Fetal heart rate Uterine contraction occlusion Complete occlusion IIIIIIIIII I: Partial occlusion Umbilical vein Umbilical artery Fetal systolic BP Umbilical cord FIGURE 24-18 Schematic representation ofthe fetal heart rate efects with partial and complete umbilical cord occlusion. Uterine pressures generated early in a contraction cause cord compres-sion predominantly ofthe thin-walled umbilical vein. The resulting decrease in fetal cardiac output leads to an initial compensatory rise in fetal heart rate. As cord compression intensifies, umbilical arteries are then also compressed. The resulting rise in fetal systolic blood pressure leads to a vagal-mediated fetal heart rate deceleration. As the contraction abates and compression is relieved first on the umbilical arteries, elevated fetal systolic blood pressures drop and the deceleration resolves. A final increase in fetal heart rate is seen as a result of persistent umbilical vein occlusion. With completion of the uterine contraction and cord compression, the fetal heart rate returns to baseline. BP = blood pressure. (Adapted with permission from Lee (V, DiLaretto pc, Lane JM: A study offetal heart rate acceleration patterns, Obstet Gynecol. 1975 Feb;45(2):142-146.) Other fetal heart rate patterns have been associatedwith umbilical cord compression. Saltatoy baseline heart rate (Fig. 24-19) was first linked o umbilical cord complications during labor (Hammacher, 1968). he pattern consists ofrapidlyrecurringcouplets of acceleration and deceleration causing relatively large oscillations of the baseline fetal heart rate. We also observed a relationship between cord occlusion and the saltatory pattern in postterm pregnancies (Leveno, 1984). In the absence of other fetal heart rate finings, these do not signal fetal compromise. Lamba is a pattern involving an acceleration followed by a variable deceleration with no acceleration at the end ofthe deceleration. This pattern typically is seen in early labor and is not ominous (Freeman, 2003). This lambda pattern may result from mild cord compression or stretch. Overshootis a variable deceleration followed by acceleration. The clinical significance ofthis pattern is controversial (Westgate, 2001). Prolonged Deceleration This pattern, which is shown in Figure 24-20, is deined as an isolated deceleration ::15 bpm that lasts ::2 minutes but
FIGURE 24-19 Saltatory baseline fetal heart rate showing rapidly recurring couplets ofacceleration combined with deceleration.
< 10 minutes from onset to return to baseline. Prolonged decelerations are diicult to interpret because they are seen in many diferent clinical situations. Some of the more frequent causes are cervical examination, uterine hyperactivity, cord entanglement, and maternal supine hypotension.
Epidural, spinal, or paracervical analgesia may induce a prolonged deceleration (Eberle, 1998). Hill and associates (2003) observed prolonged deceleration in 1 percent of women given epidural analgesia during labor at Parkland Hospital. Other causes of prolonged deceleration include maternal hypoperfusion or hypoxia from any cause, placental abruption, umbilical
FIGURE 24-20 Prolonged fetal heart rate deceleration due to uterine hyperactivity. Approximately 3 minutes of the tracing are shown, but the fetal heart rate returned to normal after uterine hypertonus resolved. Vaginal delivery later ensued.
Loss of variability pH 6.9
FIGURE 24-21 Cord-compression fetal heart rate decelerations in second-stage labor associated with tachycardia and loss of variability. The umbilical cord arterial pH was 6.9.