acidbase动物报告毛细血管95ul

ANGELABORCHERS,DVM,DACVIM,BLOOD I-STATsystem,AbbotPointofSTATprofile,pHOx,NovaABL800,RadiometerAmericaRAPID CobasB221,RocheOptiCCATS,OptiMedical 血氧

电解COMMONSAMPLING引起样本有误差的常见因Commonerrorsofarterial/venoussampling/动脉或静脉样本血引起的一般影Airinsample/PCO2↓,pH↑,PO2↑Excessanticoagulant(dilution)/（样本被稀释）PCO2↓,pH↑,PO2Metaboliceffects/代谢产物的影响:PCO2↑,pH↓,PO2↓ACIDBASE酸碱生pH=AlkalemiapH升高=碱血pH=AcidemiapH降低=酸血ACID-BASE酸-碱生Acid=H+donor/酸性物质H+提供BaseHacceptor/碱性物质H+pH=-logIncreasedH+ decreasedpH(acidosis)H+增加=pH升高（酸血症）DecreasedH+=increasedpH(alkalosis)H+减少=pH降低（碱血症）WHYISITIMPORTANTAltersbiologicfunction改变生物学功IndicatorofdiseaseMayaffectefficacyofsome可能会影响某些药物的功Helpstoguidetherapy可以指导临床治PHYSIOLOGICEFFECTSOFACIDEMIA酸血症对机体生理的影Myocardialdepression,cardiac心肌抑制，降低心肌的Sympatheticoverstimulation过度刺激交感经Cardiacarrhythmias心律tocatecholamines(pH当pH<7.1时，就会抑制儿茶Peripheralvasodilation,引起周围血管扩Cerebralvasodilation(脑血管扩张（颅内压升高Hyperventilation换气PHYSIOLOGICEFFECTSOF碱血症对机体生理的影Myocardialdepression心肌Cardiacarrhythmias心率Cerebralvasoconstriction引起外周血管收缩（颅内压降低Mentalconfusion,产生意识模糊 的症Inacuterespiratoryalkalosis<6急性呼吸性 6小时IncreasedneuromuscularMusclespasm肌肉痉Inacuterespiratoryalkalosis<6急性呼吸性 6小时PHpH值的调ImmediatechemicalActivecontrolofHH的调KidneyLungsCHEMICALWeakacidsorconjugatePreventchangesinpHbybindingexcessH+orreleasingH+ ExcessH+(acidosis)H+增加（ BufferbindsH+缓冲物质结合 ）LossofH(alkalosis)H+减少（）Buffer HCO3/CO2BUFFERCarbonicacid碳酸氢根离子中和酸性物HCO3+H+↔H2CO3↔CO2+HCO3mEq/LorRegulatedbykidneysCO2RegulatedbylungsPH值计算方pH=6.1+ Acidity(pH) BicarbonateCarbondioxideAcidity(pH) BicarbonateCarbondioxideAlkalosis

pH值

AcidosisIncreasedDecreasedcarbonBoth

DecreasedIncreasedcarbon-BothPCO2INFLUENCEONCARBONICACIDEQUATIONHCO3concentrationvarieswithchangesinPCO2HCO3+H+↔H2CO3↔CO2+Siggard-AndersenPCO2of20PCO2of80

HCO321HCO327BASEEXCESSUsuallycalculatedbybloodgas通常需要由血气分析仪Purestmarkerofmetabolic代谢性变化的标ReflectsstrongacidorbaseneededtoarterialplasmatopH NegativeSBE=metabolic剩余碱为负数时，代表PositiveSBE=metabolic剩余碱为正数时，代表 BASE酸碱紊紊乱类异pHMetabolicDecreasedDecreasedpHMetabolicIncreasedIncreasedpHRespiratoryIncreasedDecreasedpHRespiratoryDecreasedIncreasedpHAPPROACHTOBLOOD血气分pH=Acidemia酸血PCO2=38HCO3=12ic/ssPrimarymetabolic性代谢性

(32-45(18-24(-4METABOLIC代谢性酸碱平衡紊LowpHandlow低pHGainofacidHighaniongapLossof碳酸氢盐NormalanionANIONAniongap=determinesunmeasured阴离子间隙=还未测定的阴离子浓Na+K=HCO3+Cl+unmeasuredNaKHCO3Cl还未测定的阴离子浓AG/=(Na+K)–(HCO3Normal/正常值=12-20mmol/L13-22mmol/LMETABOLICHighaniongapmetabolic阴离子间隙值升高的代谢性Na+K=HCO3+ Non-aniongapmetabolic

rmalHIGHAGMETABOLIC高阴离子间隙的代谢性Acidgain:Ketones(Diabetic 引起的酮 Uremicacids(kidneyEthyleneglycolLacticLACTATELactateproducedbyallbodytissuesapyruvatebyproductof DuringanaerobicmetabolismpyruvateisnotincorporatedintotheKreb’scycle.在进行厌氧酵解时 Pyruvateisconvertedtolactatetoregeneratenicotinamideadeninedinucleotide(NAD) LACTATETYPEALACTICDecreasedoxygendelivery供氧量下HypovolemiaAnemiaCardiogenicshockSepticshockSeverehypoxemiaCarbonmonoxidepoisoningIncreasedoxygendemand氧的需求增Seizures,shivering,TYPEBLACTICInadequateOxygenUtilization氧气利用不SystemicinflammatoryresponseSepsisRenalfailureDiabetesNeoplasiaTotalparenteralnutrition全肠外营养供Thiaminedeficiency硫胺素（VB1）CongenitalErrorsof 性代谢Drugs/Toxins药物或AG=37.1mmol/L(18-21mmol/Ldog)Primarymetaboliclacticacidosis性代谢性乳酸血NORMALANIONGAPLossofbicarbonate碳酸氢盐的丢Renallosses(renalIntestinallosses肠道丢失（腹泻NORMALANIONGAPMETABOLICpH=Acidemia酸血pCO2=38Chloride=128Na=155K=3.7HCO3=11.2AG=

(7.35-(32-43(110-120(145-153(3.5-4.8(18-24RESPIRATORYIncreasedPCO2anddecreased二氧化碳分压升高和pH值降Decreasedpulmonary肺通气降BraindiseaseCervicalspinalcorddiseasePeripheralnerveorneuromuscularRespiratorymuscleRESPIRATORY呼吸性紊pH=Acidemia酸血PCO2=56HCO3=20SBE=-1Primaryrespiratory性呼吸性

(7.35-(32-45(18-24(-4METABOLIC代谢性IncreasedHCO3andincreased碳酸氢根离子增加和pHCauses病LossofacidRenallossesGastriclosses(vomiting)肠道丢失 GainofbicarbonateMETABOLIC代谢性pH= (7.35-Alkalemia碱血pCO2=38HCO3=28SBE=+4Primarymetabolic性代谢性

(32-43(18-24(-4RESPIRATORY呼吸性DecreasedPCO2andincreased二氧化碳分压降低和pH值升Increasedventilation=Hyperventilation换气过LungdiseaseBraindisease性呼ResponseoftheopposingsystemtominimizechangesinpH抑制呼吸系统，尽可能减少pHConcurrentmetabolicacidosisandrespiratory OnecompensatesfortheReturnspHtowardsnormalbutnever恢复pH值至正常但绝不会超过正RESPIRATORY呼吸性代ChangeinPCO2inresponse lslungstochang通过大脑调控肺来改变通气量或二氧化碳迅速的发挥作RESPIRATORY紊紊乱类Primary代MetabolicDecreased碳酸氢根离子Decreased二氧化碳分压代谢性MetabolicIncreased碳酸氢根离子Increased二氧化碳分压上代谢性Metabolicacidosis:PCO2decreases0.7mmHgforevery1 Metabolicalkalosis:PCO2increases0.7mmHgforevery1increasein EXAMPLE6举例pH= (7.35-Acidemia酸血PCO2=30HCO3=12SBE=-6

(32-45(18-24(-4Primarymetabolic性代谢性Compensatoryrespiratory代偿性呼吸性METABOLIC代谢性补ChangeinHCO3inresponsetorespiratoryabnormalityKidneysconserve/excrete肾脏通过调节碳酸氢根离子的浓度来发挥StartswithinhoursCompletedindaysMETABOLIC代谢性代Disorder紊乱Primary代性紊乱类RespiratoryIncreased二氧化碳分压Increased碳酸氢根离子浓度呼吸性RespiratoryDecreased二氧化碳分压Decreased碳酸氢根离子浓呼吸性Acuterespiratoryacidosis:HCO3increasesby0.15mEq/LforeverymmHgincreasein急性呼吸性 ：二氧化碳分压每增高1mmHg，HCO3每升高Acuterespiratoryalkalosis:HCO3decreasesby0.25mEq/LforeverymmHgdecreasein ：二氧化碳分压每降低1mmHg，HCO3每降低0.15EXAMPLE7病例pH (7.35-碱血PCO2=20HCO