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FOETAL CIRCULATION
• The fetal circulation is the circulatory system of a human fetus, encompassing the entire fetoplacental circulation which includes the umbilical cord and the blood vessels within the placenta that carry fetal blood.
Umbilical Cord
• 2 umbilical arteries: return deoxygenated blood, wastes, CO2 to placenta.
• 1 umbilical vein: brings oxygenated blood and nutrients to the fetus.
Placenta
• Organ that connects the developing fetus to the uterine wall.
• Functions as respiratory centre,as a site of filtration for plasma nutrients and wastes.
• Two components: - the fetal placenta(Chorion frondosum),which develops from the fetus
- the maternal placenta(Decidua basalis), which develops from the maternal uterine tissue
• Foetal hemoglobin has higher affinity for oxygen than adult hb,
which allows diffusion of oxygen from the mother's circulatory system to the foetus.
• Water, glucose, amino acids, vitamins, and inorganic salts freely diffuse across the placenta along with oxygen.
• Foetal circulation differs from the adult one by the presence of 3 major vascular shunts :
- Ductus venosus: between the umbilical vein and IVC- Foramen ovale: between the right and left atrium - Ductus arteriosus: between the pulmonary trunk and descending aorta
4 unique FETAL CVS structures : FOUR SHUNTS
• Placenta Oxygenated blood Umbilical vein Hepatic circulation Bypasses liver & joins IVC via ductus venosus
Partially mixes with poorly oxygenated IVC blood derived from lower part of fetal body
• Combined lower body blood + umbilical venous blood flow passes through IVC to the right atrium
• Part of IVC blood with high O2 concentration goes into LA via Foramen Ovale.
• Remaining IVC blood enters RV.• Most of SVC blood goes to the RV traversing the tricuspid valve and into the pulmonary trunk.
Because the pulmonary arterial circulation is vasoconstricted, only about 10% of right ventricular outflow enters the pulmonary arteries. The rest 90% blood bypasses the lungs and flows through the ductus arteriosus into the descending aorta to perfuse the lower part of the fetal body.
• The left atrium receives blood from :- Pulmonary veins- Right atrium through the foramen ovale• This blood passes into left ventricle then into the aorta supplying head,neck,brain and upper extremities through carotid and subclavians,
then mixes with poorly oxygenated blood from the ductus arteriosus and perfuses the rest of the body through branches of descending aorta.
Overview of fetal circulatory dynamics
• Parallel arrangement of two main arterial systems and their respective ventricles.
• Mixing of venous return and preferential streaming.
• High resistance and low flow of pulmonary circulation.
• Low resistance and high flow of systemic circulation.
• Presence of shunts.
At birth
Mechanical expansion of lungs Increase in arterial PO2
Rapid DECREASE in pulmonary vascular resistance
Removal of the low-resistance placental circulation
INCREASE in systemic vascular resistance.
Perinatal circulatory transition
1. High arterial PO2
Constriction of ductus arteriosus
It closes, becoming the ligamentum arteriosum.
• Right ventricle output now flows entirely into the pulmonary circulation.
• Pulmonary vascular resistance becomes lower than systemic vascular resistance
Shunt through ductus arteriosus reverses & becomes left to right.
2. Increased volume of pulmonary blood flow returning to left atrium
Increases left atrial volume and pressure
Closure of foramen ovale (functionally)
Becomes Fossa Ovalis.
• CLOSURE of :
- Foramen ovale : Functional Closure: 3rd month of life. Anatomical closure of septum primum & septum secundum by 1 year of age.
- Ductus arteriosus : Functional Closure: By 10–15 hr in a normal neonate.Anatomic closure: May take several weeks. In a full-term neonate, oxygen is the most important factor controlling ductal closure.
When the PO2 in the blood passing through the ductus reaches about 50 mm Hg , the ductal wall constricts.
3. Removal of the placenta from the circulation
Also results in closure of the ductus venosus.
• The left ventricle is now coupled to the high-resistance systemic circulation its wall thickness begins to increase.
• In contrast, the right ventricle is now coupled to the low-resistance pulmonary circulation its wall thickness decreases slightly.
FETAL NEWBORNGas exchange Placenta Lungs
RV,LV circuit Parallel Series
Pulmonary circulation Vasoconstricted Dilated
Fetal myocardiumContractility,Compliance Less Good
Dominant ventricle Right Left
Change in Structure Umbilical vein Ligamentum teres Umbilical artery Medial umb ligament Ductus venosus Ligamentum venosum Ductus arteriosus Ligamentum arteriosum Foramen ovale Fossa ovalis
Persistent Pulmonary Hypertension of the Newborn (PPHN)
• Disruption of normal transition of fetal circulation to neonatal circulation
• “Persistent fetal circulation”• Suprasystemic resistance in the pulmonary vasculature
PVR > SVR
• Leading to perpetuation of R->L shunt through foramen ovale and/or ductus arteriosus
• Resulting in diminished pulmonary perfusion and systemic hypoxemia
• Incidence is 1-2 /1000 live births• More common among full term and post term neonates
• In preterm neonates,RDS may be complicated by PPHN
RISK FACTORS
• Maternal : fever,anemia,pulmonary disease,UTI,DM,drugs like aspirin/NSAID’s/SSRI’s,smoking(antenatally)
• Foetal : 1.Birth asphyxia – prolonged hypoxemia leads to release of humoral factors which cause vasoconstriction and remodelling of pulmonary vasculature
(abnormal muscularization of arterial wall with >> medial thickness)
decreased cross sectional area of the vessels >> PVR.
2.Parenchymal lung diseases like pneumonia,surfactant deficiency,meconium aspiration – reversible,due to vasospasm.
3.Pulmonary developmental abnormalities likeCDH,Potter syndrome (parenchymal hypoplasia)Alveolar capillary dysplasia (malalignment of pulmonary veins and arteries).
4. Congenital heart disease (left and right sided obstructive lesions),myocardial dysfunction,myocarditis,intrauterine constriction of DA.
5.Infections- viral/bacterial pneumonias,sepsis cause vasospasm by release of thromboxanes,by suppressing endogenous NO production and by direct endotoxin mediated myocardial depression.
6. Genetic predisposition – low levels of NO metabolites,arginine,diminished endothelial NOS expression.
7. Mechanical factors like low cardiac output,hyperviscosity,polycythemia.
Vascular remodelling with smooth muscle hyperplasia
TYPES
• PRIMARY PPHN
• SECONDARY PPHN
DIAGNOSIS• Presents within 18 hours of birth• Respiratory distress• Marked cyanosis• Differential cyanosis between regions perfused by preductal and postductal vasculature
• Prominent precordial impulse• Loud,single or narrowly split S2• Systolic murmur• A gradient of 10% or more in oxygen saturation between preductal and postductal areas
• CXR appears normal or shows associated parenchymal lung disease
• ECG shows RV strain or hypertrophy• ECHO shows hemodynamic shunting,helps to evaluate ventricular function,tricuspid insufficiency and to exclude congenital heart disease
• Color doppler shows presence of intracardiac/ductal shunting
MANAGEMENT• Case fatality rate of 30-60%• Requires immediate intervention to reverse hypoxemia,improve pulmonary and systemic perfusion,preserve end organ function
• Supplemental oxygen(postductal SaO2 is > 90% and < 98%)• Intubation,mechanical ventilation(persisting hypoxemia,hypercapnea,acidosis)
o In the absence of pulmonary disease -> mechanical ventilation with rapid,low pressure and short inspiratory time
o PPHN + parenchymal lung disease -> High frequency oscillatory ventilation/High frequency jet ventilation (MAS,air leak)
• Sildenafil
o PDE-5 inhibitoro Inhibits metabolism of NOo >> available NOo Dose : 0.4mg/kg/dose IV over 3hrs followed by a continuous infusion of 1.6mg/kg/24hrs
for upto 7days
• iNO
diffuses into smooth muscle cells
>>cGMP
relaxes vascular smooth muscle
pulmonary vasodilation
o Started at a dose of 20ppm.o Delivered via the ventilator circuit.oMost effective when administered after adequate alveolar recruitment(by use of HFOV / surfactant).
oWhen the condition improves,dose is slowly tapered by halving.
o Stopped when SaO2 is adequate on FiO2 of < 50% and i NO dose of 1ppm.
o High doses lead to methemoglobinemia.o Abruptly stopping iNO leads to rebound hypoxemia.
• ECMO
o Extra Corporeal Membrane Oxygenation o Used when conventional therapy and iNO treatment fails
o Criteria to start ECMO : oxygenation index of >30 in 2 ABG’s taken 30 minutes apart
& alveolar-arterial oxygen difference > 600
• Intravascular volume support• Dobutamine and vasopressors • Correct hypoglycemia,hypocalcemia(to provide adequate substrates to the myocardium)• Neutral/alkalotic pH reduces PVR (by sodium bicarbonate boluses)• Sedation and analgesia with fentanyl/morphine(prevents release of catecolamines which activate pulmonary adrenergic receptors)
• Muscle relaxants like pancuronium
• Correct polycythemia,hyperviscosity (partial exchange transfusion with normal saline to maintain HCT between 50-55%)• Other therapies : Magnesium sulfate , adenosine , tolazoline , calcium channel blockers , inhaled prostacyclin , inhaled ethyl nitrite
PROGNOSIS
• Neurodevelopmental sequelae in 15-20%• Hyperventilation reduces cerebral perfusion, leads to sensorineural hearing loss
• Prolonged ventilation leads to development of chronic lung disease
• 20% risk of rehospitalization within 1 year of discharge
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