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ACaseofHeartFailure AssociatedHyponatremia China JapanUnionHospital JilinUniversityYangPing杨萍 aman 63yearsoldAwareofhypertensionsince1992 withtheBP170 110mmHg andkeptitaround130 90mmHgbyoraldosesofCandesartanDiagnosedoftype2diabetesmellitussince2002 Glycemiccontrolwassatisfactorythroughprescribedhumulin70 30 Previoushistory1 Previoushistory2 Symptoms Hereferredtothelocalhospitalforchesttightness shortnessofbreath andpalpitationinFeb 2012 UCG LVEF38 3 CAG DiffusevascularstenosisLAD Diffuseinfiltrationwithplaque withalocal65 stenosis LCX Proximal middlesegmentsub occlusion RCA Diffuseinfiltrationwithplaque withalocal40 stenosis A70 stenosisinproximalsegmentofPDA Treatment After2 stentsimplantation circulationimproving cardiacnutritionandtreatmentbasedonthesymptoms clinicalsymptomswereimprovedandhedischarged MainComplains Hereferredtoourdepartmentforchesttightnessandbreathshortnessafteractivity dyspneawhenlying orthopneaandbilaterallowerlimbsedemainAug 2012 Physicalexamination BP 120 90mmHg P 96pulse min BMI 29 3kg m2 lipscyanosis jugularveincongestion diffuseralesoverthelungfields cardiacshadowenlargementmainlyonthelateralside atrialfibrillationrhythm a3 6holosystolicmurmerintheapicalareaandradiatingtothearmpit Severepittingedemaofthelowerlimbs Presenthistory XRayoftheChest Cardio thoracicindex 0 68Hilarshadowdensified ECG Atrialfibrillation ventricularrate 104beats min NotetheQwaves V1 V2 andtheinversedTwaves V4 V6 Relativelylowvoltage LA 48 1mm IVS 11 2mm LVD 56 0mm EF 33 3 Leftventricularmyocardiumwasnotthickening motionabnormality withasignificantlyreduceoftheinferiorwallmovement andtherestoftheleftventricularmyocardiumreducedslightly Pulmonaryarterypressurewashigher withthesystolicpressureupto51 6mmHg Severemitralregurgitation andmoderatetricuspidregurgitation UCG2012 8 7 RBS 8 7mmol L BUN 6 9mmol L Scr 75 4mmol L Na 139 7mmol L K 4 2mmol L BNP 5330pg ml Aug 6 Laboratorydata Diagnosis HypertensionCoronaryheartdiseaseIschemiccardiomyopathytypeCardiacfunctionlevelIVCoronarystentimplantationType2diabetesmellitusDiabeticcardiomyopathy Therapy Intravenoussodiumnitroprussideeveryday 3 6mg h Intermittentusedcedilanid0 2mgiv torasemide20 40mgivSpironolactone20mgqdpo furosemide20mgBidpo perindopril4mgqdpo metoprololsustained releasetablets23 75mgqdpo humulin70 30forbloodglucosecontroling PotassiumcitrateContinuedualantiplatelettherapy Post dischargefollow up1 Heartfailuresymptomswerereleased andhedischargedonAug 20 andcontinuetotakemedicine 7daysafterdischarge hehadchestpain shortofbreathafteractivities dyspneawhenlying severepittingedemaofthelowerlimbs andreadmittedinourhospital Emergenttestofserumfactors K 5 1mmol L Na 133 6mmol L UCG 2012 8 29 EF loweredto18 4 andotherfactorsdidn tchangemuch MetoprololwasdiscontinuedduetoworseningsymptomsofheartfailureafterhospitalizationTheresttherapieswereessentiallythesame Features AggravationofheartfailureDeteriorationofrenalfunction 8 30 Hyponatremia severeedema pleuralandperitonealeffusion Afterduretictreatmentofhypertonicsalineandalbuminsupplements serumsodiumwaselevatedby1 2mmol L andthedailyurineoutputwas800 1000ml beforetreatment 200 400ml However drugresistanceappearedafter2days serumsodiumwasreducedto128mmol L urineoutput400 500mlperday andtherewasseverepittingedemaofthelowerlimbs 1g 10g Serumsodiumprogressivelydecreasedto128 9mmol LTolvaptanpillsorally aselectiveV2receptorantagonist 15mg RecheckedNa 9 22 133 4mmol L Na 9 24 135 2mmol L Urineoutputreachedto1000mlperday Sep20 Sep22 Sep24 Thepatientstoppedtakingdrugsbecauseofeconomicreasons Urineoutputdecreasedafterthat 2012 10 11 illnessgrewworse urineoutputwas200 300ml day andtherewashydrosarcaanasarca TwodaysofCRRT 4000mlliquidwasfilteredout butnoremissionofanasarca andoliguriawasprogressivelywores andevencameanuria The4thdayofCRRT BUN 27 7mmol L Scr 201 0mmol L UA 847mmol L cystatinc 2 33mg L Na 126mmol L Symptomsofchesttightnessanddyspneawereaggravated 2012 10 21 diedofobstinateheartfailure BMIwaslarger andsweatingwasheavier Somesodiumwaslostduetothelong termhigh doseofdiuretics Low saltdietandthegastrointestinaltractcongestionmadethesodiumlessabsorbed RAASactivated AngIIandaldosteronesecretedmore atrialstretchreceptorssensitivityloweredandcausedAVPsecretionincreased thoseallleadtosodiumwaterretention andcontributedtodilutionalhyponatremia FunctionofinactivationADHandaldosteronewasweakenduetothelivercongestionandedemacausedbyCHF Reasonsofhyponatremia Hyponatremiatoheartfailure 1 RBCsareswellingwhenserumsodiumdecreases andcausesbloodstasis whichaggravatestissuehypoxia 2 Plasmacrystalosmoticpressuredecreases watertransfersintothecellsandtissueandreducedtheeffectivecirculatingbloodvolume 3 Whenserumsodium myocardialexcitability thesystolicpowerandtheeffectivecirculatingbloodvolumedecrease renalbloodflowandglomerularfiltrationratedecrease 1receptorofjuxtaglomerularapparatusisisstimulatedandRAASisfinallyactivited Meanwhile lesssodiumforthemaculadensamakesthesensoryreceptormorestimulated andthusactivatetheRAAS Hyponatremiaisacharacteroftheendstageofheartfailure Pancirolietalproposedthathyponatremiawasapredictorofheartfailuremortality Afteranalyzedformorethan30clinical hemodynamicandbiochemistryfactors Leeetalsuggestthatserumsodiumisastrongpredictorofmortality Hyponatremia associatedfactorsofdeatharehypotension shock waterpoisoningencephalopathyandseverearrhythmiaaswell TolvaptanisaselectiveV2receptorantagonistwithanaffinityfortheV2receptorthatis1 8timesthatofnativeAVP Forsingleoraldosesrangingfrom15to60mg tolvaptanhasanadverseeffectofAVP increasestheclearanceoffreewaterandexcretionofurine reducestheurineosmoticpressure andfinallyincreasestheserumsodium OraldosesoftolvaptanincreasesserumsodiuminstageIIIandIVheartfailurepatients Experimentaldataonimprovingtheprognosishasnotbeenannouncedyet 1 Effectivecirculatingbloodvolumedeclinedinashortperiodoftime reducedth
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