Foetal Circulation

7/31/2019 Foetal Circulation

1/107

FETAL CIRCULATION

IN HEALTH AND DISEASE


2/107

Flow Chart of Fetal Circulation


3/107


4/107


5/107

Characteristics of fetal circulatory

dynamics

Parallel arrangement of two main arterialsystems and their respective ventricles.

Mixing of venous return and preferentialstreaming.

High impedance and low flow of pulmonarycirculation.

Low impedance and high flow of placentalcirculation.

Presence of shunts.


6/107

Cardiac output and its distribution

Fetal lamb

CVO is 450 ml/kg/wt

RV ejects 2/3 and LV ejects 1/3 of CVO

UV flow is 200 ml/mt/kg [45% of CVO]

Of this,110 ml/mt [24%] passes through DVand 90 ml/mt[21%] passes through hepatic

circulation


7/107


Fetal lamb

Portal venous flow forms 7% and of CVOand abdominal IVC blood forms 30% ofCVO.

Total venous return to heart from IVC is 315ml/mt and represents 70% of CVO.

Of this 115 ml/mt [25% of CVO] passesthrough FO and and 200 ml/mt [44%]passes through TV.


8/107


Fetal lamb

Venous return to heart from SVC is 90ml/mt/ and represents 21% of CVO most ofthis passes through tricuspid valve.

RV ejects about 300 ml/mt or about 66% ofCVO.

About 35 ml/mt [8% of CVO] enters thepulmonary circulation


9/107


Fetal lamb

About 265 ml/mt [60%]passes throughductus arteriosus.

LV ejects 150 ml/kg [ 33% ]. Of this,90 ml/mt [20%] distributed to head

and upper half and 45 ml/mt [10%]passes

through isthmus. 3% of CVO enters coronary circulation.


10/107

8%

66%

70%

55%

24

1828 19

20%AA 33%

3245%

21%

24%70%

21%

60%


11/107

35%

50% 65%

55%

65%


12/107


human fetus

Limited data only is available based ondoppler studies.

Umbilical blood flow is 180 ml/mt /kg ofestimated fetal weight.

Pulmonary blood flow is estimated to be 75

ml/kg of fetal weight


13/107


human fetus

CVO appears to be similar to that in lamb,450 ml/mt/kg fetal weight

Ratio of RV output to LV output is only 1.2 to1.3 as compared to 2:1 in fetal lamb


14/107

220

140

15

125

95

200250

140

175

45

75

220

180

40

75

15


15/107

49

31

3

21 28

58 44

39

31

10

17

49

39

10

17

3


16/107

Venous return to heart

Umbilical vein gives branches to left lobe ofliver and then divides into DV and arcuatevien.

Arcuate vien joins the portal vein and thengives of branches to right lobe of liver.

Left hepatic vein joins the DV at its entry to

IVC and Right hepatic vein joins the IVCdirectly.


17/107


Right lobe of liver poorly oxygenated portalvenous blood and left lobe receives welloxygenated umbilical venous blood.

Both lobes receive small contribution ofblood from hepatic artery.

Saturation of RHV is lower than that of LHV.


18/107


Posterior and left stream of IVC bloodcarries oxygenated blood while anterior andright stream carries poorly oxygenatedblood.

Preferential streaming of DV and LHV bloodacross the foramen ovale and abdominal

IVC and RHV blood across the TV.


19/107


Eustechian valve helps to direct the IVCblood to cross the foramen ovale.

The lower margin of septum secundum[christa dividens] helps to direct the leftposterior stream to preferentially across theforamen ovale.

SVC blood is directed aross the TV.


20/107

Shunts in fetal circulation

Ductus venosus

Foramen ovale

Ductus arteriosus or aortic isthmus


21/107


The blood returning to heart through venacavaeand then redistributed to tissues without beingdelivered to placenta represents effective R to L

shunt. The blood which passes through DV and then

reaches DA and goes to placenta without gettingdistributed to tissues represent effective L to R

shunt. Combined R to L and L to R shunts forms 33% of

CVO.


22/107

PULMONARY CIRCULATION

Fetal lung does not serve gas exchangefunction.

PVR is high and PBF is low. This helps to reduce workload of fetal heart.


23/107


MPA continues as Ductus and RPA andLPA arise as branches.

Medial layer is composed of smooth musclepredominantly in small pre acinar and largeacinar level arteries.

Further branches have no muscularcomponent.


24/107


PA pressure rises gradually paralleling therise in aortic pressure.

TPR falls gradually but this fall whencorrelated with rise in lung weight, there isactually an increase in PVR towards term .

PBF increases gradually.


25/107


MPA has forward flow throughout systolewith a short period of backflow at end ofsystole.

DA also has forward flow throughoutsystole.

BPA has forward flow only through initial

one third of systole followed by back flowthrough rest of systole and diastole.

In humans forward flow is more prolonged.


26/107


Experiments show fetal PBF increasesdramatically in response to increase inmaternal PO2.

This response is evident only in latter part ofgestation.

Doppler studies indicate similar changes inhumans as well.


27/107


Fetal pulmonary endothelium behaves in asimilar fashion as adult endothelium tovasodilators.

Adrenomedullin has a potent and prolongedvasodilatory effect.

Leukotriens may be responsible formaintaining high fetal PVR.


28/107


Breathing at birth is associated with amarked fall in PVR and rise in PBF.

PA pressure does not fall as rapidly andremain elevated till the Ductus is widelypatent.

Once the ductus is closed, PA pressure canvary independent of systemic pressure.


29/107

Oxygen exchange function

Higher hemoglobin level in fetus ascompared to mother facilitates oxygenuptake by the fetus in the placenta.

Oxygen dissociation curve of fetal red cellsis shifted to left as compared to adult redcells.

HbF has less affinity towards organicphosphates like 2,3 DPG and ATP.


30/107


These phosphates that are present in redcells compete with oxygen for binding tohemoglobin.

Affinity of reduced hemoglobin to 2,3 DPG ishigher than that of oxyhemoglobin and thisfacilitates oxygen delivery at tissue site.

This is not significant in fetal hemoglobin.


31/107


As CO2 crosses placenta from fetus tomother,it creates a local acidosis.

In the face of decreasing Ph,mothershemoglobin shows less affinity towards Hband oxygen release is enhanced.[Bohreffect]

This supports diffusion of more oxygenacross the diffusion membrane to fetus.


32/107


As O2 is released,maternal Hb acts as abuffer that removes H+ from localenvironment.

This encourages production of bicarbonatefrom H2O and CO2 thereby reducing localPC02 and facilitating diffusion of CO2 from

fetus.


33/107

Post natal changes

Gas exchange function is transferred fromplacenta to the lungs.

Separation of systemic and pulmonarycirculations

Increased metabolism to maintain bodytemperature and hence increased cardiacoutput.


34/107

FETAL CIRCULATION VIII: Conversion to post-natal*

PulmonaryveinsVena cava Right

ATRIUM

Pulmonaryarteries

RightVENTRICLE

LeftVENTRICLE

Aorta

LUNGS

SYSTEMICCAPILLARIES

HEART

Umbilicalarteries

Ductus arteriosus

IVC

OLef tATRIUM

Closure of Foramen ovale

DUCTUS VENOSUS

means that blood expelled from the

right ventricle has to go to the lungs

Closure of

Closure of

Stops use of umbilicalvessels, & converts all

vena cava blood todeoxygenated

Forces venous blood (now all deoxygenated) intothe right ventricle for expulsion to the lungs

Closure of

Stops use ofumbilical vessels


35/107

Post natal changes in various circulatory

beds

Coronary Blood flow decreases dramaticallyas the oxygen content increases.

Cerebral circulation also behaves in thesame fashion as coronary circulation.


36/107


beds

Skin blood flow is high in utero as thevessels are dilated because the skin isexposed to warm amniotic fluid.

Cutaneous vasoconstriction occurs postnatally as evaporation from skin starts.

Cutaneous flow falls and the vascularresistance increaes.


37/107


beds

Hepatic blood flow falls rapidly post natallywith reduction in umbilical venous return andthen increases as the GI flow is re

established. Hepatic blood flow progressively increases

after birth and by 7 days after birth reaches

a level of 250 ml/minute /100 g by whichtime there is no flow through ductusvenosus.


38/107

Changes in Cardiac output

Oxygen consumption increases from 6-8ml/mt/kg body weight pre natally to 1520ml/mt/kg post natally.

CVO of fetal lamb is 450 ml/mt/kg.

C.O of neonatal lamb is 300 -425ml/mt/kg.So the CVO will be 600 -850ml/mt/kg.

So the increase is 1.5 to 2 times.


39/107


Mechanisms

Neonate has to increase the metabolism toincrease the body temperature as it isexposed to external temperature.

Improved diastolic function due to removalof compression by maternal organs anduterus causes increased cardiac filling and

hence the cardiac output.


40/107

Characteristics of fetal circulatory

dynamics

Parallel arrangement of two main arterialsystems and their respective ventricles.

Mixing of venous return and preferential

streaming. High impedance and low flow of pulmonary

circulation.

Low impedance and high flow of placentalcirculation.

Presence of shunts.


41/107


Fetal lamb

CVO is 450 ml/kg/wt

RV ejects 2/3 and LV ejects 1/3 of CVO

UV flow is 200 ml/mt/kg [45% of CVO] Of this,110 ml/mt [24%] passes through DV

and 90 ml/mt[21%] passes through hepatic

circulation


42/107


Fetal lamb

Portal venous flow forms 7% and of CVOand abdominal IVC blood forms 30% ofCVO.

Total venous return to heart from IVC is 315ml/mt and represents 70% of CVO.

Of this 115 ml/mt [25% of CVO] passesthrough FO and and 200 ml/mt [44%]passes through TV.


43/107


Fetal lamb

Venous return to heart from SVC is 90ml/mt/ and represents 21% of CVO most ofthis passes through tricuspid valve.

RV ejects about 300 ml/mt or about 66% ofCVO.

About 35 ml/mt [8% of CVO] enters thepulmonary circulation


44/107


Fetal lamb

About 265 ml/mt [60%]passes throughductus arteriosus.

LV ejects 150 ml/kg [ 33% ].

Of this,90 ml/mt [20%] distributed to headand upper half and 45 ml/mt [10%]passesthrough isthmus.

3% of CVO enters coronary circulation.


45/107


human fetus

Limited data only is available based ondoppler studies.

Umbilical blood flow is 180 ml/mt /kg ofestimated fetal weight.

Pulmonary blood flow is estimated to be 75ml/kg of fetal weight


46/107


human fetus

CVO appears to be similar to that in lamb,450 ml/mt/kg fetal weight

Ratio of RV output to LV output is only 1.2 to1.3 as compared to 2:1 in fetal lamb


47/107


Umbilical vein gives branches to left lobe ofliver and then divides into DV and arcuatevien.

Arcuate vien joins the portal vein and thengives of branches to right lobe of liver.

Left hepatic vein joins the DV at its entry to

IVC and Right hepatic vein joins the IVCdirectly.


48/107


Right lobe of liver poorly oxygenated portalvenous blood and left lobe receives welloxygenated umbilical venous blood.

Both lobes receive small contribution ofblood from hepatic artery.

Saturation of RHV is lower than that of LHV.


49/107


Posterior and left stream of IVC bloodcarries oxygenated blood while anterior andright stream carries poorly oxygenated

blood.

Preferential streaming of DV and LHV bloodacross the foramen ovale and abdominal

IVC and RHV blood across the TV.


50/107


Eustechian valve helps to direct the IVCblood to cross the foramen ovale.

The lower margin of septum secundum[christa dividens] helps to direct the leftposterior stream to preferentially across theforamen ovale.

SVC blood is directed aross the TV.


51/107


Ductus venosus

Foramen ovale

Ductus arteriosus or aortic isthmus


52/107


The blood returning to heart through venacavaeand then redistributed to tissues without beingdelivered to placenta represents effective R to Lshunt.

The blood which passes through DV and thenreaches DA and goes to placenta without gettingdistributed to tissues represent effective L to Rshunt.

Combined R to L and L to R shunts forms 33% ofCVO.


53/107


Fetal lung does not serve gas exchangefunction.

PVR is high and PBF is low.

This helps to reduce workload of fetal heart.


54/107


MPA continues as Ductus and RPA andLPA arise as branches.

Medial layer is composed of smooth musclepredominantly in small pre acinar and largeacinar level arteries.

Further branches have no muscularcomponent.


55/107


PA pressure rises gradually paralleling therise in aortic pressure.

TPR falls gradually but this fall whencorrelated with rise in lung weight, there isactually an increase in PVR towards term .

PBF increases gradually.


56/107


MPA has forward flow throughout systolewith a short period of backflow at end ofsystole.

DA also has forward flow throughoutsystole.

BPA has forward flow only through initial

one third of systole followed by back flowthrough rest of systole and diastole.

In humans forward flow is more prolonged.


57/107


Experiments show fetal PBF increasesdramatically in response to increase inmaternal PO2.

This response is evident only in latter part ofgestation.

Doppler studies indicate similar changes inhumans as well.


58/107


Fetal pulmonary endothelium behaves in asimilar fashion as adult endothelium tovasodilators.

Adrenomedullin has a potent and prolongedvasodilatory effect.

Leukotriens may be responsible formaintaining high fetal PVR.


59/107


Breathing at birth is associated with amarked fall in PVR and rise in PBF.

PA pressure does not fall as rapidly andremain elevated till the Ductus is widelypatent.

Once the ductus is closed, PA pressure canvary independent of systemic pressure.


60/107


Higher hemoglobin level in fetus ascompared to mother facilitates oxygenuptake by the fetus in the placenta.

Oxygen dissociation curve of fetal red cellsis shifted to left as compared to adult redcells.

HbF has less affinity towards organicphosphates like 2,3 DPG and ATP.


61/107


These phosphates that are present in redcells compete with oxygen for binding tohemoglobin.

Affinity of reduced hemoglobin to 2,3 DPG ishigher than that of oxyhemoglobin and thisfacilitates oxygen delivery at tissue site.

This is not significant in fetal hemoglobin.


62/107


As CO2 crosses placenta from fetus tomother,it creates a local acidosis.

In the face of decreasing Ph,mothershemoglobin shows less affinity towards Hband oxygen release is enhanced.[Bohreffect]

This supports diffusion of more oxygenacross the diffusion membrane to fetus.


63/107


As O2 is released,maternal Hb acts as abuffer that removes H+ from localenvironment.

This encourages production of bicarbonatefrom H2O and CO2 thereby reducing localPC02 and facilitating diffusion of CO2 from

fetus.


64/107

Post natal changes

Gas exchange function is transferred fromplacenta to the lungs.

Separation of systemic and pulmonarycirculations

Increased metabolism to maintain bodytemperature and hence increased cardiac

output.

P t t l h i i i l t


65/107


beds

Coronary Blood flow decreases dramaticallyas the oxygen content increases.

Cerebral circulation also behaves in thesame fashion as coronary circulation.



66/107


beds

Skin blood flow is high in utero as thevessels are dilated because the skin isexposed to warm amniotic fluid.

Cutaneous vasoconstriction occurs postnatally as evaporation from skin starts.

Cutaneous flow falls and the vascular

resistance increaes.



67/107


beds

Hepatic blood flow falls rapidly post natallywith reduction in umbilical venous return andthen increases as the GI flow is re

established. Hepatic blood flow progressively increases

after birth and by 7 days after birth reachesa level of 250 ml/minute /100 g by whichtime there is no flow through ductusvenosus.


68/107


Oxygen consumption increases from 6-8ml/mt/kg body weight pre natally to 1520ml/mt/kg post natally.

CVO of fetal lamb is 450 ml/mt/kg.

C.O of neonatal lamb is 300 -425ml/mt/kg.So the CVO will be 600 -850

ml/mt/kg.

So the increase is 1.5 to 2 times.



69/107


Mechanisms

Neonate has to increase the metabolism toincrease the body temperature as it isexposed to external temperature.

Improved diastolic function due to removalof compression by maternal organs anduterus causes increased cardiac filling and

hence the cardiac output.



70/107


Mechanisms

Perinatal but not post natal increase inthyroid hormones is the principalmechanism for increase in cardiac output.

Improvement in myocardial growth andmaturation brought about by cortisol may

also play important role.

Changes in hemoglobin and tissue


71/107

Changes in hemoglobin and tissue

oxygen delivery

Human new born has a high hemoglobin level(about 16g/dl) so that the oxygen carrying capacityis quiet high and the total amount of oxygentransported to tissues is quiet high.

Since the Hb F levels are still high facilitation attissue site is not as great as in adults.

Over the first 8-10 weeks after the birth,Hb

concentration falls to 10-11 g/dl. This isaccompanied by loss of Hb F and almost 100% isadult type.


72/107

Regulation of fetal circulation

Arterial baroreceptors are funtional in fetusfrom early in the gestation

Near term, it is as sensitive as adults in fetallambs.

Chemoreceptors are active only in latter partof gestation.

Fetal circulation in pathological


73/107


conditions



74/107


conditions

Development of a structural abnormality willmodify the fetal circulation.

This will affect the development of othercomponents and can lead to other defects.

The impact of a defect will depend on its

severity and time of gestation at which it

occurs.



75/107


conditions

Many of the defects, though it modifies thecirculation, will not significantly affect fetalperfusion and hence the growth and development.

This is because of the presence of shunts andmixing of blood.

Fetus tolerates the obstructive lesions very much.

Fetal circulation is jeopardized by regurgitant

lesions and myocardial disease.


76/107

Septal defects

They in general do not modify the fetalcirculation significantly.

VSD may have a transient left to right shuntin systole.

In OP ASD, due to close proximity of defectwith TV, more than normal amount of SVC

blood may enter the LA.


77/107

Septal defects

In atrioventricular septal defects, theobligatory flow from LV to RA will result indecrease in LV output and an increase in

RV output. This will reduce the flow across the isthmus

and can predispose to coarctation.

It is the degree of severity of AV valve lesionand regurgitation which will determine theoutcome.


78/107

LVOT Obstruction

Severe obstruction developing early result ina small LV with an increased mass.

RV is able to compensate fully if LVOTOdevelops slowly.


79/107

LVOT Obstruction

SVC flow courses normally.

Majority of IVC blood flow crosses TV to RV.

Flow across the ductus increases.

PBF has higher than normal saturation.

LVOT obstruction


80/107

LVOT obstruction

Decrease in saturation between DA and AA.

LV systolic pressure increases slightly butnot EDP.

A retrograde flow in arch and ascendingaorta indicates severe obstruction.


81/107

70

6065

62

60

75/4 90/

5

75/50

70/45


82/107

Aortic arch abnormalities

Most of the alteration in the circulation aredue to co existing intra cardiac defects.

Common features are, reduced flow in to

ascending aorta, increased flow in to thepulmonary trunk and greater proportion ofCVO carried across ductus to descendingaorta.

The decreased volume loading of LV maypossibly interfere with its development.

Mi l d i i


83/107

Mitral and aortic atresia

All blood must pass through RV and ductus has toprovide for both AA and DA blood flow.

Complete mixing of blood occurs in RA and

saturation in PA,AA and DA are all same. If the foramen ovale is sufficiently large and ductus

accomodates whole of systemic blood flow, therewill be no significant interference with intrauterine

development and survival.


84/107

70

40

60 60

60

70/2

70/40

Mi l d i i


85/107

Mitral and aortic atresia

If the foramen ovale is restrictve, severepulmonary venous hypertension develops.

If the ductus does not enlarge to

accommodate the whole of systemic bloodflow increased blood flow to lungs andpulmonary hypertension develops.

Both these can lead to increaseddevelopment of smooth muscle in thepulmonary vasculature.

RVOTO i h i IVS


86/107

RVOTO with intact IVS

In rapidly developing RVOTO,RV and LVcannot compensate for and the CVO falls.

If RVOTO developing slowly,both LV and

RV can compensate for and CVO ismaintained.

In pulmonary atresia, total cardiac output is

carried by the left heart.


87/107

70

40

63

63

63

63100/4

70/3


88/107


In pulmonary atresia, all systemic venousblood is carried to left side through foramen

ovale and all blood supply to DA is providedthrough isthmus.

Larger than normal foramen ovale, left sided

chambers,AA and aortic isthmus.

RVOTO i h i IVS


89/107


If severe RVOTO develops early ingestation,the flow through the ductus isreversed and carries only 8 to 10 % of

cardiac output. The ductus will be narrower and will make

an acute inferior angle with aorta.

The ductus will remain patent for longer thannormal duration.

RVOTO i h i IVS


90/107


If the fetus develops significant TR,RVpressure remains low and myocardialsinusoids and coronary fistulae do not

develop. If TR does not develop,significant RV

systolic pressure develops and if occurs

early in gestation, intramyocardial sinusoidsand coronary fistulae develop.

TAPVC


91/107

TAPVC

Usually does not affect the development offetus.

If whole of PV return drains to SVC,LV will

be totally free of PV blood and hence will beof higher saturation.

Left atrium and left ventricle will be relatively

small in TAPVC.

TOF d l t d di d


92/107

TOF and related disorders

Does not appear to affect fetal circulationadversely.

The volume and direction of flow across the

PA and ductus are dependant on theseverity of obstruction.

Total flow through the ductus will be

reduced considerably.

TOF d l t d di d


93/107

TOF and related disorders

This can markedly reduce the diameter offetal ductus and also reduce thedevelopment of smooth muscle in its wall.

If blood flows from aorta to PA in fetallife,the orientation of ductus changes and itforms an acute inferior angle with aorta.

AA and the isthmus carries large thannormal amount of blood and they tend to belarger.


94/107

70

55 65

63

60

70/4 70/4

70/45

TOF ith absent PV


95/107

TOF with absent PV

Ductus is frequently either atretic or notdeveloped.

RV would be subjected to both volume and

pressure overload and can develop in utero. Significant pulmonary regurgitation can

seriously affect perfusion of pulmonaryvessels and cause abnormal developmentof intrapulmonary vessels.

Aortopulmonary transposition


96/107


Compatible with fetal survival and normalintrauterine development.

Does not affect the pattern of venous return.

Blood with higher oxygen saturation will goto lungs. This will reduce the PVR andhence increase in PBF.



97/107


This will reduce the blood flow across theductus and increases the flow across theisthmus.

Blood with lower oxygen saturation perfusescoronary and cerebral circulation.

Hence cerebral and coronary blood flow are

increased considerably.


98/107

70

40

55 70

55

65

70/4 70/3

70/45

70/45

TGA with VSD


99/107

TGA with VSD

Bi directional shunting occur depending onafter load of each ventricle.

The difference in saturation between AA andDA will be lesser.

TGA with VSD and PS


100/107

TGA with VSD and PS

Almost complete admixture of SVC and IVCstreams in RV.

AA and DA will have similar oxygen

saturations.

Blood flow in the ductus will be from aorta toPA.


101/107

70

40

55

65 65

6570/4

70/4

70/45

Truncus arteriosus


102/107

Truncus arteriosus

Various degree of mixing occurs just abovethe semilunar valve.

Degree of mixing depends on morphology.In

type 1,there is differential streaming of bloodand in others there will be complete mixing.

Ductus is usually small or absent andincreased flow traverses through isthmusand it is large.

Ebsteins anomaly


103/107

Ebstein s anomaly

Severe TR can manifest as in utero cardiacfailure especially if foramen ovale isrestrictive.

Marked enlargement of RA and atrialisedRV can cause septal displacement andcompromise LV output.

Functional pulmonary atresia can result andductal flow may be reversed.

Ebsteins anomaly


104/107

Ebsteins anomaly

Marked enlargement of right atrium cancause pulmonary hypoplasia

Severe TR alters the preferential drainage of

venacaval blood and causes completemixing of blood in right atrium.

Tricuspid atresia


105/107

Tricuspid atresia

All of the venous return traverses foramenovale and it is considerably larger thannormal .

Complete admixture of blood in the leftatrium

It is compatible with normal intrauterine

development and survival.

Tricuspid atresia


106/107

Tricuspid atresia

If IVS is intact, whole PBF is from aortathrough ductus and ductal flow is lesser thannormal.

75% of combined VO traverses the isthmusand it tends to be larger.

In the presence of VSD,the flow pattern is

decided by the size of the defect andpresence of pulmonary stenosis.


107/107

Foetal Circulation

Documents

Transcript of Foetal Circulation