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It is the fetal heart and not the mother's heart that builds up the fetal blood pressure to drive its blood through the fetal circulation. Intracardiac pressure remains identical between the right and left ventricles of the human fetus. [15] The blood pressure in the fetal aorta is approximately 30 mmHg at 20 weeks of gestation, and increases ...
Persistent fetal circulation is a condition caused by a failure in the systemic circulation and pulmonary circulation to convert from the antenatal circulation pattern to the "normal" pattern. Infants experience a high mean arterial pulmonary artery pressure and a high afterload at the right ventricle.
In pregnancy, it is the fetal heart and not the mother's heart that builds up the fetal blood pressure to drive blood through the fetal circulation. The blood pressure in the fetal aorta is approximately 30 mmHg at 20 weeks of gestation, and increases to approximately 45 mmHg at 40 weeks of gestation. [27]
Blood pressure readings should range from 60 to 80 mm Hg systolic and 40–50 mm Hg diastolic. Mean arterial pressure should be the same as the weeks of gestation at birth. Within the first hour after birth, there may be a drop of up to 15 mm Hg in the systolic blood pressure. [1]
The umbilical arteries are one of two arteries in the human body, that carry deoxygenated blood, the other being the pulmonary arteries. The pressure inside the umbilical artery is approximately 50 mmHg. [4] Resistance to blood flow decreases during development as the artery grows wider. [5]
The unpaired umbilical vein carries oxygen and nutrient rich blood derived from fetal-maternal blood exchange at the chorionic villi.More than two-thirds of fetal hepatic circulation is via the main portal vein, while the remainder is shunted from the left portal vein via the ductus venosus to the inferior vena cava, eventually being delivered to the fetal right atrium.
Blood Pressure: Unaffected; Cardiac output increases throughout early pregnancy, and peaks in the third trimester, usually to 30-50% above baseline. [6] Estrogen mediates this rise in cardiac output by increasing the pre-load and stroke volume, mainly via a higher overall blood volume (which increases by 40–50%). [22]
In addition, vessel direction tends to follow the direction of the normal to the steepest stress gradient. [5] Additionally, biomechanic forces inside embryonic vessels have important remodelling effects. Pressure fluctuations lead to stress and strain fluctuations, which can "train" the vessels to bear loads later in the organism's development ...