Congenital heart disease and foetal circulation Flashcards
Q: How does blood flow between the fetus and the placenta?
A: The fetal heart pumps blood to the placenta via the umbilical arteries( low oxygen) , and blood from the placenta returns to the fetus via the umbilical vein(high oxygen).
Q: What are the functions of the placenta in fetal circulation?
A: The placenta performs several functions, including
* homeostasis,
* gas exchange,
* transportation of nutrients,
* hormone production (including prostaglandin E2), and the transport of IgG, which provides passive immunity to the fetus.
Pressure of the right side of the heart > left side of the heart
Q: What is the function of the placenta in gas exchange?
A: The placenta facilitates the exchange of gases between the mother and the fetus through simple diffusion.
Oxygen delivery to the fetus occurs through placental blood flow.
Q: What are the components of the umbilical cord?
A: The umbilical cord consists of
- two umbilical arteries that carry deoxygenated blood away from the fetus and
- one umbilical vein (left) that carries oxygenated blood from the placenta to the fetus. Additionally, there is
- Wharton’s jelly, a gelatinous substance that protects and supports the blood vessels in the umbilical cord.
Q: What happens to the fetal lungs during labor and birth?
A:
* When hormones are released during labor, the fetal lungs stop producing fluid and start being able to absorb fluid.
* The fetus takes a big breath and cries, which pushes the fluid out of the lungs.
* The fluid then enters the lymphatic system and is drained.
Q: How do the circulatory changes occur at birth?
A:
- Pulmonary vascular resistance (PVR) decreases as the lungs physically expand upon breathing in, and there is an increase in circulating oxygen, which acts as a vasodilator.
- The PVR reaches “normal” adult-type levels by 2-3 months.
- Systemic vascular resistance increases when the umbilical cord is clamped and cut, redirecting more of the cardiac output to the lungs.
Q: What causes the closure of the foramen ovale?
A:
- The closure of the foramen ovale occurs as the pulmonary vascular resistance falls and the systemic vascular resistance rises.
- When the left atrial pressure exceeds the right atrial pressure,the flap of the foramen ovale is pushed closed.
Q: What causes the closure of the foramen ovale?
A:
* The closure of the foramen ovale occurs as the pulmonary vascular resistance falls and the systemic vascular resistance rises.
* When the left atrial pressure exceeds the right atrial pressure,** the flap of the foramen ovale is pushed closed.**
Q: How does the ductus arteriosus constrict and eventually close?
A: The ductus arteriosus undergoes functional closure within hours to days and anatomical closure within 7-10 days after birth.
- The increase in oxygen tension causes the vascular smooth muscle of the duct to constrict. With more blood flowing to the lungs and aorta and less flowing through the duct, it eventually closes.
- The reduction in prostaglandin E2 (PGE2) levels, which is metabolized by the lungs and is no longer connected to the placenta, also contributes to the closure.
- The increase in Bradykinin level also causes its closure.
- The ductus arteriosus ends up as a fibrous ligament known as the ligamentum arteriosum.
Q: What are cyanotic defects in congenital heart abnormalities?
A: Cyanotic defects are conditions that cause deoxygenated blood to bypass the lungs and enter systemic circulation
or result in a mixture of oxygenated and deoxygenated blood entering circulation.
Examples include
truncus arteriosus,
tetralogy of Fallot,
transposition of the great vessels, and many others.
Q: What is the characteristic feature of Tetralogy of Fallot?
A: Tetralogy of Fallot is characterized by the presence of four heart abnormalities:
* ventricular septal defect,
* pulmonary stenosis,
* overriding aorta, and
* right ventricular hypertrophy.
Q: What are acyanotic defects in congenital heart abnormalities?
A:
Acyanotic defects involve left-to-right shunting or no shunting of blood.
Examples include
* atrial septal defects (ASD),
* ventricular septal defects (VSD),
* atrioventricular septal defects (AVSD), and conditions such as
* patent ductus arteriosus (PDA),
* aortic stenosis, and
* pulmonary stenosis.
Q: How are congenital heart defects detected antenatally?
A: Congenital heart defects can be detected antenatally through ultrasound scans (USS) performed between 18-22 weeks of pregnancy.
If a duct-dependent lesion is diagnosed antenatally, management typically involves prostaglandin E2 (PGE2) infusion.
Q: What is involved in the newborn screening for congenital heart defects?
A: Newborn screening for congenital heart defects involves a clinical examination performed around 24 hours after birth.
It includes assessing
* femoral pulses,
* heart sounds,
* the presence of murmurs, and, in some regions,
* pre-ductal (arms) and post-ductal (legs) ductal saturations.
Q: When does cyanosis become evident in infants with congenital heart defects?
A: Cyanosis, a bluish discoloration of the skin, becomes evident shortly after birth in infants with certain congenital heart defects.
However, it can also be a symptom of respiratory disease and persistent pulmonary hypertension of the newborn.
Q: What is meant by duct-dependent circulation in infants?
A:
.
- refers to a condition where a baby has a congenital heart defect that relies on the ductus arteriosus (a blood vessel connecting the pulmonary artery and the aorta) to supply oxygenated blood to the body.
- The ductus arteriosus stays open longer than normal but will eventually close, leading to circulatory collapse.
Q: What are the clinical signs and symptoms of duct-dependent circulation presenting around day 4-7 after birth?
A:
severe cyanosis (bluish discoloration),
pallor,
distress,
prolonged capillary refill time,
poor or absent pulses,
hepatomegaly (enlarged liver),
crepitations (abnormal lung sounds), and
increased work of breathing.
Q: How is duct-dependent circulation managed until an alternative shunt or definitive surgery can be established?
A:
Intravenous prostaglandin E2 (PGE2) can be used to keep the ductus arteriosus open until an alternative shunt can be established or definitive surgery is carried out.
Q: What is cardiac failure in infants, and when does it typically present?
A:
is a condition characterized by inadequate pumping of blood by the heart.
It is commonly seen around 6-8 weeks of age and can be caused by conditions such as hypoplastic left heart and pulmonary atresia.
