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ACUTE RESPIRATORY DISTRESS SYNDROME急性呼吸窘迫综合征,Michael L. Fiore, MD Fellow in Critical Care Medicine Mary W. Lieh-Lai, MD, Director, ICU and Fellowship Program Division of Critical Care MedicineChildrens Hospital of Michigan/Wayne State University,A.K.A.另外的名字,Adult Respiratory Distress Syndrome （成人呼吸窘迫综合征） Da Nang Lung（） Transfusion Lung（输液肺） Post Perfusion Lung（灌注肺） Shock Lung Traumatic Wet Lung（创伤后湿肺）,HISTORICAL PERSPECTIVES历史回顾,Described by William Osler in the 1800sAshbaugh, Bigelow and Petty, Lancet 196712 patientspathology similar to hyaline membrane disease in neonatesARDS is also observed in childrenNew criteria and definition,ORIGINAL DEFINITION最初的定义,Acute respiratory distress（急性呼吸窘迫）Cyanosis refractory to oxygen therapy （氧疗无法改善的发绀）Decreased lung compliance（肺顺应性下降）Diffuse infiltrates on chest radiograph （胸牌提示弥漫浸润）Difficulties:lacks specific criteria（缺乏特异的标准）controversy over incidence and mortality（）,REVISION OF DEFINITIONS订正的定义,1988: four-point lung injury scoreLevel of PEEP（呼气末压水平）PaO2 / FiO2 ratio （氧分压与吸入氧浓度的比率）Static lung compliance（静态肺顺应性）Degree of chest infiltrates （肺部浸润的程度）1994: consensus conference simplified the definition,1994 CONSENSUS1994年达成一致看法,Acute onset（）may follow catastrophic event（）Bilateral infiltrates on chest radiograph（）PAWP 18 mm Hg（肺动脉楔压）Two categories（两个分类）Acute Lung Injury - PaO2/FiO2 ratio 300ARDS - PaO2/FiO2 ratio 200,EPIDEMIOLOGY流行病学,Earlier numbers inadequate (vague definition)Using 1994 criteria（使用94年标准）17.9/100,000 for acute lung injury （肺损伤发病率）13.5/100,000 for ARDSCurrent epidemiologic study underway （流行病学研究进行中）In children: approximately 1% of all PICU admissions （儿童：接近1%的PICU病人发生急性肺损伤或ARDS）,INCITING FACTORS引起ARDS的因素,ShockAspiration of gastric contents （胃内容物吸入）Trauma（创伤）Infections（感染）Inhalation of toxic gases and fumes （吸入有毒气体）Drugs and poisons（药物、毒物）Miscellaneous（其它原因）,STAGES（阶段）,Acute, exudative phase（严重渗出时期）rapid onset of respiratory failure after trigger （在触发后呼吸衰竭快速启动）diffuse alveolar damage with inflammatory cell infiltration（由于炎症细胞的浸润导致弥漫性肺泡损伤）hyaline membrane formation（透明膜形成）capillary injury（毛细血管损伤）protein-rich edema fluid in alveoli （肺泡里充满含丰富蛋白质液体）disruption of alveolar epithelium（肺泡上皮破裂）,STAGES（另一阶段）,Subacute, Proliferative phase （亚急性增殖阶段）persistent hypoxemia（顽固的低氧血症）development of hypercarbia （进展的高碳酸血症）fibrosing alveolitis（肺泡纤维化）further decrease in pulmonary compliance 肺顺应性进一步减低pulmonary hypertension（肺动脉高压）,STAGES第三、四阶段,Chronic phase（慢性期）obliteration of alveolar and bronchiolar spaces and pulmonary capillaries 肺泡、细支气管和肺毛细血管塌陷Recovery phase（恢复期）gradual resolution of hypoxemia 低氧血症逐步改善improved lung compliance（肺顺应性改善）resolution of radiographic abnormalities X线异常改变消失,MORTALITY死亡率,40-60%Deaths due to:死亡原因multi-organ failure多器官衰竭Sepsis脓毒症Mortality may be decreasing in recent years 近几年死亡率减少better ventilatory strategies 更好的通气策略earlier diagnosis and treatment（早期诊断及治疗）,PATHOGENESIS发病机制,Inciting eventInflammatory mediators炎症介质Damage to microvascular endothelium 损伤微血管内皮Damage to alveolar epithelium 损伤肺泡上皮Increased alveolar permeability results in alveolar edema fluid accumulation 增加肺泡通透性导致肺泡内液体增多肺泡水肿？,NORMAL ALVEOLUS,ACUTE PHASE OF ARDS,PATHOGENESIS,Target organ injury from hosts inflammatory response and uncontrolled liberation of inflammatory mediators 因为机体炎症应答和炎症介质不受控制的释放导致目标器官的损伤Localized manifestation of SIRS（ SIRS的局部表现）Neutrophils and macrophages play major roles 中性粒细胞和巨噬细胞扮演重要角色Complement activation补体激活Cytokines: TNF-a, IL-1b, IL-6细胞因子Platelet activation factor血小板活化因子Eicosanoids: prostacyclin, leukotrienes, thromboxane 类花生酸类：前列环素、白三烯类、血栓素Free radicals自由基Nitric oxide一氧化氮,PATHOPHYSIOLOGY病理生理学,Abnormalities of gas exchange 气体交换畸形Oxygen delivery and consumption 氧输送耗损Cardiopulmonary interactions 心肺互相影响Multiple organ involvement 多器官受累,ABNORMALITIES OF GAS EXCHANGE气体交换异常情况,Hypoxemia: HALLMARK of ARDS 低氧血症：ARDS的标志Increased capillary permeability 毛细血管渗透性增加Interstitial and alveolar exudate 肺泡及间质的渗出物Surfactant damage肺表面活性物质损伤Decreased FRC功能残气量？储气量？减少Diffusion defect and right to left shunt 气体弥散减少和右向左分流？,OXYGEN DELIVERY氧输送,DO2 = Q X CaO2DO2 = Q X (1.34 X Hb X SaO2) X 10,Q = cardiac output心排量,CaO2 = arterial oxygen content动脉血氧含量Normal DO2: 520-570 ml/min/m2Oxygen extraction ratio = (SaO2-SvO2/SaO2) X 100Normal O2ER = 20-30%,HEMODYNAMIC SUPPORT血流动力学的支持两个图表的区别？,Max O2extraction,Critical DO2,Abnormal Flow Dependency,DO2,VO2,Septic Shock/ARDS,OXYGEN DELIVERY & CONSUMPTION,Pathologic flow dependency 病理学的依存关系Uncoupling of oxidative dependency ？Oxygen utilization 氧利用by non-ATP 没有ATPproducing 产生oxidase systems？Increased diffusion distance for O2 between capillary and alveolus肺泡与毛细血管间增加氧扩散距离,CARDIOPULMONARY INTERACTIONS,A = Pulmonary hypertension resulting in increased RV afterload肺动脉高压导致右心室后负荷增加B = Application of high PEEP resulting in decreased preload高PEEP的应用导致前负荷减少A+B = Decreased cardiac output心输出量减少,RESPIRATORY SUPPORT呼吸支持,Conventional mechanical ventilation 常规机械通气Newer modalities:新的方式High frequency ventilationECMOInnovative strategies创新的策略Nitric oxide一氧化氮Liquid ventilation液体通气Exogenous surfactant外源的肺表面活性物质,MANAGEMENT处理,Monitoring:Respiratory呼吸Hemodynamic血液动力学Metabolic代谢的Infections感染Fluids/electrolytes液体/电解质,MANAGEMENT处理,Optimize VO2/DO2 relationship优化两者关系DO2Hemoglobin 血红蛋白mechanical ventilation 机械通气oxygen/PEEP 氧/PEEPVO2Preload 前负荷Afterload 后负荷Contractility 心肌收缩力,CONVENTIONAL VENTILATION常规通气,OxygenPEEPInverse I:E ratio 反比呼吸Lower tidal volumeVentilation in prone position俯卧位通气,RESPIRATORY SUPPORT呼吸支持,Goal: maintain sufficient oxygenation and ventilation, minimize complications of ventilatory management 目标：维持充足的氧气和交换，最大可能减少机械通气并发症Improve oxygenation: PEEP, MAP, Ti, O2 改善氧合：PEEP, MAP, Ti, O2Improve ventilation: change in pressure 改善通气：压力改变,Mechanical Ventilation Guidelines机械通气指导方针,American College of Chest Physicians Consensus Conference 1993Guidelines for Mechanical Ventilation in ARDSWhen possible, plateau pressures 20 and failure to decrease OI by 20% at six hours predicted death with 88% (7/8) sensitivity and 83% (19/23) specificity, with an odds ratio of 33 (p= .0036, 95% confidence interval 3-365) 高频通气前氧指数大于20，,STUDY CONCLUSIONS研究结论,In patients with potentially reversible underlying diseases resulting in severe acute respiratory failure that is unresponsive to conventional ventilation, high frequency ventilation improves gas exchange in a rapid and sustained fashion.无效的常规通气可能使某些患有可逆性疾病的患者导致严重的急性呼吸衰竭，而高频通气能迅速、持久的改善患者的气体交换。The magnitude of impaired oxygenation and its improvement after high frequency ventilation can predict outcome within 6 hours.氧合作用损伤的大小和改善的程度在高频通气6小时内可以预知。,High Frequency Oscillating Ventilation (HFOV) Pediatric ARDS儿科ARDS病儿高频振荡通气,Arnold JH et al. Crit Care Med 1994; 22:1530-1539.Prospective, randomized clinical study with crossover of 70 patientsHFOV had fewer patients requiring O2 at 30 daysHFOV patients had increase survivorSurvivors had less chronic lung disease,New England Journal of Medicine 2000;342:1301-8,STUDY CONCLUSION,In patients with acute lung injury and the acute respiratory distress syndrome, mechanical ventilation with a lower tidal volume than is traditionally used results in decreased mortality and increases the number of days without ventilator use,Prone Position,Improved gas exchangeMore uniform alveolar ventilationRecruitment of atelectasis in dorsal regionsImproved postural drainageRedistribution of perfusion away from edematous, dependent regions,Prone Position,Nakos G et al. Am J Respir Crit Care Med 2000;161:360-68Observational study of 39 patients with ARDS in different stages Improved oxygenation in prone (PaO2/FiO2 18934 prone vs. 8314 supine) after 6 hoursNo improvement in patients with late ARDS or pulmonary fibrosis,Prone Position,NEJM 2001;345:568-73Prone-Supine Study GroupMulticenter randomized clinical trial304 adult patients prospectively randomized to 10 days of supine vs. prone ventilation 6 hours/dayImproved oxygenation in prone positionNo improvement in survival,Exogenous Surfactant,Success with infants with neonatal RDSExosurf ARDS Sepsis Study. Anzueto et al. NEJM 1996;334:1417-21Randomized control trialMulticenter study of 725 patients with sepsis induced ARDSNo significant difference in oxygenation, duration of mechanical ventilation, hospital stay, or survival,Exogenous Surfactant,Aerosol delivery system only 4.5% of radiolabeled surfactant reached lungsOnly reaches well ventilated, less severe areasNew approaches to delivery are under study, including tracheal instillation and bronchoalveolar lavage,Inhaled Nitric Oxide (iNO),Pulmonary vasodilatorSelectively improves perfusion of ventilated areasReduces intrapulmonary shuntingImproves arterial oxygenationT1/2 111 to 130 msecNo systemic hemodynamic effects,Inhaled Nitric Oxide (iNO),Inhaled Nitric Oxide Study Group Dellinger RP et al. Crit Care Med 1998; 26:15-23Prospective, randomized, placebo controlled, double blinded, multi-center study177 adults with ARDSImprovement in oxygenation indexNo significant differences in mortality or days off ventilator,Inhaled Aerosolized Prostacycli