• Explain The Difference Between Circulatory And Foetal Lungss

Neonatal RDS is a condition of increasing respiratory distress commencing at or shortly after birth (BAPM-2006). It’s the single most important cause of morbidity and mortality in preterm infants (Greenough, et al 2004). Typically RDS affects preterm infants with the incidence being inversely proportional to the gestational age (Stewart 2005) Approximately 60% of those born before 28 weeks gestation are affected (Fraser, et al 2004) Incidence also increases in infants of diabetic mothers those born via elective caesarean section (Fraser, et al 2004) and perinatal asphyxia (Rodriguez, 2003).

Lung development takes place while a child is in their mother’s womb. A baby’s lungs take twenty-three weeks to fully expand. At this point in the baby’s life, he is ready to start breathing air when he or she is born. Some children are born with developed lungs but others are not. Scientists believe that there is a molecule in vegetables such as broccoli that helps with lung development.

Premature birth has been linked to a vast array of lungs problems, the earlier the birth the greater risk of health complications(Davis R and Mychaliska G, 2013). A majority of the health problems will affect the infant for the rest of their life (Davis R and Mychaliska G, 2013). Infants born between the canalicular and the saccular period (week 25) have lung development that is unsuitable for gas exchange (Davis R and Mychaliska G, 2013). Two major complications that arise with undeveloped lungs is bronchopulmonary dysplasia, and pulmonary arterial hypertension (Mahgoub L. et al. 2017).

In the foetal circulation, the primary role of the ductus arteriosus (DA) is to divert the ventricular output away from the lungs towards the placenta in utero by its connection between the pulmonary artery and the descending aorta. The patency of the ductus is mainly regulated by low oxygen tension present in the foetal lung and prostaglandin, which is known for its vasodilating effect in the placental circulation. Prostaglandin levels are usually high as a result of placental production and low clearance ability of the foetal lung (Gardner, Carter, Enzman Hines, Hernandez,2016).

Patent Ductus Arteriosus is a common condition seen in preterm infants. PDA may cause congestive heart failure, respiratory distress, necrotizing enterocolitis, and renal impairment. Cyclooxygenase (COX) inhibitors and surgical interventions for ligation of PDA are widely used in management of this condition. In small infants, surgical closure can be difficult, therefore medical closure offers a great advantage.

As we breathe in, the muscles in the chest wall force the thoracic area, ribs and connective muscles to contract and expand the chest. The diaphragm is contracted and moves down as the area inside the chest increases as air enters the lungs. The lungs are forced open by this expansion and the pressure inside the lungs becomes enough that it pulls

The Fetal circulatory route different from the systemic or portal circulatory route is that the fetal circulatory carries fetal blood thru the umbilical cord and circulation thru the blood vessel in the placenta. In the fetus, the lungs are not in use so oxygen exchange and nutrients are obtained from the mother through the placenta and the umbilical cord. While pregnant the lungs in the fetus are not in the use so oxygen is shared and the nutrients are obtained from mother through the placenta and the umbilical cord. The placenta acts as a respiratory center for the fetus the uterine arteries carry oxygenated blood to the placenta. In the fetus there is an opening between the right and left atrium and most of the blood flows through this

Respiratory distress is common, affecting up to 70% of all premature newborns, and is increasingly common in even modest prematurity. Preventive and therapeutic measures for some of the most common underlying causes are well studied and when implemented can reduce the burden of disease. Failure to readily recognize symptoms and treat the underlying cause of respiratory distress in the newborn can lead to short- and long-term complications, including chronic lung disease, respiratory failure, and even death.

The respiratory system undergoes major changes as the newborn’s lungs fill with air during the first breath, and gas exchange across the pulmonary circulation abruptly replaces placental transfer.

When premature babies are born they do not have fully developed lungs because the lungs are one of the last organs in the body to be produced. The alveoli in the baby’s lungs have not yet started making surfactant, which is typically produced when the baby is 34-36 weeks’ gestation. When the alveoli do not have surfactant, the alveoli want to naturally collapse. Surfactant helps to keep the alveoli open and create more surface area for gas exchange. If you were to look at the infant’s lungs using a microscope, you can see that lungs look as though they are solid from the areas where the alveoli have collapsed, also known as atelectasis. To try to compensate for the atelectasis, “the respiratory bronchioles, alveolar ducts, and some of the alveoli dilate to decrease airway resistance and increase gas exchange” (Jardins 476). As the disease worsens, the walls of the alveoli become lined with a hyaline membrane that is made up of dead cells and proteins that make it nearly impossible for gas exchange to occur. It makes the lungs stiff and much harder to ventilate. With the lungs being noncompliant, the baby starts to become hypoxic. When the infant becomes hypoxic, blood is shunted away from the other organs in the body and venous return and cardiac output are decreased. “Hypoxemia is common in pulmonary hypertension (PH) and may be partly related to ventilation/perfusion mismatch, low diffusion

When the newborn takes its first breath there are several things that take place. The lungs expand for the first time increasing oxygenation. Also there is a reduction in prostaglandins that have been provided by the mother via the placenta. These two things force the ductus arteriosus to clothes. The ductus arteriosus connects the pulmonary artery to the aorta. This allows the circulatory system to bypass the lungs during pregnancy. When the infant takes its first breath, it is supposed to close so pulmonary blood will only flow to the lungs. When this does not take place, it causes blood from the pulmonary artery and blood from the aorta to mix between the two systems. This mixing of blood is squeezed out both ways resulting in a murmur that

The fetal circulatory system is different in the way that it sends and receives blood throughout the body. The fetus is dependent on the mother while in the womb for blood circulation. The fetus will receive blood through the placenta, attached to the umbilical card, which sends the oxygenated blood to the fetus’s lungs. Through this process the fetus receives all nutrients and oxygen it needs to survive. Waste from the fetus is then sent back to the mother through the umbilical cord and placenta to the mother’s circulation for proper elimination. Then the process is repeated until the fetus is born. Once the fetus is born the lungs start to do the job that the mother was doing for the fetus. It is now the fetus’s job to circulate oxygenated

The placenta is a major source of fetal prostaglandins and its removal after birth allows for the lungs to expand and become metabolically active, where most prostaglandins are degraded. This, in combination with increased pulmonary oxygen tension, in healthy full-term infants, normally causes functional closure of the ductus arteriosus within 15 hours after birth.

In the course of the essay, literature on physiology of the intrauterine circulation and adaptation of foetus to extra uterine life will be examined. An emphasis will be laid on the necessity of neonatal examination, why? When? and how?.

Preterm infants are born during the late cannalicular to early saccular stages of lung development, which corresponds to the period when respiratory bronchioles capable for gas exchange and type II alveolar