Two types ofvariable decelerations are shown in Figure 24-17. The deceleration denoted by "A" is very much like that seen with complete umbilical cord occlusion in experimental animals (see Fig. 24-16). Deceleration "B," however, has a diferent configuration because of the "shoulders" of acceleration before and ater the deceleration component. Lee and coworkers (1975) proposed that this form of variable deceleration was caused by difering degrees of partial cord occlusion. In this physiological scheme, occlusion of only the vein reduces fetal blood return, thereby triggering a baroreceptor-mediated c'Eii. 40
FIGURE 24-15 A. The effects oF 25-second cord compression compared with those of 40 seconds in panel (8). (Redrawn with permission from Hon EH: The fetal heart rate patterns preceding death in utero, Am J Obstet Gynecol. 1959 Jul;78(l ):47-56.) acceleration. With increasing intrauterine pressure and subsequent complete cord occlusion, fetal systemic hypertension develops due to obstruction of umbilical artery flow. This stimulates a baroreceptor-mediated deceleration. Presumably, the aftercoming shoulder of the acceleration represents the same events occurring in reverse (Fig. 24-18).
Ball and Parer (1992) concluded that variable decelerations are mediated vagally and that the vagal response may be due to chemoreceptor or baroreceptor activity or both. Partial or complete cord occlusion produces an increase in afterload (baroreceptor) and a drop in fetal arterial oxygen content (chemoreceptor). These both result in vagal activity leading to deceleration. In fetal monkeys, the baroreceptor relexes appear to operate during the first 15 to 20 seconds of umbilical cord occlusion followed by decline in P02 at approximately 30 seconds, which then serves as a chemoreceptor stimulus (MuellerHeubach, 1982).
Thus, variable decelerations represent fetal heart rate reflexes that relect either blood pressure changes due to interruption of umbilical flow or changes in oxygenation. It is likely that most fetuses have experienced brief but recurrent periods of hypoxia due to umbilical cord compression during gestation. The frequency and inevitability of cord occlusions undoubtedly have provided the fetus with these physiological mechanisms as a means of coping. The great dilemma for the obstetrician in managing variable fetal heart rate decelerations is determining when variable decelerations are pathological. According to the American College of 0bstetricians and Gynecologists (2017 a), recurrent variable decelerations with minimal-to-moderate beat-to-beat variability are indeterminate, whereas those with absent variability are abnorma.
FIGURE 24-16 Total umbilical cord occlusion (arrow) in the sheep fetus is accompanied by an increase in fetal aortic blood pressure. Blood pressure changes in the umbilical vessels are also shown. (Redrawn with permission from Kunzel W: Fetal heat rate alterations in partial and total cord occlusion. In Kunzel W (ed): Fetal Heart Rate Monitoring: Clinical Practice and Pathophysiology. Berlin, Springer, 1985.)
FIGURE 24-17 Varying (variable) fetal heart rate decelerations. Deceleration (8) exhibits "shoulders" of acceleration compared with deceleration (A).