ARDS肺复张的临床实施-医学课件.ppt

BP 70/50，HR 170,cvp 8.NE 5 PHE 5 FiO2 70%,PEEP 12 Ph24 SaO2 90%ARDSARDS常见的临床综合征常见的临床综合征内容提要病理生理特点病理生理特点肺泡塌陷的危害肺泡塌陷的危害如何实施肺复张如何实施肺复张?肺复张疗效的判断肺复张疗效的判断影响肺复张实施的因素影响肺复张实施的因素30 kg 猪肺灌洗复制ARDS模型压力控制通气PCVPaw 13 cmH2O PEEP 5 cmH2OARDS-肺泡塌陷广泛存在肺泡塌陷广泛存在肺容积明显降低肺容积明显降低(a)肺泡水肿肺泡水肿(b)肺泡表面活性物质的消耗或不足肺泡表面活性物质的消耗或不足(c)肺间质水肿压迫远端细支气管肺间质水肿压迫远端细支气管肺顺应性明显降低肺顺应性明显降低通气通气/血流比例失调血流比例失调 肺内分流和死腔样通气肺内分流和死腔样通气ARDS的病理生理的病理生理CT scan70-80%的肺野呈现高密度区的肺野呈现高密度区分布：下垂部位分布：下垂部位(dependent field)提示：提示：1.参与通气的肺泡区域明显减少参与通气的肺泡区域明显减少(20-30%)2.肺损伤具有不均一性肺损伤具有不均一性肺容积减少肺容积减少Small lung Baby Lung肺顺应性明显降低肺顺应性明显降低Reduced range of volume excursion:Low complianceFlattening at low and high volumes:Lower and upper inflection pointsVolumePressureNORMALARDS顺应性曲线明显向右下移位顺应性曲线明显向右下移位肺内分流增加肺内分流增加肺泡塌陷：肺泡塌陷：ARDS重力依赖区重力依赖区 炎症或不张区炎症或不张区生理性低氧缩血管反应：障碍生理性低氧缩血管反应：障碍HEARTSPARDS-Gattinoni分区分区1.1.过度通气区或过度通气区或“干区干区”“baby lungbaby lung2.2.可复张区或湿区可复张区或湿区3.3.实变实变区区内容提要病理生理特点病理生理特点肺泡塌陷的危害肺泡塌陷的危害如何实施肺复张如何实施肺复张?肺复张疗效的判断肺复张疗效的判断影响肺复张实施的因素影响肺复张实施的因素PEEP肺复张与肺复张与低氧血症改善低氧血症改善Gattinoni L,Caironi P,Pelosi P,et al.Am J Respir Crit Care Med,2001,164:1701-1711 A.低氧血症低氧血症PressureVolumePressure wedgeShear forceB.剪切力剪切力(Shear force)DR-RM 盐水灌肺制造家兔盐水灌肺制造家兔ARDSARDS模型模型低流速法测定低流速法测定LIPLIP水平水平肺保护通气肺保护通气3 3h,Vt6ml/kg,PEEP=LIPh,Vt6ml/kg,PEEP=LIPDRDR后予后予SI SI的的RMRMDRDR后予后予PCVPCV的的RMRM每小时的每小时的0 0、1010、2020、3030、4040分钟分钟将呼吸机脱开将呼吸机脱开1 1分钟分钟制造肺泡的重复去复张制造肺泡的重复去复张(DR)DR)动物处死，取肺病理检查、测湿动物处死，取肺病理检查、测湿/干重比、测干重比、测TNF-mRNATNF-mRNA表达、表达、转录因子转录因子NF-BNF-B的活性的活性 、MPOMPO及及MDAMDA活性活性对照组对照组ARDSARDS组组LPLP组组DRDR组组PCVPCV组组SI SI组组动物准备动物准备1 2 3 456 1、2、3、4、5和和6泳道分别为正常、泳道分别为正常、ARDS、DR、LP、SI和和PCV组组肺复张手法对重复去复张肺复张手法对重复去复张ARDSARDS家兔家兔肺组织肺组织NF-NF-B B 活性的影响活性的影响肺复张手法对重复去复张肺复张手法对重复去复张ARDSARDS家兔家兔 肺组织肺组织TNFmRNA TNFmRNA 表达的影响表达的影响 01 23 45 6 1、2、3、4、5和和6泳道泳道分别为分别为Normal、ARDS、LP、DR、SI和和PCV组组0泳道为分子质量标准泳道为分子质量标准肺复张手法对重复去复张肺复张手法对重复去复张ARDS ARDS 家兔家兔PaO2 PaO2 的影响的影响C.C.感染与肺不张感染与肺不张全麻-肺不张的发生率 90%择期腹部手术：肺不张肺部感染9.6%择期心脏手术：肺不张肺部感染5.7%肥胖病人手术：25%-30%发生肺不张肺部感染 CHEST 1997;111:564-71Qiu Haibo.Chin J Emerg Med,2001,10(5):293-294 气压伤气压伤气压伤气压伤 生物伤生物伤生物伤生物伤启动炎症反应启动炎症反应启动炎症反应启动炎症反应炎症介质移位炎症介质移位炎症介质移位炎症介质移位细菌毒素移位细菌毒素移位细菌毒素移位细菌毒素移位MODS/MOFD.气压伤、生物伤与气压伤、生物伤与MODSFrom SluskyARDSmotor of MODS邱海波邱海波.中华急诊医学杂志中华急诊医学杂志,2001,10(5):293-294 Biotrauma Barotrauma initiate a cascade of proinfla mediators肺是炎症细胞激活和聚积的重要场所肺是炎症细胞激活和聚积的重要场所肺实质细胞可释放炎症介质肺实质细胞可释放炎症介质 Mediator translocationBacteria and LPS translocationMODS/MOFDuggan M.Am J Respir Crit Care Med.2003,167:1633-1640.持续肺泡塌陷持续肺泡塌陷-预后不良预后不良临床研究临床研究:塌陷肺泡越多塌陷肺泡越多,病死率越高病死率越高N Engl J Med 2006;354:1775-86内容提要病理生理特点病理生理特点肺泡塌陷的危害肺泡塌陷的危害如何实施肺复张如何实施肺复张?肺复张疗效的判断肺复张疗效的判断影响肺复张实施的因素影响肺复张实施的因素20406080100Pressure cmH2O102030406050Total Lung Capacity%R=22%R=81%R=100%R=93%肺复张是压力依赖性过程肺复张是压力依赖性过程00R=0%R=59%From Pelosi et alAJRCCM 20011/5 of“Recruitable”Units肺复张是压力依赖性过程肺复张是压力依赖性过程 40 SECONDS肺复张的常用方法肺复张的常用方法l控制性肺膨胀控制性肺膨胀(SI)lPEEP递增法递增法l压力控制法压力控制法(PCV)45 for 40 s 35 Peak45/16 and 1:2 for 120 sPCV Advantages-Same Recruiting Pressure-Repeated Maneuvers-Lower Mean Pressure-Preserved Ventilation1.CPAP模式模式:PS 0,PEEP 30-40 cmH2O,20-50s 2.BIPAP:Ph/PL 30-40cmH2O,20-50s 3.Insp Hold:将吸气保持键按住，持续将吸气保持键按住，持续20-40s控制性肺膨胀控制性肺膨胀(SI)法法内容提要病理生理特点病理生理特点肺泡塌陷的危害肺泡塌陷的危害如何实施肺复张如何实施肺复张?肺复张疗效的判断肺复张疗效的判断影响肺复张实施的因素影响肺复张实施的因素肺泡完全复张的临床标准肺泡完全复张的临床标准氧合标准CT标准EIT标准肺泡完全复张的临床标准肺泡完全复张的临床标准-PaO2/FiO21.PaO2/FiO2400 PaO2+PaCO2 400 2.PaO2/FiO2 降低降低5%lPaO2+PaCO2 400(at 100%oxygen):维持肺开放的可靠指标维持肺开放的可靠指标l达到达到PaO2+PaCO2 400时：时：CT显示只有显示只有5%的肺泡塌陷的肺泡塌陷l PaO2+PaCO2 400对塌陷肺泡的对塌陷肺泡的预测：预测：ROC曲线下面积曲线下面积 0.943Borges JB,Amato MBP.Am J Respir Crit Care Med Vol 174.pp 111,2006肺泡完全复张的临床标准肺泡完全复张的临床标准-CT肺泡完全复张的临床标准肺泡完全复张的临床标准-CTBorges JB,Amato MBP.Am J Respir Crit Care Med Vol 174.pp 111,2006l动脉氧合与塌陷肺组织重量明显呈负相关动脉氧合与塌陷肺组织重量明显呈负相关(R=0.91)Lower vs higher Lower vs higher Percentage of Potentially Recruitable LungPercentage of Potentially Recruitable LungARDSARDS塌陷肺泡都能重新开放吗塌陷肺泡都能重新开放吗?N Engl J Med 2006;354:1775-86PEEP 5cmH2O Ppla 20cmH2OPEEP 17cmH2O Ppla 40cmH2OPEEP 25cmH2O Ppla 40cmH2OPEEP 25cmH2O Ppla 60cmH2OCorrespondence:Amato,N Engl J Med 2006,355:319内容提要病理生理特点病理生理特点肺泡塌陷的危害肺泡塌陷的危害如何实施肺复张如何实施肺复张?肺复张疗效的判断肺复张疗效的判断影响肺复张实施的因素影响肺复张实施的因素Prespective,randomized study:Effect of RM on ARDSPrespective,randomized crossover study34 ICU at 19 hospRM:CPAP over 510 s to 35 cm H2OPEEP:FIO2/PEEPstep to maintain SpO2 8895%.CCM,2003,31(11):2592-7肺泡复张的决定因素肺泡复张的决定因素(1):肺内肺内 vs 肺外源性肺外源性ARDS ARDS Trial Network,Crit Care Med 2003;31(11):2592-2597Starting Conditions For the ARDSnet Recruiting TrialPrimary为什么为什么RMRM改善氧合不明显？改善氧合不明显？病人的特点：病人的特点：l入组时入组时Ppla 26.4Ppla 26.4l肺内原因肺内原因ARDSARDS占占65%65%Paw cmH2O%05 10 15 20 25 30 35 40 45 5001020304050Crotti et al.AJRCCM 2001.PPLATPRECRUITOpening Pressures:Primary ARDS RM能够实现能够实现ARDS肺完全开放肺完全开放实现实现 open the lung and keep the lung open in the 24/26 patsBorges JB,Amato MBP.Am J Respir Crit Care Med Vol 174.pp 111,2006麻醉导致的非炎症性肺泡塌陷麻醉导致的非炎症性肺泡塌陷肺泡复张的决定因素肺泡复张的决定因素(2):病理特征病理特征Rothen HU.Dynamics of reexpansion of atelectasis during general anaesthesia.Br J Anaesth1999;82:5516Lim,et,al.Anesthesiology 2003;99:71ARDS导致的炎症性肺泡塌陷导致的炎症性肺泡塌陷SuperimposedPressureOpeningPressureInflated0Alveolar Collapse(Reabsorption)20-60 cmH2OSmall AirwayCollapse10-20 cmH2OConsolidation(modified from Gattinoni)Regional Spectrum of Opening Pressures肺泡复张的决定因素肺泡复张的决定因素(3):压力与时间压力与时间实现实现 open the lung and keep the lung open in the 24/26 patsBorges JB,Amato MBP.Am J Respir Crit Care Med Vol 174.pp 111,2006Multiple maneuvers-获得理想的复张效应获得理想的复张效应Fujino et al,Crit Care Med 2001;29(8):1579-1586肺泡复张的决定因素肺泡复张的决定因素(4):ARDS病程病程(早期早期vs 后期后期)N=17 ARDS with a lung protective ventEarly ARDS(n=9)vs Late ARDS(n=8,7d)RM:PCV 2min at PIP 50cmH2O/PEEP PUIPAm J Respir Crit Care Med,2002,165:165170不同不同RM方法的肺复张效应不同方法的肺复张效应不同PCVPCVVolume increments at 15 min Post-RM in VILI ModelPaw cmH2O%Opening and Closing Pressures0510152025303540455001020304050 Opening pressureClosing pressure5 patients,ALI/ARDSFrom Crotti et alAJRCCM 2001.Some units cantbe kept open by any reasonable PEEP!肺泡复张的决定因素肺泡复张的决定因素(5):循环耐受情况循环耐受情况An RM Can Profoundly Depress COAveraged Data from 3 ModelsS-C Lim,et al 2004RM导致的血流动力学改变导致的血流动力学改变ARDS pats n=10 SI的实施：的实施：30cmH2O，20s SI时时vPAP、CVP、PAWP、PVRI和和RVSWI均显著增加均显著增加(P 12%RM面临的循环困境面临的循环困境LMRs:40 cmH2O for 10 s or 20 s lCO reduction 50%lLV end-diastolic area 45%lMean arterial pressure drop 20%Of course,hemodynamic status return stable within 3minIntensive Care Med(2005)31:11891194lProspective randomized cross-over studylPats with CABGlRM(40 cmH2O X 10 s/20sRM循环干扰的机制：循环干扰的机制：Effect of RM on LV preloadIntensive Care Med(2005)31:11891194TEE:transgastric ED short axis view of the LVA before a 10s LRMB at the end of a 10-s LRMC before a 20s LRMD at the end of a 20-s LRMRM循环干扰的机制：循环干扰的机制：Effect of RM on RV afterloadIncrease in RV afterloadlAlveolar overdistention of aerated lung areaslHypoxic vasoconstriction in atelectatic lung areasAtelectasis causes vascular leak and lethal right ventricular failure in uninjured rat lungs.Am J Respir Crit Care Med 2003,167:1633-1640.Ventilation above closing volume reduces pulmonary vascular resistance hysteresis.Am J Respir Crit Care Med 1998,158:1114-1119.RM效应lRandomized,controlled,cross-over studylPig ARDS model by lung-lavagelRM:12s-s X 40 cm H2O OR 30-s X 40 cm H2ORM循环干扰的机制：循环干扰的机制：Effect of RM on Leftward septal shiftEchocardiogram:via the short axis end-diastolic view of the RV and LVBefore RM and at the end of a 30-s RMIntensive Care Med(2006)32:585594RM Effect on CO Varies Among Injury ModelsAveraged data for 3 RM Methods PNMPNMVILIVILIS-C Lim,CCM 2004突破循环限制血流动力学干扰 vs ARDS病因(a)Pigs with BAL vs LPS-induced ALIRM for 1 minvital capacity manoeuvres(ViCM)at SI30 OR SI40 cmH2OPCRM with peak airway pressure PIP/PEEP30/15 OR 40/20 Volume expansion:dextran 8 ml/kgIntensive Care Med(2005)31:112120Aortic blood flow(ABF)Mesenteric blood flow(QPV)BAL-ARDSLPS-ARDS突破循环限制血流动力学干扰 vs ARDS病因(a)1.RM使三种使三种 ARDS模型模型 CI均明显下降均明显下降2.CI盐酸组降低盐酸组降低37%油酸组油酸组 19%生理盐水组生理盐水组 23%3盐酸组盐酸组5min后接近后接近 RM前水平前水平 不同病因的不同病因的ARDS vs RM对对CI的影响的影响Effect of RM Method on CO in Pneumonia ModelSISIPCVPCVS-C Lim,CCM 2004突破循环限制血流动力学干扰 vs RM方法(b)*nHCI吸入复制模型吸入复制模型nCI降低程度不同降低程度不同pPCV:降低降低25%pSI:降低降低46%pIP:降低降低39%RM方法不同对方法不同对CI的影响的影响Pigs with BAL vs LPS-induced ALIRM for 1 minvital capacity manoeuvres(ViCM)at SI30 OR SI40 cmH2OPCRM with peak airway pressure PIP/PEEP30/15 OR 40/20 Volume expansion:dextran 8 ml/kgIntensive Care Med(2005)31:112120Aortic blood flow(ABF)Mesenteric blood flow(QPV)BAL-ARDSLPS-ARDS突破循环限制血流动力学干扰 vs RM方法(b)突破循环限制血流动力学干扰 vs RM方法(b)Intensive Care Med(2006)32:585594突破循环限制血流动力学干扰 vs Volume expansion(c)Volume status in pats with ARDS Intensive Care Med(2006)32:585594Pigs with ARDS,RM for 1 minvital capacity manoeuvres(ViCM)at SI30 OR SI40 cmH2OPCRM with peak airway pressure PIP/PEEP30/15 OR 40/20 Volume expansion:dextran 8 ml/kgIntensive Care Med(2005)31:112120Aortic blood flow(ABF)Mesenteric blood flow(QPV)BAL-ARDSLPS-ARDS突破循环限制血流动力学干扰 vs Volume expansion(c)lRandomized,controlled,cross-over studylPig ARDS model by lung-lavagelRM:12s-s X 40 cm H2O OR 30-s X 40 cm H2OlVolume status:under hypovolemia,normovolemia and hypervolemiaEffect of volume status on Leftward septal shiftlEchocardiogram Screen:via the short axis end-diastolic view of the left and right ventricleslBefore RM and at the end of a 30-s RMIntensive Care Med(2006)32:585594突破循环限制血流动力学干扰 vs Volume/septal shift(d)hypovolemia,normovolemia and hypervolemia突破循环限制血流动力学干扰 vs Volume/septal shift(d)Anesthetized pigsA bronchial blocker was inserted in the right lower lobe,which was selectively lavaged to create a dense lobar collapse.Randomized into two groupsSelective lung RM(using the inner lumen of the bronchial blocker)General lung RMRM 40cmH2O for 30 s突破循环限制血流动力学干扰 vs Selective RM(e)Before(A)and after(B)selective lobar recruitmentANESTH ANALG 2006;102:150410突破循环限制血流动力学干扰 vs Selective RM(e)ANESTH ANALG 2006;102:150410Hemodynamic effectlSelective RM:no circulatory changeslGeneral lung RM:lmABP decreased significantly by 36(21,41)mm HglCO decreased by 2.1(1.6,2.5)L/min lLVED area decreased by 4.4(3.5,4.5)cm2.Transthoracic end-diastolic short axis view of the LV at baseline(A),after recovery(B),at the end of a selectiveLRM (C),and at the end of a general LRM(D)突破循环限制血流动力学干扰 vs Selective RM/Low volume(e)Anesth Analg 2007;105:729 34Hemodynamic effectlNormovolemia and 20%hypovolemia:no circ changesl40%hypovolemia:l CO:unchangedlmABP(mmHg)pBefore RM:48 pEnd of RM:40(P0.05)p3 min after RM:47lAnesthetized pigslA bronchial blocker was inserted in the right lower lobelS-LRM 40cmH2O for 30 slat normovolemia,lafter venesection of 20%of the blood volume,lafter venesection of 40%of the blood volume,小结小结l肺复张是肺复张是ARDS降低肺不张降低肺不张,减少肺内分流的重要减少肺内分流的重要手段手段l塌陷肺泡是否能够开放受多种因素影响塌陷肺泡是否能够开放受多种因素影响-肺复张的方法肺复张的方法(手段手段,压力压力,时间时间,次数次数)-原发病原发病(pul vs non-pul)与病理特征与病理特征-ARDS病程病程-肺泡过度膨胀肺泡过度膨胀(VILI)与循环干扰与循环干扰l多数多数ARDS患者通过高条件的肺复张可实现塌陷肺患者通过高条件的肺复张可实现塌陷肺泡的复张泡的复张