Introduction
Intrapartum fetal heart rate monitoring is intended to assess the adequacy of fetal oxygenation during labor. To that end, three central concepts of evidence-based FHR interpretation provide the foundation for a systematic approach to the decision-making process underlying FHR management.
All clinically significant FHR decelerations reflect interruption of oxygen transfer from the environment to the fetus at one or more points along the oxygen pathway. Interrupted fetal oxygenation does not result in neurologic injury unless it progresses at least to the stage of significant metabolic acidemia (umbilical artery pH <7.0 and base deficit ≥12 mmol/L) [1].
Moderate variability and/or accelerations reliably predict the absence of metabolic acidemia at the time they are observed [2,3].
General considerations
Reliable information is vital to the success of intrapartum FHR monitoring. Therefore, it is essential to confirm that the monitor is recording the FHR and uterine activity accurately. Ultrasound might be necessary to locate the FHR or to confirm that the observed rate is fetal and not maternal. If external monitoring is not adequate for interpretation, a fetal scalp electrode and/or intrauterine pressure catheter might be necessary.
Evaluate the FHR tracing
After confirming that the monitor is accurately and adequately recording the necessary information, the FHR tracing is evaluated. Thorough evaluation of the FHR tracing includes assessment of five FHR components: baseline rate, variability, accelerations, decelerations, and changes or trends in the tracing over time. If necessary, fetal stimulation should be used to provoke accelerations and/or improve FHR variability.
Evaluation of five FHR components
If all five FHR components are normal, there is a very low probability of interrupted fetal oxygenation. As long as there are no other reasons to review the FHR tracing more frequently (such as pre-eclampsia or fetal growth restriction), routine intrapartum surveillance is appropriate. In low-risk patients, the FHR tracing should be reviewed at least every 30 minutes during the first stage of labor and every 15 minutes during the second stage [3,4]. If one or more of the five FHR components is abnormal, further evaluation is necessary. Corrective measures may be needed before making a decision regarding management. A practical approach can be summarized as follows.
“A” – assess the oxygen pathway
Rapid, systematic assessment of the oxygen pathway from the environment to the fetus can identify possible sources of interrupted oxygenation. This pathway includes the maternal lungs, heart, vasculature, uterus, placenta and umbilical cord.
“B” – begin corrective measures
At each point along the pathway, appropriate corrective measures should be initiated to optimize oxygen delivery. Specific measures are summarized below.
Supplemental oxygen
Fetal oxygenation is dependent upon the oxygen content of maternal blood perfusing the intervillous space of the placenta. Administration of supplemental oxygen by nasal cannula or facemask can increase the PO2 of inspired air, increasing both the partial pressure of oxygen dissolved in maternal blood and the amount of oxygen bound to hemoglobin. This can increase the oxygen concentration gradient across the placental blood–blood barrier and lead to increased fetal PO2 and oxygen content. Several studies have reported resolution of FHR abnormalities after administration of supplemental oxygen to the mother, providing indirect evidence of improved fetal oxygenation [5–9]. Fetal pulse oximetry studies have demonstrated increased fetal hemoglobin saturation following maternal administration of oxygen. Available data support the use of a nonrebreather facemask to administer oxygen at a rate of 10 L/min for approximately 15–30 minutes [5,10–12].
Maternal position changes
Supine positioning increases the likelihood that pressure on the inferior vena cava will impair venous return, cardiac output and perfusion of the intervillous space. It also increases the likelihood that pressure on the descending aorta and/or iliac vessels will impede the delivery of oxygenated blood to the intervillous space. Fetal pulse oximetry data confirm that lateral positioning results in higher fetal hemoglobin saturation levels than does supine positioning [5,13,14]. In the setting of suspected umbilical cord compression, maternal position changes may result in fetal position changes and relief of pressure on the umbilical cord.
Intravenous fluid administration
Optimal uterine perfusion depends upon optimal cardiac output and intravascular volume. An intravascular bolus of isotonic fluid can improve cardiac output by increasing circulating volume and increasing venous return, left ventricular end diastolic pressure, ventricular preload and stroke volume. Simpson & James [5] demonstrated a significant increase in fetal oxygen saturation following an intravascular isotonic fluid bolus approximating 10–20% of blood volume (500–1000 cc). Boluses were administered over 20 minutes to normotensive women without evidence of hypovolemia. The maximum effect was achieved with a 1000 cc bolus, and the beneficial impact on fetal oxygen saturation lasted for more than 30 minutes after the bolus.
Correct maternal blood pressure
A number of factors predispose laboring women to transient episodes of hypotension. These include inadequate hydration, insensible fluid losses, supine position resulting in compression of the inferior vena cava, and peripheral vasodilation due to sympathetic blockade during regional anesthesia. Maternal hypotension can reduce uterine perfusion and fetal oxygenation. Hydration and lateral or Trendelenberg positioning usually correct the blood pressure. However, medication may be necessary. Ephedrine is a sympathomimetic amine with weak α- and β-agonist activity. The primary mechanism of action is displacement of norepinephrine from presynaptic storage vesicles, resulting in release of norepinephrine and stimulation of postsynaptic adrenergic receptors.
Reducing uterine activity