（体外膜肺ECMO课件）-Physiologic-Basis-for-the-Managemen.ppt

1、Physiologic Basis for the Management of Acute Respiratory Disorders in the NewbornMarc Collin,MD18 November 2003Developmental Anatomy Alveoli-developed by 25th week -increase in#until 8 yr.-from 20 to 300 million -surface area:2.8 m2 birth 32 m2 8 yr.75 m2 adulthood -diameter:150-300 um(NB-Adult)Dev

2、elopmental Anatomy Airways-cartilaginous -relatively weak in infancy -dynamic compression -bronchiolitis(RSV)-RAD -crying!Developmental Anatomy airways enlarge in diameter/length distal airways lag in first 5 yr.high peripheral resistance in infancy Resistance=1/R4Pulmonary Physiology Compliance=Cha

3、nge in Volume Change in PressureStatic Lung Volumes Mechanics of Infant v.Adult LungPulmonary Physiology Alveoli at birth fluid-filled v.air-filled v.air-liquid interface pressures up to 80 cm H2O birth alveolar rupturePressure-Volume Curves after Air v.Liquid Lung ExpansionPulmonary Physiology LaPl

4、ace relationship:P=2T/R P=distending pressure T=wall tension R=radius(alveolar)Pressure-Volume Curves of First 3 BreathsDevelopmental Biochemistry of Alveoli History:Avery&Mead-1959 -RDS secondary to surfactant deficiency -Treatment:CPAPSurfactant Phospholipids -phosphatidylcholine -phosphatidylglyc

5、erol Surfactant proteins -A,B,CSurfactant ComponentsSurfactant Type II alveolar epithelial cells-responsible for synthesis,storage,secretion,and reuptake Lamellar bodies -intracellular storage form of surfactant -secreted via exocytosis -forms tubular myelin in extracellular spaceSurfactant and Type

6、 II CellsSurfactant Inactivation by:-alveolar-capillary leak -pulmonary edema -hemorrhage(hemoglobin)-alveolar cell injury -meconiumSurfactant Recycling -spent forms taken up/reused by Type II cells.-process facilitated by SP-A,B,and C -half-life=3.5 daysRDS US incidence:30,000/yr.Inversely related

7、to gestational age Onset-shortly after birth Signs-grunting,flaring,retracting Duration-1 weekRDSRDS Progressive atelectasis V/Q mismatch Decreased FRC Impaired ventilation(weak respiratory ms,compliant chest wall)Increased PVR due to hypoxia,acidosisRDS Right to left shunting leading to further hyp

8、oxemia Left to right shunting leading to pulmonary edemaExogenous Surfactants Replacement therapy/Fujiwara,Japan,1980 Human(from C/S)Artificial(Exosurf)Bovine(Survanta)Calf(Infasurf)Pig(Curosurf)Compliance Before and After SurfactantBefore surfactantAfter surfactantVOLUMEPRESSUREAir Leaks Pulmonary

9、interstitial emphysema(PIE)Pneumomediastinum Pneumothorax Pneumopericardium PneumoperitoneumSubtle left pneumothoraxLeft pneumothorax now more obviousLeft pneumothorax?pneumothoraxTransillumination of left pneumothoraxpneumomediastinumPneumopericardium(note air under heart)Air Leaks initiating facto

10、r:PIE(alveolar rupture into perivascular and peribronchial spaces)dissection into mediastinum further dissection into pleural,pericardial space rupture from surface blebs direct lung rupture-VERY rareAir Leak Risk Factors RDS:12-26%MAS/other aspirations SpontaneousAir Leak Management early recogniti

11、on(esp.in preterms)nitrogen wash-out(term/near-term)needle aspiration v.tube thoracotomy limit barotrauma HFOV positioning selective ET intubationMeconium Aspiration Syndrome(MAS)GI secretions,cellular debris,bile,pancreatic juice,mucus,lanugo hairs,vernix;blood.incidence:15%(30%42 wks)cause v.resul

12、t of asphyxiaMAS Asphyxia intestinal ischemia anal sphincter relaxation meconium passageMAS Asphyxia fetal gasping enhanced meconium entry into respiratory tractMAS-Presentation Respiratory distress -tachypnea -prolonged expiratory phase -hypoxemia Increased A-P diameter(barrel chest)Pulmonary hyper

13、tensionMAS-Radiographic Findings coarse alveolar infiltrates consolidation/hyperaeration pleural effusion(30%)pneumothorax/pneumomediastinumMeconium aspiration syndromeMeconium aspiration syndromeMAS-Pathophysiology Acute small airway obstruction -increased expiratory resistance -increased FRC -regi

14、onal atelectasis -V/Q mismatchingMAS-Pathophysiology Surfactant inactivation -decreased compliance -hypoxia Pulmonary hypertensionMAS-Treatment Intubation/tracheal suction delivery Saline lavage?Surfactant therapyMAS-Ventilatory Support CPAP/PEEP(be careful)Air leak due to ball-valve phenomenon Decr

15、eased I/E ratio(more E time)Hyperventilation(CMV)HFOV iNO ECMOPersistent Pulmonary Hypertension of the Newborn(PPHN)Etiology:Primary v.Secondary Failure of transition from high to low PVR after birth PFO and PDA rightleft shunting Intrapulmonary shunting,esp.w/pulmonary parenchymal diseasePPHN PVR d

16、ecreases secondary to:-mechanical distention of pulmonary vascular bed improved oxygenation of pulmonary vascular bed prostacyclin and NO productionPPHN Remodeling of pulmonary vascular musculature Normally,fully muscularized preacinar arteries extend to terminal bronchiolar level.Muscularization be

17、gins to decrease w/in days,complete w/in months.Regression process delayed by hypoxia Chronic hypoxia stimulates further muscularizationPPHN Differential Diagnosis:-Primary (chronic hypoxia)-Parenchymal disease(MAS,pneumonia,RDS,hemorrhage)-Cyanotic heart disease(TGV,critical PS,HLHS,severe coarctat

18、ion)-Pulmonary hypoplasia(Potters S.,Oligohydramnios,CDH,CCAM)Congenital cystic adenomatoid malformationCongenital diaphragmatic herniaThoracic hypoplasiaHypoplastic right lungHypoplastic lungsPPHN-Treatment/Medical Intravascular volume Correct metabolic acidosis Pressors(be careful!)Sedation(for lability)v.paralysisPPHN-Treatment/Respiratory induction of respiratory alkalosis pressure support/barotrauma risk depending on etiology(compliance)very labile.SLOW wean(maintain relative HYPERoxia,if possible)iNO ECMO