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Blood is not shunted from the right ventricle to the aorta through the foramen ovale. That function is carried out by the ductus arteriosus, which connects the pulmonary artery to the descending aorta, not by the foramen ovale.

The ductus venosus, not the foramen ovale, bypasses the liver by channeling oxygenated blood from the umbilical vein directly to the IVC. The foramen ovale plays no role in hepatic circulation.

The umbilical arteries return deoxygenated blood to the placenta, not the foramen ovale. These arteries arise from the internal iliac arteries and transport waste-laden blood to the placenta for oxygen exchange.

The umbilical arteries carry deoxygenated, nutrient-poor blood from the fetus back to the placenta. They originate from the internal iliac arteries and are responsible for eliminating waste and carbon dioxide via placental exchange.

The pulmonary artery carries blood from the right ventricle to the fetal lungs. However, in fetal life, the lungs are nonfunctional, and most of this blood is diverted through the ductus arteriosus to the descending aorta. This blood is deoxygenated.

The aorta distributes mixed oxygenated blood to the fetal body. Although it carries blood to systemic tissues, it does not deliver blood from the placenta and is not the most oxygenated vessel.

The ductus venosus connects the umbilical vein to the inferior vena cava, bypassing the hepatic circulation. It plays no role in pulmonary or aortic circulation.

The foramen ovale is an interatrial opening that allows blood to shunt from the right atrium to the left atrium, bypassing the lungs. It does not connect the pulmonary artery to the aorta.

The umbilical vein carries oxygenated blood from the placenta to the fetus. It enters the ductus venosus and does not connect to either the pulmonary artery or aorta.

The foramen ovale is an atrial-level shunt that bypasses the fetal lungs by directing blood from the right atrium to the left atrium. It plays no role in hepatic circulation.

The ductus arteriosus connects the pulmonary artery to the descending aorta, bypassing the lungs. It does not affect liver perfusion.

The ligamentum teres is the fibrous remnant of the umbilical vein after birth. It does not function as a shunt and is not present during fetal circulation as a bypass mechanism.

Pulmonary vascular resistance decreases, not increases, after birth due to lung aeration and increased alveolar oxygen. A decrease in PVR facilitates increased left atrial return, contributing to closure—not an increase.

Oxygen levels rise after birth, not decrease. Increased oxygen tension is essential for pulmonary vasodilation and shunt closure. Decreased oxygen would maintain fetal circulatory pathways, not close them.

Clamping of the umbilical arteries contributes to systemic vascular resistance but does not directly trigger foramen ovale closure. It affects ductus venosus and arterial pressures, not atrial-level dynamics directly.

Increase of ≥10 bpm for ≥10 seconds defines an acceleration only in fetuses <32 weeks. In a term fetus, this threshold is too low and does not qualify as a valid acceleration under standard criteria.

A decrease in fetal heart rate of ≥15 bpm for ≥15 seconds defines a deceleration, not an acceleration. It may indicate cord compression, placental insufficiency, or uterine hypertonicity depending on its timing and morphology.

A decrease of ≥10 bpm for ≥10 seconds also constitutes a mild deceleration pattern and cannot be interpreted as an acceleration. Such decreases do not reflect fetal well-being but may warrant clinical observation.

The umbilical arteries do not deliver oxygenated blood. Instead, oxygenated blood is supplied to the fetus by the umbilical vein, which carries blood from the placenta with saturation levels around 70–80%. This blood bypasses hepatic circulation via the ductus venosus en route to systemic circulation.

The fetal lungs are bypassed by other shunting mechanisms—not the umbilical arteries. Structures like the foramen ovale and ductus arteriosus direct blood away from nonfunctional fetal lungs. The umbilical arteries are peripheral and not directly involved in this bypass system.

Nutrient absorption occurs via the placenta and maternal supply, not through the umbilical arteries. These arteries merely transport deoxygenated blood to the placenta, where nutrient and gas exchange occurs. They have no absorptive role.

Fetal distress is typically associated with absent accelerations, decreased variability, or late decelerations. A reactive NST, by definition, rules out distress at the time of testing and suggests normal fetal acid–base balance.

Uteroplacental insufficiency manifests as absent accelerations, decreased variability, or late decelerations. These would lead to a non-reactive NST, not a reactive one, which implies that placental perfusion is adequate.

Cord compression leads to variable decelerations, not accelerations. If present, these would be noted during monitoring and may signal concern depending on frequency and severity. A reactive NST lacks these deceleration patterns.Take home points

● Reactive NST suggests adequate fetal oxygenation and neurologic status.

● Requires 2 accelerations of ≥15 bpm lasting ≥15 seconds in 20 minutes.
● Non-reactive NST may signal placental or umbilical pathology.

Hemoglobin size does not influence oxygen affinity. Both HbF and HbA have tetrameric structures and comparable molecular weight (~64 kDa). Oxygen binding characteristics are not determined by molecular size but by subunit interactions and responsiveness to modulators like 2,3-BPG.

Carbon dioxide transport is mediated through different mechanisms including carbamino formation and bicarbonate buffering. HbF does not demonstrate superior carbon dioxide carriage over HbA. The increased oxygen affinity of HbF is unrelated to carbon dioxide handling.

While HbF concentration in fetal blood is higher than HbA concentration in adults (about 70–90% of total hemoglobin in the fetus), oxygen affinity is not determined by quantity. It is a function of molecular structure and reduced modulation by 2,3-BPG. Concentration influences oxygen-carrying capacity, not affinity.

An oxygen saturation of 20% is far below physiological levels for umbilical venous blood. Saturation this low would indicate profound hypoxia incompatible with fetal survival. Venous blood from the placenta is enriched and never falls to this range under normal conditions.

A saturation of 50% is typical of mixed blood seen in fetal systemic circulation or the pulmonary artery, not the umbilical vein. This value reflects oxygen levels after blood mixing with deoxygenated venous return, not direct placental transfer.

A saturation of 100% is unattainable in the umbilical vein due to low placental PaO₂ (~50 mmHg) and diffusion limitations. Maternal arterial oxygen saturation may be near 98–100%, but fetal venous saturation remains substantially lower due to fetal metabolic activity and limited oxygen gradient.