Oxygen fetal arterial

Severe, acute reduetion in oxygenation, for example by complete arrest of uterine flow or complete umbiheal cord occlusion, is not associated with a decrease in eerebrovascular resistance, as is seen in more mild insults. This suggests that the ability of the fetus to adapt to hypoxia has been overwhelmed. The rate at which the fetal arterial O2 content falls may be a determinant of the response elicited whether it be a rapid onset of ECoG isoelectricity (32,120), reduced regional cerebral blood flows (17), a failure of cardiovascular adaptive responses (139), an increase in eerebral lactate production (140), or a 50% reduction in cerebral metabolic rate... 

IV. Fetal Arterial Oxygen Tension Implications for Carotid Chemoreceptor Maturation... 

Zourabian, A, Chance, B., Ramanujam, N., Martha, R. David, AB. 2000. Trans-abdominal monitoring of fetal arterial blood oxygenation using pulse oximetry. J. Biomed. Opt. 5 391-405. 

In addition, the metabolic effects of insulin ultimately increase fetal oxygen consumption. The circulation of the fetus is unique specifically, because blood in the fetal descending aorta contains a portion of venous return after tissue perfusion, the increased rate of consumption of oxygen by fetal tissues decreases the arterial oxygen concentration of the fetus. The fetal tissues supplied by this circulation (which include most of the mass of the fetus) are then at risk for inadequate tissue oxygenation. 

In the placenta a volume of oxygen sufficient for fetal needs must diffuse across the membranes from maternal to fetal blood during the short time the two circulations are in close contact. This oxygen transfer is a function of several factors which include uterine and umbilical arterial 02 partial pressures, maternal and fetal placental blood flow rates, the 02 capacity and 02 affinity of maternal and fetal hemoglobin, the diffusing capacity of the placenta, the amount of C02 exchanged, and the vascular arrangement of maternal to fetal vessels. 

After it was determined that changing the linear velocity of the maternal or fetal blood stream did not affect the equilibration pressure, it was possible to determine the maternal to fetal volumetric flow rate ratio that would result in an equilibration pressure which matched experimentally determined values of umbilical vein and artery oxygen partial pressures (37). As the maternal to fetal volumetric flow rate ratio is increased, the partial pressure of oxygen at which equilibration... 

Figures 17 and 18 shows the effects produced on maternal and fetal blood when the arterial oxygen partial pressure of maternal blood is decreased.

The fetal and maternal flow rates were set at 40-80 ml/min and 450 ml/min, respectively, and an amniotic fluid pressure of 15 mm Hg was maintained over the placenta throughout the experiment. Oxygen tensions were 60-160 mm Hg in the maternal artery and 14-28 mm Hg in the fetal vein. Glucose was added at the beginning of the perfusion to help maintain placental viability. 

In late gestation, the fetal cardiovascular response to hypoxia is typified by a rapid, transient bradycardia and increased heart rate variability (21,22). The bradycardia reaches a nadir approximately 1-2 min after the onset of the hypoxic insult (15,23) and, presumably, economizes on myocardial oxygen consumption. Fetal hypoxic bradycardia occurs at the onset of hypoxic hypoxia (5), umbilical cord occlusion (24,25), and uterine artery occlusion (26)— the three most common experimental hypoxic challenges. 

Metabolic data from fetal brain studies indicate that moderate hypoxia or asphyxia can be adapted to by increases in cerebral blood flow and/or fractional oxygen extraction (15,111,135-138). Acutely, reductions in cerebral oxygen consumption are small eompared to the reduction in arterial oxygen content (34) however, during severe or prolonged asphyxia, reductions in cerebral oxygen consumption become apparent. 

Figure 7 Relationship between arterial O2 content and plasma adenosine concentration in the near-term fetal sheep in utero. Under normal fetal oxygenation, adenosine remains constant at approximately 1 pM adenosine rises with falling oxygenation, reaching 3—4 pM. (From Ref. 155.)...

Peeters L, Sheldon R, Jones M, Makowski E, Meschia G. Blood flow to fetal organs as a function of arterial oxygen content. Am J Obstet Gynecol 1979 135(5) 637-646. Johnson G, Palahniuk R, Tweed W, Jones M, Wade J. Regional cerebral blood flow changes during severe fetal asphyxia produced by slow partial umbilical cord compression. Am J Obstet Gynecol 1979 135(l) 48-52. 

Fig. P-66. The growing fetus depends on its mother for nutrients and removal of wastes. The mother s heart pumps blood through the uterine arteries into the placenta nutrients and oxygen diffuse through the placental membranes into the fetal bloodstream by way of the umbilical cord and wastes pass in the reverse direction to the maternal bloodstream through the uterine veins.

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