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ESRA19-0659 Fetal bradycardia and neuraxial techniques…who is the real culprit?
  1. K Theodoraki
  1. Aretaieion University Hospital, Department of Anaesthesiology, Athens, Greece


Fetal well-being during labor is of paramount importance. Feta heart rate (FHR) monitoring during labor can detect fetal distress and guide therapeutic interventions. Three parameters are most commonly evaluated: baseline FHR, baseline FHR variability and accelerations or decelerations. Loss of beat to beat variability and deceleration patterns are associated with fetal distress. Decelerations and fetal bradycardia have been described after all types of effective labor analgesia (epidural, spinal and combined spinal-epidural (CSE), and intravenous opioids). Several hypotheses have been advocated in the literature as to the origin of the FHR changes and fetal bradycardia observed with labor analgesia. One of the most popular theories is that the profound analgesia achieved with intrathecal opioids leads to a decrease in sympathetic nervous system output and circulating epinephrine levels. Epinephrine is in itself an effective tocolytic due to β2 activity. Therefore, the reduction in epinephrine levels leads to unopposed norepinephrine activity, which increases uterine tone and consequently placental blood flow. If placental blood flow is decreased enough, fetal bradycardia will ensue due to fetal compromise. Alternatively, the profound analgesia achieved with intrathecal techniques leads to a decrease in maternal blood pressure, which leads to a compensatory increase of norepinephrine levels, vasoconstriction of placental blood vessels and consequently reduced placental blood flow and fetal compromise with the aforementioned mechanism. This theory however has been questioned since it has been shown that the intrathecal administration of 2.5 mg bupivacaine can also lead to profound analgesia without however affecting the fetal heart rate. Therefore, it has been argued that the intrathecal administration of opioids rather than profound analgesia is the contributing factor in the loss of fetal heart rate variability and fetal decelerations. An alternative pathophysiologic mechanism might be that the rostral spread of intrathecally administered opioids could lead to an elevation of oxytocin secretion and increased uterine activity. Strangely enough, epidurally administered opioids do not seem to affect fetal heart rate the way intrathecal opioids do. Regarding epidurals, it seems that hypotension is the main responsible factor that contributes to FHR abnormalities, since it has been shown that volume preloading or vasoconstricting agents decrease the incidence of fetal decelerations. Maternal positioning and inferior vena cava syndrome seem to also play a role. Other factors that can also be present when labor analgesia is offered to the parturient, which are often disregarded are induction of labor with oxytocin, prolongation of the first and/or second stage of labor (maybe as a result of epidural analgesia and the presence of ruptured membranes for a prolonged period of time. A common factor in the above situations is the high catecholamine levels and increased pain scores. Fortunately, in the majority of studies, FHR changes do not seem to be associated with an increased incidence of emergency cesarean section or with an untoward effect on neonatal outcome. As to ways of dealing with FHR abnormalities, the use of uterine displacement and changing the maternal position in order to relieve any aortocaval compression has been advocated. Any hypotension should be corrected using phenylephrine in 50 μg – 100 μg increments (or ephedrine in 5 mg – 10 mg increments) and intravenous fluids. Extra oxygen should be administered and administration of oxytocin should be discontinued because of the association of FHR changes with uterine hyperstimulation. Administration of a tocolytic agent should also be considered. In conclusion, FHR abnormalities during labor should not always be attributed to labor analgesia (since the regional technique could sometimes be the innocent bystander...) and the possibilities of hypotension, inferior vena cava syndrome and uterine hyperactivity should be taken into consideration. However, high doses of intrathecal opioids should most probably be avoided.

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