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1、酸碱平衡和酸碱平衡紊乱 Acid BasebalanceandDisturbance 相加型 pHH2CO3HCO3 代酸 呼酸 代偿 原发 原发 代偿 N N 综合 代碱 代偿 原发 呼碱 原发 代偿 综合 N N 二重型酸碱平衡紊乱 相消型 pHH2CO3HCO3 代酸 代偿 原发 呼碱 原发 代偿 N 综合 代碱 代偿 原发 呼酸 原发 代偿 综合 N pHH2CO3HCO3 代酸 代偿 代碱 代偿 原发 混合 N N N 三三重型酸碱平衡紊乱 pHH2CO3HCO3 代酸 代碱 呼酸 代酸 代碱 呼碱 不定 不定 不定 不定 不定 不定 原发 pHH2CO3HCO3 代酸 代偿 代碱
2、代偿 原发 混合 N N N 三三重型酸碱平衡紊乱 pHH2CO3HCO3 代酸 代碱 呼酸 代酸 代碱 呼碱 不定 不定 不定 不定 不定 不定 原发 NormalLevelsofSubstancesintheArterialBlood pH 7 40 0 05 病历分析 彭某 男 冠心病左心衰 肺感染呼吸困难用利尿剂 速尿 抗感染治疗 pH 7 7 血浆HCO3 20mmol L PaCO216 6mmHg Na 120mmol L Cl 70mmol L 判断上述病人发生了何重类型的酸碱平衡紊乱 AG 120 70 20 30 代酸 PaCO2 16 6mmHg 40mmHg 呼碱 HC
3、O3 0 5 PaCO2 2 5 0 5 40 16 6 2 5 11 7 2 5 9 2 14 2 实际上HCO3 20mmol L 只降低了约4mmol L 存在增高因素 代碱 代碱的机制何在 A14 year oldgirlwithcysticfibrosishascomplainedofanincreasedcoughproductiveofgreensputumoverthelastweek Shealsocomplainedofbeingincreasinglyshortofbreath andsheisnoticeablywheezing 喘息 onphysicalexamina
4、tion Arterialbloodwasdrawnandsampled revealingthefollowingvalues pH7 30PCO250mmHgPO255mmHb O2saturation45 HCO3 24meq li 1 Cysticfibrosis CF themostcommoninheriteddiseaseamongCaucasians isanautosomalrecessivedisorderthatismarkedbytheproductionofexcessivelythickmucusintherespiratorytract pancreaticduc
5、ts andbiliarytree IndividualswithCFproduceafaultyversionofachloridechannelproteincalledcysticfibrosistransmembraneconductanceregulator CFTR Thenormalversionofthisproteinhelpstransportchlorideionsoutofexocrineglandcells Inthisprocess waterusuallyfollowsbyosmosis thusdecreasingtheviscosityofmucussecre
6、tionsfromtheseexocrinecells However inCFthefaultyCFTRproteinisnotabletoadequatelypumpchlorideoutthroughthecellmembraneandthusthemucussecretionsfromexocrinecellsareexcessivelyviscous i e thick Thethickmucusisdifficulttoclearfromtherespiratorytract anditprovidesanutrient richbreedinggroundforbacteria
7、IndividualswithCFarethereforesubjectedtorepeatedboutsoflowerrespiratorytractinfections Questions Whatcausescysticfibrosis Describethepathophysiologicmechanismsofthedisease 2 Howwouldyouclassifythisgirl sacid basestatus Thisgirlisinrespiratoryacidosis asisevidentfromherdecreasedarterialbloodpH elevat
8、edarterialbloodpCO2 andnormalarterialHCO3 concentration Howdoescysticfibrosiscausethisacid baseimbalance Thepoolingofexcessivelythickmucusobstructsthesmallandlargeairways Thisreducesthepatient sminuteventilation causinghypoventilation Asshehypoventilates thepCO2levelrisesandtheexcessCO2reactswithH2O
9、inthebloodstreamtoproducecarbonicacid H2CO3 whichdissociatesintoH ionsandHCO3 ions loweringthepHoftheblood Whenherairwaysbecomeinfected whichwillhappenrepeatedlyoverherlifetime theinflammatoryresponsethatfollowsincludestheactivationofmacrophagesandneutrophils Whilethiswhitebloodcellresponsehelpstoge
10、tridoftheinfection italsocreateslong termdamagetothelungtissueasneutrophilsreleasefreeradicals elastase andotherlysosomalenzymes Thislong termdamagecauseslossofviablelungtissue hyperinflationofthelungs andfurtherairwayobstruction PatientswithCFcometoresembleolderindividualswithemphysemaduetotheexces
11、siveair trappinganddevelopmentofthebarrel shapedchest SinceindividualswithCFsofrequentlydeveloppulmonaryinfectionsthatrequireantibiotictreatment thetypesofbacteriathatinvadethelungsbecomeresistanttoeventhemostpotentantibiotics Thus theStaphylococcusaureus Hemophilusinfluenzae andPseudomonasaeruginos
12、abacteriathatmostcommonlyinfectthepatient slungsareverydifficulttotreat Hospitalizationwithintravenousantibiotics inhaledmucolyticagents andaregularscheduleofchestpercussiontherapyaretheprincipaltenetsoftreatmentinsuchcases Howwouldthekidneystrytocompensateforheracid baseimbalance Thekidneyswouldcom
13、pensateforthisprimaryrespiratoryacidosisbyincreasingtherateoftubularsecretionofhydrogenionsintotherenaltubules Thishastwopurposes A Itallowsallofthefilteredbicarbonateiontobeconvertedtocarbondioxideinthetubularlumenandabsorbedintothetubularliningcells Herethecarbondioxidecanbereconvertedtobicarbonat
14、eionandaddedtothebloodstreamintheperitubularcapillaries Theneteffectofthismulti steppedprocessisthatthekidneysreabsorballofthebicarbonateionoriginallyfilteredoutintotheBowman scapsules addingitbacktothebloodstreamtopreventthebloodpHfromdecreasingevenfurther B Theexcesshydrogenionremaininginthenephro
15、ntubuleafterallofthebicarbonateionhasbeenconvertedtoCO2canbindtoammonia NH3 toproduceammoniumion NH4 andtomonohydrogenphosphate HPO4 2 toproducedihydrogenphosphate H2PO4 ThesecompoundsdonotgetreabsorbedandthusprovideavehiclefortheexcretionofexcessH ionsfromthebody Thereisanotherwaythatthekidneyshelp
16、compensateforrespiratoryacidosis InadditiontothereabsorptionoffilteredHCO3 ions therenaltubulecellscanproducenewHCO3 ionstoaddtothebloodstream aneffectequivalenttoremovinghydrogenionsfromthebloodstream ThenewHCO3 formsinthetubuleliningcellsfrom A theconversionofmetabolicallyproducedCO2 and B thebreakdownofglutamine Incidentally thefactthatthispatient sbloodHCO3 levelsarestillnormalsuggeststhatthekidneyshavenotyetbeguntocompensateforherrespiratoryacidosis Listsomeothercausesofthistypeofacid based
