Download - Foetal Circulation
-
7/31/2019 Foetal Circulation
1/107
FETAL CIRCULATION
IN HEALTH AND DISEASE
-
7/31/2019 Foetal Circulation
2/107
Flow Chart of Fetal Circulation
-
7/31/2019 Foetal Circulation
3/107
-
7/31/2019 Foetal Circulation
4/107
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
7/107
Cardiac output and its distribution
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.
-
7/31/2019 Foetal Circulation
8/107
Cardiac output and its distribution
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
-
7/31/2019 Foetal Circulation
9/107
Cardiac output and its distribution
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.
-
7/31/2019 Foetal Circulation
10/107
8%
66%
70%
55%
24
1828 19
20%AA 33%
3245%
21%
24%70%
21%
60%
-
7/31/2019 Foetal Circulation
11/107
35%
50% 65%
55%
65%
-
7/31/2019 Foetal Circulation
12/107
Cardiac output and its distribution
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
-
7/31/2019 Foetal Circulation
13/107
Cardiac output and its distribution
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
-
7/31/2019 Foetal Circulation
14/107
220
140
15
125
95
200250
140
175
45
75
220
180
40
75
15
-
7/31/2019 Foetal Circulation
15/107
49
31
3
21 28
58 44
39
31
10
17
49
39
10
17
3
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
17/107
Venous return to heart
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.
-
7/31/2019 Foetal Circulation
18/107
Venous return to heart
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.
-
7/31/2019 Foetal Circulation
19/107
Venous return to heart
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.
-
7/31/2019 Foetal Circulation
20/107
Shunts in fetal circulation
Ductus venosus
Foramen ovale
Ductus arteriosus or aortic isthmus
-
7/31/2019 Foetal Circulation
21/107
Shunts in fetal circulation
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.
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
23/107
PULMONARY CIRCULATION
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.
-
7/31/2019 Foetal Circulation
24/107
PULMONARY CIRCULATION
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.
-
7/31/2019 Foetal Circulation
25/107
PULMONARY CIRCULATION
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.
-
7/31/2019 Foetal Circulation
26/107
PULMONARY CIRCULATION
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.
-
7/31/2019 Foetal Circulation
27/107
PULMONARY CIRCULATION
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.
-
7/31/2019 Foetal Circulation
28/107
PULMONARY CIRCULATION
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.
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
30/107
Oxygen exchange function
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.
-
7/31/2019 Foetal Circulation
31/107
Oxygen exchange function
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.
-
7/31/2019 Foetal Circulation
32/107
Oxygen exchange function
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.
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
36/107
Post natal changes in various circulatory
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.
-
7/31/2019 Foetal Circulation
37/107
Post natal changes in various circulatory
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.
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
39/107
Changes in Cardiac output
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.
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
41/107
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 DV
and 90 ml/mt[21%] passes through hepatic
circulation
-
7/31/2019 Foetal Circulation
42/107
Cardiac output and its distribution
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.
-
7/31/2019 Foetal Circulation
43/107
Cardiac output and its distribution
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
-
7/31/2019 Foetal Circulation
44/107
Cardiac output and its distribution
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.
-
7/31/2019 Foetal Circulation
45/107
Cardiac output and its distribution
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
-
7/31/2019 Foetal Circulation
46/107
Cardiac output and its distribution
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
-
7/31/2019 Foetal Circulation
47/107
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.
-
7/31/2019 Foetal Circulation
48/107
Venous return to heart
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.
-
7/31/2019 Foetal Circulation
49/107
Venous return to heart
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.
-
7/31/2019 Foetal Circulation
50/107
Venous return to heart
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.
-
7/31/2019 Foetal Circulation
51/107
Shunts in fetal circulation
Ductus venosus
Foramen ovale
Ductus arteriosus or aortic isthmus
-
7/31/2019 Foetal Circulation
52/107
Shunts in fetal circulation
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.
-
7/31/2019 Foetal Circulation
53/107
PULMONARY CIRCULATION
Fetal lung does not serve gas exchangefunction.
PVR is high and PBF is low.
This helps to reduce workload of fetal heart.
-
7/31/2019 Foetal Circulation
54/107
PULMONARY CIRCULATION
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.
-
7/31/2019 Foetal Circulation
55/107
PULMONARY CIRCULATION
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.
-
7/31/2019 Foetal Circulation
56/107
PULMONARY CIRCULATION
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.
-
7/31/2019 Foetal Circulation
57/107
PULMONARY CIRCULATION
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.
-
7/31/2019 Foetal Circulation
58/107
PULMONARY CIRCULATION
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.
-
7/31/2019 Foetal Circulation
59/107
PULMONARY CIRCULATION
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.
-
7/31/2019 Foetal Circulation
60/107
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.
-
7/31/2019 Foetal Circulation
61/107
Oxygen exchange function
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.
-
7/31/2019 Foetal Circulation
62/107
Oxygen exchange function
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.
-
7/31/2019 Foetal Circulation
63/107
Oxygen exchange function
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.
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
65/107
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.
Post natal changes in various circulatory
-
7/31/2019 Foetal Circulation
66/107
Post natal changes in various circulatory
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.
Post natal changes in various circulatory
-
7/31/2019 Foetal Circulation
67/107
Post natal changes in various circulatory
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.
-
7/31/2019 Foetal Circulation
68/107
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 -850
ml/mt/kg.
So the increase is 1.5 to 2 times.
Changes in Cardiac output
-
7/31/2019 Foetal Circulation
69/107
Changes in Cardiac output
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.
Changes in Cardiac output
-
7/31/2019 Foetal Circulation
70/107
Changes in Cardiac output
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
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
73/107
Fetal circulation in pathological
conditions
Fetal circulation in pathological
-
7/31/2019 Foetal Circulation
74/107
Fetal circulation in pathological
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.
Fetal circulation in pathological
-
7/31/2019 Foetal Circulation
75/107
Fetal circulation in pathological
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.
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
81/107
70
6065
62
60
75/4 90/
5
75/50
70/45
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
84/107
70
40
60 60
60
70/2
70/40
Mi l d i i
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
87/107
70
40
63
63
63
63100/4
70/3
-
7/31/2019 Foetal Circulation
88/107
RVOTO with intact IVS
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
-
7/31/2019 Foetal Circulation
89/107
RVOTO with intact IVS
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
-
7/31/2019 Foetal Circulation
90/107
RVOTO with intact IVS
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
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
94/107
70
55 65
63
60
70/4 70/4
70/45
TOF ith absent PV
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
96/107
Aortopulmonary transposition
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.
Aortopulmonary transposition
-
7/31/2019 Foetal Circulation
97/107
Aortopulmonary transposition
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.
-
7/31/2019 Foetal Circulation
98/107
70
40
55 70
55
65
70/4 70/3
70/45
70/45
TGA with VSD
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
101/107
70
40
55
65 65
6570/4
70/4
70/45
Truncus arteriosus
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
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
-
7/31/2019 Foetal Circulation
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.
-
7/31/2019 Foetal Circulation
107/107