Ebook Fluids and electrolytes made incredibly easy (6/E): Part 2

339 17 0
  • Loading ...
1/339 trang
Tải xuống

Thông tin tài liệu

Ngày đăng: 22/01/2020, 20:41

(BQ) Part 2 book Fluids and electrolytes made incredibly easy has contents: Heart failure, respiratory failure, acute pancreatitis, renal failure, heat related health alterations, total parenteral nutrition, when acids and bases tip the balance,... and other contents. Chapter9 Whenphosphorustipsthebalance Justthefacts Inthischapter,you’lllearn: ♦ therolethatphosphorusplaysinthebody ♦ thebody’smechanismsforregulatingphosphorus ♦ waystoassessapatientforaphosphorusimbalance ♦ managementofhypophosphatemiaandhyperphosphatemia Alookatphosphorus Phosphorusistheprimaryanion,ornegativelychargedion,foundinintracellularfluid It’s containedinthebodyasphosphate (Thetwowords—phosphorusandphosphate—are commonlyusedinterchangeably.)About85%ofphosphorusexistsinboneandteeth,combinedin a1:2ratiowithcalcium About14%isinsofttissue,andlessthan1%isinextracellularfluid Whyit’simportant Anessentialelementofallbodytissues,phosphorusisvitaltovariousbodyfunctions Itplaysa crucialroleincellmembraneintegrity(phospholipidsmakeupthecellmembranes);muscle function;neurologicfunction;andthemetabolismofcarbohydrates,fat,andprotein Phosphorusis aprimaryingredientin2,3-diphosphoglycerate(2,3-DPG),acompoundinredbloodcells (RBCs)thatpromotesoxygendeliveryfromRBCstothetissues Phosphorusalsohelpsbufferacidsandbases Itpromotesenergytransfertocellsthroughthe formationofenergy-storingsubstancessuchasadenosinetriphosphate(ATP) It’salsoimportant forwhitebloodcell(WBC)phagocytosisandforplateletfunction Finally,withcalcium, phosphorusisessentialforhealthybonesandteeth Thelowdownonlowphosphoruslevels Normalserumphosphoruslevelsinadultsrangefrom2.5to4.5mg/dl(or1.8to2.6mEq/L) In comparison,thenormalphosphoruslevelinthecellsis100mEq/L Becausephosphorusis locatedprimarilywithinthecells,serumlevelsmaynotalwaysreflectthetotalamountof phosphorusinthebody Forexample,it’simportanttodistinguishbetweenadecreaseinthelevel ofserumphosphate(hypophosphatemia)andadecreaseintotalbodystorageofphosphate (phosphatedeficiency) Howthebodyregulatesphosphorus Thetotalamountofphosphorusinthebodyisrelatedtodietaryintake,hormonalregulation, kidneyexcretion,andtranscellularshifts Foradults,therangefortherecommendeddaily requirementofphosphorusis800to1,200mg Phosphorusisreadilyabsorbedthroughthe gastrointestinal(GI)tract,withtheamountabsorbedproportionaltotheamountingested (See Dietarysourcesofphosphorus.) Dietarysourcesofphosphorus Majordietarysourcesofphosphorusinclude: • dairyproducts,suchasmilkandcheese • driedbeans • eggs • fish • nutsandseeds • organmeats,suchasbrainandliver • poultry • wholegrains(Shutoetal.,2009) Mostingestedphosphorusisabsorbedthroughthejejunum Thekidneysexcreteabout90%of phosphorusastheyregulateserumlevels (TheGItractexcretestherest.)Ifdietaryintakeof phosphorusincreases,thekidneysincreaseexcretiontomaintainnormallevelsofphosphorus A low-phosphorusdietcausesthekidneystoconservephosphorusbyreabsorbingmoreofitinthe proximaltubules BalancingitoutwithPTH Theparathyroidglandcontrolshormonalregulationofphosphoruslevelsbyaffectingtheactivity ofparathyroidhormone(PTH) (SeePTHandphosphorus.)Changesincalciumlevels,rather thanchangesinphosphoruslevels,affectthereleaseofPTH Youmayrecallthatphosphorus balanceiscloselyrelatedtocalciumbalance PTHandphosphorus ThisillustrationshowshowPTHaffectsserumphosphorus(P)levelsbyincreasingphosphorus releasefrombone,increasingphosphorusabsorptionfromtheintestines,anddecreasingphosphorus reabsorptionintherenaltubules Normally,calciumandphosphorushaveaninverserelationship Forinstance,whentheserum calciumlevelislow,thephosphoruslevelishigh Thiscausestheparathyroidglandtorelease PTH,whichcausesanincreaseincalciumandphosphorusresorptionfrombone,raisingboth calciumandphosphoruslevels Phosphorusabsorptionfromtheintestinesalsoincreases (ActivatedvitaminD—calcitriol—alsoenhancesphosphorusabsorptionintheintestines.) Kidneysentertheequation PTHalsoactsonthekidneystoincreaseexcretionofphosphorus TherenaleffectofPTH outweighsitsothereffectsontheserumphosphoruslevel,particularlythatofreturningthe phosphorusleveltonormal ReducedPTHlevelsallowforphosphorusreabsorptionbythe kidneys Asaresult,serumlevelsrise(Connor,2009) Shiftybusiness Certainconditionscausephosphorustomove,orshift,inandoutofcells Insulinmovesnotonly glucosebutalsophosphorusintothecell Alkalosisresultsinthesamekindofphosphorusshift Thoseshiftsaffectserumphosphoruslevels (SeeElderlypatientsatrisk,page170.) Agesandstages Elderlypatientsatrisk Elderlypatientsareparticularlyatriskforalteredelectrolytelevelsfortwomainreasons First,they havealowerratioofleanbodyweighttototalbodyweight,whichplacesthematriskforwater deficit Second,theirthirstresponseisdiminishedandtheirrenalfunctiondecreased,whichmakes maintainingelectrolytebalancemoredifficult Age-relatedrenalchangesincludechangesinrenal bloodflowandglomerularfiltrationrate Medicationscanalsoalterelectrolytelevelsbyaffectingtheabsorptionofphosphate Somakesure youaskelderlypatientsifthey’reusingsuchover-the-countermedicationsasantacids,laxatives, herbs,andteas Hypophosphatemia Hypophosphatemiaoccurswhentheserumphosphoruslevelfallsbelow2.5mg/dl(or1.8 mEq/L) Althoughthisconditiongenerallyindicatesadeficiencyofphosphorus,itcanoccur undervariouscircumstanceswhentotalbodyphosphorusstoresarenormal Severe hypophosphatemiaoccurswhenserumphosphoruslevelsarelessthan1mg/dlandthebody can’tsupportitsenergyneeds Theconditionmayleadtoorganfailure Howithappens Threeunderlyingmechanismscanleadtohypophosphatemia:ashiftofphosphorusfrom extracellularfluidtointracellularfluid,adecreaseinintestinalabsorptionofphosphorus,andan increasedlossofphosphorusthroughthekidneys Somecausesofhypophosphatemiamayinvolve morethanonemechanism Severalfactorsmaycausephosphorustoshiftfromextracellularfluidintothecell Herearethe mostcommoncauses Whenhyperventilationhappens Respiratoryalkalosis,oneofthemostcommoncausesofhypophosphatemia,canstemfroma numberofconditionsthatproducehyperventilation,includingsepsis,alcoholwithdrawal,heat stroke,pain,anxiety,diabeticketoacidosis,hepaticencephalopathy,andacutesalicylate poisoning Althoughthemechanismthatpromptsrespiratoryalkalosistoinducehypophosphatemia isunknown,theresponseisashiftofphosphorusintothecellsandaresultingdecreaseinserum phosphoruslevels Sugarhigh Hyperglycemia,anelevatedserumglucoselevel,causesthereleaseofinsulin,whichtransports glucoseandphosphorusintothecells Thesameeffectmayoccurinapatientwithdiabeteswho’s receivinginsulinorinasignificantlymalnourishedpatient;atparticularriskformalnourishment areelderly,debilitated,oralcoholicpatientsandthosewithanorexianervosa Failuretoaddphosphorus Afterinitiationofenteralorparenteralfeedingwithoutsufficientphosphorussupplementation, phosphorusshiftsintothecells Thisshift—calledrefeedingsyndrome—usuallyoccurs3ormore daysafterfeedingsbegin Patientsrecoveringfromhypothermiacanalsodevelop hypophosphatemiaasphosphorusmovesintothecells Abnormalabsorption Malabsorptionsyndromes,starvation,andprolongedorexcessiveuseofphosphorus-binding antacidsorsucralfateareamongthemanycausesofimpairedintestinalabsorptionofphosphorus BecausevitaminDcontributestointestinalabsorptionofphosphorus,inadequatevitaminDintake orsynthesiscaninhibitphosphorusabsorption Chronicdiarrheaorlaxativeabusecanalsoresult inincreasedGIlossofphosphorus Decreaseddietaryintakerarelycauseshypophosphatemia becausephosphateisfoundinmostfoods Callingthekidneystoaccount Diureticuseisthemostcommoncauseofphosphoruslossthroughthekidneys Thiazides,loop diuretics,andacetazolamidearethediureticsthatmostcommonlycausehypophosphatemia (See Drugsassociatedwithhypophosphatemia.) Drugsassociatedwithhypophosphatemia Thefollowingdrugsarecommonlyassociatedwithhypophosphatemia: • acetazolamide,thiazidediuretics(chlorothiazideandhydrochlorothiazide),loopdiuretics (bumetanideandfurosemide),andotherdiuretics • antacids,suchasaluminumcarbonate,aluminumhydroxide,calciumcarbonate,andmagnesiumoxide • insulin • laxatives Thesecondmostcommoncauseisdiabeticketoacidosis(DKA)indiabeticpatientswhohave poorlycontrolledbloodglucoselevels InDKA,highglucoselevelsinduceanosmoticdiuresis Thisresultsinasignificantlossofphosphorusfromthekidneys Ethanolaffectsphosphorus reabsorptioninthekidneyssothatmorephosphorusisexcretedinurine AbuildupofPTH,whichoccurswithhyperparathyroidismandhypocalcemia,alsoleadsto hypophosphatemiabecausePTHstimulatesthekidneystoexcretephosphate Finally, hypophosphatemiaoccursinpatientswhohaveextensiveburns Althoughthemechanismis unclear,theconditionseemstooccurinresponsetotheextensivediuresisofsaltandwaterthat typicallyoccursduringthefirst2to4daysafteraburninjury Respiratoryalkalosisand carbohydrateadministrationmayalsoplayarolehere Whattolookfor Mildtomoderatehypophosphatemiadoesn’tusuallycausesymptoms Noticeableeffectsof hypophosphatemiatypicallyoccuronlyinseverecases Thecharacteristicsofsevere hypophosphatemiaareapparentinmanyorgansystems Signsandsymptomsmaydevelopacutely becauseofrapiddecreasesinphosphorusorgraduallyastheresultofslow,chronicdecreasesin phosphorus Hypophosphatemiaaffectsthemusculoskeletal,centralnervous,cardiac,andhematologic systems Becausephosphorusisrequiredtomakehigh-energyATP,manyofthesignsand symptomsofhypophosphatemiaarerelatedtolowenergystores Weakandweary Withhypophosphatemia,muscleweaknessisthemostcommonsymptom Othersymptomsmay includediplopia(doublevision),malaise,andanorexia Thepatientmayexperienceaweakened handgrasp,slurredspeech,ordysphagia Healsomaydevelopmyalgia(tendernessorpaininthe muscles) Respiratoryfailuremayresultfromweakenedrespiratorymusclesandpoorcontractilityofthe diaphragm Respirationsmayappearshallowandineffective Inlaterstages,thepatientmaybe cyanotic Keepinmindthatitmaybedifficulttoweanamechanicallyventilatedpatientwith hypophosphatemiafromtheventilator Withseverehypophosphatemia,rhabdomyolysis(skeletalmuscledestruction)canoccurwith alteredmusclecellactivity Muscleenzymessuchascreatinekinasearereleasedfromthecells intotheextracellularfluid Lossofbonedensity,osteomalacia(softeningofthebones),andbone painmayalsooccurwithprolongedhypophosphatemia Fracturescanresult Logicalneurologiceffects Withoutenoughphosphorus,thebodycan’tmakeenoughATP,acornerstoneofenergymetabolism Asaresult,centralnervoussystemcellscanmalfunction,causingparesthesia,irritability, apprehension,memoryloss,andconfusion Theneurologiceffectsofhypophosphatemiamay progresstoseizuresorcoma Whentheheartisn’thardy Theheart’scontractilitydecreasesbecauseoflowenergystoresofATP Asaresult,thepatient maydevelophypotensionandlowcardiacoutput Severehypophosphatemiamayleadto cardiomyopathy,whichtreatmentcanreverse Oxygendeliverydrop-off Adropinproductionof2,3-DPGcausesadecreaseinoxygendeliverytotissues Because hemoglobinhasastrongeraffinityforoxygenthanforothergases,oxygenislesslikelytobegiven uptothetissuesasitcirculatesthroughthebody Asaresult,lessoxygenisdeliveredtothe myocardium,whichcancausechestpain Hypophosphatemiamayalsocausehemolyticanemiabecauseofchangesinthestructureand functionofRBCs Patientswithhypophosphatemiaaremoresusceptibletoinfectionbecauseof theeffectoflowlevelsofATPinWBCs LackofATPresultsinadecreasedfunctioningof leukocytes Chronichypophosphatemiaalsoaffectsplateletfunction,resultinginbruisingand bleeding,particularlymildGIbleeding Whattestsshow Thesediagnostictestresultsmayindicatehypophosphatemiaorarelatedcondition: • serumphosphorusleveloflessthan2.5mg/dl(or1.8mEq/L);severehypophosphatemia,less than1mg/dl • elevatedcreatinekinaselevelifrhabdomyolysisispresent • X-raystudiesthatrevealtheskeletalchangestypicalofosteomalaciaorbonefractures • abnormalelectrolytes(decreasedmagnesiumlevelsandincreasedcalciumlevels) Howit’streated Treatmentvarieswiththeseverityandcauseofthecondition Itincludestreatingtheunderlying causeandcorrectingtheimbalancewithphosphorusreplacementandahigh-phosphorusdiet The routeofreplacementtherapydependsontheseverityoftheimbalance Mildermeasures Treatmentformildtomoderatehypophosphatemiaincludesadiethighinphosphorus-richfoods, suchaseggs,nuts,wholegrains,organmeats,fish,poultry,andmilkproducts However,if calciumiscontraindicatedorthepatientcan’ttoleratemilk,heshouldinsteadreceiveoral phosphorussupplements OralsupplementsincludeNeutra-PhosandNeutra-Phos-Kandcanbe usedformoderatehypophosphatemia Dosagelimitationsarerelatedtotheadverseeffects,most notablynauseaanddiarrhea (SeeWhendietarychangesaren’tworking.) It’snotworking Whendietarychangesaren’tworking Ifyourpatient’sphosphorus-richdiethasn’traisedserumphosphoruslevelsasyouhadhoped,it’s timetoaskthesequestions: • IsaGIproblemmakingphosphorusdigestiondifficult? • Isyourpatientusingaphosphate-bindingantacid? • Isyourpatientabusingalcohol? • Isyourpatientusingathiazidediuretic? • Isyourpatientcomplyingwiththetreatmentregimenfordiabetes? Sternersteps ForpatientswithseverehypophosphatemiaoranonfunctioningGItract,I.V phosphorus replacementistherecommendedchoice Twopreparationsareused:I.V potassiumphosphateand I.V sodiumphosphate Dosageisguidedbythepatient’sresponsetotreatmentandserum phosphoruslevels Potassiumphosphaterequiresslowadministration(nomorethan10mEq/hour) Adverse effectsofI.V replacementforhypophosphatemiaincludehyperphosphatemiaandhypocalcemia Howyouintervene Ifyourpatientbeginstotalparenteralnutritionorisotherwiseatriskfordeveloping hypophosphatemia,monitorhimforsignsandsymptomsofthisimbalance Ifthepatienthas alreadydevelopedhypophosphatemia,yournursingcareshouldfocusoncarefulmonitoring, safetymeasures,andinterventionstorestorenormalserumphosphoruslevels (SeeTeaching F First-degreeburns,317 Fluidaccumulationphaseofburns,320–322 Fluidandelectrolytebalance diureticsand,30,31i drugeffects,31i I.V fluideffects,30 kidneyregulation,28,29i organandglandinvolvement,27 Fluidbalance,3–20 measurement,61 mechanismtomaintain,11–18 Fluidcompartments,5i Fluidoverload,inI.V therapy,345 Fluidremobilizationphaseofburns,322 Fluidreplacementformula,burnpatients,324 Fluidvolume,55–62 cuffmeasurement,55–58,56i Fluids seealsoFluidandelectrolytebalance agingeffects,6,12 balancing,3–20 insensiblelosses,3 movement withinthecells,8 throughcapillaries,10i withinthevascularsystem,10 reabsorption,10 sensiblelosses,4 sitesinvolvedinloss,4i solutemovementand,27 types,6–8 Fourth-degreeburns,317 G Gallstones,acutepancreatitisand,284–285,286t GIfluidloss,272–281 adolescents,275 causes,272 diagnosis,276 documentation,278 imbalancescausedby,273 nursingintervention,277–278 signsandsymptoms,276 teachingpatients,277 treatment,277 Glomerularfiltrationrate(GFR),12,302–303 H Heart,roleinfluidandelectrolytebalance,27 Heartfailure,248–261 advanced,255 causes,249,253–254 compensatoryresponses,250–251 diagnosis,255 documentation,257 drugsusedin,256–257 imbalancescausedby,252–253 left-sided,250i,254 nursingintervention,257–258 right-sided,251i,254–255 signsandsymptoms,254 surgery,257 teachingpatients,258 treatment,255–256 Heartrate,248 Heatcramps,237,241 Heatexhaustion,237,242 Heatrash,237,241 Heat-relatedhealthalterations,235–247 age-relatedrisks,240,241 diagnosis,240 documentation,244 drugsthatcause,237 nursingintervention,243 prevention,244 risks,238–239 signsandsymptoms,238,239t teachingpatients,244 treatment,241–242 types,237–238 Heatstroke,238,242 Heatsyncope,238,242 Hydrostaticpressure,10 Hyperactivedeeptendonreflexes(DTRs) grading,132i hypomagnesemiaand,128,131 Hypercalcemia,157–162 causes,157–159 dangersigns,160 diagnosis,160 documentation,162 drugsassociatedwith,159 nursingintervention,161–162 signsandsymptoms,159–160 teachingpatients,162 treatment,160–161 whentreatmentdoesn’twork,161 Hyperchloremia,193–197 causes,193 diagnosis,194 diuretics,194 drugsassociatedwith,193 nursingintervention,196 signsandsymptoms,194 teachingpatients,196 treatment,194–195 Hyperchloremicmetabolicacidosis,aniongapand,195i Hyperglycemia,hypophosphatemiaand,170 Hyperkalemia,114–120 inburnpatients,321 calciumchlorideorcalciumgluconate,118 causes,114–115 diagnosis,116–117,116i diet,120 documentation,120 drugsassociatedwith,115 elderlypatients,115 emergencytreatment,309 heartfailureand,253 intervention,118–119 prematureinfants,115 renalfailureand,303–304,309 respiratoryfailureand,263 signsandsymptoms,116 teachingpatients,120 treatment,117 Hypermagnesemia,136–143 causes,136–138 diagnosis,139 documentation,142 drugsandsupplementsassociatedwith,138 nursinginterventions,140–142 renalfailureand,303–305 signsandsymptoms,138–139,139t teachingpatients,141 treatment,139–140 Hypernatremia,94–99 inburnpatients,322 causes,94–95 diagnosis,98 documentation,99 drugsassociatedwith,97t elderlypatients,96 excessivesodiumintake,96–97 fluidmovementin,95 nursinginterventions,98–99 renalfailureand,303–304 signsandsymptoms,97–98 teachingpatients,99 treatment,98 waterdeficit,96 Hyperphosphatemia,175–181 calcification,177,178i causes,176–177 cow’smilkand,177 diagnosis,178 documentation,181 drugsassociatedwith,177 nursingintervention,180 renalfailureand,303–304 signsandsymptoms,177 teachingpatients,180 treatment,178–179 Hyperthermia,239t Hypertonicdehydration,62 Hypertonicfluids,7,7i Hypertonicsolutions,336,337i,339–340t Hyperventilation carbondioxideand,42i hypophosphatemiaand,170 respiratoryalkalosisand,210 Hypervolemia,71–77 inburnpatients,322 CRRT,75,75i diagnosis,73 documentation,77 edema,72–73 heartfailureand,252 nursingcare,76 renalfailureand,303–304 respiratoryfailureand,263 signsandsymptoms,72–73 teachingpatients,76 treatment,74–75 Hypervolemichyponatremia,89 Hypoalbuminemia,acutepancreatitisand,287 Hypocalcemia,150–157 acutepancreatitisand,287 inburnpatients,322 causes,150–152 diagnosis,153–154,154i documentation,157 drugsassociatedwith,152 elderlypatients,151 I.V administrationofcalcium,156i signsandsymptoms,153 teachingpatients,157 treatmentandinterventions,154–155 Hypochloremia,188–192 causes,188–190,189i diagnosis,191 documentation,192 drugsassociatedwith,189 excessiveGIfluidloss,273 nursingintervention,191–192 signsandsymptoms,190 teachingpatients,192 treatment,191 Hypochloremicalkalosis,189,189i infants,190 Hypokalemia,108–114 acutepancreatitisand,287 inburnpatients,322 commoncauses,108–109 dangersigns,110 diagnosis,110,110i diet,120 disordersassociatedwith,109 documentation,120 drugsassociatedwith,109 elderlypatients,108 excessiveGIfluidloss,273 heartfailureand,253 monitoringandintervention,111–112 renalfailureand,303–304 respiratoryfailureand,263 signsandsymptoms,109–110,240 teachingpatients,120 whentreatmentdoesn’twork,112 Hypomagnesemia,128–137 acutepancreatitisand,287 alcoholismand,129 causes,128–130 diagnosis,134 documentation,137 drugsassociatedwith,130 excessiveGIfluidloss,273 heartfailureand,253 identificationof,131 signsandsymptoms,130–134 teachingpatients,136 treatmentandintervention,134–135 Hyponatremia,87–94 acutepancreatitisand,287 inburnpatients,321,322 causes,88 criticalsteps,93 diagnosis,92 documenting,99 drugsassociatedwith,89t excessiveGIfluidloss,273 fluidmovementin,88i heartfailureand,252–253 hypervolemic,89 hypovolemic,89 isovolemic(dilutional),90 nursinginterventions,93 renalfailureand,303–305 signsandsymptoms,91–92,240 teachingpatients,99 treatment,92–93 Hypophosphatemia,169–175 causes,170 diagnosis,173 documentation,175 drugsassociatedwith,171 elderlypatients,170 malabsorptionsyndromesand,170–171 nursingintervention,173–174 signsandsymptoms,171–172 teachingpatients,174 treatment,173 Hypotonicdehydration,62 Hypotonicfluids,7,7i Hypotonicsolutions,337,337i,339t Hypoventilation,207 Hypovolemia,65–71 acutepancreatitisand,286–287 inburnpatients,320,321 causes,66 dangersigns,68t diagnosis,68 documentation,71 excessiveGIfluidloss,273 heartfailureand,252 nursingresponsibilities,69–70 renalfailureand,303–304 respiratoryfailureand,263 signsandsymptoms,67 teachingpatients,70 treatment,68–69 Hypovolemichyponatremia,89 Hypovolemicshock,67–68 hemodynamicvaluesin,70 Hypoxia,respiratoryalkalosisand,210 I Infants seealsoPediatricpatients;Prematureinfants respiratoryacidosis,205 Infection,inI.V therapy,343 Infiltration,inI.V therapy,343 Insensiblefluidlosses,3 Intracellularfluids(ICF),4,5i Intrapulmonaryshunting,263i Intravenousfluids(I.V.) comparingfluidtoxicity,337i complications,343–346 components,32t deliverymethods,338–343 documentation,347 effectsonfluidandelectrolytebalance,30 nursingintervention,346–347 replacement,335–351 severedcatheter,344 teachingpatients,347 tubingsystems,342–343 typesofsolutions,336–338(seealsospecifictype) Ions,21,22i Isotonicdehydration,62 Isotonicfluid,6,6i Isotonicsolutions,336,337i,339t Isovolemichyponatremia(dilutional),90 I.V seeIntravenousfluids J Juxtaglomerularcells,13 K Kidneys seealsoRenalfailure acid-baseregulationand,40,42–44 hyperphosphatemiaand,176 hypophosphatemiaand,171 roleinfluidandelectrolytebalance,28,29i roleinfluidbalance,11–12 Kussmaul’srespirations,metabolicacidosisand,217 L LactatedRinger’ssolution,electrolytecontent,32t Lacticacidosis,219i heartfailureand,253 Laxatives,excessiveGIfluidlossand,274 Lipidemulsions adversereactionsto,355t inTPN,355 Lipids,componentofTPNsolutions,353 Lund-Browderclassification,inestimatingextentofburns,319i M Magnesium,125–146 absorptionproblems,129 dangersignsoflowlevels,128 dietarysources,127i functions,23,25 gaugingstatuswithpatellarreflex,141i GIproblems,129 levels,126 levelsatdifferentages,126 regulation,127 urinaryproblems,129 Magnesiumsulfate infusion,136 injection,134 preventingmedicationerrors,136 Majorburns,318 Metabolicacidosis,214–221 inburnpatients,322 causes,215,216–217i diagnosis,218 documentation,221 dopamineand,220 excessiveGIfluidloss,273 nursinginterventions,220–221 renalfailureand,303–305 respiratoryfailureand,265 signsandsymptoms,217–218 teachingpatients,221 treatment,219–220 Metabolicalkalosis,222–227 causes,222–223,223–224i diagnosis,225 documentation,227 drugsassociatedwith,224 excessiveGIfluidloss,273 nursingintervention,226–227 renalfailureand,303–305 signsandsymptoms,225 teachingpatients,227 treatment,226 Micronutrients,componentofTPNsolutions,353 Minorburns,318 Moderateburns,318 ModifiedParklandformula,324 Multiorgansystemfailure(MOSF),inacutepancreatitis,289–290 Myoglobin,inburnpatients,321 N Necrotizingpancreatitis,284 O Oliguric-anuricphase,renalfailure,302 Osmosis,9i P Pancreas,functions,283 Pancreatitis acute,282–299 causes,284–285,286t complications,288t diagnosis,288–289 documentation,296 edematousvs necrotizing,284 imbalancescausedby,286–287 nursingintervention,293–295 painrelief,292 severityscoring,289 signsandsymptoms,287 teachingpatients,294 treatment,290–293 chronic,285 Parathyroidhormone(PTH) calciumlevelsand,148 hyperphosphatemiaand,176 hypophosphatemiaand,171 phosphorusand,168,169i Partialpressureofcarbondioxideinarterialblood,44 Partialpressureofoxygeninarterialblood,44 Patellarreflex,testsformagnesiumlevels,141i Pediatricpatients dehydrationand,63 estimatingextentofburns,319i excessiveGIfluidlossand,275 hyperkalemia,115 hypernatremia,96 hypochloremicalkalosisininfants,190 hypokalemia,108 PeripheralI.V therapy,340–341 Peripheralparenteralnutrition(PPN),354 pH arterialblood,45 normal,38i understandingof,37–39 Phlebitis,inI.V therapy,344 Phosphate seePhosphorus Phosphatebuffersystem,41 Phosphorus,167–185 calciumlevelsand,149 dietarysources,168 functions,23,25 parathyroidhormoneand,168,169i regulation,168–169 Plasmacolloidosmoticpressure,11 Potassium,105–124 dietarysources,107 drugsassociatedwithdepletion,109 functions,23,25 guidelinesforadministration,113 regulation,107 roleinacid-basebalance,106i Preload(volume),248 increased,251,253 Prematureinfants,hyperkalemia,115 Proteinbuffers,41 Pulmonaryarterycatheter bloodpressuremeasurement,59–61,60i ports,60i Pulmonaryarterypressure(PAP),55 Pulmonaryedema,74i inburnpatients,323 R Radiation,235 Ranson’scriteria,inacutepancreatitis,289,290t Reabsorption,fluids,10 Refeedingsyndrome,170 Renalfailure,300–314 acuteorchronic,300 agingeffects,308 cardiovascularsigns,306t,307 causes,300,301i,302–303 diagnosis,308 diureticphase,302 documentation,311 genitourinarysigns,306t GIsigns,306t,307 imbalancescausedby,303–304 integumentarysigns,306t,307 laboratoryresults,305 musculoskeletalsigns,306t,307 neurologicsigns,306t nursingintervention,309–311 phase1(oliguric-anuricphase),302 pulmonarysigns,306t,307 recoveryphase,302 signsandsymptoms,305–306 teachingpatients,310 treatment,308–309 Renin-angiotensin-aldosteronesystem,27 fluidbalanceand,13–15,14–15i Respiratoryacidosis,202–209 inburnpatients,322 causes,202–206,203–204i diagnosis,206–207 documentation,209 drugsassociatedwith,204 nursingintervention,207–208 respiratoryfailureand,264 signsandsymptoms,206 teachingpatients,208 treatment,207–208 Respiratoryalkalosis,209–214 causes,210 diagnosis,212–213 documentation,214 drugsassociatedwith,210 nursingintervention,214 respiratoryfailureand,264 signsandsymptoms,210–213,211–212i teachingpatients,214 treatment,213 Respiratorychanges,inburnpatients,320 Respiratoryfailure,262–271 causes,262–263,264t diagnosis,266 nursingintervention,267–268 signsandsymptoms,265 teachingpatients,268 treatment,266–267 worsening,266 Respiratorysystem,acid-baseregulationand,40,41–42,42i Ringer’ssolution,electrolytecontent,32t RuleofNines,inestimatingextentofburns,319i S Second-degreeburns,317 Sensiblefluidlosses,4 Serumelectrolytetestresults,26t SerumpH,calciumlevelsand,149 Severedcatheter,inI.V therapy,344 Sodium,84–104 dietarysources,85 excessiveintake,96–97 functions,23,25 regulation,85–87,86i Sodiumchloride,electrolytecontent,32t Sodium-potassiumpump,85–87,87i,107 Speedshock,inI.V therapy,345 Stressulcers(Curling’sulcers),inburnpatients,321 Suctioningofstomachcontents,excessiveGIfluidloss,273 Sympatheticnervoussystem,heartfailureand,250 Syndromeofinappropriateantidiuretichormone(SIADH)secretion,77–78,90,91i T Thermalburns,316 Third-degreeburns,317 Third-spacefluidshifts,67 Thirst,fluidbalanceand,16–17 Thrombophlebitis,inI.V therapy,344 Totalparenteralnutrition(TPN),352–362 commonadditives,353 documentation,359 infusionfacts,356 nursingintervention,356–358 signsandsymptomsofproblems,357 teachingpatients,356 technique,358 timingout,358–359 uses,352–353 Trousseau’ssign,hypocalcemia,154i V V/Qmismatch,263i Vasopressin seeAntidiuretichormone(ADH) VitaminD,calciumlevelsand,149 Vitamins,componentofTPNsolutions,353 Vomiting characteristicsandcauses,274 excessiveGIfluidloss,273 W Waterintoxication,77–79 causes,77 diagnosis,78 documentation,79 nursingcare,79 signsandsymptoms,78 teachingpatients,79 treatment,78 ... JournaloftheAmericanSocietyofNephrology, 20 (2) , 388–396 Ketteler,M (20 11) PhosphatemetabolisminCKDstages3-5:Dietary and pharmacologicalcontrol InternationalJournalofNephrology, 20 11,97 024 5 Kling,J (20 13) Newphosphatebinderforrenalfailurelowerspillburden... Buffersacids and bases,promotesenergytransferbyformingATP, and isessentialforhealthybones and teeth • Normalrange: 2. 5to4.5mg/dl(1.8to 2. 6mEq/L) Phosphorusbalance • Dietaryintake and renalexcretionmaintainnormallevels;ifintakeincreases,renalexcretionalso... About85%foundinbones and teeth,combinedwithcalciumina1 :2 ratio • Crucialtocellmembraneintegrity,muscle and neurologicfunction, and metabolismofcarbohydrates, fats, and proteins • PromotesoxygendeliveryfromRBCstotissues
- Xem thêm -

Xem thêm: Ebook Fluids and electrolytes made incredibly easy (6/E): Part 2, Ebook Fluids and electrolytes made incredibly easy (6/E): Part 2

Gợi ý tài liệu liên quan cho bạn