transitional circulation

Transitional

circulation

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FETAL CIRCULATION

• DEFINITION: the circulation of blood from the placenta to and through the fetus and back to the placenta .

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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

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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.


• DUCTUS ARTERIOSUS: • 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


• DUCTUS ARTERIOSUS:

-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 pressuremean 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 performanceThe 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 PAPFunctional 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. www.cardiacanaesthesia.in|DrAmarja

• 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 HLHSTo maintain pulm circulation – PA Critical PS TA TOFWherein syst & pulm circ – separate -TGA


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


Response of fetal circulation to stress circulatory redistributional

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


Response of fetal circulation to 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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