENTTERM TREATMENT

Treatment of chronic renal failure may include dietaryTreatment of chronic renal failure may include dietarypotassium restriction. "Loop diuretics" may bepotassium restriction. "Loop diuretics" may beprescribed to reduce potassium and fluid levels .prescribed to reduce potassium and fluid levels .

Medications that may causeMedications that may cause hyperkalemiahyperkalemia should beshould bereviewed. These medications may be stopped, reducedreviewed. These medications may be stopped, reducedin dose, or substituted by another medication.in dose, or substituted by another medication.

Salt substitute, often used by people on a low salt diet,Salt substitute, often used by people on a low salt diet,should not be used by those with renal failure or ashould not be used by those with renal failure or ahistory ofhistory of hyperkalemiahyperkalemia..Docu

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ReferenceReference

Applied therapeutics: The clinical use ofApplied therapeutics: The clinical use ofdrugs,8thed,2004drugs,8thed,2004

Pharmacotherapy: APharmacotherapy: A pathophysiologicpathophysiologic approach, 6thapproach, 6thed.,2005ed.,2005

ACS Surgery: Principles& Practice(2006)ACS Surgery: Principles& Practice(2006) HarrisonHarrison’’s Internal Medicines Internal Medicine Current Critical Care Diagnosis &Current Critical Care Diagnosis &

Treatment ,2Treatment ,2ndnd--ED(2003)ED(2003) MD consultMD consult--American Family physician(2004)American Family physician(2004)Docu

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THE ENDTHE END

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