急性呼吸窘迫综合征英文教学课件教学课件

1、急性呼吸窘迫综合征-英文课件A.K.A. Adult Respiratory Distress Syndrome Da Nang Lung Transfusion Lung Post Perfusion Lung Shock Lung Traumatic Wet LungHISTORICAL PERSPECTIVESDescribed by William Osler in the 1800sAshbaugh, Bigelow and Petty, Lancet 196712 patientspathology similar to hyaline membrane disease in ne

2、onatesARDS is also observed in childrenNew criteria and definitionORIGINAL DEFINITIONAcute respiratory distressCyanosis refractory to oxygen therapyDecreased lung complianceDiffuse infiltrates on chest radiographDifficulties:lacks specific criteriacontroversy over incidence and mortalityREVISION OF

3、DEFINITIONS1988: four-point lung injury scoreLevel of PEEPPaO2 / FiO2 ratioStatic lung complianceDegree of chest infiltrates1994: consensus conference simplified the definition1994 CONSENSUSAcute onsetmay follow catastrophic eventBilateral infiltrates on chest radiographPAWP 18 mm HgTwo categories:A

4、cute Lung Injury - PaO2/FiO2 ratio 300ARDS - PaO2/FiO2 ratio 200EPIDEMIOLOGYEarlier numbers inadequate (vague definition)Using 1994 criteria:17.9/100,000 for acute lung injury13.5/100,000 for ARDSCurrent epidemiologic study underwayIn children: approximately 1% of all PICU admissionsINCITING FACTORS

5、ShockAspiration of gastric contentsTraumaInfectionsInhalation of toxic gases and fumesDrugs and poisonsMiscellaneousSTAGESAcute, exudative phaserapid onset of respiratory failure after triggerdiffuse alveolar damage with inflammatory cell infiltrationhyaline membrane formationcapillary injuryprotein

6、-rich edema fluid in alveolidisruption of alveolar epitheliumSTAGESSubacute, Proliferative phase:persistent hypoxemiadevelopment of hypercarbiafibrosing alveolitisfurther decrease in pulmonary compliancepulmonary hypertension STAGESChronic phaseobliteration of alveolar and bronchiolar spaces and pul

7、monary capillariesRecovery phasegradual resolution of hypoxemiaimproved lung complianceresolution of radiographic abnormalitiesMORTALITY40-60%Deaths due to:multi-organ failuresepsisMortality may be decreasing in recent yearsbetter ventilatory strategiesearlier diagnosis and treatmentPATHOGENESISInci

8、ting eventInflammatory mediatorsDamage to microvascular endotheliumDamage to alveolar epitheliumIncreased alveolar permeability results in alveolar edema fluid accumulationNORMAL ALVEOLUSType I cellEndothelialCellRBCsCapillaryAlveolarmacrophageType IIcellACUTE PHASE OF ARDSType I cellEndothelialCell

9、RBCsCapillaryAlveolarmacrophageType IIcellNeutrophilsPATHOGENESISTarget organ injury from hosts inflammatory response and uncontrolled liberation of inflammatory mediatorsLocalized manifestation of SIRSNeutrophils and macrophages play major rolesComplement activationCytokines: TNF-a, IL-1b, IL-6Plat

10、elet activation factorEicosanoids: prostacyclin, leukotrienes, thromboxaneFree radicalsNitric oxidePATHOPHYSIOLOGYAbnormalities of gas exchangeOxygen delivery and consumptionCardiopulmonary interactionsMultiple organ involvementABNORMALITIES OF GAS EXCHANGEHypoxemia: HALLMARK of ARDSIncreased capill

11、ary permeabilityInterstitial and alveolar exudateSurfactant damageDecreased FRCDiffusion defect and right to left shuntOXYGEN EXTRACTIONVO2 = Q x Hb X 13.4 X (SaO2 - SvO2)ArterialInflow (Q)capillaryO2O2O2O2O2O2O2VenousOutflow (Q)CellO2(Adapted from the ICU Book by P. Marino)OXYGEN DELIVERYDO2 = Q X

12、CaO2DO2 = Q X (1.34 X Hb X SaO2) X 10Q = cardiac outputCaO2 = arterial oxygen contentNormal DO2: 520-570 ml/min/m2Oxygen extraction ratio = (SaO2-SvO2/SaO2) X 100Normal O2ER = 20-30%HEMODYNAMIC SUPPORTMax O2extractionCritical DO2VO2 = DO2 X O2ERDO2VO2NormalMax O2extractionCritical DO2Abnormal Flow D

13、ependencyDO2VO2Septic Shock/ARDSOXYGEN DELIVERY & CONSUMPTIONPathologic flow dependencyUncoupling of oxidative dependencyOxygen utilization by non-ATP producing oxidase systemsIncreased diffusion distance for O2 between capillary and alveolusCARDIOPULMONARY INTERACTIONSA = Pulmonary hypertension res

14、ulting in increased RV afterloadB = Application of high PEEP resulting in decreased preloadA+B = Decreased cardiac outputRESPIRATORY SUPPORTConventional mechanical ventilationNewer modalities:High frequency ventilationECMOInnovative strategiesNitric oxideLiquid ventilationExogenous surfactantMANAGEM

15、ENTMonitoring:RespiratoryHemodynamicMetabolicInfectionsFluids/electrolytesMANAGEMENTOptimize VO2/DO2 relationshipDO2hemoglobinmechanical ventilationoxygen/PEEPVO2preloadafterloadcontractilityCONVENTIONAL VENTILATIONOxygenPEEPInverse I:E ratioLower tidal volumeVentilation in prone positionRESPIRATORY

16、 SUPPORTGoal: maintain sufficient oxygenation and ventilation, minimize complications of ventilatory managementImprove oxygenation: PEEP, MAP, Ti, O2Improve ventilation: change in pressureMechanical Ventilation GuidelinesAmerican College of Chest Physicians Consensus Conference 1993Guidelines for Me

17、chanical 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)STUDY CONCLUSIONSIn patients with potentially rever

18、sible 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.The magnitude of impaired oxygenation and its improvement after high frequency ventilation can p

19、redict outcome within 6 hours.High Frequency Oscillating Ventilation (HFOV) Pediatric ARDSArnold 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

20、had less chronic lung diseaseNew England Journal of Medicine 2000;342:1301-8STUDY CONCLUSIONIn 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 num

21、ber of days without ventilator useProne PositionImproved gas exchangeMore uniform alveolar ventilationRecruitment of atelectasis in dorsal regionsImproved postural drainageRedistribution of perfusion away from edematous, dependent regionsProne PositionNakos G et al. Am J Respir Crit Care Med 2000;16

22、1:360-68Observational 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 fibrosisProne PositionNEJM 2001;345:568-73Prone-Supine Study GroupMulticenter randomized

23、clinical trial304 adult patients prospectively randomized to 10 days of supine vs. prone ventilation 6 hours/dayImproved oxygenation in prone positionNo improvement in survivalExogenous SurfactantSuccess with infants with neonatal RDSExosurf ARDS Sepsis Study. Anzueto et al. NEJM 1996;334:1417-21Ran

24、domized control trialMulticenter study of 725 patients with sepsis induced ARDSNo significant difference in oxygenation, duration of mechanical ventilation, hospital stay, or survivalExogenous SurfactantAerosol delivery system only 4.5% of radiolabeled surfactant reached lungsOnly reaches well venti

25、lated, less severe areasNew approaches to delivery are under study, including tracheal instillation and bronchoalveolar lavageInhaled Nitric Oxide (iNO)Pulmonary vasodilatorSelectively improves perfusion of ventilated areasReduces intrapulmonary shuntingImproves arterial oxygenationT1/2 111 to 130 m

26、secNo systemic hemodynamic effectsInhaled 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 ventilatorInhaled Aerosolized Prostacyclin (IAP)Potent selective pulmonary vasodilatorEffective for pulmonary hypertensionShort half-life (2-3 mi