anatomy of foetal circulation

Indraprastha Apollo Hospital 1

Anatomy of Foetal Circulation

Dr Leena Tayshete (Jr Reg)Dr Anil K Sharma (Moderator)

28-10-2014


Objectives

• Review of Fetal Circulation• Changes at Birth• Postnatal circulation• Defects

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Indraprastha Apollo Hospital 328-10-2014


– Begins to develop toward the end of 3rd wk– Heart starts to beat at the beginning of 4th wk– Critical period of heart development- day 20 to

day 50 aft fertilization.

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‘Shunt-Dependent’ Circulation

• PaO2 in the umbilical vein around 4.7 kPa & foetal blood saturation 80–90%.

• 50–60% of this placental venous flow bypasses the hepatic circulation via the ductus venosus (DV) to enter the inferior vena cava (IVC).

• Venous blood, which is returning from the lower portions of the body SVO2 of around 25–40%.

• Eustachian valve -flap tends to direct the more highly oxygenated blood, streaming along the dorsal aspect of the IVC, across the foramen ovale (FO).

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• In LA, O2 saturation of foetal blood is 65%. Majority of the LV blood is delivered to the brain and coronary circulation.

• Desaturated blood(SO2 25–40%),from SVC & coronary sinus, in addition to the IVC’s anteriorly streamed flow (comprised mainly of venous return from lower body and hepatic circulation) directed across tricuspid valve.

• Due to high pulmonary vascular resistance (PVR) about 12% of the RV output pulmonary circulation; remaining 88% crossing the ductus arteriosus (DA)descending aorta

• Lower half of the body supplied with relatively desaturated blood (PaO2 2.7 kPa).

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• Three shunts in foetal circulation– Ductus arteriosus

protects lungs against circulatory overload� allows the right ventricle to strengthen � hi pulmonary vascular resistance, low pulmonary �

blood flow carries mostly � medium oxygen saturated blood.

– Ductus venosus connecting the umbilical vein to IVC� blood flow regulated via sphincter� carries mostly � highly oxygenated blood.

– Foramen ovale shunts � highly oxygenated blood from RA LA.

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Foetal circulation is characterized by

• High PVR (fluid filled lungs and a hypoxic environment).

• Low systemic vascular resistance (SVR) (large surface area of low resistance utero-placental bed).

• Most oxygenated blood from the umbilical vein perfuses the brain and heart preferentially by shunting across Ductus Venosus & Foramen Ovale.

• Lesser oxygenated blood perfuses the lower body by shunting across the Ductus Arteriosus.

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Physiology of Foetal Hb

• Umbilical vein PaO2 30-35 mmHg.• Approximately 80% of foetal haemoglobin is Hb F• Hb F (P50 19mmHg) is left shifted in comparison to Hb

A (P50 26mmHg), which improves oxygen uptake at the placenta.

• Foetal pH (normal values 7.25-7.35) is lower than in adults. Low foetal pH improves oxygen unloading at tissue level.

• Foetal Hb is high compared to adult levels (raises oxygen carrying capacity).

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• CaO2 (ml O2/dl blood) = (SaO2 x Hgb x 1.34) + (PaO2 x 0.003)

• Umbilical vein PaO2 30-35 mmHg. Foetal Hb 70%-80% saturated at this PaO2 in (comparison adult Hb SaO2 50-60%).

• CaO2 for foetus - Hb 18 grams/dl & SaO2 75% in the umbilical vein yields: CaO2 = 0.75 x 18 x 1.34 = 18.1 ml O2/ dl blood

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• Foetal Hb conc. - 16 g dl/1 at term, with high % of haemoglobin F (HbF), which has a lower content of 2,3-DPG (shifting the oxygen dissociation curve to the left) favours oxygen uptake in placenta.

• After birth, presence of HbF becomes a disadvantage.• The P50 fetal blood-3.6 kPa compared with adult blood-4.8

kPa.• When PO2 is 5.3 kPa (approximates to normal neonatal

venous value), the oxygen content of fetal blood is much higher than that of adult blood. Thus, in the neonate, HbF impairs oxygen extraction at tissue level.

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Combined ventricular output (CVO)

• SV of foetal LV ≠SV of RV.• The RV receives about 65% of the venous return and

the LV about 35%.• In the shunt dependent circulation of the foetus, the

situation is much more complex.• The cardiac output of the foetus determined as

combined ventricular output (CVO)₂.• About 45% of the CVO is directed to the placental

circulation with only 8- 12% of CVO entering the pulmonary circulation.

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Review of changes at birth

• Overview-– As soon as the baby is born– Increasing uptake of oxygen by lungs (first and

subsequent breaths) vasoconstriction of ductus venosus and ductus arteriosus.

– The sphincter in ductus venosus constricts blood entering liver diverts to the hepatic sinusoids).

Occlusion of placental circulation � BP fall in the IVC & RA.

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• Aeration of the lungs at birth1. ↓ in PVR due to lung expansion.2. ↑ in pulmonary blood flow (thus raising LA pr > IVC pr)3. progressive thinning of walls of the pulmonary arteries (due to stretching).

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Factors affecting Pulmonary Vasculature

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The first breath:

Pulmonary alveoli open up:– pressure in pulmonary tissues decrease.– Blood from right heart rushes to fill the alveolar

capillaries.– Pressure in right side of heart ↓.– Pressure in the left side of the heart ↑ (as more

blood is returned from pulmonary tissue via pulmonary veins to the LA).

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• Resulting circulatory changes:– blood pressure is now high in the aorta and systemic circulation is

well established• Control of circulation is a reflex function regulated:

– Peripheral baroreceptors in aortic arch & carotid sinus.– Central baroreceptors in cardiovascular center of medulla (close

proximity to chemoreceptors that regulate respiration).• Respiratory and circulatory reflexes are usually strong in the

healthy full-term newborn, but efficiency in controlling cardiovascular function is susceptible to environmental factors.

• Parasympathetic > sympathetic activity.

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• Foramen ovale- Closes at birth– Decreased flow from placenta & IVC to hold open

foramen and;– Increased pulmonary blood flow & pulmonary

venous return to left heart causing pressure in the LA > RA.

• Other changes in the heart-– The RV wall is thicker than LV wall in foetus and

newborn infants. By the end of the first month the left ventricular wall is thicker than the right.

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Ductus Arteriosus-– DA constricts at birth, often a small shunt from the aorta to

the left pulmonary artery for a few days in a healthy, full-term infant.

– In premature infants and in those with persistent hypoxia the DA may remain open longer.

– Oxygen, most important factor in controlling closure of DA in full-term infants.

– Closure of DA appears to be mediated by bradykinin.– PO2 of blood passing through DA reaches about 50 mm Hg,

the wall of the DA constricts. (May be mediated directly or by Oxygen effect on decreasing PG E2 & prostacyclin secretion.

– Implication- Coarctation of aorta requires PGE2 infusion to reopen the DA for blood flow.

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• Umbilical Arteries constrict at birth– To prevent loss of infant’s blood.– Umbilical cord is not tied for 30-60s; transferring

blood from placenta to infant.• The closure of the foetal vessels and foramen

ovale is initially a functional change; later anatomic closure (from proliferation of endothelial and fibrous tissues).

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UMBILICAL CORD CLAMPINGEXPOSURE TO ROOM AIR

TRANSITIONAL CIRCULATION

↓↓PVR↑ SVR

↑ PULMONARY BLOOD FLOW↑ OXYGENATION

RESPONDS TO CHANGES IN PaO2, PaCO2, pH & CIRCULATING FACTORSSVR – systemic vascular resistance PVR – pulmonary vascular resistance

↑ SVR ↓PVR

MECHANICAL INFLATION OF LUNGS(↑ alveolar O2 tension,↑PaO2,↓PaCO2) EDRF & PGs

↑ LT. ATRIAL FLOW↓FORAMEN OVALE SHUNTF.O. CLOSURE

DUCTUS ARTERIOSUS CONSTRICTION


FETAL CIRCULATION VIII: Conversion to post-natal*

Pulmonary veinsVena cava Right

ATRIUM

Pulmonary arteries

Right VENTRICLE

Left VENTRICLE

Aorta

LUNGS

SYSTEMIC CAPILLARIES

HEART

Um bilical arteries

Ductus arteriosus

IVC

OLef t ATRIUM

Closure of Foramen ovale

DUCTUS VENOSUS

means that blood expelled from the right ventricle has to go to the lungs

Closure of

Closure of

Stops use of umbilical vessels, & converts all vena cava blood to deoxygenated

Forces venous blood (now all deoxygenated) into the right ventricle for expulsion to the lungs

Closure of

Stops use of um bilical vessels


Adult Derivatives of Fetal Vascular Structures

Fetal Structure Adult Structure

Foramen Ovale Fossa Ovalis

Umbilical Vein (intra-abdominal part) Ligamentum Teres

Ductus Venosus Ligamentum Venosum

Umbilical Arteries and Abdominal Ligaments

Medial Umbilical Ligaments,Superior Vesicular Artery (supplies bladder)

Ductus Arteriosum Ligamentum Arteriosum

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Persistent Foetal Circulation

• Neonate to revert back to foetal type circulation, pathophysiological state- PFC.

• Causes- Hypothermia, hypercarbia, acidosis, hypoxia and sepsis.

• One major difference—NO PLACENTA for oxygenation vicious cycle of worsening hypoxia and acidosis.

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Patent Ductus Arteriosus• Female: Male, 2-3:1.• Aortic blood shunted into Pulmonary Artery(shunt in

opposite direction to that in foetus). The magnitude of the shunt increases as PVR continues to fall.

• Increased volume and workload left heart failure.• Associated with maternal rubella infection during early

pregnancy.• Premature infants usually have a PDA due to hypoxia and

immaturity.• Surgical closure of PDA is achieved by ligation and division

of the DA.

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Patent Foramen Ovale

• Most common form of an ASDs• Small isolated patent foramen ovale (no

hemodynamic significance); but if other defects present (e.g. pulmonary stenosis or atresia), blood is shunted through the foramen ovale into LV cyanosis.

• Probe patent foramen ovale, in up to 25% of people (superior part of the floor of the fossa ovalis). Though not clinically significant, may be forced open because of other cardiac defects.

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Ventricular Septal Defects

• Ventricular septal defects (VSD) are one of the most common forms of CHD.

• Well-tolerated in the fetus, as LV and RV pressures are equal.

• After birth, circulatory effects are dependent on size of the defect and balance between PVR & SVR.

• In neonates with large VSD, as SVR rises and PVR falls, L R shunt through VSD develops. As PVR continues to fall during the first weeks of life, this shunt increases CCF.

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Tetralogy of Fallot• TOF, one of the most common congenital heart malformations.• Most important features-

1. RV outflow obstruction, with hypoplastic pulmonary artery;2. large subaortic VSD with malalignment of conal septum.

• In foetus, depending on severity of the obstruction to pulmonary blood flow, the aorta will carry percentage of CVO. If obstruction to pulmonary blood flow is very severe, blood flow to the lungs will be supplied via the DA from descending aorta (i.e. the reverse of normal).

• After birth- If pulmonary obstruction is severe, the neonatal circulation is ‘duct-dependent’ and duct closure severe cyanosis.

• Re-establishment of ductal flow- prostaglandin infusion.

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Transposition of Great Arteries• Abnormal rotation & septation of the arterial truncus during

embryogenesis.• The aorta arises from the RV and the pulmonary artery from the LV

(pulmonary and systemic circulations are arranged in parallel ).• The FO and DA develop as normal(no major circulatory consequences of

this lesion in utero).• After birth, survival depends on presence of ASD, VSD or PDA between

the two circulations.• Newborns with TGA & intact ventricular septum (IVS) who have small

PFO or ASD will be severely cyanosed after closure of the DA. • Immediate management- establishing ductal patency (PGE1 infusion)

and, if necessary, balloon atrial septostomy.• Complete surgical repair- electively later.

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Anaesthetic Agents

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Propofol• For induction/ procedural sedation. • In healthy children without CHD, decrease in blood pressure of 30% due

to decreases in SVR (15%) and heart rate (10-20%).• Children with CHD - primary effect is drop in BP through decrease in

SVR. Systemic cardiac output increased without a change in heart rate or PVR.

• In children without shunt there was a small decrease in Pa02 (decreased respiratory drive), but no increase in PVR.

• In children with shunts the decrease in SVR L-to-R shunting decreased and R-to-L shunting increased.

• Used with caution as the sole agent in R-to-L shunts and in those for whom a decrease in systemic afterload is dangerous (aortic stenosis, hypertrophic cardiomyopathy, severe ventricular dysfunction).

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Ketamine• Anesthesia, analgesia, cardiovascular stability and lack of respiratory

depression with maintenance of airway reflexes. • Drawbacks- prolonged action, emergence and dissociative anesthetic state.• Anesthetic dose 50-75 mcg/kg/min, analgesic dose 5-10 mcg/kg/min.• In children with CHD, ketamine (50-75 mcg/kg/min) maintenance of the

relationship between SVR and PVR. Systemic blood pressure increased through an increase in cardiac output with little change in heart rate.

• Increased inotropy- beneficial for children with significant ventricular dysfunction.

• Sympathomimetic increased PVR??? In the setting of normocarbia with supplemental oxygen , PVR is not increased.

• Combined with 0.5 minimal alveolar concentration (MAC) sevoflurane in spontaneously breathing children with severe PHTN, ketamine did not raise PVR.

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Etomidate

• Few studies.• Bolus dosing of 0.3 mg/kg well tolerated-

maintenance of systemic BP & preservation of balance between SVR and PVR.

• Drawbacks- Transient adrenal suppression, pain on injection, vomitting.

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Volatile Agents• Halothane- equivalent MAC to isoflurane and sevoflurane,

greater myocardial depression and suppression of baroreceptor mediated increase in heart rate.

• The Qp:Qs ratio is unchanged with halothane, sevoflurane or isoflurane if ventilation is controlled even with high Fi02.

• Isoflurane- CO was maintained even at 1.5 MAC (decrease in SVR and increase in HR counters reduced inotropy).

• Sevoflurane- similar, but overall decrease in CO (lack of compensatory increase in HR with reduced inotropy).

• Children with significant ventricular dysfunction may not hemodynamically tolerate MAC levels of volatile anesthesia.

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Fentanyl/ Midazolam

• Limited to sick children who will remain intubated at the end of procedure.

• The ratio of Qp:Qs is unchanged in controlled ventilation.

• Fentanyl 25 mcg/kg maintains SVR, PVR and systemic blood pressure. Caution- Avoid bradycardia.

• The general tone of the sympathetic nervous system influences BP.

• Sympatholytic- combination of synthetic opioids with volatile anesthetics, midazolam or propofol.

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Dexmedetomidine• Selective α-2 agonist.• Analgesic and sedative with minimal respiratory depression.

Similar to natural sleep state.• Decreased sympathetic outflowrelative bradycardia and

stable blood pressure.• Side effects detrimental to children with CHD - hypertension

(peripheral α-2 agonist effect), bradycardia and hypotension. • Poorly tolerated in heart rate dependent neonates and infants.• Lack of respiratory depression ICU sedation in children at risk

for OSA such as Down syndrome.

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anatomy of foetal circulation

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