Fetal well-being is dependent on the adequate delivery of oxygen from maternal blood to the fetus. This requires an intact oxygen conduit from the maternal arterial system to fetal tissue (most importantly, the fetal brain). Blood flow must therefore be maintained from the maternal aorta to the uterus, from the uterus to the placenta/umbilical cord, within the umbilical cord, and then to the fetus and fetal brain. Additionally, adequate maternal oxygen must be present to insure oxygen transfer across the utero-placental interface down a concentration gradient.

Fetal injury or stress occurs when inadequate levels of oxygen are delivered. There are numerous causes that may lead to decreased fetal oxygenation. As previously discussed, these may involve maternal causes (hypotension, hypoxemia), disruption at the uterine-placental surface, prolonged uterine activity, and compression of the umbilical cord.

When a non-reassuring pattern is observed, this suggests inadequate fetal oxygenation. Measures to improve this condition are therefore directed at correcting the potential causes. Depending on the cause, any or all of the measures discussed below may be taken.

Improving uterine perfusion

Increasing maternal cardiac output will improve uterine perfusion. This in turn may lead to improved oxygen delivery to the fetus.

Lateral positioning of the mother. During the third trimester the combined weight of the fetus and uterus may compress the vena cava if the mother is supine (supine compression syndrome). This compression decreases venous return and leads to decreased maternal cardiac output. Decreased cardiac output will lower uterine perfusion pressure. Moreover, the lower aorta may also be compressed further decreasing utero-placental perfusion. To remedy this situation, the mother is placed in the right or left lateral position to decrease the pressure from the gravid uterus on the great vessels.

Correction of maternal hypotension. Hypotension may occur as a result of sympathetic blockade from regional anesthesia, supine positioning, or maternal hypovolemia from hemorrhage. Corrective measures are aimed at improving maternal cardiac output. These steps include:

Administration of intravenous fluids. Provision of intravenous fluids (500-1000 cc) may improve maternal cardiac output which will in turn increase uterine perfusion.

Administration of pressor agents (ephedrine 5-10mg IV push). Ephedrine is a direct and indirect sympathominetic and increases cardiac output via its action on beta and alpha sympathetic receptors. It also causes the release of endogenous epinephrine.

Elevation of the legs or Trendelenberg position. This action increases venous return to the heart and increases cardiac output.

Reduction of uterine activity

Increased uterine activity can decrease oxygen transfer due to the effect of contractions on uterine capillary flow. Decreasing uterine contractions may increase uterine perfusion and allow for fetal recovery. Therefore if any drugs are being administered that increase uterine activity (Pitocin, Cervidil, Cytotec) they should be decreased or discontinued. Tocolytics, such as terbutaline, are agents that relax uterine muscle. They may be given as necessary to reduce uterine activity.

Increasing oxygen transfer

If the mother is hypoxemic or there is a problem with oxygen transfer across the uterine-placental interface, providing supplemental oxygen (10L /minute by non-rebreather mask) to the mother may increase the oxygen tension in maternal blood. This will increase the gradient across the uterine-placental interface and may result in increased oxygen transfer to the fetus.

Promoting umbilical cord flow

Compression of the umbilical cord will affect oxygen delivery to the fetus. This can occur due to compression of the cord due to maternal or fetal position. Cord compression can happen at any time during labor and may worsen with pushing during the second stage of labor. Additionally, oligohydramnios, or decreased levels of amniotic fluid may increase the risk of cord compression. Measures that can be taken include:

Maternal position change. This may relieve compression of the cord. The mother is assisted to other positions such as side-lying and/or knee-chest until improvement is seen.

Stop pushing or change frequency of pushing to every second or third contraction.

Amnioinfusion. For non-reassuring patterns that are associated with oligohydramnios, infusion of amniotic fluid during the first stage of labor may alleviate cord compression.

Increasing fetal cerebral blood flow

Pushing during the second stage of labor may increase excessively intracranial pressure in the fetus. This may result in decreased cerebral blood flow if fetal mean arterial pressure falls below intracranial pressure. Halting pushing or decreasing the frequency of pushing to every other or third contraction will allow for fetal recovery and relieve fetal cerebral hypoxia. This rationale for decreasing the frequency of pushing is currently an area of controversy.

Other Measures

Provider evaluation

If the patient’s provider is not immediately available when intrauterine resuscitation measures begin, he or she should be notified about maternal and fetal status and which intervention measures are in progress. The necessity of prolonged and/or repeated intervention requires a bedside evaluation by the provider.

Emergent delivery

If the above interventions do not alleviate the non-reassuring fetal rate patterns, consideration should be given to expedient delivery of the fetus. An operative vaginal or cesarean section delivery may be considered depending on maternal and fetal status and labor progress.

Summary of actions for non-reassuring fetal status

  1. Repositioning or lateral positioning of mother
  2. Reversal of hypotension (elevate legs or Trendelenberg, ephedrine, fluids)
  3. Cessation of oxytocics
  4. Consider tocolytics
  5. Administration of oxygen
  6. Decrease frequency of pushing
  7. Re-evaluation of mother by provider
  8. Urgent or emergent delivery