Presentation on theme: "Neonatal Physiology Teka Siebenaler RRT Cardiopulmonary Services"— Presentation transcript:
1Neonatal Physiology Teka Siebenaler RRT Cardiopulmonary Services University of Minnesota Amplatz Children’s Hospital
2Fetal Lung Stages of Development Embryonic Stage 3rd-8th weekNeural Tube closureDiaphragm and lung bud formationInternal organs in primitive formationstomach, liver, pancreas, gall bladder,bladder and intestinal loopVascular systems appears
3Most congenital malformations occur during the 4th-8th weeks Anencephaly/Spina BifidaExtremity deformitiesDiaphragmatic hernia (85% on the left side)
4Fetal Lung Development 7-16 weeks the formation of the bronchial tree17-24 weeks primitive gas exchange surface forms24-40 weeks alveolar development continues35 weeks stable surfactant production
5Postnatal Lung Development NewbornAirway branching completeAlveolar formation is not completeAge 1-10 years number of alveoli increaseAge 10 to young adult lung grows larger with little alveolar growth
6Fun FactsSurfactant is produced by alveolar epithelial cells (type II)Surfactant production increases 2 weeks prior to normal birthWe are born with on 1/6th the number of alveoli we will need as an adult.
7Surfactant Replacement Creates a layer between the alveolar surface and the alveolar gas and reduces alveolar collapse by decreasing surface tension within the alveoli.Given to patients with immature lungs, MAS, RDS, Pulmonary Hypoplasia and CDHCurosurf vs. Infasurf vs. Survanta……
8Cardiac Formation By 22 days a endocardial tube has formed At 28 days aortic roots, primitive left atrium, pericardial cavity, left ventricle have formedBlood begins to shunt from left to right during the 4th and 5th weeks of development“Abnormalities in heart formation, the most common form of human birth defects, afflict nearly 1% of newborns, and their frequency in spontaneously aborted pregnancies is estimated to be tenfold higher”Hoffman, J.I. Incidence of congenital heart disease: II. Prenatal incidence. Pediatr. Cardiol. 16, (1995).
9Fetal Circulation Fetal Circulation Oxygenated blood from placenta via umbilical vein66% shunted past liver by DUCTUS VENOSUS to IVC50% of this blood shunted from right atrium to left atrium via FORAMEN OVALEThis blood continues to left ventricle, ascending aorta, and arteries feeding head and right arm
10Fetal Circulation cont’d Venous blood from head (SVC) is directed via right atrium to right ventricle into the pulmonary artery90% of blood in PA is shunted away from lungs and into descending aorta via the DUCTUS ARTERIOUS and returns to the placenta via the umbilical arteries.
12Changes in Circulation, Respiration After Birth Pulmonary vascular resistance decreases after birth due to:Increased alveolar and arterial oxygen tensions, which increase nitric oxideLung expansionDecrease in PaCO2Increase in arterial pHPulmonary artery pressure decreases below systemic pressure; pulmonary blood flow increasesLeft and right ventricles pump in series rather than in parallel as in the fetal circulatory pattern
13“Normal Circulation”Closure of Umbilical arteries w/in minutes after birthLigation of umbilical vein (clamped cord)Closure of PDA (minutes to days)Closure of Foramen Ovale due to increased pressure in Left Atrium and Decreased pressures in Right Atrium
14Pulmonary Hypertension (PPHN) Occurs in 2 out of every 1,000 born live infantsComplicates the course of 10% of infants with respiratory distressTypically seen in infant’s >34 weeksMore common in babies that were hypoxic and acidemic around the time of birth (Venous cord Ph <7.20 and BE -8)More prevalent in infants whose mothers took NSAIDS or SSRI’s during the 3rd trimester
15“Due to a patent foramen ovale and patent ductus arteriosus, which are normally present early in life, elevated pulmonary vascular resistance in the newborn produces extrapulmonary shunting of blood, leading to severe and potentially unresponsive hypoxemia. With inadequate pulmonary perfusion, neonates are at risk for developing refractory hypoxemia, respiratory distress, and acidosis.”Robin Steinhorn, MD
17PPHN3 types:Result of abnormally constricted pulmonary vasculature due to lung parenchymal diseases leading to hypoxia (mec aspiration, pneumonia, RDS)Idopathic (10-20% of all affected infants)Pulmonary hypoplasia or structural defects (CDH, PROM)How do you know its PPHN? Hyperoxia test (PO2 >150 on 100% is good) and pre/post difference >5% and fetal echo
18How do you know it is PPHN? CyanosisTachypneaGruntingPre/post ductal splitHypoxia/hypercapnea/acidosisResponse to oxygen and iNOCardiac Ultrasound
19Treatment for PPHN Oxygen therapy Inhaled Nitric Oxide Normal Lab ValuesBlood Pressure support if neededMechanical VentilationECMOTime!
20PPHN and ECMO Can be V-A or V-V ECMO Typically a short run (3-5 days) Survival rates greater than 68% as compared with 40% in infants treated with conventional non-ECMO therapyPatient needs time for the pulmonary vasculature to relax and for the patient’s heart is able to pump blood to the lungs
21Congenital Diaphragmatic Hernia Occurs in 1 of every live births and accounts for 8% of all major congenital anomalies. Mortality rates are 25-60%....The diaphragm initially develops as a septum between the heart and liver, progresses posterolaterally, and closes at the left Bochdalek foramen at approximately 8-10 weeks' gestation.
22A severe CDH is believed to occur during the pseudoglandular stage of lung development. Weeks 7-17 and this is when pulmonary circulation develops.Lung compression results in pulmonary hypoplasia (both lungs may be abnormal). Pulmonary hypoplasia is associated with fewer bronchial generations, alveoli, and arterial generations.
25CDH and ECMO Typically VA ECMO Can be a difficult cannulation due to small vessels and cardiac anatomyAverage run time hours and 50% of patients with a CDH are treated with ECMOPatients are often decannulated and immediately repaired on the NICUIf patient is not repaired by 14 days-survival rates rapidly decline
26ECMO and Respiratory Failure Meconium Aspiration SyndromeSepsisPneumoniaAlveolar Capillary Dysplasia****All have a component of PPHN******
27Alveolar Capillary Dysplasia Very rare lethal congenital anomalyFailure of formation of the normal air-blood diffusion barrier in the newborn lung. Alveolar Capillary Dysplasia is usually associated with "misalignment" of the pulmonary veins.
28Patient will not repond to mechanical ventilation, iNO or ECMO 75% of these patients will have other organs affectedLongest reported survival is 2 months post ECMO run