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
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
5.
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 RVLV
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
10.
11.
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
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
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
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
39.
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
Hinweis der Redaktion
Pulmonary blood flow is represented by RVO minus ductus arteriosus flow. Pulmonary blood flow has also been calculated from direct measurement of right and left branch pulmonary arteries insome studies
Pulmonary blood flow is represented by RVO minus ductus arteriosus flow. Pulmonary blood flow has also been calculated from direct measurement of right and left branch pulmonary arteries insome studies
Pulmonary blood flow is represented by RVO minus ductus arteriosus flow. Pulmonary blood flow has also been calculated from direct measurement of right and left branch pulmonary arteries insome studies
(Blood going from RV->PA to Des Ao through PDA – none of this passes retrograde to ascending aorta)