Foetal Circulation

Question 1

What is the function of the foetal CVS

Answer 1

The foetal cardiovascular system is designed to serve prenatal needs and permit modifications at birth that establish the neonatal circulatory pattern.

Question 2

What are the peculiarities of the foetal circulation?

Answer 2

In the foetal circulation, the right and left ventricles exist in a parallel circuit as opposed to the series circuit of a newborn or adult.

In the foetus, the gas exchange is provided by the placenta and not the lungs as the pulmonary vessels are vasoconstricted.

Question 3

Mention the shunts in the foetal circulation

Answer 3

Ductus venosus
Foramen ovale
Ductus arteriosus
Umbilical artery

Question 4

What are the functions of each of the shunts

Answer 4

The ductus venosus joins the placental venous return to the systemic venous return

The ductus arteriosus connects the pulmonary arterial circulation directly to the systemic arterial circulation

The umbilical artery joins the systemic arterial circulation with the placental arterial circulation

The foramen ovale joins the left and right sides of the heart.

Question 5

Where is the highest partial pressure of oxygen in the fortis found - why and what is its range

Answer 5

Blood from the umbilical veins.

The placenta is not as efficient as the lungs as an O2 exchange organ, so umbilical venous PO2 is 30-35mmHg.

Question 6

What part of the heart does more work in the foetus

Answer 6

In the foetus, the right ventricular output is 1.3 times left ventricular output. As a result, the right ventricle does more work than the left ventricle

Question 7

What are the transitional circulatory changes that occur at birth

Answer 7

Mechanical expansion of the lungs
Removal of the placenta

This results in a shift of gaseous exchange from the placenta to the lungs

Question 8

What happens when the lungs are aerated at birth

Answer 8

There is increase in arterial pO2 and a dramatic fall in pulmonary vascular resistance.

There is a marked increase in pulmonary blood flow with progressive thinning of the pulmonary arteries.

Because of increased pulmonary blood flow, the pressure in the left atrium becomes higher than that in the right atrium resulting in functional closure of the foramen ovale.

The increased arterial oxygen saturation leads to the constriction and eventually closure of the Patent Ductus Arteriosus.

Question 9

What happens after removal of the placenta

Answer 9

Increase in Systemic Vascular Resistance
Cessation of blood flow through the umbilical veins
Closure of the ductus venosus

Question 10

What is another name for persistent foetal circulation

Answer 10

Persistent pulmonary hypertension of the newborn

Question 11

Describe the pathophysiology of persistent pulmonary hypertension of the newborn

Answer 11

In utero, the pulmonary vascular resistance is high due to the increased amount of smooth muscle in the walls of the pulmonary arterioles and alveolar hypoxia.

However, after birth, pulmonary vascular resistance normally declines rapidly as a result of the vasodilating effect of oxygen on the pulmonary vasculature.

However, some neonatal conditions causing inadequate oxygenation may interfere with the natural maturation/ thinning of the pulmonary arterioles resulting in a delay in the fall of the pulmonary vascular resistance- thus leading to persistence of the foetal circulation/ persistent pulmonary hypertension.

Question 12

Mention the causes of PPH of the newborn

Answer 12

Maladaption of the vessels due to acute injury

Chronic fetal hypoxia so muscles become thickened and extends into the non-muscular layers

Pulmonary hypoplasia - diaphragmatic hernia, potters syndrome

Obstruction - TAPVR

Question 13

What are the predisposing factors for PPH

Answer 13

Birth asphyxia
Meconium aspiration syndrome
Early onset sepsis
Respiratory distress syndrome
Hypoglycaemia
Polycythemia
Pulmonary hypoplasia resulting from diaphragmatic hernia, amniotic fluid leak, oligohydramnios or pleural effusion.
Idiopathic

Question 14

What are the clinical manifestations of PPH

Answer 14

cyanosis, grunting, flaring, retraction, tachycardia and shock.

There may be multi-organ involvement

Myocardial ischemia, papillary muscle dysfunction and biventricular dysfunction leads to cardiogenic shock with decreased pulmonary blood flow, tissue perfusion and oxygen delivery.

The hypoxia is often out of proportion to findings on chest x-ray

Question 15

What investigations would you carry out for PPH

Answer 15

Depending on the underlying cause- FBC, B/C, E/U, arterial blood gases, CXR

Echocardiography - right to left shunting of blood across a patent foramen ovale and ductus arteriosus.

Question 16

How would you make a diagnosis of PPH

Answer 16

PPHN should be suspected in all term infants who have cyanosis, with or without foetal distress, intra-uterine growth restriction, meconium stained amniotic fluid, hypoglycaemia, polycythemia, diaphragmatic hernia, pleural effusion and birth asphyxia.

Hypoxia is unresponsive to 100% oxygen given by oxygen hood but may respond transiently to hyperoxic hyperventilation after endotracheal intubation or to the use of bag and mask

Question 17

What are the diffential diagnosis of PPH

Answer 17

Cyanotic congenital heart disease
Hypoglycaemia
Polycythemia
Sepsis

Question 18

How would you treat PPH

Answer 18

Correction of the predisposing disease
Improving poor tissue oxygenation
Reduction of pulmonary vascular pressure by measures such as hyperventilation, forced alkalosis (with sodium bicarbonate) inhaled nitric oxide.
Use of inotropic therapy to support blood pressure and tissue perfusion. Dopamine is frequently used as a first line agent.