急性肺损伤ALI.ppt

第二十二章急性肺损伤（ALI）急性呼吸窘迫综合征（ARDS）ACUTE LUNG INJURY ACUTE LUNG INJURY ACUTE RESPIRATORY DISTRESS SYNDROMEACUTE RESPIRATORY DISTRESS SYNDROME 概述lDAD:diffuse alveolar damage（弥漫性肺泡损害）lEtiology:shock,infection,trauma,aspiration,drugs,inhalation etc.lALI&ARDS:a syndrome of pulmonary vasoconstriction,inflammation and greater permeability of both the alveolar capillary endothelium and epithelium that results in both arterial hypoxemia,resistant to oxygen therapy and the appearance of diffuse infiltrates on chest X-rays.Synonyms for Acute(adult)Respiratory Distress SyndromeSynonyms for Acute(adult)Respiratory Distress SyndromelAdult hyaline membrane diseaselAdult respiratory insufficiency syndromelCongestive atelectasislDa Nang lunglHemorrhagic atelectasislHemorrhagic lung syndromelHypoxic hyperventilationlPostperfusion lunglPost-traumatic atelectasislPost-traumatic pulmonary insufficiencylProgressive pulmonary consolidationlProgressive respiratory distresslPump lung、Shock lunglTransplant lunglTraumatic wet lung、Wet lung、White lungFrom Taylor RW,Duncan CA:The adult respiratory distress syndrome.Resident Med 1983;1:17ALI&ARDSl病理生理改变：急性肺损伤反应，肺泡的弥漫性损害（血管内皮和肺泡上皮细胞的损伤，肺泡的实变，成纤维细胞的增生和胶原纤维的沉着）。ALI&ARDSlCLINICALFEATURES（临床表现）呼吸急促，呼吸音改变进行性呼吸困难，低氧血症双侧肺部浸润影心动过速等ALI&ARDSViolent and choatic immunologic reactionPulmonary microvascular thrombosis Aggregation of inflammatory cells Stagnation of blood flow through the lungs Intensive hypoxemia Pulmonary arterial hypertension Radiographic evidence:pulmonary edemaStiff lung ALI&ARDSlARDS is not a single disease,l but rather a pathophysiologic syndrom.1.病因 etiologyetiologylSepsis&MODSlTraumalAspiration(误吸)lBlood transfusionletc.2.病理生理 pathophysiologypathophysiologyl基本病理改变：acute exudative phase proliferative phase chronic fibrotic phase PATHOPHYSIOLOGYl非心源性高通透性肺水肿lNon-cardiac pulmonary edema with increased permeabilityl肺呼吸功能改变lChanges of lung respiratory functionl肺循环功能改变lChanges of lung circulatory functionPATHOPHYSIOLOGYlInflammatory ResponseInflammatory ResponseAcute alveolar and endothelial damageVascular permeabilityLung waterproteinGas exchangeincreasedecreaseInflammatory Mediators in ARDSInflammatory Mediators in ARDSlCytokinesInterleukinsTumor necrosis factorInterfornslComplement proteinslContact activation proteinsBradykininlCoagulation proteinsThrombinFibrin degradation productsProgtaglandinsLeukotrienesVasoactive peptidesSerotoninHistaminePlatelet-activating factorsFrom Foner BJ,Norwood S,Taylor RW:The acute repiratory distress syndrome In:Critical Care.3rd ed.Civetta JM,Taylor RW,Kirby RR(Eds).Philadelphia,Lippincott-Raven,1997,pp 18251839PATHOPHYSIOLOGYlPulmonary edema formation and microcirculatory injury:Pulmoanry edema formationEndothelial injuryEpithelial injuryVentilator induced pulmoary edemaPATHOPHYSIOLOGYlHistologic changeslSurfactant AlterationlLung mechanics and Gas exchangelExtrapulmonary organ failureComponents and Individual Values of the Lung Injury ScoreComponents and Individual Values of the Lung Injury ScorelComponent ValuelChest roentgenogram score l No alveolar consolidation 0l Alveolar consolidation confined to 1 quadrant 1l Alveolar consolidation confined to 2 quadrant 2l Alveolar consolidation confined to 3 quadrant 3l Alveolar consolidation in all 4 quadrant 4lHypoxemia scorel PaO2/FiO2 300 0l PaO2/FiO2 225299 1l PaO2/FiO2 175224 2l PaO2/FiO2 100174 3l PaO2/FiO2 100 4lPEEP scorel PEEP 5 cmH2O 0l PEEP 68 cmH2O 1l PEEP 911 cmH2O 2l PEEP 1214 cmH2O 3l PEEP 15 cmH2O 4The final value is obtained by dividing the aggregate sum by the number of components that were used.No lung injury:0Mild to moderate:0.12.5Severe:2.5From Murray JF,Mathay MA,Luce JM,et al:An expanded definition of the adult respiratory distress syndrome.Am Rev Respir Dis 1988;138:720.临床分期ARDS分期：分期：第一期：原发病临床表现第一期：原发病临床表现第二期：轻度呼吸困难第二期：轻度呼吸困难第三期：呼吸窘迫第三期：呼吸窘迫第四期：严重呼吸窘迫第四期：严重呼吸窘迫4.Diagnosis CriterialALI:PaO2/FiO2300(whatever PEEP)l Bilateral infiltrates on chest radiographl PAWP18mmHg or no clinical findings suggestive of increased LAPlARDS:PaO2/FiO2200(whatever PEEP)l Bilateral infiltrates on chest radiographl PAWP18mmHg or no clinical findings suggestive of increased LAP From Bernard GR,Artigas A,Brigham KL,et al:The American-European consensus conference on ARDS definitions.Am J Respir Crit Care Med 1994;149:818患者，女性，患者，女性，63，误吸。，误吸。38mmHg,100%9h后后：56mmHg,50%13h后：后：65mmHg,50%20h后：后：79mmHg,50%34h后：后：73mmHg,50%5.治疗治疗 therapy or treatmenttherapy or treatment1.积极治疗原发疾病7.部分液体通气2.控制感染8.表面活性物质替代3.机械通气支持9.免疫疗法的应用4.降低肺血管阻力 10.营养代谢支持疗法5.肾上腺糖皮质激素 12.循环功能的支持6.体外膜肺氧合 Fluid TherapylConventional Approach:Aims of resuscitation in ARDS:1.Attain normal vital signs while PAWPis kept as low as possible.2.Fluid restriction and diuretic administration.(1)Input and output records of large amount of fluids given befor the diagnosis of ARDS was given.(2)Clinical evidence of excessive fluid retention,such as peripheral edema.(3)Clinical radiologic evidence of pulmoary congestive and edema(4)Improvement in arterial blood gas values after diuretic therapyFluid TherapylCritique of conventional approach:Pulmonary edema may be caused by so many diseases.In postoperative,posttrauma and sepsis patients,pulmonary edema is due to overexpansion of the interstitium,not to plasma volume overload.Peripheral and pulmonary edema reflect:interstitial fluid volumes increase,plasma oncotic pressure decrease,nutritional failure,endothelial permeability increase,lung hypoxia or anaphylactoid reactions(过敏反应)Hypovolumia is a major pathophysiologic factor of ARDS;pulmonary edema is an effect,not the cause of,ARDS.Fluid TherapylFluid therapeutic goals values:CI4.5 L/min.m2DO2 600 ml/min.m2VO2 170ml/min.m2Blood volume 500 ml greater than normall3.2 L/min.m2(men)l2.7 L/min.m2(women)lAll these values should be reached within 812h postoperatively or after trauma From Shoemaker WC,Ayres SM,Ake Grenvik,Holbrook PR.Textbook of Critical Care,4th Edition.Harcourt Publishers Limited.2000.1397.Fluid TherapylFor patients with severe lung injury,less is more.l in a news release from the National Heart,Lung and Blood Institute with this headline.lFluid management is a complex issue,and,until now,it was not clear whether providing more or less fluids was more beneficial.Current trends in usual care appear to more closely resemble the liberal fluid management arm of this study-the stdy arm with worse outcomes.l Gordon Bemard,chair of NIH ARDS Network Steering CommitteeMechanical VentilationlLung-protective strategies(肺保护策略):Permissive hypercapnia(允许性高碳酸血症)Low tidal volume+high PEEPlRecruitment maneuver(肺复张法)lProne position(俯卧位)lNO inhalationlExtracorporeal gas exchange(体外气体交换)ECMO(体外膜肺氧合)ECCO2OR(体外CO2清除)Lung protective ventilationlLow tidal volume:6 ml/kg vs 1012 ml/kglPeak airway pressure 30 cmH2OlDriving pressure 20 cmH2OlPaCO2 60 mmHglpH 7.20lHigh PEEP than conventional valuesLung protective ventilation-physiologic consequencies of hypercapnia-physiologic consequencies of hypercapnialCellular effects:intracellular acidosisIn the absence of hypoxemia,intracellular acidosis appears to be well tolerated in critical ill patients.lCardiovascular effects:high sympathetic activityIncrease:HR,BP,PVRDecrease:SVRlCNS effects:CBF and ICP increaseConsciousness:severe agitation,seizure,coma.Lung protective ventilation-recruitment maneuver-recruitment maneuverOpen the lung and keep the lung openLung protective ventilation-stepwise recruitment maneuver-stepwise recruitment maneuverlPEEP titration depend on:Pdeflex、PaCO2、CompliancelPEEP in crement:23 cmH2OlMaintain:12 minuteslPEEP target:16/1st RM;20/2nd RM;26-30/3rd RMlPIPmax:40 cmH2OlInterval:twice a dayProne position 俯卧位lPhysiologic effects:Reexpand consolidated depedent lung regionImprove V/Q matchingReduce the compressive force of the heart to lunglComplications:Accidental extubation,removal of invasive catheters,facial injury,retinal ischemia,blindness from pressure on the eyeball,peripheral neuropathy,etc.再见l