Transitional circulation

Transitional
circulation
www.cardiacanaesthesia.in | DrAmarja

FETAL CIRCULATION
• DEFINITION: the circulation of blood
from the placenta to and through the fetus
and back to the placenta .
www.cardiacanaesthesia.in|DrAmarja

FETAL CIRCULATION
 O2 uptake occurs in the placenta
 PREFERENTIAL STREAMING : Delivery of
highly oxygenated blood to the metabolically
active tissues(brain & heart) and of less
oxygenated blood to the placenta
 SHUNTS exists in the venous system, heart &
arterial system.
 PARALLEL CIRCULATION :
various organs receive portions of their blood
supply from either ventricles

Preferential pattern of
ventricular output.
•The left ventricle (LV) directs
most of its highly saturated blood
(red arrow) via the ascending
aorta (AAo) to the highly
metabolic heart and upper body.
• The right ventricle (RV)
primarily ejects less oxygenated
blood (purple arrow) via the main
pulmonary artery (MPA)
primarily down the ductus
arteriosus (PDA) and via the
descending aorta (DAo) to the
placenta for oxygen uptake.

FETAL CIRCULATION
Major difference
– DUCTUS VENOSUS
– FORAMEN OVALE
– DUCTUS ARTERIOSUS

The left umbilical vein
• Highly oxygenated
PO2-32 mmHg
nutrient rich blood
• Much of this blood is
diverted into ductus
venosus, which
connects the left
umbilical vein to IVC
in the liver
left umbilical veinwww.cardiacanaesthesia.in|DrAmarja

Sphincter mechanism in the liver
• This regulates the flow of remaining blood
from umbilical vein into IVC through
hepatic veins.
• A physiological sphincter exists and
prevents overloading of heart when the
venous flow in the left.umb.vein is high
(uterine contractions)

Ductus Venosus
• DV - slender shunt connecting the intra-
abdominal umbilical vein to the IVC
• 30-50% of the umbilical blood is shunted
through the DV

• Ductus venosus
blood has…
– the highest oxygenation
– the highest kinetic energy
in the IVC and
– predominantly presses open
the foramen ovale valve to
enter the left atrium, i.e
‘preferential streaming’

 Ductus venosus
• The shunt obliterates within 1-3 weeks of birth in term
infants
• takes longer time in :
• premature births
• persistent pulmonary hypertension
• various forms of cardiac malformations.
• In contrast to the DA where increased oxygen tension
triggers the closure, no trigger for DV
• Although PGE1 may keep it open , thromboxane may close
it .

Preferential pattern of venous return to the
right (RV) and left (LV) ventricles.
•More highly saturated blood (red
arrow) from the umbilical vein (UV)
passes via the ductus venosus (DV)
and left hepatic vein (LHV) to the left
atrium (LA) and LV.
• Less saturated blood (blue arrows)
from the lower body via the inferior
vena cava (IVC, not shown), from the
main and right portal veins (MPV and
RPV) via the right hepatic vein
(RHV), from the coronary sinus (CS),
and from the superior vena cava
(SVC) passes to the right atrium (RA)
and RV.

• FORAMEN OVALE:
– Formed by the
overlapping edge of the
septum secundum against
the ruptured upper
portion of the septum
primum.
– Acts like a flap valve for
preferential blood flow
from the right atrium to
the left atrium.

• FORAMEN OVALE:
• the inferior venous inlet to the
heart could be viewed as a
column of blood that ascends
between the two atria from
below.
• This column hits the interatrial
ridge, the crista dividens, and
is divided into a left and right
arm….

• FORAMEN OVALE:
– The left arm fills the
‘windsock’, formed
between the foramen ovale
valve and the atrial septum,
to enter the LA.
– The right arm is directed
towards the TV and joins
the flow from the SVC and
coronary sinus.

• DUCTUS ARTERIOSUS:
– Connects the left branch of the pulmonary trunk to arch
of aorta(beyond the origin of left subclavian artery)
– It protects the lungs from circulatory overloading.
– The blood that arrives via IVC reaches the LA-LV-
Aorta-carotid circulation-brain.
– The blood that arrives via the SVC reaches the RA-RV-
Pulmonary artery-Ductus arteriosus-Aorta- to the lower
portion of the body.

• 40% or less of the CO is directed through
the ductus arteriosus
• The lungs receive 13% of the CO at mid-
gestation and 20-25% after 30 weeks

• DA – circularly arranged smooth muscles ,
localized intimal cushions .
• Active muscular contraction opposes
cushions : functionally closes
• Stimulus – 02 – inhibition of potassium
channels , mito – ROS
• Preterms – deficient in K channels

-Influence of circulating substances PGE2 , which is
crucial in maintaining patency.
-Sensitivity to prostaglandin antagonists is highest in
third trimester and is enhanced by glucocorticoids and
fetal stress.
-The increased reactivity of the DA makes it vulnerable to
prostaglandin synthase inhibitors, such as
indomethacin.
-Nitric oxide has a relaxing effect on it

Umbilical arteries
• About 65%of blood in the descending aorta
goes to umbilical arteries(right and left) ,
direct branches of fetal internal iliac arteries
• Remaining 35% of blood supplies the lower
half of the body and viscera

Pulmonary Vascular Resistance
High PVR restricts PBF to 10 % of CO
• Causes – thick muscular layer
HPV
decreased NO synthetase
increased endothelin 1
mechanical – fluid filled alveoli
• Initial rapid fall – O2 , Slower fall –
thinning of medial layer ( 6-8 wks) – 2 yrswww.cardiacanaesthesia.in|DrAmarja

Blood volume
• The blood volume - fetus : 10-12% BW
7-8% in adults.
• The estimated volume of 80 ml/kg is > that
in adults.

• Arterial and venous blood pressure
mean arterial pressure - 15 mmHg at
gestational weeks 19-21.
systemic systolic pressure increases from
15-20 mmHg at 16 weeks to 30-40 mmHg
at 28 weeks.
• There is no obvious difference between the
left and right ventricles.

• This increase is also seen for diastolic
pressure, which is <5 mmHg at 16-18
weeks and 5-15 mmHg at 19-26 weeks.
• Umbilical venous pressure, increased from
4.5 mmHg at 18 weeks to 6 mmHg at term.

The fetal heart
• Fetal and neonatal myocardial cells
– are smaller in diameter
– contain relatively more non-contractile mass (primarily mitocondria, nuclei &
surface membrane).
– force generation , extent and velocity of shortening are low
– stiffness and water content of ventricular myocardium are high
• The fetal heart is surrounded by fluid-filled rather than air-filled
lungs.
• Hence the fetal and neonatal heart has limited ability to increase CO
in presence of volume load or a lesion that increases resistance to
emptying.
• CO is more dependent on changes in heart rate : bradycardia is poorly
tolerated by the fetus.

• Cardiac performance
The myocardium grows by cell division
until birth, and growth beyond birth is due
to cell enlargement. The density of
myofibrils increases particularly in early
pregnancy and the contractility continues to
improve during the second half of
pregnancy.

• The fetal heart has limited capacity to
increase stroke volume by increasing
diastolic filling pressure, the right ventricle
even less than the left.
• Increased heart rate may be the single most
prominent means of increasing cardiac
output in the fetus.

• The two ventricles pump in parallel and the
pressure difference between them is
minimal compared with postnatal life.
• Fetal myocardium is more stiff attributed to
the constraint of the pericardium, lungs and
chest wall, all of which have low
compliance before air is introduced.

Cardiac output & distribution:
• The right ventricular
output is slightly larger
than that of the left
ventricle, and pulmonary
flow in the human fetus is
13-25%, at 28-32 weeks
when the pulmonary blood
flow reaches a maximum.

• Cardiac output &
distribution:
• The lowest saturation is
found in the abdominal
IVC, and the highest
saturation is found in the
umbilical vein

Postnatal changes
• The changes in the central circulation at
birth are primarily caused by
– the rapid and large decrease in pulmonary
vascular resistance and
– the disruption of the umbilical-placental
circulation.

Postnatal changes
Placenta is cutoff
Peripheral resistance suddenly rises
Aortic pressure exceeds PA pressure
Fetal asphyxia
Infant gasps- lungs expand
Decrease in PVR , Increase in PBF , Fall in PAP
Functional closure of FO , Closure of DA.

Postnatal changes
Lungs expand
Pulmonary resistance falls
PBF increases
Blood returning to LA increases
PFO closes

Postnatal changes
• Once the child takes the first
breath,pulmonary circulation begins
and the right and left hearts become
completely independent of each other.
• All the by-pass channels having served
their purpose,obliterate.
• Foramen ovale is closed and becomes
fossa ovalis in the right atrium
• closure of the foramen ovale at birth is
entirely passive, secondary to
alterations in the relative return of
blood to the right and left atria.

Postnatal changes
• Ductus arteriosus
constricts in a few minutes
• Functional closure begins
by 10-15 hrs.
• Anatomical closure
complete by 2 weeks(by
probe patency).
• Ligamentum arteriosum by
3 weeks.
• Arterial o2, bradykinin
play a critical role in the
closure after birth.

• Postnatal closure of the ductus arteriosus is effected in two
phases:
• Immediately after birth:
– contraction and cellular migration of the medial smooth muscle in
the wall of DA
– intimal cushions or mounds
– functional closure within 12 hours after birth in full-term human
infants.
• The second stage :
– completed by 2 to 3 weeks in human infants
– produced by infolding of the endothelium,
– disruption and fragmentation of the internal elastic lamina
– proliferation of the subintimal layers
– hemorrhage and necrosis in the subintimal region.

• Patency or closure of the ductus arteriosus represents a
balance between
– the constricting effects of oxygen, vasoconstrictive substances, and
– the relaxing effects of several prostaglandins

Ligamentum venosum
• Ductus venosus becomes a fibrous band called
ligamentum venosum which is seen in continuation with
ligamentum teres(obliterated left umbilical vein)

Other changes and clinical aspects
• The umbilical arteries become umbilical ligaments
attached to the internal iliac arteries upto superior
vesical arteries.
• The left umbilical vein remains patent for
considerable time and can be used for exchange
transfusions.

Fetal pulmonary circulation
• Fetal mean PAP increases progressively
with gestation and at term is about 50 mm
Hg, exceeds mean aortic blood pressure .

Fetal pulmonary circulation
• Total pulmonary vascular resistance early in
gestation is extremely high ,owing to the
small number of small arteries present.
• It decreases progressively - last half of
gestation, with growth of new arteries and
an overall increase in cross section.

Transitional Circulation
• with initiation of pulmonary
ventilation:
– pulmonary vascular resistance
decreases rapidly
– eightfold to tenfold increase in
pulmonary blood flow.
– by 24 hours of age, mean
pulmonary arterial blood pressure
is half systemic.
– adult levels reached after 2 to 6
weeks
– This is due to vascular
remodeling, muscular involution,
and rheologic changes.

Regulation of Pulmonary
Vascular Resistance
• state of oxygenation
• the production of vasoactive substances:
– oxygen modulates the production of both
prostacyclin and endothelium-derived nitric
oxide (EDNO)
– Direct potassium channel activation
– Physical expansion
– Changes in alveolar surface tension

Control of the perinatal
pulmonary circulation
• balance between factors producing
– active pulmonary vasoconstriction (leukotrienes, low
oxygen, and possibly even ET-1 acting through the ETA
receptor) and
– those leading to pulmonary vasodilation (EDNO, ET-1
acting through the ETB receptor, bradykinin, and
prostaglandins).

Persistent fetal circulation
• Also called Persistent Pulmonary Hypertension of the
Newborn (PPHN)
• Most common - full term infants.
• Causes :
• Meconium aspiration
• Severe respiratory distress syndrome
• Pneumonia caused by Group B beta streptococci
• Episodes of asphyxia
• Progressive increase in RV afterload  RV dysfunction.
• results in right to left shunting through the PFO and / or
PDA.

• tachypnoea & acidosis
• a parasternal heave, loud S2 and a systolic
murmur.
• CXR – decrease vascular flow
no parenchymal disease
• Echo and Doppler evaluation to rule out TAPVC.
• 3 forms are described
– Hypertrophic type
– Hypoplastic type
– Reactive type

Treatment
• increase in the inspired O2 level
• correction of acidosis - NaHCo3.
• artificial ventilation
• inhaled NO - reduce PVR
• IV Prostaglandins
• Treatment of severe disease - ECMO

Duct Dependent Circulations
To maintain systemic circulation – Co-arct
Critical AS
HLHS
To maintain pulm circulation – PA
Critical PS
TA
TOF
Wherein syst & pulm circ – separate -TGAwww.cardiacanaesthesia.in|DrAmarja

Response of fetal circulation to
stress
• A hypoxic insult - activates a chemoreflex mediated by
the carotid bodies - vagal effect - reduced heart rate and a
sympathetic vasoconstriction
• endocrine responses (e.g. adrenaline and noradrenaline)
– maintaining vasoconstriction (a-adrenergic),
– increasing heart rate (b-adrenergic) and
– reducing blood volume with renin release and increased
angiotensin II concentration

stress
circulatory redistributional
pattern that maintains
placental circulation and
gives priority to the
adrenal glands,
myocardium and brain

stress
• Sustained hypoxia forces an adaptational shift to
– less oxygen demand,
– reduced DNA synthesis and growth
– a gradual return towards normal concentrations of blood gases and
endocrine status

Premature Newborns
• Pulmonary vascular smooth muscles – not
developed – rapid fall in PVR – early onset
of L-R shunt & CHF
• DA – open as no developed constrictor
response , high levels of PGE2 ( more
production less degradation ) , deficient in
K+ channels

Oxygen
• O2 - dilates PA constricts DA
• Acidosis – increases HPV

PA
Dilated by
• O2
• Vagus
• Beta – stimulation
• Bradykinin
Constricted by
• Hypoxia
• Acidosis
• Sympathetic stimulation
• Alpha adren stimulation

DA
Dilated by
• Hypoxia
• Acidosis
Constricted by
• Oxygen

Thank you

Transitional circulation

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