ecmo course 4

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Neonatal Physiology

Teka Siebenaler RRT

Cardiopulmonary Services

University of Minnesota Amplat Children!s "ospital



#etal $ung Stages of

%evelopment• &mbryonic Stage 'rd()th *eek

• Neural Tube closure

• %iaphragm and lung budformation

• +nternal organs in primitiveformation

stomach, liver, pancreas, gallbladder,

bladder and intestinal loop

• -ascular s stems a ears



• Most congenital malformationsoccur during the .th()th *eeks

• Anencephaly/Spina 0i1da• &2tremity deformities

• %iaphragmatic hernia 3)45 on the

left side6



#etal $ung %evelopment

• 7(89 *eeks the formation of thebronchial tree

• 87(:. *eeks primitive gase2change surface forms

• :.(.; *eeks alveolar development

continues• '4 *eeks stable surfactant

production



Postnatal $ung

%evelopment• Ne*born

– Air*ay branching complete

– Alveolar formation is not complete

Age 8(8; years number of alveoli

increase Age 8; to young adult lung gro*s

larger *ith little alveolar gro*th



#un #acts

• Surfactant is produced by alveolarepithelial cells 3type ++6

• Surfactant production increases :*eeks prior to normal birth

• <e are born *ith on 8/9th the

number of alveoli *e *ill need asan adult=



Surfactant Replacement• Creates a layer bet*een the

alveolar surface and the alveolargas and reduces alveolar collapse

by decreasing surface tension*ithin the alveoli=

• >iven to patients *ith immature

lungs, MAS, R%S, Pulmonary"ypoplasia and C%" – Curosurf vs= +nfasurf vs= Survanta??



Cardiac #ormation

• 0y :: days a endocardial tube has formed• At :) days aortic roots, primitive left atrium,

pericardial cavity, left ventricle have formed

• 0lood begins to shunt from left to right during the

.th

and 4th

*eeks of development• @Abnormalities in heart formation, the most

common form of human birth defects, aict nearly85 of ne*borns, and their freBuency inspontaneously aborted pregnancies is estimated to

be tenfold higher – "oDman, E=+= +ncidence of congenital heart diseaseF ++= Prenatal

incidence= Pediatr. Cardiol. 89, 844(894 38GG46=



#etal Circulation

• #etal Circulation – H2ygenated blood from placenta via

umbilical vein

– 995 shunted past liver by %UCTUS

-&NHSUS to +-C – 4;5 of this blood shunted from right

atrium to left atrium via #HRAM&N H-A$&

– This blood continues to left ventricle,

ascending aorta, and arteries feeding headand right arm



#etal Circulation cont!d

• -enous blood from head 3S-C6 isdirected via right atrium to right

ventricle into the pulmonary artery• G;5 of blood in PA is shunted a*ay

from lungs and into descending aorta via the %UCTUS ART&R+HUS and

returns to the placenta via theumbilical arteries=



Changes in Circulation, Respiration After0irth

•

Pulmonary vascular resistance decreases afterbirth due toF – +ncreased alveolar and arterial o2ygen tensions, *hich

increase nitric oxide

– $ung e2pansion

– %ecrease in PaCH:

– Increase in arterial pH

• Pulmonary artery pressure decreases belo* systemicpressureI pulmonary blood Jo* increases

• $eft and right ventricles pump in series rather thanin parallel as in the fetal circulatory pattern



@Normal Circulation• Closure of Umbilical arteries */in

minutes after birth

• $igation of umbilical vein

3clamped cord6

• Closure of P%A 3minutes to days6

• Closure of #oramen Hvale due toincreased pressure in $eft Atriumand %ecreased pressures in Right

Atrium



3PP"N6

–

Hccurs in : out of every 8,;;; bornlive infants

– Complicates the course of 8;5 ofinfants *ith respiratory distress

– Typically seen in infant!s K'. *eeks – More common in babies that *ere

hypo2ic and acidemic around the

time of birth 3-enous cord Ph L7=:;and 0& ()6

– More prevalent in infants *hosemothers took NSA+%S or SSR+!s

during the 'rd trimester



• @%ue to a patent foramen ovale and

patent ductus arteriosus, *hich arenormally present early in life, elevatedpulmonary vascular resistance in thene*born produces e2trapulmonary

shunting of blood, leading to severeand potentially unresponsivehypo2emia= <ith inadeBuate pulmonaryperfusion, neonates are at risk for

developing refractory hypo2emia,respiratory distress, and acidosis=

» Robin Steinhorn, M%

http://emedicine.medscape.com/article/156863-overview












Cardiac Complications• Persistent

pulmonaryhypertension

• Normal Circulation



PP"N•

' typesF• Result of abnormally constricted

pulmonary vasculature due to lungparenchymal diseases leading tohypo2ia 3mec aspiration,pneumonia, R%S6

• +dopathic 38;(:;5 of all aDectedinfants6

• Pulmonary hypoplasia orstructural defects 3C%", PRHM6



"o* do you kno* it is

PP"N• Cyanosis

• Tachypnea

•

>runting• Pre/post ductal split

• "ypo2ia/hypercapnea/acidosis

•

Response to o2ygen and iNH• Cardiac Ultrasound



Treatment for PP"N• H2ygen therapy

• +nhaled Nitric H2ide

• Normal $ab -alues

• 0lood Pressure support if needed

• Mechanical -entilation

•

&CMH• Time



PP"N and &CMH• Can be -(A or -(- &CMH

• Typically a short run 3'(4 days6

• Survival rates greater than 9)5 ascompared *ith .;5 in infants treated*ith conventional non(&CMH therapy

• Patient needs time for the

pulmonary vasculature to rela2and for the patient!s heart is ableto pump blood to the lungs



Congenital %iaphragmatic

"ernia• Hccurs in 8 of every :;;;(';;;live births and accounts for )5 ofall maOor congenital anomalies=

Mortality rates are :4(9;5====• The diaphragm initially develops

as a septum bet*een the heart

and liver, progressesposterolaterally, and closes at theleft 0ochdalek foramen at

appro2imately )(8; *eeks



• A severe C%" is believed to occur

during the pseudoglandular stageof lung development= <eeks 7(87and this is *hen pulmonary

circulation develops=• $ung compression results in

pulmonary hypoplasia 3both lungs

may be abnormal6= Pulmonaryhypoplasia is associated *ithfe*er bronchial generations,alveoli, and arterial generations=



$eft Sided Congenital

%iaphragmatic "ernia



$eft C%"



C%" and &CMH

• Typically -A &CMH• Can be a diDicult cannulation due

to small vessels and cardiac

anatomy• Average run time 8)8(8G7 hours

and 4;5 of patients *ith a C%"

are treated *ith &CMH• Patients are often decannulated

and immediately repaired on the

N+CU



&CMH and Respiratory

#ailure• Meconium Aspiration Syndrome

• Sepsis

• Pneumonia

• Alveolar Capillary %ysplasia

QQQQAll have a component ofPP"NQQQQQQ



Alveolar Capillary

%ysplasia• -ery rare lethal congenital

anomaly

• #ailure of formation of the normalair(blood diDusion barrier in thene*born lung= Alveolar Capillary

%ysplasia is usually associated*ith misalignment of thepulmonary veins=



• Patient *ill not repond tomechanical ventilation, iNH or

&CMH• 745 of these patients *ill have

other organs aDected

• $ongest reported survival is :months post &CMH run



• uestions

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