酸碱平衡紊乱及分析PPT课件.ppt

Acid-baseBalanceandImbalance,酸碱平衡紊乱及其分析,Acid-basebalance,Thebasicmeaningofacid-basebalanceisthestableH+inthebodyfluid.pH:7.357.45Compatiblewithlife6.8-8.0,因酸碱负荷过度、不足或调节机制障碍导致体液酸碱度稳定性失衡的病理过程。,Acid-basedisturbance：,Indisease,becauseofoverload,lossordeficiencyanddisorderinregulationofacidandbase,thehomeostasiscanbedestroyed.,Normalacid-basebalance,Section1,1.Acid-H+donor,volatileacid(挥发酸)Nonvolatileacid/fixedacid(固定酸),dailyproduction：300-400L/d,volatileacidH2CO3,CO2,H2O,H2CO3,CA,H+HCO3-,Reabsorptioninkidney,RBC、kidneytubules-epithelium、alveolarepithelialcell、gastricmucosa,Sourceofacid,volatileacid,Pco2ismostimportantfactorinpHofbodytissues,Fixedacid(nonvolatileacid),(50-100mmol/d),Base-H+acceptor,碱性氨基酸分解Endogenous：deaminationNH3Lessthanacidproduction有机酸盐转变Exogenousinput：vegetables,andfruits,Regulationofacid-basebalance,Buffersystems(体液缓冲)Respiratoryregulation(肺)Renalregulation(肾)Cellularregulation(细胞调节),1.Buffersystemsinbodyfluid,弱酸及其共轭碱构成的具有缓冲酸或碱能力的缓冲对,HCO3-/H2CO3isthemostimportantbufferpair,themostimportantbufferpair(50%)。fixedacidandbasebuffersystemPHisdermatiedbyHCO3-/H2CO3,特点：OpenBufferSystem反应快；但被消耗，不持久；不彻底，直接受肾、肺调节。,2.Respiratoryregulation,PaCO2(N:40mmHg)pHofCSFtostimulatecentralchemoreceptortherespiratorycenterPulmonaryventilationvolumePaCO260mmHg(8kPa)Pulmonaryventilationvolume10timesPaCO280mmHg(10.7kPa)inhibitrespiratorycenter，namedascarbondioxidenarcosis,特点：作用较快(数分钟内开始发挥作用，30分钟达到高峰)；代偿能力大；只对挥发性酸有效。,3.Renalregulation,“排酸保碱”起效慢，1224h作用强大持久,NaHCO3重吸收(bicarbonateconservation),磷酸盐酸化(phosphateacidification),氨的排泄(ammoniaexcretion),Renalregulation,Bicarbonateconservation(NaHCO3重吸收),Phosphateacidification(磷酸盐酸化),K+,K+,Cl-,Ammoniaexcretion(氨的排泄),4.Cellularregulation,红细胞肌细胞,HHb,特点：缓冲强于细胞外液；24h起效；引起血钾改变。,组织细胞,血液,H,K,Na,肝脏细胞,NH3,H,OH-,NH4,NH3,尿素,骨骼,Ca3(PO4)2,H,Ca2,PO43-,Ca2,PO43-,H,H2PO4-,Parametersofacid-basebalance,Section2,1.pH,pH:acidosispH:alkalosis,7.357.45,kassier,pH正常,NodisturbsnceCompletecompensationAcidosis+Alklosis,2.PaCO2-“respiratoryfactor”.(Partialpressureofcarbondioxide),正常值:40mmHg(3346mmHg)H2CO3:40X0.03=1.2mmol/L,HigherPaCO2isduetotheinhibitionofrespiration.LowerPaCO2isduetooverventilation.,PaCO2是物理溶解在动脉血中的CO2产生的张力。,PaCO246mmHgPrimaryincrease:respiratoryacidosisSecondaryincrease:metabolicalkalosis(compensatedbylung)PaCO2SB(CO2retention)respiratoryacidosisABSBPaCO210mmHgHCO3代偿性1mmol/L,Chronic:pHPaCO2ABSBPaCO210mmHgHCO3代偿性3.5mmol/L,(4)Changesofparametersandelectrolytes,案例4-2：患者：男，15岁，因溺水窒息。查血气：PH7.15，PaCO280mmHg，HCO3-27mmol/L。分析？,与代酸相同，但CNS症状更明显,?,Why?,(5）Alterationsofmetabolismandfunction,CO2直接弥散进入脑组织,Carbondioxidenarcosis:PaCO280mmHg,Celebralvasculardilationcerebralbloodflowincrease,Hypoxia,肺性脑病,(Pulmonaryencephalopathy),intracranialhypertensionandbrainedema.,增加肺泡通气量(Increasealveolarventilation),应用碱性药物(supplementofbase),(6)Principlesofpreventionandtreatment,Becarefultoalkalinedrug(NaHCO3)THAM,85,案例4-3：,一男性患者，60岁，因进食即呕吐10天而入院。近20天明显消瘦，卧床不起。精神恍惚，嗜睡，皮肤干燥松弛，眼窝深陷，呈重度脱水征。呼吸17次/min，血压120/70mmHg，诊断为幽门梗阻。血液生化检验：K+3.4mmol/L,Na+158mmol/L，Cl-90mmol/L；血气：pH7.50，PaO262mmHg，PaCO249mmHg，BE8.0mmol/L，HCO3-45mmol/L。思考题：该患者属于何种类型的酸碱平衡紊乱？原因和机制如何？该患者有无水电紊乱？,3.Metabolicalkalosis,MetabolicalkalosisisdefinedasanincreaseofpHinducedbyprimaryincreaseinplasmabicarbonate(HCO-3).,(1)Etiology,1)Hloss,vomiting(HCl),Lossfromstomach：,Lossfromkidney:,长期应用袢利尿剂（抑制髓袢升支对Cl-、Na+和H2O的重吸收）远端肾小管H+-Na+交换排H+、排Cl-，HCO3-重吸收血HCO3-、Cl-Diuretics-furosemide低氯性碱中毒醛固酮增多或糖皮质激素使用过多肾排H+、K+-重吸收NaHCO3,PrimaryhyperaldosteronismSecondaryhyperaldosteronismcausedby:hypovolemiaCushingssyndrome,低氯性碱中毒,利尿剂,2)Excessiveintakeofalkalinesubstances,3)Hypokalemia/hypochloremia低钾/低氯性碱中毒paradoxicalacidicurine,ExcessiveintakeofNaHCO3orstoredblood,4)Misuseofmechanicalventilationinchronicrespiratoryacidosis,原因呕吐丢失HCl；脱水造成浓缩性HCO3；低钾碱中毒,案例4-3：一男性患者，60岁，因进食即呕吐10天而入院。近20天明显消瘦，卧床不起。精神恍惚，嗜睡，皮肤干燥松弛，眼窝深陷，呈重度脱水征。呼吸17次/min，血压120/70mmHg，诊断为幽门梗阻。血液生化检验：K+3.4mmol/L,Na+158mmol/L，Cl-90mmol/L；血气：pH7.50，PaO262mmHg，PaCO249mmHg，BE8.0mmol/L，HCO3-45mmol/L。,(2)Clasification,Chloride-responsivealkalosis盐水反应性碱中毒Chloride-resistantalkalosis盐水抵抗性碱中毒,(3)Compensation,4)Renalregulation,SecreteH+SecreteNH3ReabsorbHCO3-UrinepH,细胞外液H,肾小管腔,碱中毒低血钾,3)Intracellularregulation,原发性:pHSBABBBBE继发性:PaCO2血K,正值,(4)Changesofparametersandelectrolytes,案例4-3,血气：pH7.50，PaO262mmHg，PaCO249mmHg，BE8.0mmol/L，HCO3-45mmol/L分析：患者幽门梗阻呕吐丢失HCl等而导致HCO3-pH，BE正值，继发性PaCO2，PaO2，属于失代偿型代谢性碱中毒。患者低Cl-、脱水应属于盐水反应性碱中毒,(1)CentralNervousSystem,-氨基丁酸(GABA),(5）Alterationsofmetabolismandfunction,restlessness，mentalderangement，delirium.,2)Neuromuscularexcitability(神经肌肉应激性升高),机制:pH，血中游离Ca2+,手足搐搦(CarpopedalSpasm),3)Hypoxia(left-shiftofoxygen-Hbdissociationcurve),4)Hypokalemia,治疗原发病(treatmentofprimarydisease),saline-responsivealkalosisKClsaline-resistantalkalosis,(6)Principlesofpreventionandtreatment,Replenish0.9%NaClNa+Cl-(mmol/L)-0.9%NaCl154154Plasma140104-a)DilutetheHCO3-b)Increasethebloodvolume,reducethereabsorptionofHCO3-.c)increasedCl-indistaltubuleleadstoincreasedexcretionofHCO3-incollectingduct.,103,案例4-4,4.Respiratoryalkalosis,RespiratoryalkalosisisdefinedasanincreaseofpHinducedbyPrimarydecreaseinplasmH2CO3Concentration.,(1)Etiology,CO2排出过多,Psychogenicfactors:Nervousness,anxiety,hysteria,etc.(2)Braindiseases:Encephalitis,meningitis,etc.(3)Reflectivestimulation:Hypoxemia,fever,pain,NH3,salicylateetc.(4)Misuseofmechanicalventilation,案例4-4原因发热、肺炎、肺水肿、低氧血症等刺激呼吸频率CO2呼出过多,(2)ClassificationandCompensation,Acuterespiaratoryalkalosis24h,血H2CO3,血K,1）Acuterespiaratoryalkalosis,RBC,plasma,2）Chronicrespiaratoryalkalosis,泌H+泌氨HCO3-重吸收尿pH,急性:pHPaCO2ABSBPaCO210mmHgHCO3代偿性2mmol/L,慢性:pHPaCO2ABSBPaCO210mmHgHCO3代偿性4mmol/L,(4)Changesofparametersandelectrolytes,案例4-4血气：pH7.52,PaCO230mmHg，PaO257mmHg，BE-1.2mmol/L，HCO3-23.3mmol/L，K+、Na+、Cl-正常。分析：患者发热、肺炎、肺水肿并缺氧，引起呼吸急促，使PaCO2原发性pH，继发性HCO3-，属于失代偿型呼吸性碱中毒。,眩晕、四肢感觉异常、意识障碍、抽搐等碱中毒症状,(5）Alterationsofmetabolismandfunction,CNSdysfunction：GABA，cerebralbloodflow,(6)Principlesofpreventionandtreatment,TreatmentofprimarydiseasePreventmis-operationofmechanicalventilator5CO2mixtruegasinhalationormask,115,各型酸碱平衡紊乱指标的变化,代酸,呼酸,代碱,呼碱,小结,117,单纯型ABD小结1、概念：根据原发变化因素及方向命名。2、代偿变化规律：代偿变化与原发变化方向一致。3、血气特点：呼吸性ABD，血液pH与其它指标变化方向相反；代谢性ABD，血液pH与其它指标变化方向相同。4、原因和机制：代酸：固定酸生成及HCO3-丢失HCO3-降低。呼酸：CO2排出减少吸入过多，使血浆H2CO3升高。代碱：丢失，过量负荷，血增多。呼碱：通气过度CO2呼出过多，使血中H2CO3降低。,118,5、对机体的影响：CNS离子改变其它酸中毒抑制性紊乱血钾增高血管麻痹，心律失常收缩力降低碱中毒兴奋性紊乱血钾降低肌肉痉挛6、代偿调节(1)代谢性ABD,各调节机制都起作用，尤其是肺和肾；呼吸性ABD,细胞内外离子交换是急性紊乱的主要机制（两对离子交换），肾调节是慢性紊乱的主要机制。（2）代偿是有限度的。（3）pH值取决于代偿能否维持HCO3-/H2CO3比值为20/1。,例一、患者腰痛3月入院，诊断为肾盂肾炎，血液生化测定pH=7.32,PaCO2=20mmHg,BE=-15.3mmol/L，SB=19.2mmol/L。该病人发生何种酸碱平衡紊乱？,代酸,例二、糖尿病患者，血液生化测定pH=7.30,PaCO2=34mmHg,SB=16mmol/L，Na+=140mmol/L,K+=4.5mmol/LCL-=104mmol/L，HCO3-=21mmol/L该病人发生何种酸碱平衡紊乱？,AG增高性代酸,综合举例,例三某溃疡病患者,因反复呕吐入院,血气分析为pH7.49，PaCO248mmHg，HCO-36mmol/L。该病人酸碱失衡类型为：A代酸B代碱C呼碱D呼碱例四某肝性脑病患者,血气分析为pH7.47，PaCO226.6mmHg，HCO-.3mmol/L。应诊断为：A代碱B呼碱C呼酸D代酸,Mixedacid-baseDisturbance,Section4,Amixedacid-basedisturbanceisdefinedasthesimultaneousexistanceoftwoormoresimpleacid-basedisturbanceinthesamepatient.,Concept,酸碱一致型（相加型）酸碱混合型（相消型）,Doubleacid-basedisturbance(二重性),呼吸心跳骤停肺疾患并心衰或休克,pHPaCO2HCO3-,Respiratoryacidosis+metabolicacidosis,Causes,Characteristics,通气障碍（CO2潴留）伴有产酸（固定酸潴留）。,高热合并呕吐肝硬化应用利尿剂,pHPaCO2HCO3-,Respiratoryalkalosis+metabolicalkalosis,Causes,Characteristics,慢性肺疾患应用利尿剂或合并呕吐,pHPaCO2HCO3-,Respiratoryacidosisplusmetabolicalkalosis,Causes,Characteristics,(-)、,水杨酸中毒或肾衰合并通气过度,Metabolicacidosis+respiratoryalkalosis,Causes,Characteristics,pHPaCO2HCO3-,(-)、,肾衰伴呕吐酮症酸中毒伴呕吐呕吐伴有腹泻,Metabolicacidosis+metabolicalkalosis,Causes,Characteristic,pH、PaCO2、HCO3-不定,呼酸+代酸(AG)+代碱呼碱+代酸(AG)+代碱,Tripleacid-basedisturbance（三重性),Section5,Judgmentofacid-basedisorders,“一划五看”简易判断法,一划：将多种指标简化成三项，并用箭头表示其升降,SBABBB，BE(-),HCO3-,H2CO3,PaCO2,pH,H+,五看：一看pH定酸碱,1.pH升高：失偿型碱中毒pH降低：失偿型酸中毒2.pH正常可能是（1）酸碱平衡（2）代偿性单纯性（3）混合性相消型,病史中有获酸，失碱或相反情况，为代谢性ABD病史中有肺过度通气或相反情况，为呼吸性ABD,二看原发因素定代呼,HCO-3H2CO3,pHN,病史？,1.继发性变化的方向(1)与原发性变化方向一致：,三看“继发性变化”定单混,PaCO2HCO-3pH接近正常,单纯型ABD或混合型(相消型)ABD,PaCO2,HCO-3，pH,(2)与原发性变化方向相反,混合型(相加型)ABD,“继发性变化”的数值(代偿预计值）（1）数值在代偿预计值范围内，为单纯型（2）数值明显超过或低于代偿预计值，为混合型,代偿预计值（见书中表格）,如：慢性呼酸代偿预计公式：HCO-3=0.4PaCO23,单纯性酸碱失衡常用代偿预测公式,Acid-BaseDisturbance,一位慢性肺心病人，其PaCO2为60mmHg/L，这位病人HCO-3的代偿最大限值是多少？,HCO-3=0.4x(60-40)+243=32mmol/L3=2935mmol/L,例5,一位肝性脑病病人，pH=7.