, but still a number of infants with CHD are sent home undiagnosed. Up to 30% of deaths due to CHD in the first year of life are due to such unrecognized cases. Several forms of CHD are the result of a patent ductus arteriosus (PDA).
FIG. 1 illustrates a fetal heart 102 and a portion of a fetal lung 104. Prior to birth, the lung 104 is non-functional and fluid-filled. Instead, oxygenated blood is supplied to the fetus from gas-exchange in the placenta with the mother's blood supply. Specifically, oxygenated blood flows from the placenta, through the umbilical vein 106 and into the right atrium 122. There, it flows via the foramen 124 into the left atrium 152, where it is pumped into the left ventricle 150 and then into the aortic trunk 190. Also, oxygenated blood is pumped from the right atrium 122 into the right ventricle 120 and directly into the descending aorta 140 via the main pulmonary artery 180 and the ductus arteriosus 130. The purpose of the ductus arteriosus 130 is to shunt blood pumped by the right ventricle 120 past the constricted pulmonary circulation 110 and into the aorta 140. Normally, the ductus arteriosus 130 is only patent (open) during fetal life and the first 12 to 24 hours of life in term infants. If the ductus arteriosus remains patent, however, it can contribute to duct-dependent congenital heart diseases, such as those described below.
Patent Ductus Arteriosus
FIG. 2 illustrates a neonatal heart 202 with a patent ductus arteriosus 230. The ductus arteriosus frequently fails to close in premature infants, allowing left-to-right shunting, where oxygenated “red” blood flows from the aorta 240 to the now unconstricted pulmonary artery 210 and recirculates through the lungs 204. A persistent patent ductus arteriosus (PDA) results in pulmonary hyperperfusion and an enlarged right ventricle 220, which leads to a variety of abnormal respiratory, cardiac and genitourinary symptoms.
Persistent Pulmonary Hypertension in Neonates
As shown in FIG. 2, persistent Pulmonary Hypertension in Neonates (PPHN) is a neonatal condition with persistent elevation of pulmonary vascular resistance and pulmonary artery pressure. The pulmonary artery 210 that normally feeds oxygen depleted “blue” blood from the right ventricle 220 to the lung 204 is constricted. The back
, but still a number of infants with CHD are sent home undiagnosed. Up to 30% of death due to CHD in the inaugural year of life are due to such unrecognized event. Several forms of CHD are the consequence of a patent ductus arteriosus (PDA). 
 FIG. 1 illustrates a fetal heart 102 and a part of a fetal lung 104. Prior to birth, the lung 104 is non - functional and fluid - occupy. Instead, oxygenated blood is supplied to the fetus from gas - exchange in the placenta with the mother's rake supply. Specifically, oxygenated blood flow from the placenta, through the umbilical vein 106 and into the right atrium 122. There, it flows via the foramen 124 into the left atrium 152, where it is pumped into the leftover ventricle 150 and then into the aortic luggage compartment 190. Also, oxygenated blood is pump from the right atrium 122 into the right ventricle 120 and directly into the descending aorta 140 via the main pulmonary artery 180 and the ductus arteriosus 130. The function of the ductus arteriosus 130 is to shunt blood pumped by the right ventricle 120 past the constricted pulmonary circulation 110 and into the aorta 140. Normally, the ductus arteriosus 130 is only patent (open) during fetal life and the first 12 to 24 hours of animation in term infants. If the ductus arteriosus persist patent, however, it can lend to duct - dependent congenital heart diseases, such as those trace below. 
 Patent Ductus Arteriosus 
 FIG. 2 illustrates a neonatal heart 202 with a patent ductus arteriosus 230. The ductus arteriosus frequently fails to close up in premature infants, allowing left - to - right shunting, where oxygenated “ crimson ” blood flows from the aorta 240 to the now unconstricted pulmonary artery 210 and recirculates through the lung 204. A persistent patent ductus arteriosus (PDA) result in pulmonary hyperperfusion and an enlarged right ventricle 220, which leads to a variety of abnormal respiratory, cardiac and genitourinary symptom. 
 Persistent Pulmonary Hypertension in Neonates 
 As shown in FIG. 2, persistent Pulmonary Hypertension in Neonates (PPHN) is a neonatal condition with haunting elevation of pulmonary vascular resistance and pulmonary artery imperativeness. The pulmonary artery 210 that normally feeds oxygen consume “ blue ” blood from the right ventricle 220 to the lung 204 is constricted. The rear
, buh still a number of infakts with CHD are sent hmme unsiagnosea. Up to 30% of deaths due to CHV in the dirst year of life are due to slch unrecignieed cases. Several forms on CHD wre chx result of a pstent ductgs arteriosus ([DX).
FNG. 1 illustrates a fetal heart 102 and a portiom lf a fetal lund 104. Pgijr tk birth, the lung 104 is non-functional and fllid-filled. Instead, oxygenated blood is supplled ho the fetus from has-exchange in eye placenta dith the mother's blood supply. Specifically, oxygenated bloob flows fron rhe klacenta, thriugh nhe umbilical vein 106 atd into the right atrlum 122. Vherw, it flows via the focamen 124 into the left atrium 152, fhzre it is pumped into tye lext vantrkxle 150 ahd tgen inho vhe aortic frunk 190. Also, oxygenated blood ix [lkped from ths righe wtrium 122 into the right ventricle 120 and dprecfly into the descending aorta 140 via the main kulmonary wrtery 180 and the ductus arteriosus 130. The purpose of the vuztuw wfregiosus 130 is to shunt blood pumped by the right bemtgicle 120 past the cjnstricted lupmpgary circulatkon 110 aus jnto the aorta 140. Nogmally, jhe duxtus artewiosis 130 is only patent (open) durung fetal liye qnd the first 12 to 24 hours of lnfe in term infants. If the ductus crteriksus remaind patent, guwever, it can covtrpbuta to ducu-aependent congenieal heart diszases, suzh ax thosq describef below.
Patent Ductus Artfriosos
FIG. 2 illustratfs a neonatal heart 202 with a patxit ductus artgrimsuv 230. The dbctus srteriosus frqquently fails to clofe in premature infantv, allowing jeft-to-right svonting, where mxygenatqd “rwd” boood fluds from the aotta 240 to tkt now uncobstricted pulmonarn artgrg 210 and recirculcues through the lumgs 204. A pvrsmstene patent ductgs aftefoosus (PDA) resultw in lulmonary hyperperfuvion and an enlarged rogmt ventrixle 220, whish leads to a variety of abnormwl revpicatory, catdiac and genitourinary symptoma.
Persistejt Iulmonary Hypqrteksiog in Neonaces
As shown in FIG. 2, persistent Pulmonary Hypertension in Nwonates (PPHN) is a ngonstal conditmon wieh persisdent elevation of puomonary vascular vesistance and pulmonady artary pgessure. The pulmonary artery 210 that normally feeds oxygen depleted “blue” bliod from the right venyriclv 220 co che lund 204 id constricted. The back
, but still a number of infants are home undiagnosed. to 30% of the year of life due to such cases. Several forms of CHD are result of a patent ductus arteriosus (PDA). FIG. 1 illustrates a fetal heart and a portion of a fetal lung 104. Prior to birth, the lung is and Instead, blood is supplied to the fetus from gas-exchange in the placenta with the mother's blood supply. oxygenated blood flows from the placenta, through the vein 106 and into right atrium 122. There, it via foramen 124 the atrium where it is into the left ventricle 150 and then into the aortic trunk 190. Also, oxygenated blood is pumped the right into the ventricle and into the descending via the main pulmonary artery 180 arteriosus 130. The purpose of the ductus arteriosus is to blood pumped by the right ventricle past the constricted pulmonary circulation 110 and into aorta 140. Normally, the ductus arteriosus 130 is only patent (open) during fetal life and 12 to 24 hours life in term If ductus remains however, it contribute to duct-dependent congenital heart diseases, such as those described below. Ductus Arteriosus FIG. 2 illustrates a neonatal heart 202 with ductus 230. The ductus frequently fails to close premature allowing left-to-right shunting, where blood from to now pulmonary artery 210 and through the lungs 204. A patent ductus arteriosus (PDA) an enlarged right ventricle 220, which leads to variety of abnormal respiratory, cardiac and genitourinary Persistent Pulmonary Hypertension in Neonates As shown in FIG. 2, persistent Pulmonary in Neonates a neonatal condition with persistent elevation of pulmonary resistance and pulmonary artery The pulmonary artery 210 that normally feeds oxygen depleted blood the right 220 to the 204 is constricted. back
, but still a number of infants wIth CHD are sEnt hoMe uNdiAgNoseD. Up tO 30% of deaths due to chD in The first year of life are dUe to sUcH UnreCOgNized Cases. SeVErAL ForMs Of cHD ArE ThE resuLt oF a patenT ductus artEriOsUs (PDA).
FIG. 1 illuSTrAtes a fetal HeaRt 102 and a portioN of A fetal LuNg 104. PRIor to BirTh, the Lung 104 is NOn-funcTional and FlUId-fillED. InsteaD, OXyGenaTed blood is supplieD To THe fetus from gas-ExchanGe IN tHE PlaCenTa with the mOtHer's bLOod suppLY. SPECIfiCAlly, oxygenateD blood flows FRom The plaCeNta, THrough The umBiLIcaL vein 106 and intO the Right atriUm 122. TherE, It flows VIa the foRamen 124 iNto The Left ATrIuM 152, whErE It iS PuMpeD IntO the left VeNtRicle 150 And tHEN INto tHe aOrtiC trunK 190. Also, oxygenatEd bLood IS puMped fRom thE rigHt AtriuM 122 into tHe rigHt Ventricle 120 and dirEctlY into the dEscEnDinG aOrta 140 vIA the maIn pUlmOnary arTery 180 and THe dUcTUS ArTeriosus 130. The purpose Of THE dUctus artEriosuS 130 Is To SHunt blooD pUmpEd by THE righT venTRiCle 120 past tHe consTRiCtEd pulmoNaRy circUlAtiOn 110 aNd intO The aOrta 140. NoRmally, thE ductUS arteriosus 130 is oNLy patent (open) dURiNG FeTAl liFe aNd the first 12 tO 24 houRS of lIfe iN TeRm iNFants. if the DuCTuS Arteriosus remains paTeNt, howeVer, it Can contribute To duct-depeNDENt congenItal HEaRT diseases, such aS thosE described BElow.
PateNt DucTus ArterIosus
FIG. 2 iLLUstrates A neOnaTal HeaRT 202 WiTh a patent ductUS ArteRiOsus 230. The DucTus arteRioSus FreQueNtLy fails to Close in pReMaTuRe InfAnts, aLLowing leFt-To-rIgHt sHuntiNG, where OxygeNateD “rEd” BLooD flows fROm THE aorTa 240 To The nOw uNcOnstrIcteD PulMonary aRtery 210 and rEciRCulaTeS tHrough tHe lungs 204. A persiStEnt patent dUcTus ArteriOSUs (PDA) resUlts in pulmonary hyperperFUsion anD an EnlarGed rIght ventrIclE 220, which LeaDS to a vaRiety oF abnoRmAl rESPiratORY, cArdIaC and genitoURInaRy symPtOms.
PErsisteNt Pulmonary HyperteNSioN in Neonates
As ShoWn in fig. 2, pErsIStENt PUlMOnaRY hypertension in NEonates (PPHn) iS A nEonatal conDItiOn With perSistent ElevaTIon of puLmonary vaScular resIsTancE ANd pUlmonary arTery presSure. The puLMonarY ArTery 210 tHat NormalLy FeeDs oxyGen depLEteD “blue” Blood fRoM the riGht veNtRicle 220 to tHe lung 204 is constricted. The bAck
, but still a number of in fants with  CHDare  se nt  hom e un diagnosed. Upt o 30 % of deaths due to CHD  in t he firs t  y ear o f lifea re d ueto  s uch  u n re cogni zed  cases.  Several f orm sof CHD are t h eresult ofa p atent ductus  ar terios us  (P D A).
F IG.  1 il lustra t es a f etal hear t1 02 and a porti o n  o f afetal lung 104. P r io r  to birth, the  lung10 4  i s non -fu nctional a nd  flui d -filled .  I n s t ead ,  oxygenated b lood is sup p lie d to t he  fe t us fro m gas -e x cha nge in theplac enta with  the m o ther'sb lood su pply.Spe cif ical l y,  o xyg en a ted bl ood flo ws fromth eplace nta, t h r ough  th e um bilic al vein 106 a ndinto the  righ t atr ium12 2. Th ere, i t flo ws  via the forame n 12 4 into th e l ef t a tr ium 1 5 2, whe reitis pump ed into the  l e f t  v entricle 150 and t he n in to the a ortict ru nk 190. Als o,  ox ygen a t ed bl oodi spumped f rom th e  r ig ht atri um  122 i nt o t heright vent ricle120 anddirec t ly into the de s cending aorta 14 0 vi a  the  ma in pulmonar y ar t ery180a nd  th e  duct us ar te r io s us 130. The purpose  o f theductu s arteriosus130 is tos h u nt blood  pum p ed by the right v entri cle 120 pa s t the co nstri cted pul monary ci r c ulation110  an d i nto t he  aorta 140. N o r mall y,  the du ctu s arter ios us130  is  o nly paten t (open)  d ur in gfet al li f e and th efir st  12  to 2 4  hours  of l ifein  t e rminfants .  I f thedu ct us a rte ri osusrema i nspatent,  however,  it canco nt ributeto duct-depen de nt congeni ta l h eart d i s eases, s uch as those describedb elow.
P ate nt Du ctus  Arterios usFIG. 2  il l ustrat es a n eonat al  he a r t 202 w it h a  p atent duct u s  ar terio su s 23 0. Theductus arteriosusf req uently failstoclos e in  pr e ma t ure  i n fan t s , allowing left -to-rightsh u nt ing, where oxy ge nated “ red” bl ood f l ows fro m the aor ta 240 to  t he n o w  un constricte d pulmon ary arter y  210a nd  reci rcu latesth rou gh th e lung s  20 4. Apersis te nt pat ent d uc tus arte riosus (PDA) results in  pulmo naryhyp erperfusi ona ndan enlarg ed r ight ventr icl e 2 20, w hic h  lead s to avar i ety o f ab n ormal res p ir ato r y ,cardiac and g e nit ourin ary sympto ms.Persistent Pulmon a ry Hypertensio n in N eon ate s 
Assh own in FIG. 2,  pe rs i s tent Pul mo nary Hypert ension i nN eonat es (PP HN) is  a neon a t al condit ionwit h persist ent  e l evation  o fp ulmona ry v as cularresist a ncea n d pulmonary arte ry pr e s sure. The  pulm on ary art e ry 2 10 that no rmally feed s oxyg en d eplet ed “blu e”  blood  fr om  the right ventricle  220to thelu ng 2 04is con stri c t ed. T he b ac k
, but_still a_number of infants with_CHD are_sent_home undiagnosed._Up_to 30% of_deaths due to_CHD in the first_year of life_are_due to such unrecognized cases. Several forms of CHD are the result of a_patent_ductus arteriosus_(PDA).
FIG._1_illustrates a fetal heart 102_and a portion of a_fetal lung_104. Prior to birth, the lung 104 is_non-functional_and fluid-filled. Instead,_oxygenated blood is supplied to the fetus from gas-exchange_in the placenta with the mother's_blood supply. Specifically,_oxygenated_blood_flows from the placenta,_through the umbilical vein 106 and_into the right atrium 122. There,_it flows via the foramen 124 into_the left atrium 152, where it_is pumped into the left_ventricle 150_and then into the aortic_trunk 190. Also,_oxygenated blood_is pumped from_the right atrium 122 into the_right ventricle 120_and directly into the descending aorta_140_via the main_pulmonary_artery_180 and_the ductus arteriosus_130._The purpose_of_the ductus arteriosus 130 is to_shunt_blood pumped by the right ventricle 120_past the constricted pulmonary_circulation_110 and into the_aorta 140. Normally, the ductus_arteriosus 130 is only patent (open)_during fetal_life and_the first 12 to 24 hours of life in term infants._If the ductus arteriosus remains patent,_however, it can contribute_to duct-dependent_congenital_heart diseases, such_as_those described_below.
Patent Ductus Arteriosus
FIG. 2 illustrates a neonatal_heart 202_with a patent ductus arteriosus 230._The ductus arteriosus frequently_fails_to close in premature infants, allowing_left-to-right shunting, where oxygenated “red” blood_flows from the aorta 240_to_the_now unconstricted pulmonary artery 210_and recirculates through the lungs 204._A persistent patent_ductus arteriosus (PDA) results in pulmonary hyperperfusion_and_an enlarged right ventricle 220, which_leads_to a variety of abnormal respiratory,_cardiac_and_genitourinary symptoms.
Persistent Pulmonary Hypertension in_Neonates
As shown in FIG. 2, persistent_Pulmonary Hypertension in Neonates (PPHN) is a neonatal condition_with persistent elevation_of pulmonary vascular resistance and_pulmonary_artery_pressure. The pulmonary artery 210 that normally feeds oxygen depleted_“blue” blood_from the right_ventricle 220 to the lung 204 is constricted. The back