Fetal Circulation & Hemodynamics of

Congenital Heart Diseases

Dr. Mythili Bhaskaran,

Professor, Madras Medical College, Chennai
Dr. S. Chidambaranathan, Chidambaram
Dr. J. Saravanan, Chennai
 Development of Heart
• Mesodermal germ layer gives rise to the entire
cardiovascular system
• Two paramedian endothelial tubes fuse to form primitive
heart
• This heart has 3 parts: Cranial portion, Caudal portion and
bulbus cordis.
• Cranial portion  aortic sac which will give rise to the
aortic arch and its branches
• Caudal  dilates to form the early embryonic ventricle &
Sinus Venosus
• Bulbus cordis – 3 parts
 Development – Contd..
• In course of development this tube will form four
parts
• Sinus venosus – part of RA, IVC, SVC, Coronary
sinus & oblique vein of LA
• Primitive atrium – RA, LA, part of endocardial
cushion
• Primitive ventricle – RV, LV, Part of Endocardial
cushion
• Bulbus Cordis
 Development – Contd..
• Bulbus cordis which has three distinct areas

• Proximal one-third  body of the right ventricle RVIT

• Distal-most section  Truncus arteriosus  aortic root ,
parts of the ascending aorta & Pulmonary trunk
• Mid-portion   Conus cordis and connects the primitive
right ventricle to the truncus arteriosus.
• The conus cordis partitions to form the outflow tracts of the
right and left ventricles.
 Embryological Timetable
Weeks Days Somites Length in mm Cardiac events

1-2 0-20 1 1.5 No heart or great vessels

3 20 2 1.5 Cardiogenic plate

3 21 5 1.5 Endocardial tubes

4 22 10 2 Fusion of endocardial tubes

4 23 12 2 Single median cardiac tube,first contraction

( ineffective)
4 25 17 2.5 Cardiogenic loop

4 26 20 3 Single atrium

5 29 25 4 Bilobed atrium

5 30 26 4 Beginning of circulation

7 49 20 4-chambered heart, Absorption of pulmonary veins

Fetal Circulation
Fetal Circulation

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 Peculiarities of Fetal Circulation
• Lungs not functional
• Right to Left shunts - Foramen Ovale to supply
oxygenated blood to the systemic circulation
• Through Ductus Arteriosis to divert blood from non
functional lungs

• Two sides of the heart work in parallel

 SVC

Fetal Circulation LA

RA
From Placenta
LV
to Fetus
RV

Liver
IVC
Umbilical Vein

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 UPPER BODY

Fetal Circulation
Pulmonary Artery
From Fetus to
LA Placenta
RA
LV

RV

Umblical Artery
Placenta

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% change in CO 300 Cardiac reserve

25
Resting cardiac output

Fetus Adult
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 Reason for Low Cardiac Output (CO)
• The Cardiac fibers are small
• Proportionately more non-contractile elements
• Force generation & extent of shortening small
• Sympathetic functionally not matured until after
birth.
• Cardiac reserve small
 Changes takes place soon after birth

• Expansion of the lungs  ↓Pul vascular resistance

 ↑Pul blood flow  ↑Left atrial pressure 
Closure of foramen ovale
• Clamping of umblical cords  ↑Systemic
resistance  ↑ Systemic pressure
• The 2 sides of the heart work in series.
• Closure of ductus venosus and ductus arteriosus
Circulation
after Birth
AFTER BIRTH
Pulmonary Capillary

LUNGS

LA

First few breaths Click and watch graphics

AFTER BIRTH
Pulmonary arterial Capillary Venous Cap.

LA

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 AFTER BIRTH

Pulmonary Vein

Foramen Ovale LA

LV

Umbilical Artery

clamped Click and watch graphics

 Ligamentum
Ductus Arteriosus
Arteriosus

Pulmonary Vein

LA

LV

AFTER BIRTH
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 Normal Pressure Before & After Birth
Site Before After
(mm of Hg) (mm of Hg)

Right Atrium 10 0–6

Right Ventricle 60 / 10 25 / 0 – 6
Pulmonary Artery 60 / 40 25 / 10
Left Atrium 10 6 – 12
Left Ventricle 60 / 10 60 - 120 / 0 – 12
Aorta 60 / 40 60 - 120 / 40 - 75
 Pressures
Pressure = Flow x Impedance

Systemic Blood Pressure = Systemic flow (Cardiac output) x

Systemic impedance (systemic vascular resistance)

Pulmonary artery pressure = pulmonary blood flow x

pulmonary vascular impedance (pulmonary vascular
resistance)
 Pulmonary artery pressure (PAP)
PAP = Pulmonary blood flow (PBF) X
Pulmonary vascular resistance (PVR)

Pulmonary Artery Hypertension (PAH) may be due to ↑ PBF or ↑ PVR

↑ PBF  PAH  Hyperkinetic PAH  in large left to right shunts

↑ PVR  PAH  Obstructive PAH  Small left to right shunts

Changes in PAH  hypertrophy of musculature of the pulmonary

arteries
 PAH – Contd..
Long standing PAH  intimal hyperplasia & fibrosis
 Irreversible changes  Pulmonary Vascular
Obstructive disease (PVOD)  inoperable &
incurable

Eisenmenger Syndrome  Severe PAH with Right to

left shunt at atrial, ventricular or pulmonary artery
level.
 How to differentiate Hyperkinetic &
Obstructive PAH
Hyperkinetic Obstructive PAH
PAH
Heart Size Large Normal (except in ASD)

Parasternal Hyperkinetic Forcible of Heaving in ASD, Mild

in VSD & PDA
Impulse
Click of PAH Absent Present
Shunt Murmur Loud Short or Absent
Flow Murmur Present Absent
HEMODYNAMICS
IN
CONGENITAL
HEART
DISEASE.
 Congenital Cardiovascular Disease usually results
from altered embryonic development or persistence
of a fetal structure.

The altered structure might influence the functional

development of the reminder of the circulation
 Prenatal survival is not
endangered by major cardiac
anomalies as long as one side of the
heart can drive the blood from the
great veins to the aorta
 Left To Right Shunt

Determining Factors:
• Size of the defect
• Pressure difference between the two compartments.
• Systemic & Pulmonary Vascular resistance.
 Atrial Septal Defect

• The Pressure in the Atria is decided by the

compliance of the Ventricles.
• As the Pulmonary vascular resistance decreases
with age, hence the shunt increases
• Preferential shunting of blood from Right lung
• Irreversible Pulmonary hypertension uncommon.
 Ventricular Septal Defect
Three types
• Small defect without
Pulmonary resistance
• Large defect with
moderate Pulmonary
resistance.
• Large defect with high
Pulmonary resistance.
 1. Small defect without Pulmonary resistance
2. Large defect with moderate Pulmonary resistance.

Rt Vent.

VSD

Pulm.Outlet

L Vent.
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 Large defect with high Pulmonary resistance
Rt Vent.

VSD
Pulm.Outlet

L Vent.
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 Small defect with low vas. Resis.
• Continuous left to right shunt thro the Cardiac
Cycle.
• Holosystolic murmur due to large press. grad. in
vent. Systole.
• Absence of murmur in Diastole thorough flow
present, due to absence of turbulence
 Diastole

Systole
Small defect with Low Pulmonary Resistance.

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Diastole

Isovolumic Contraction

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 Early Ejection Late Ejection

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Isovolumic Relaxation
 Ventricular Septal Defect
• Increased pulmonary flow  Increased pulmonary
vascular resistance  Pulmonary Hypertension
develops

• Inflow into the Left Atrium & L Ventricle

increases  Left Ventricular Failure
PATENT DUCTUS ARTERIOSIS
Ductus Arteriosis to Ligamentum arteriosum
Pulmonary Artery

Ductus Arteriosis
Ligamentum Arteriosum
Oxygen

Aorta
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Pulmonary Artery
Ductus Arteriosis

Aorta
Pulmonary Vein

LA

Volume over load

LV

Hemodynamics in PDA
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 With Atrial volume Load

Closure of the LA
foramen ovale
Inc in LAP

Stretch of the foramen

LV Inc. in EDP

LEFT HEART FAILURE

PULMONARY EDEMA
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 Compensatory mechanism PDA
• Frank Starling’s mechanism.
• Increased sympathetic stimulation
Inc. in HR
Inc. in force of contraction.
• Myocardial hypertrophy if vol. load persists
Relationship b/n Gestational age & Ductus
600
Term
Percent increase
in resistance

30wks
300

24wks

0
PO2
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Relationship b/n Gestational age & Ductus

With advancing gestation, the level of PO2

required to initiate constriction falls
&
The extent of constriction increases
 PDA
• Prolonged patency seen in prematurity due to
immaturity.
• Prolonged PDA in hypoxic states like high altitude,
lung diseases.
• PDA in term infants due to congenital malformation,
defect of the elastic tissue.
The physiologic features associated with (L) to
(R) shunt thro. a PDA
will depend on
the magnitude of the shunt
&
the ability of the infant to handle the extra
volume load.
Hemodynamics of Pulmonary Atersia with PDA
Pulmonary Artery

Pulmonary Atresia
Ductus Arteriosis

Aorta Click and watch graphics

 AORTIC STENOSIS
• Pressure Gradient between LV & Aorta increases
• Normal aortic orifice  2cm2/m2
• LV Hypertrophy takes place to maintain the Cardiac
Output.
• Failure supervenes when hypertrophy not able to
over come the pressure gradient.
 AORTIC STENOSIS

Aorta
Low CO

Aortic Orifice
LV

Vent. Hypertrophy

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 AORTIC STENOSIS
Inc. compression of coronary artery due to
hypertrophy
Aortic head pressure low during diastole
Though coronary arteries are normal & dilated
the supply & demand do not balance.
Ischemia results.
 Pulmonary Stenosis
• The hemodynamics depends on the severity of stenosis &
Degree of development of right ventricle
• If the ventricular septum is intact, right ventricular mass &
pressure increase
• (R) to (L) shunt occurs through Foramen ovale or ASD
Cyanosis, polycythemia & clubbing.
• Pulmonary blood flow is better if associated with PDA
• In severe PS Rt. sided failure develops
 During inspiration

Pulm.Valve
Pulm.Orifice

Ejection sound soft

or absent
Rt.Ven.
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 During expiration

Ejection sound loud.

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Tetrology of Fallot
 Hemodynamics in TOF
• During activity → ↑ respiration (hyperpnea) →
Venous return increases but Pulmonary flow cannot
increase → Right to Left shunt → Cyanosis
• On squatting, venous return decreases →
Systemic vascular resistance increases, therefore
less or no right to left shunt → decreases cyanosis
Hemodynamics in TOF

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Thank you