Mechanisms of late decelerations of the fetal heart rate during hypoxia.
Transient maternal aortic occlusion decreases uterine blood flow and results in the delayed deceleration of the fetal heart rate. The response to this maneuver was examined in the hypoxic fetus. Pregnant ewes and their fetuses at 0.8 gestation were catheterized for chronic study. A blood flow transducer was placed around the common umbilical artery, and a Fogarty balloon-tipped catheter was placed in the maternal abdominal aorta distal to the renal arteries. The ewes were made hypoxic by breathing a hypoxic gas mixture through a mask placed over their faces. Transient maternal aortic occlusion resulted in a delayed and transient deceleration of the fetal heart rate in hypoxic fetuses, associated with a significant decrease in mean arterial pressure and umbilical blood flow. Infusion of atropine into the fetus before maternal aortic occlusion modified but did not abolish the fetal heart rate response. The deceleration was associated with the significant decrease in the "double-product" index of myocardial oxygen consumption. The conclusion is that late decelerations result from two mechanisms: chemoreceptor vagal reflex mechanisms and hypoxic myocardial depression.
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure; D005260:Female; D005312:Fetal Blood / Q000502:physiology; D005318:Fetal Heart / Q000503:physiopathology*; D005311:Fetal Hypoxia / Q000503:physiopathology*; D006339:Heart Rate; D006863:Hydrogen-Ion Concentration; D009206:Myocardium / Q000378:metabolism; D010100:Oxygen / Q000097:blood; D011247:Pregnancy; D012018:Reflex; D012756:Sheep; D014630:Vagus Nerve / Q000502:physiology
D001285:Atropine; D010100:Oxygen