Fetal heart rate nadir during bradycardia and umbilical artery acidemia at birth.

Abstract

Fetal bradycardia due to sentinel events such as placental abruption, cord prolapse or uterine rupture is associated with an increased risk of acidemia at birth. In the absence of a sentinel event, data regarding neonatal prognosis are scarce, and it seems plausible that the depth of bradycardia might be associated with an increased risk of acidosis at birth. The objective was to determine whether the depth of bradycardia is associated with a higher risk of umbilical artery acidemia at birth in term singleton pregnancies requiring cesarean delivery during labor. A retrospective comparative study of all cesarean deliveries for bradycardia in an academic tertiary center in the 6-year period of 2013-2018, among term singleton pregnancies. Bradycardia associated with a sentinel event such as placental abruption, cord prolapse or uterine rupture, were excluded. The nadir of the bradycardia was defined as the lowest fetal heart rate baseline lasting at least 3 minutes during bradycardia. Women who delivered an infant with an umbilical pH at birth <7.00 (acidosis group) were compared with women who delivered an infant with an umbilical pH at birth ≥7.00 (non-acidosis group). Among 111 eligible cases, 32 women in the acidosis group were compared with 79 in the non-acidosis group. The median nadir of the bradycardia was lower in the acidosis than in the non-acidosis group (60bpm, interquartile range [56-65] vs 70 [60-76], P<.01). A bradycardia nadir <60bpm emerged as the optimal threshold for predicting acidemia and was more frequently observed in the acidosis than in the non-acidosis group (10 [31%] vs 10 [13%], P=.02). In the multivariable analysis, a nadir <60bpm was independently associated with an umbilical artery pH <7.00 (adjusted OR 3.16, 95% CI 1.10-9.04). A bradycardia nadir <60bpm was associated with a tripled risk of umbilical artery acidemia at birth.