动脉血气分析六步法作者杜斌

1、动脉血气分析六步法-作者杜斌作者:日期:动脉血气分析六步法(6- S te P Appr o a ch inABGs)摘录翻译自：错误！未定义书签。引自CSCC M;整理及讲解：杜斌；WOR D制作：KI WI,ICU同仁，向杜斌表示致 敬。第一步根据H en de rse o n-Ha s s e Iba c h公式评估血气数值的内在一致H"o如果pH和=24 x ( Pa CO 2 )/ HCO 3 h"数值不一致，该血气结果可能是错误的pH估测H+(mmol/L)7.001007.05897.10797.15717.20637.25567.30507.35457.40

2、407.45357.50327.55287.60257.6522第二步是否存在碱血症或酸血症?pH < 7.35酸血症pH >7 .45碱血症记住:即使pH值在正常范围(通常这就是原发异常7. 3 5- 7. 4 5 ),也可能存在酸中毒或碱中毒你需要核对 PaC Q, H C 03和阴离子间隙:第三步是否存在呼吸或代谢紊乱?p H值改变的方向与 P aCO改变方向的关系如PaCO2改变方向相反;在原发代谢障碍时，P H值在原发呼吸障碍时，pH值和 和Pa CO改变方向相同酸中毒呼吸性pH JPaCO酸中毒代谢性pHJPaCO碱中毒呼吸性pHfPaCO碱中毒代谢性pHfPaCO第四

3、步针对原发异常是否产生适当的代偿通常情况下，代偿反应不能使PH恢复正常（7.3 5 7.45 ）异常预期代偿反应校正因 子代谢性酸中毒PaCO= ( 1.5 x HCO3- ) +8± 2急性呼吸性酸中毒HCO3-升高=? PaCQ /10± 3慢性呼吸性酸中毒（3-5 天）HCO3- 升高=3.5 x (? P aCQ /10 )代谢性碱中毒PaCO 升高=0.6 x (? HCO-)急性呼吸性碱中毒HCO 下降=2 x ( ? PaCQ / 10 )慢性呼吸性碱中毒HCO 下降=5 x ( ? PaCQ / 10 ) 至 7 x (? PaCQ / 10 )o如果观察到

4、的代偿程度与预期代偿反应不符，很可能存在一种以上的酸碱异常第五步 计算阴离子间隙（如果存在代谢性酸中毒）丰-AG = Na （: Cl + H CO : ） = 12± 2正常的阴离子间隙约为12 m Eq /L对于低白蛋白血症患者阴离子间隙正常值低于12 mEq/L低白蛋白血症患者血浆白蛋白浓度每下降约 2. 5 mEq/L1 gm/dL,阴离子间隙“正常值”下降（例如，血浆白蛋白下降 2.0 gm/dL患者AG约为7 mEq / L）如果阴离子间隙增加，在以下情况下应计算渗透压间隙?. AG升高不能用明显的原因（DKA ,孚L酸酸中毒，肾功能衰竭）解释?.怀疑中毒O SM间隙测定

5、 OSM - ( 2 x Na 血糖/ 1 8BUN / 2.8 )?. OSM间隙应当 10第六步如果阴离子间隙升高，评价阴离子间隙升高与HC O 3降低的关系o计算阴离子间隙改变（？ AG与 HCO3-改变（? HCO 3-）的比值:? AG / ? HC O-如果为非复杂性阴离子间隙升高代谢性酸中毒 之间,此比值应当介于1.0和2. 0如果这一比值在正常值以外，则存在其他代谢紊乱如果 ？ AG /?: HCC3- < 1.0,则可能并存阴离子间隙正常的代谢性酸中毒?.如果？ A G / ? HCO 3- > 2.0,则可能并存代谢性碱中毒记住患者阴离子间隙的预期“正常值”非常

6、重要，且这一正常值须根据低白蛋白血 症情况进行校正（见第五步）表1 :酸碱失衡的特征异常pH原发异常代偿反应代谢性酸中毒HCO JPaCO J代谢性碱中毒HCO TPaCO T呼吸性酸中毒PaCO THCO T呼吸性碱中毒PaCO JHCO J表2 :呼吸性酸中毒部分病因气道梗阻?.上呼吸道?.下呼吸道COPD哮喘 其他阻塞性肺疾病CNS抑制睡眠呼吸障碍（OSA或OHS）神经肌肉异常通气受限CO2产量增加；震颤，寒战，癫痫，恶性高热，高代谢，碳水化合物摄入增加错误的机械通气设置表3 :呼吸性碱中毒部分病因CNS刺激:发热，疼痛，恐惧，焦虑,CVA,脑水肿，脑创伤, 脑肿瘤，CNS感染 低氧血症

7、或缺氧：肺疾病，严重贫血，低FiO2 化学感受器刺激：肺水肿，胸腔积液，肺炎，气胸， 肺动脉栓塞 药物，激素：水杨酸，儿茶酚胺，安宫黄体酮，黄 体激素 妊娠，肝脏疾病，全身性感染，甲状腺机能亢进 错误的机械通气设置表4:代谢性碱中毒部分病因 低血容量伴Cl -缺乏GI丢失H + ：呕吐，胃肠吸引，绒毛腺瘤，腹泻时丢 失富含Cl的液体染肾脏丢失H+:袢利尿剂和噻嗪类利尿剂，CO2猪留后（尤其开始机械通气后） 低血容量肾脏丢失H+:水肿状态（心功能衰竭，肝硬化，肾病 综合征），醛固酮增多症，皮质醇增多症，ACTH过量，外源性皮质激素，高肾素血症，严重低钾血症，肾动脉狭窄，碳酸盐治疗表5:代谢性酸中

8、毒部分病因 阴离子间隙升高甲醇中毒尿毒症糖尿病酮症酸中毒a，酒精性酮症酸中毒，饥饿性 酮症酸中毒 三聚乙醛中毒 异烟肼 尿毒症 甲醇中毒 乳酸酸中毒 乙醇b或乙二醇b中毒 水杨酸中毒a阴离子间隙升高代谢性酸中毒最常见的原 b常伴随渗透压间隙升高阴离子间隙正常：Cl 一升高GI丢失HCO-腹泻，回肠造痿术，近端结肠造痿术, 尿路改道 肾脏丢失HCO-近端RTA 碳酸酐酶抑制剂（乙酰唑胺）肾小管疾病ATN慢性肾脏疾病，远端 RTA醛固酮抑制剂或缺乏，输注NaCl，TPN输注NH4+表6:部分混合性和复杂性酸碱失衡异常特点部分病因i呼吸性酸中毒谢性酸中毒伴代pHJHCOP aCOT?心跳骤停?中毒?

9、多器官功能衰竭?肝硬化应用利尿剂呼吸性碱中毒伴代pHTHCOP aCOJ?妊娠合并呕吐谢性碱中毒? COPD过度通气? COPD应用利尿剂，呼吸性酸中毒谢性碱中毒伴代pH正常HCOP aCOT呕吐? NG吸引?严重低钾血症?全身性感染呼吸性碱中毒谢性酸中毒伴代pH正常HCOP aCOJ?水杨酸中毒?肾功能衰竭伴CHF或肺炎?晚期肝脏疾病?尿毒症或酮症酸中代谢性酸中毒谢性碱中毒伴代pH正常HCO正常毒伴呕吐，NG吸引，利尿剂等:建议阅读文献 ? Rose, B.D. and T.W. Post. C li n i c al ph y siolo gy of ac i d - b ase and

10、e lec t r o lyte diso r de r s, 5th ed.Ne w Yo r k:McG ra w Hill Medi c a l Publis h ing Division,? Fidk ow ski, C And J. Helst ro m Diagill:br idg i ng the a n ion ga p ,n osing met abolic ac i d o sis in the c riticallySt e wa r t a n d b as e exces s meth o ds . Can J A nest h 2009; 5 6: 2 47-256

11、.e ning a cid-base dis2 6 - 34.r eate n ing acid - base? Adrogu e, H.J. and N. E . Madi as. Mana gement of li f e- t hre a to r de rs firs t o f two par t s. N En gl J Med 1998;3 3 8： ? Adrog ue, H.J . an d N.E . Mad i a s . Managem ent o fl if e-thdi s orde rs se c ond of t wo pa r ts. N Engl J Med

12、19 9 8;338:10 7 -111 .病例1Case 1K亠"H V = &PO> 二 102BG = 5：4A 22yr4i qI叮 ai'AH 诃 raUitiis 蘭赳。严 A sevwif' tipper rfjpiraTCrV iijlrcciortNa -Cl F 勺4PCO j 二 15 pH s 7 flAif ihr (Ifin iiPniiiilly i niid>：rir E i>e piheut j昭w ilkaJemic? li llif prinwr- diSOtJfr rt碎iralQfV? Is line

13、ibi Then>etaboLic acilos is appicpnate Suicf the pilirnT has a mclbolic AciJoqif, is Ths a liypcrf hlcneiiijf or Ugji auKJii 阿 type 谕jhaUc aciJoJiJ?s ilieiaimliFT (atenboaif Jitatcsis) aciJ d：£tiijk9Btr p:eseiit' Wliai u dlr ilrkd iiEiiuu 別Q (也别prWhiii wf rhf- fJiisrs of ukyp/bf m ajiiQi

14、q gips e?吟uUv ill tins pitiit -Step 1: Internal ConsistencyM Hcndcrscn-Hassclbach equationM H = 24x PCO2/HCO3pH|ir)(mAin)7.001007<0897JC797.15717-2CU7J5号7M507,35457«074535ISO32W528zee2576522Slo* FrwKA6r CMmm祝 Ovc ci C«f«、一 :r- »*' -K*.，乞,Case 1: Internal Consistency22- _ 一

15、、HJ=24 X PCO. / HCOj = 24x 15/6 = 60I'hc data are internally consistentpH1iHMmz"!)7001007,05697107971571rx1 «7QX730SO7.354570407©»730327.S5287M2>7fcSStep 2: Alkalemia or AcidemiaIs there alkalemia or acidemia present? pH V 7,35 acidcinia pH > 7.45 dlkalemiaThis is usual

16、ly the primary disoiderRemember: an acidosis or alkaJusis may be present even if the pH is in the normal range (7.35 - 7.45) Need to check the PaCO?， HCO. and anion gapCase 1: Acidemia or Alkalemiap? The arterial pH = 7.19 < 7.400 The patients is acidemic3fry CNn«M So<Mx *53Cor*砂祥门J,-tnV&

17、amp;. etCOaw What is the relationship between direction of change in【he pH and the direction of change in ihe PaCO,?AcidosisResp iratoryMetabolicAlkalosisRespiraioryMetabolicpHFaV()>Step 3: Respiratory orMetabolicCase 1: Respiratory orMetabolic(ApH = 7.19, PaCO. = 15 The primary disorder is a met

18、abolic acidosispHHaC(>2AcidosisRespimton*MeUbolic*AlkalosisRespirauxyt0Metbolivtt-p trStep 4: CompensationAppr op riate?DiwrdvrExpected CumpensjUlunCormtig FactorMetabolic addosisPM?O? (1 $x(HCOJ) + 8±2Acute respiratory* acidosisHg、 = 24 + APaCO； / 10Chronic res;vatory acidosis (3 to 5 4ay$H

19、CO, = 24 + APaCOj / 3Meuboliv alkalosisPaCO?二(0.7 X+ 21± rsAcute respiratory alkalosis卩 ICO J 二 24 - QRiCO? / 5)Chronic respiratory alkalosisHCOJ = 24-(APaCO； /2)Case 1: CompensationAppropriate?essaeDisorderExpected CompensalinnCorrection FactorMeulv>lic aeidnnisPaCO2-(l 5xn(?Oy|) 1 8±2

20、The expecied PaCO> 二 1.5x6 + 8±2Ihc expected PaCO? =17 + 2Therefore, the measured P382 of 15 is within the predicted nnge<15 to 19) finr normal compensalion-2n -'-厂MA b<nipot*mV < f W# #* < veof C or* 2" a*Step 5: Anion GapAG = Na* Cl - HCOJ = 12*2A normal AG is approxim

21、ately 12 mEq/L lu patients with hypoalbuminemia, the normal AG is about 2.5 mEq/L lower for each 1 gm/dL decrease in the plasma albumin enneenrrationMSyrmMhffP » ChhM”Co AMc.: r T 件w、j e ' r*. CICCMCase 1: Anion Gapess&eAG = Na q - Cl - HCO3 = 12 ± 200GRAG = 128 94 - 6 = 28The norm

22、al AG is 10 to 12Therefore, the patient has a high anion gap metabolic acidosis“d S«x>-/r«nc/i SyrrVMAO byotCsr* AHSux以下两张图片很重要!Step 6: AAGr 7 AAG 琴 measured AG = nonnal AG"2 Predicted starling HCO, = AAG + ineasured HCO, JII < 22, non-anion yap metabolic acidosisw II > 26i n

23、ieL<bulit alkalosisStep 6: A AGexCAI1A = IP +A ir + HCO3 = 1I2CO3 H2CO3 = CO2 + HQIncrease of A=decrease of HCOjAAG = AHCOiI AGHCO,Naa>* * ' ' 八 jfcftbh "乞! nA _ sc*' bCase 1: AAGGQraAAG = 28-10= 18Predicted starting HCO3 = 18 + 6 = 24There is no underlying metabolic alkalosis

24、This, then, is a simple compensaied metabolic acidosisIbqqLS：J-如和>77科-F- '.-7些IJUCase 1: Causes"C咼use? of anian gapmctAholic dc 1110515 Diabetic kcroLKidosis. alcoholic kcioaddoais, lactic acidosisf肩 Drug'i and loxins； toxic akohuls (ineUirinoL cthylcnc l>col :1 he most likclv enu

25、sc ofmetabolic acidosis in ih岳 patient is diabeticCbilscs of Anic'i Gap AcidosisKbfHCjdrt百isPiAbftesEthdiLolNLeEhanolETh*ue gy<olEdkyt 日P.ii.lMrlLVxTr病例2Case 2eeeeA 33 year oU nun wirhh/o chrocuc alcohol use is trough: to the eorrgnry center oAer 3 4iy$ of nausea, vomiting* bdnuul piiit Four

26、bxin Jo be took "somrthinj" to bea wth the |>AUL lie u <w«ke and akif, <ih1 pliyskcal exMiiiuTioo bunmuikabk.E0CM(HntKi =132K = 35C4a=83HCOj = 42PCO,= IOPO.= 110pH =725BG"BUN= MMood okobol s IOt><X111Vrinalrus: 00 procrai or krtoocs, -tw for aystakntQtArc tbc data

27、insrroaly coesutest? Is tbe pftbnil andraiic or dkakmic? Is the pruoiry disorder mptfatcry?Is the cxspeoMtioQ (or the metibohc Acidew apptc|*;ule?Since the patim tusamrabolk acidosu, a this a liypeiclilcirieiuk- or high anioo jip type mubdk acidosis?b thm JAOtbe (meubobc aUeXosts) Mid base disorder

28、presenl? Wliai is the Wp?Wtur areibeausesof Miincreue tnaniocIW-How doe) one make die dujoods of ethyfene ghrol bffstKX?VlTui are possible ouses of mcubolk aflcjlosis?S- W'Ff«f>c/>by CMmw fo«Mx «f Cn2 Core；. I J? RO >、eX* - 'MCase 2: Internal ConsistencyH*<4= 24x P

29、CO./ HCO3 =24 X 10 / 4 = 60The data are internally consistentpHjH'l (snBol/L)7.001007,05897.1079115717.M65701X750135457.0407-453573O327.552876025g22、Case 2: Acidemia or Alkalemia0 The arterial pH = 7.25 < 7.40 心 The patienls is acidemict：V* ? - MCase 2: Respiratory orMetabolic3 pH = 7.25, PaC

30、O2 = 10Q? Theprimary disorder is a metabolic acidosis as the PaCOj is not elevated1pH1 PaCOjAcidosisRespiratoryMetabolic I1 *AlkalosisResp iralory4MeUiboIictDisorderI Expected CompensationCorrection FttctorCase 2: CompensationAppropriate?Metabolic acidosisPaCO2 =(1.5x IlCOy) I SThe expected PaCO? =

31、1.5 x 4 + 8 ± 2The expected PaCO? = 14 ± 2As the measured PaCO? is IQ the compensation is dose enough to say that it is appropnate.Q一竹弋 Case 2: Anion GapAG = NaJ - Cl - HCO31 = 12±2AG= 132-82 4 = 46The normal AG is 10 to 12C This is a highanion gap type metabolic acidosis Z人I申XLCase 2: AAGAAG = 46-10= 36The potential* fate of ihis anion is lo become bicarbonate. The bicarbonate level before the acid base disturbance was 36 + 4 = 40.Therefore, there is an underlying metabolic alkalosis