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

電解COMMONSAMPLING引起樣本有誤差的常見因Commonerrorsofarterial/venoussampling/動脈或靜脈樣本血引起的一般影Airinsample/PCO2↓,pH↑,PO2↑Excessanticoagulant(dilution)/（樣本被稀釋）PCO2↓,pH↑,PO2Metaboliceffects/代謝產物的影響:PCO2↑,pH↓,PO2↓ACIDBASE酸堿生pH=AlkalemiapH升高=堿血pH=AcidemiapH降低=酸血ACID-BASE酸-堿生Acid=H+donor/酸性物質H+提供BaseHacceptor/堿性物質H+pH=-logIncreasedH+ decreasedpH(acidosis)H+增加=pH升高（酸血癥）DecreasedH+=increasedpH(alkalosis)H+減少=pH降低（堿血癥）WHYISITIMPORTANTAltersbiologicfunction改變生物學功IndicatorofdiseaseMayaffectefficacyofsome可能會影響某些藥物的功Helpstoguidetherapy可以指導臨床治PHYSIOLOGICEFFECTSOFACIDEMIA酸血癥對機體生理的影Myocardialdepression,cardiac心肌抑制，降低心肌的Sympatheticoverstimulation過度刺激交感經Cardiacarrhythmias心律tocatecholamines(pH當pH<7.1時，就會抑制兒茶Peripheralvasodilation,引起周圍血管擴Cerebralvasodilation(腦血管擴張（顱內壓升高Hyperventilation換氣PHYSIOLOGICEFFECTSOF堿血癥對機體生理的影Myocardialdepression心肌Cardiacarrhythmias心率Cerebralvasoconstriction引起外周血管收縮（顱內壓降低Mentalconfusion,產生意識模糊 的癥Inacuterespiratoryalkalosis<6急性呼吸性 6小時IncreasedneuromuscularMusclespasm肌肉痙Inacuterespiratoryalkalosis<6急性呼吸性 6小時PHpH值的調ImmediatechemicalActivecontrolofHH的調KidneyLungsCHEMICALWeakacidsorconjugatePreventchangesinpHbybindingexcessH+orreleasingH+ ExcessH+(acidosis)H+增加（ BufferbindsH+緩沖物質結合 ）LossofH(alkalosis)H+減少（）Buffer HCO3/CO2BUFFERCarbonicacid碳酸氫根離子中和酸性物HCO3+H+?H2CO3?CO2+HCO3mEq/LorRegulatedbykidneysCO2RegulatedbylungsPH值計算方pH=6.1+ Acidity(pH) BicarbonateCarbondioxideAcidity(pH) BicarbonateCarbondioxideAlkalosis

pH值

AcidosisIncreasedDecreasedcarbonBoth

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

HCO321HCO327BASEEXCESSUsuallycalculatedbybloodgas通常需要由血氣分析儀Purestmarkerofmetabolic代謝性變化的標ReflectsstrongacidorbaseneededtoarterialplasmatopH NegativeSBE=metabolic剩余堿為負數時，代表PositiveSBE=metabolic剩余堿為正數時，代表 BASE酸堿紊紊亂類異pHMetabolicDecreasedDecreasedpHMetabolicIncreasedIncreasedpHRespiratoryIncreasedDecreasedpHRespiratoryDecreasedIncreasedpHAPPROACHTOBLOOD血氣分pH=Acidemia酸血PCO2=38HCO3=12ic/ssPrimarymetabolic性代謝性

(32-45(18-24(-4METABOLIC代謝性酸堿平衡紊LowpHandlow低pHGainofacidHighaniongapLossof碳酸氫鹽NormalanionANIONAniongap=determinesunmeasured陰離子間隙=還未測定的陰離子濃Na+K=HCO3+Cl+unmeasuredNaKHCO3Cl還未測定的陰離子濃AG/=(Na+K)–(HCO3Normal/正常值=12-20mmol/L13-22mmol/LMETABOLICHighaniongapmetabolic陰離子間隙值升高的代謝性Na+K=HCO3+ Non-aniongapmetabolic

rmalHIGHAGMETABOLIC高陰離子間隙的代謝性Acidgain:Ketones(Diabetic 引起的酮 Uremicacids(kidneyEthyleneglycolLacticLACTATELactateproducedbyallbodytissuesapyruvatebyproductof DuringanaerobicmetabolismpyruvateisnotincorporatedintotheKreb’scycle.在進行厭氧酵解時 Pyruvateisconvertedtolactatetoregeneratenicotinamideadeninedinucleotide(NAD) LACTATETYPEALACTICDecreasedoxygendelivery供氧量下HypovolemiaAnemiaCardiogenicshockSepticshockSeverehypoxemiaCarbonmonoxidepoisoningIncreasedoxygendemand氧的需求增Seizures,shivering,TYPEBLACTICInadequateOxygenUtilization氧氣利用不SystemicinflammatoryresponseSepsisRenalfailureDiabetesNeoplasiaTotalparenteralnutrition全腸外營養供Thiaminedeficiency硫胺素（VB1）CongenitalErrorsof 性代謝Drugs/Toxins藥物或AG=37.1mmol/L(18-21mmol/Ldog)Primarymetaboliclacticacidosis性代謝性乳酸血NORMALANIONGAPLossofbicarbonate碳酸氫鹽的丟Renallosses(renalIntestinallosses腸道丟失（腹瀉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二氧化碳分壓升高和pH值降Decreasedpulmonary肺通氣降BraindiseaseCervicalspinalcorddiseasePeripheralnerveorneuromuscularRespiratorymuscleRESPIRATORY呼吸性紊pH=Acidemia酸血PCO2=56HCO3=20SBE=-1Primaryrespiratory性呼吸性

(7.35-(32-45(18-24(-4METABOLIC代謝性IncreasedHCO3andincreased碳酸氫根離子增加和pHCauses病LossofacidRenallossesGastriclosses(vomiting)腸道丟失 GainofbicarbonateMETABOLIC代謝性pH= (7.35-Alkalemia堿血pCO2=38HCO3=28SBE=+4Primarymetabolic性代謝性

(32-43(18-24(-4RESPIRATORY呼吸性DecreasedPCO2andincreased二氧化碳分壓降低和pH值升Increasedventilation=Hyperventilation換氣過LungdiseaseBraindisease性呼ResponseoftheopposingsystemtominimizechangesinpH抑制呼吸系統，盡可能減少pHConcurrentmetabolicacidosisandrespiratory OnecompensatesfortheReturnspHtowardsnormalbutnever恢復pH值至正常但絕不會超過正RESPIRATORY呼吸性代ChangeinPCO2inresponse lslungstochang通過大腦調控肺來改變通氣量或二氧化碳迅速的發揮作RESPIRATORY紊紊亂類Primary代MetabolicDecreased碳酸氫根離子Decreased二氧化碳分壓代謝性MetabolicIncreased碳酸氫根離子Increased二氧化碳分壓上代謝性Metabolicacidosis:PCO2decreases0.7mmHgforevery1 Metabolicalkalosis:PCO2increases0.7mmHgforevery1increasein EXAMPLE6舉例pH= (7.35-Acidemia酸血PCO2=30HCO3=12SBE=-6

(32-45(18-24(-4Primarymetabolic性代謝性Compensatoryrespiratory代償性呼吸性METABOLIC代謝性補ChangeinHCO3inresponsetorespiratoryabnormalityKidneysconserve/excrete腎臟通過調節碳酸氫根離子的濃度來發揮StartswithinhoursCompletedindaysMETABOLIC代謝性代Disorder紊亂Primary代性紊亂類RespiratoryIncreased二氧化碳分壓Increased碳酸氫根離子濃度呼吸性RespiratoryDecreased二氧化碳分壓Decreased碳酸氫根離子濃呼吸性Acuterespiratoryacidosis:HCO3increasesby0.15mEq/LforeverymmHgincreasein急性呼吸性 ：二氧化碳分壓每增高1mmHg，HCO3每升高Acuterespiratoryalkalosis:HCO3decreasesby0.25mEq/LforeverymmHgdecreasein ：二氧化碳分壓每降低1mmHg，HCO3每降低0.15EXAMPLE7病例pH (7.35-堿血PCO2=20HCO