美國重癥醫(yī)學(xué)(FCCM)的基礎(chǔ)教程 電解質(zhì)代謝紊亂

ElectrolyteandMetabolic

DisturbancesMET1

?ObjectivesReviewcausesandclinicalmanifestationsofsevereelectrolytedisturbancesOutlineemergentmanagementofelectrolytedisturbancesRecognizeacuteadrenalinsufficiencyandappropriatetreatmentDescribemanagementofseverehyperglycemicsyndromesPrinciplesofElectrolyteDisturbancesImpliesanunderlyingdiseaseprocessTreattheelectrolytechange,butseekthecauseClinicalmanifestationsusuallynotspecifictoaparticularelectrolytechange,e.g.,seizures,arrhythmiasPrinciplesofElectrolyteDisturbancesClinicalmanifestationsdetermineurgencyoftreatment,notlaboratoryvaluesSpeedandmagnitudeofcorrectiondependent

onclinicalcircumstancesFrequentreassessmentofelectrolytesrequiredHypokalemiaEtiology–renalloss,extrarenalloss,transcellularshift,decreasedintakeManifestations–cardiac,neuromuscular,gastrointestinalDeficitpoorlyestimatedbyserumlevelsHypokalemiaTitrateadministrationofK+againstserumlevelandmanifestationsCorrecthypomagnesemiaECGmonitoringwithemergentadministrationAllowablemaximumivdoseperhourcontroversialTreathypokalemiaurgentlyinacidosisHyperkalemiaEtiology–renalfailure,transcellularshifts,celldeath,drugs,pseudohyperkalemiaManifestations–

cardiac,neuromuscularHyperkalemia–TreatmentStopintakeGivecalciumforcardiactoxicityShiftK+intocell–glucose+insulin,NaHCO3,inhaled

-agonistRemovefrombody–diuretics,sodiumpolystyrenesulfonate,

dialysisPediatricConsiderations–

PotassiumReplaceatmaximumivrate<1.0mmol/kg/hr;monitorECGHyperkalemiaECGabnormality:calciumgluconateorchlorideShift:NaHCO3,glucose+insulin,inhaled-agonistsRemoval:diuretic,sodiumpolystyrenesulfonate,dialysisMET9

–?HyponatremiaHypo-osmolarhyponatremiaEuvolemicHypovolemicHypervolemicNormo-orhyperosmolarhyponatremiaPseudohyponatremiaManifestations–neurologic,muscular,gastrointestinalHyponatremia–TreatmentHypovolemic

Na–givenormalsaline,ruleoutadrenalinsufficiencyHypervolemic

Na–increasefreeH2OlossEuvolemichyponatremiaRestrictfreewaterintakeIncreasefreewaterlossNormalorhypertonicsalineCorrectslowlyduetopossibilityofdemyelinatingsyndromesHypernatremiaEtiology–

H2Oloss,

H2Ointake,

NaintakeManifestations–neurologic,muscularH2Odeficit(L)=[0.6

wt(kg)]

[obsNa-1]

140

Hypernatremia–TreatmentProvideintravascularvolumereplacementConsidergivingone-halfoffreeH2OdeficitinitiallyReduceNacautiously:0.5-1.0mmol/L/hrSecondaryneurologicsyndromeswithrapidcorrection

PediatricConsiderations–SodiumHyponatremia–seizures:titrate3%NaCl;usualdose1.5-2.5mmol/kgHypernatremia–calculateH2Odeficitas4mL/kgforeach1mmol/LserumNa>145mmol/LDecreaseserumNanofasterthan0.5mmol/L/hrMET14

?OtherElectrolyteDeficits

Ca,PO4,MgMayproduceseriousbutnonspecificcardiac,neuromuscular,respiratory,andothereffectsAllareprimarilyintracellularions,sodeficitsdifficulttoestimateTitratereplacementagainstclinicalfindings

OtherElectrolyteDisorders

HypocalcemiaCalciumchlorideorgluconateBolus+continuousinfusionHypercalcemiaRehydrationwithnormalsalineLoopdiureticsOtherElectrolyteDisordersHypophosphatemiaReplacementivforlevel<1mg/dL(0.32mmol/L)HypomagnesemiaEmergentadministrationover5–10minsLessurgentadministrationover

10–60minsAcuteAdrenalInsufficiencyNonspecificmanifestationsAbdominalpain,nausea,emesisOrthostatic/refractoryhypotensionLaboratoryfindingsHyponatremia,