FETAL CIRCULATION -CHANGES AT BIRTH / IMPLICATIONS IN CHD

1. DR ADHI ARYA
FELLOW PEDIATRIC CARDIOLOGY

2.  Circulation undergoes continuous maturation during gestation,
both morphologically and functionally, and these changes
during development may be greatly influenced by congenital
cardiac lesions
 Knowledge of fetal circulation is important to our understanding
of the manner in which various CHD influence the normal
circulation.
 Clinical manifestations of congenital heart disease are
intimately related to postnatal changes in the circulation

3. Fetal circulation
Implications in congenital malformations

4.  History
 Difference from neonatal/adult circulation
 Salient features of fetal circulation
 Normal flow/Anatomic shunts/ Admixture sites
 Concept of CVO/ distribution of CVO
 Factors affecting fetal CO and its response to
decreased CO

6.  Based on studies done on fetal lambs
 Fetal USG
 Fetal MRI
•Course and distribution same
•Quantities of blood ejected by ventricles and distributed to
various organs different
•Different gestation periods/ proportion to organs /12% vs 3%

7. Fetal USG
•Based on flow velocities and vessel
diameter.
•Heterogenous because of
measurements at different sites and
inter-observer variation .
•Diameter is squared , even small errors
lead to big errors in flow calculation

8. FETAL POSTNATAL
GAS EXCAHNGE PLACENTA LUNGS
RV/LV CIRCUIT PARALLEL SERIES
DOMINANT
VENTRICLE
RV RVLV
FETAL MYOCARDIUM LESS CONTRACTILE
ELEMENTS
LESS COMPLIANT
ADMIXTURE SITES IVC/LA
R-L
L-R Shunts
NONE

9.  Unique features of myocardium
 Preferential streaming within
the IVC between liver and heart
 Functional separation of aorta
at isthmus
 Higher O2 saturation in left
hepatic venous blood
Stiffness and impaired
relaxation of the fetal
myocardium---reflected in
pattern of Doppler
echocardiography
across the AV valves

12. Gives Br to L lobe ,
divides in to DV and
arcuate branch
Portal vein joins arcuate
Branch supplies rt side
RHV enters IVC separately
LHV joins DV and enters IVC
SVC blood to RV –
tubercle of Lower

13. Streaming in IVC , DV
vel-55 cm/s RHV blood
15 cm/s

14.  IVC
 LA
 L->R( UV blood returning to placenta without
being given to fetal body)
 R->L ( Blood from SVC or IVC distributed to
body without being delivered to placenta )
45% of SVC blood, 53% of IVC blood

15. Left to right and right to left shunts in fetus
constitute 33% of CVO of fetal heart

16. In fetus, blood distributed to palcenta and
to various parts of body –derived from
systemic as well as umblical venous return
Blood to organs derived from both
ventricles
So expressed as CVO

18. Coronary venous blood

19. Coronary circulation

24. Effects studied on fetal lambs
Heart rate –Pacing/ Vagal stimulation
Preload/Afterload
Myocardial contractility
Baroreceptors /chemoreceptors

25. PACING
RA Pacing 250-300 LVO 15 % inc, no eff
on RVO. Rates > 300 output fell,
progressively
LA pacing
LVO reduced by 50%;RVO inc
LA pressure exceeds RA and flow across
foramen ovale hampered, reducing LVO

26. VAGAL STIMULATION
Vagal stimulation
inc SVR( inc afterload) , inc intrapleural
pressure( dec VR)--decreases CVO
So fall in CO is also due to associated
changes not only decr HR

27. Fetal heart is normally operating
near the top of its ventricular
function curve, so that a fall in
preload results in a decrease in
output.
Second alternate theory is of
ventricular constraints due to
extrinsic compression of fetal
heart

28.  At constant arterial pressure
levels, progressive elevation
of left atrial pressure
increased left ventricular
stroke volume even with
atrial pressures as high as
10–15 mmHg

29. Few sarcomeres
Parallal arrangement of myofibrils absent
T tubule system less developed
Poor sympathetic innervation
Beta receptor concentration variable
So in cases of fetal bradycardia, SV cannot
be increased much

30. Mature with advancing gestation
Baroreceptors induced by arterial HT—
bradycardia, vasodilation
Chemoreceptor by hypoxemia—
brady(reflexly induced by vagal
stimulation)

31. Acute hypoxemia –brady(vagal) and HT(
catecholamine induced)
<12mm Hg- depressent effect on
myocardium
Chronic – resetting of chemoreceptor
sensitivity—HR increases but not fully
Increased systemic venous pressures –
HYDROPS

32. Hydrops (inc systemic venous pressure)
Obstruction
Volume of blood flow
Blood oxygen content

35. DA obstruction- pulmonary circulation
Maternal NSAIDs
Increased PA pressure
Increased pulmonary vascular smooth
muscles
PPHN

36. Aortic arch obstruction
 COA
 Neurodevelopmental
problems

37. 1.Ventricular development: inflow or outflow reduction
 Inflow reduction: hypoplastic chamber
 (FO, mitral atresia)
 Outflow obstruction(AS/PS): ESV inc , atrial filling
pressure increase, hypertrophy, foramen ovale diverts
the venous return to normal ventricle, CVO is maintained

38. 2.Ascending aorta and arch
 10% CVO passes through isthmus
 Aortic atresia: no forward flow, hypoplastic arch
 Pulm atresia: entire CVO through aorta, dilated
ascending aorta
3.Ductus size and angle
 Aortic atresia :Wide oblique inferior angle/ inc
size
 Pulm atresia:Acute inferior angle / dec size

40. Aortopulmonary transposition
 Ascending aortic blood flow desaturation, cerebral
malformations
 Pulmonary blood flow has high oxygen content,
pulmonary vasodilation, increased PBF, increased
venous return to LA, LA pressure higher, flap of foramen
ovale shifted to right
 Oxygenated blood from PA passing through ductus
causes its constriction