Fetal heart rate patterns in growth-restricted fetal sheep induced by chronic fetal placental embolization.

OBJECTIVE

Our purpose was to test the hypothesis that chronic placental insufficiency and intrauterine growth restriction in fetal sheep causes a decrease in the number of fetal heart rate accelerations and fetal heart rate variability.

STUDY

DESIGN

Chronically catheterized fetal sheep were embolized (n = 6) daily with 15 to 50 microns latex microspheres for 21 days between 0.74 and 0.88 of gestation into the abdominal aorta, until fetal arterial oxygen content was decreased by 40% to 50% of the preembolization value. Control animals (n = 6) received saline solution only. Signals from chest electrodes were analyzed on-line with the Sonicaid System 8000 in 2-hour epochs every 6 hours starting at 8 AM over the first 48 hours of hypoxemia and for 2 hours between 8 and 10 AM every other day from day 3 to day 21 of hypoxemia. Umbilical artery Doppler-derived resistance index and fetal plasma catecholamine concentrations were also measured.

RESULTS

Embolized fetuses had asymmetric intrauterine growth restriction and became chronically hypoxemic (p < 0.001) with a progressive increase in the umbilical artery resistance index (p < 0.001). During the first 48 hours of hypoxemia the number of accelerations and decelerations and both short- and long-term fetal heart rate variability increased initially, followed by a return to control levels by 20 hours after the onset of embolization. After 21 days of hypoxemia the number of accelerations was significantly reduced by 30% compared with controls (p < 0.05). Both short- and long-term fetal heart rate variability in control fetuses gradually increased with advancing gestational age (p < 0.001 and p < 0.01, respectively), whereas in embolized fetuses the fetal heart rate variability remained unchanged and was 20% lower than that of controls on day 21 (both p < 0.01).

CONCLUSION

Intrauterine growth restriction and long-term hypoxemia in fetal sheep are associated with a decrease in short- and long-term fetal heart rate variability, possibly because of a delay in the normal maturational changes of the autonomic control of fetal heart rate.