呼吸衰竭和急性呼吸窘迫綜合征-英文

1、UTHSCSA Pediatric Resident Curriculum for the PICURESPIRATORY FAILURE & ARDS.RESPIRATORY FAILUREInability 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 ch

2、ronic.Both types of respiratory failure can be present in the same patient.CENTRAL ETIOLOGIESTrauma: head injury, asphyxiation, hemorrhageInfection: meningitis, encephalitisTumorsDrugs: narcotics, sedativesNeonatal apneaSevere hypoxemia or hypercarbiaIncreased ICP from any of the above causes.OBSTRU

3、CTIVE ETIOLOGIESUpper 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, L

4、aryngpospasmLower AirwayAnatomic: bronchomalacia, lobar emphysemaAspiration: FB, mucus, meconium, vomitusInfection: pneumonia, pertussis, bronchiolitis, CFTumors: teratoma, bronchogenic cystBronchospasm.RESTRICTIVE ETIOLOGIESLung ParenchymaAnatomic: agenesis, cyst, pulmonary sequestrationAtelectasis

5、Hyaline membrane diseaseARDSInfection: pneumonia, bronchiectasis, pleural effusion, Pneumocystis cariniiAir leak: pneumothoraxMisc: hemorrhage, edema, pneumonitis, fibrosisChest WallMuscular: diaphragmatic hernia, myasthenia gravis, muscular dystrophy, botulismSkeletal: hemivertebrae, absent ribs, f

6、used ribs, scoliosisMisc: distended abdomen, flail chest, obesity.HYPOXEMIAV/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 diffu

7、sionOxygen must diffuse across increased distance secondary to interstitial edema, fibrosis, or hyaline membrane.Low inspired FiO2: high altitude.HYPERCARBIAPump FailureReduced central drive: apnea, metabolic alkalosis, drugs, brainstem injury, hypoxiaMuscle fatigue: muscular dystrophyIncreased pulm

8、onary workload: decreased compliance, increased obstructionIncreased CO2 production: fever, seizure, malignant hyperthermiaIncreased dead space: V/Q mismatch (ventilation of non-perfused lung).PHYSICAL EXAMTachypneaDyspneaRetractionsNasal flaringGruntingDiaphoresisTachycardiaHypertensionAltered ment

9、al statusConfusionAgitationRestlessnessSomnolenceCyanosis (need 5mg/dl of unoxygenated blood).CXR FINDINGSCXR 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.BLO

10、OD GASFor 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 of

11、ten have a normal pH because of compensatory metabolic alkalosis.MANAGEMENTREMEMBER PALSAirwayBreathingCirculation.AIRWAYRepositioningPosition of comfortJaw thrust/chin liftOral airwayUnconscious patients onlyNasal trumpetNasal or mask CPAPBag-mask ventilationUse during preparation for intubationTra

12、cheal intubation.BREATHINGDecrease respiratory workload-agonistsDecadron or steroidsAntibioticsCPAPSupplemental O2Nasal cannulaClosed face maskNon-rebreatherCounteract drug effectsBag-mask ventilationMechanical ventilation.CIRCULATIONSuppress anaerobic metabolism and acidosisCorrect anemia to improv

13、e oxygen deliveryEnsure adequate cardiac outputInotropes: oxygen, vasopressorsFluid boluses.ARDSA 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 Consens

14、us Conference on ARDS (Am J Resp Crit Care Med 149:818, 1994)The following are implied:Previously normal lungsDecreased lung complianceIncreased shuntingHypoxemic respiratory failure.ETIOLOGYARDS represents about 3% of PICU admissions.Numerous precipitating events:TraumaPneumoniaBurnsSepsisDrowningS

15、hock.PATHOPHYSIOLOGYAcute InjuryLatent PeriodEarly Exudative PhaseCellular Proliferative PhaseFibrotic Proliferative Phase.Royall and LevinJ Peds 112:169-180;335-347, 1988.PATHOLOGY OF ARDSGreen arrows point to hyaline membraneBlue arrows point to type II pneumocytes and alveolar macrophages.MANAGEM

16、ENTMeticulous 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 35 cm H2OUse pressure-control ventilationUse TV of

17、 6-10cc/kgKeep rate 7.20Limit O2 ToxicityGive enough PEEP to lower FiO2 to 90%.PEEP E) ventilation.CARDIAC OUTPUTKeep 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 SEC

18、ONDARY INFECTIONSWash 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.DRUGSDiuretics: 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, pro