Fetal compensatory responses to reduced oxygen delivery.
I have described how various maternal and fetal conditions can affect fetal oxygen delivery. It is clear from much of the recent experimental evidence that fetal oxidative metabolism can be sustained despite reductions in fetal O2 delivery of 40-50%. As long as fetal oxygen reserves are not depleted, fetal metabolic functions will continue aerobically, even though fetal hypoxemia is present. As O2 reserves are exhausted in some tissues, fetal hypoxemia will be associated with tissue hypoxia, the net result of which will be anaerobic metabolism, lactic acidosis, and tissue death. Whether a fetus is adequately oxygenated or not is a function of the quantity of oxygen reserve available. A fetus with a substantial oxygen reserve can compensate fully for most interferences in its oxygen supply and can maintain oxidative metabolism under a variety of conditions. In contrast, a fetus with minimal oxygen reserves will not tolerate even the mildest degree of O2 deficiency without developing tissue hypoxia or even death in utero. The quantity of O2 delivered to the fetus, rather than the specific condition that may be adversely affecting O2 delivery, is the important determinant of the adequacy of fetal oxygenation.
D000818:Animals; D003251:Constriction, Pathologic; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D005315:Fetal Diseases / Q000378:metabolism; D005318:Fetal Heart / Q000502:physiology; D005311:Fetal Hypoxia / Q000378:metabolism; D005333:Fetus / Q000378:metabolism* / Q000502:physiology; D006339:Heart Rate; D006801:Humans; D007022:Hypotension / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000378:metabolism; D012756:Sheep; D014470:Umbilical Cord; D014472:Umbilicus / Q000098:blood supply; D014599:Uterus / Q000098:blood supply / Q000378:metabolism
D010100:Oxygen