呼吸衰竭和急性呼吸窘迫综合征-英文课件.ppt

UTHSCSA Pediatric Resident Curriculum for the PICU,RESPIRATORY FAILURE&ARDS,RESPIRATORY FAILURE,Inability of the pulmonary system to meet the metabolic demands of the body through adequate gas exchange.Two types of respiratory failure:HypoxemicHypercarbicEach can be further divided into acute and chronic.Both types of respiratory failure can be present in the same patient.,CENTRAL ETIOLOGIES,Trauma:head injury,asphyxiation,hemorrhageInfection:meningitis,encephalitisTumorsDrugs:narcotics,sedativesNeonatal apneaSevere hypoxemia or hypercarbiaIncreased ICP from any of the above causes,OBSTRUCTIVE ETIOLOGIES,Upper AirwayAnatomic:choanal atresia,tracheomalacia,tonsillar hypertrophy,laryngeal web,vascular rings,vocal cord paralysis,macroglossiaAspiration:mucus,foreign body,vomitusInfection:epiglottitis,abscesses,laryngotracheitisTumors:hemangioma,cystic hygroma,papilloma,Laryngpospasm,Lower AirwayAnatomic:bronchomalacia,lobar emphysemaAspiration:FB,mucus,meconium,vomitusInfection:pneumonia,pertussis,bronchiolitis,CFTumors:teratoma,bronchogenic cystBronchospasm,RESTRICTIVE ETIOLOGIES,Lung ParenchymaAnatomic:agenesis,cyst,pulmonary sequestrationAtelectasisHyaline membrane diseaseARDSInfection:pneumonia,bronchiectasis,pleural effusion,Pneumocystis cariniiAir leak:pneumothoraxMisc:hemorrhage,edema,pneumonitis,fibrosis,Chest WallMuscular:diaphragmatic hernia,myasthenia gravis,muscular dystrophy,botulismSkeletal:hemivertebrae,absent ribs,fused ribs,scoliosisMisc:distended abdomen,flail chest,obesity,HYPOXEMIA,V/Q mismatchMost common reason.Blood perfuses non-ventilated lung.Seen in atelectasis,pneumonia,bronchiectasisGlobal hypoventilation:apneaRight-to-left shuntIntracardiac lesions,e.g.,tetralogy of FallotIncomplete diffusionOxygen must diffuse across increased distance secondary to interstitial edema,fibrosis,or hyaline membrane.Low inspired FiO2:high altitude,HYPERCARBIA,Pump FailureReduced central drive:apnea,metabolic alkalosis,drugs,brainstem injury,hypoxiaMuscle fatigue:muscular dystrophyIncreased pulmonary workload:decreased compliance,increased obstructionIncreased CO2 production:fever,seizure,malignant hyperthermiaIncreased dead space:V/Q mismatch(ventilation of non-perfused lung),PHYSICAL EXAM,TachypneaDyspneaRetractionsNasal flaringGruntingDiaphoresisTachycardiaHypertension,Altered mental statusConfusionAgitationRestlessnessSomnolenceCyanosis(need 5mg/dl of unoxygenated blood),CXR FINDINGS,CXR may be normal if problem is with upper airwayCan see hyperinflation,atelectasis,infiltrate,cardiomegalyAdditional studies may be needed,e.g.,chest CT,barium swallow,echocardiogram,BLOOD GAS,For any age patient,breathing room air,respiratory failure is defined as arterial pCO2 50mm Hg or arterial pO2 60mm Hg.If the patient is hyperventilating,a normal pCO2 is disturbing.The above definition assumes the absence of an anatomic shunt.Chronic hypercarbic respiratory failure will often have a normal pH because of compensatory metabolic alkalosis.,MANAGEMENT,REMEMBER PALSAirwayBreathingCirculation,AIRWAY,RepositioningPosition of comfortJaw thrust/chin liftOral airwayUnconscious patients onlyNasal trumpetNasal or mask CPAPBag-mask ventilationUse during preparation for intubationTracheal intubation,BREATHING,Decrease respiratory workload-agonistsDecadron or steroidsAntibioticsCPAPSupplemental O2Nasal cannulaClosed face maskNon-rebreatherCounteract drug effectsBag-mask ventilationMechanical ventilation,CIRCULATION,Suppress anaerobic metabolism and acidosisCorrect anemia to improve oxygen deliveryEnsure adequate cardiac outputInotropes:oxygen,vasopressorsFluid boluses,ARDS,A patient must meet all of the following:Acute onset of respiratory symptomsCXR with bilateral infiltratesNo evidence of left heart failurePaO2/FiO2 200mm Hg(regardless of PEEP)American-European Consensus Conference on ARDS(Am J Resp Crit Care Med 149:818,1994)The following are implied:Previously normal lungsDecreased lung complianceIncreased shuntingHypoxemic respiratory failure,ETIOLOGY,ARDS represents about 3%of PICU admissions.Numerous precipitating events:TraumaPneumoniaBurnsSepsisDrowningShock,PATHOPHYSIOLOGY,Acute InjuryLatent PeriodEarly Exudative PhaseCellular Proliferative PhaseFibrotic Proliferative Phase,Royall and LevinJ Peds 112:169-180;335-347,1988,PATHOLOGY OF ARDS,Green arrows point to hyaline membraneBlue arrows point to type II pneumocytes and alveolar macrophages,MANAGEMENT,Meticulous supportive care is the mainstay of therapyPrevent secondary lung injuryEnsure adequate cardiac outputLimit secondary infectionsDrugsGood nutrition,VENTILATOR STRATEGIESThe hallmark of ARDS is heterogeneous lung.,Limit BarotraumaKeep PIP 7.20,Limit O2 ToxicityGive enough PEEP to lower FiO2 to 90%.PEEP E)ventilation.,CARDIAC OUTPUT,Keep cardiac output 4.5 L/min/m2.Keep O2 delivery 600 ml O2/min/m2.Keep Hct 30%,higher if signs of heart failure.Use inotropes to augment cardiac output.Ensure adequate preload.,LIMIT SECONDARY INFECTIONS,Wash your hands.Use the gut as soon as possible for nutrition and meds.Discontinue indwelling catheters as soon as possible.Have high index of suspicion.Treat infections early,but tailor antibiotics to culture results.,DRUGS,Diuretics:a dry lung is a good lung.InotropesSteroids:2mg/kg/day begun after a week into the course may be of benefit,otherwise dont use.Pulmonary vasodilators(nitric oxide,prostaglandins,nitroprusside):of little benefit.NO may be of benefit in some patients.Surfactant replacement:probably no benefitNSAIDs:no clinical benefit,NUTRITION,Ensure adequate calories as soon as possible:50-60kcal/kg/day in infants35-45kcal/kg/day in older children.After day 4,increase calories by 25-50%above baseline.Begin enteral feeds as soon as is safe.“Pulmonary”formulas probably of little benefit.,MORTALITY/MORBIDITY,Published mortality is 50%in children.Pulmonary failure accounts for only 15%of the deaths.Lung function usually returns to normal within 18 months after leaving the hospital.,