16.4: Physiological Influences on Fetal Heart Rate Patterns
By the end of this section, you will be able to:
- Explain the influence of uteroplacental sufficiency on the FHR pattern
- Explain the influence of the fetal nervous system on the FHR pattern
- Explain the influence of the fetal cardiovascular system on the FHR pattern
- Explain the importance of fetal reserve on the FHR pattern
Multiple factors influence the FHR. The pregnant person’s influence can be positioning, blood pressure, oxygenation , and medications. Fetal influence can be nuchal cord, hypoxia , cord entanglement, and fetal movement. Other influences can be the use of uterotonics such as oxytocin (Pitocin) to increase the strength and frequency of uterine contractions. The Three Principles of Patient Safety offer a uniform explanation of abnormal FHR tracings (Miller & Miller, 2012).
- Principle 1: Variable, late, or prolonged FHR decelerations demonstrate interruption of the oxygen transfer path from the environment to the fetus at one or more points.
- Principle 2: The absence of metabolic acidemia in the fetus is reliably supported when moderate variability and/or accelerations of the FHR are observed.
- Principle 3: Neurologic injury to the fetus does not occur unless the interruption of fetal oxygenation progresses to the significant fetal metabolic acidemia (umbilical artery < 7.0 and base deficit > 12 mmol/L).
Fetal monitoring is used to assess the changes in FHR patterns associated with these influences. When determining fetal well-being , the nurse is aware of which FHR patterns are reassuring and which are nonreassuring. Understanding the physiologic influence causing the FHR pattern allows the nurse to intervene to correct the nonreassuring FHR .
Uteroplacental Insufficiency
A disruption of the delivery of oxygen and nutrients to the fetus from the placenta is called uteroplacental insufficiency . It is associated with preexisting medical conditions and lifestyle behaviors of the pregnant person. These include hypertension , obesity , diabetes , thyroid conditions, blood clotting disorders, smoking, and substance misuse. Conditions limited to pregnancy, such as preeclampsia , gestational diabetes , placenta previa , placental abruption , nutritional deficits, and fetal anomalies, are also associated with the development of uteroplacental insufficiency. These factors degrade the placenta . The placenta becomes damaged and does not function properly. Because of the placental damage, the fetus does not receive nutrients, and there is insufficient gas exchange resulting in fetal growth restriction and hypoxia (Aubin & El-Chaâr, 2022).
Intrapartum Causes
A cause of uteroplacental insufficiency in labor can be hypotension after epidural or spinal anesthesia. Anesthesia dilates the vessels, promoting hypotension. The placenta relies on blood pressure to push oxygen and nutrients across the placenta to the fetus. Hypotension decreases the transfer of these nutrients due to the decrease in pressure. Supine position can also be a cause of hypotension.
Uterine hyperstimulation is another cause of uteroplacental insufficiency in labor. The uterus contracts, and perfusion to the fetus is decreased. Uterine contractions occurring too frequently can cause a prolonged decrease in oxygen profusion. Uterine hyperstimulation is seen most commonly with the use of oxytocin or misoprostol (Cytotec) , medications that increase the frequency and intensity of uterine contractions.
Catastrophic events such as placental abruption or uterine rupture cause prolonged decelerations. These events can be immediate or occur slowly over time. Placental abruption and uterine rupture can cause brisk vaginal bleeding, which should immediately alert the nurse to the cause. In other conditions, the bleeding is covert, and the nurse must investigate to determine the cause.
Nurse:
M. Johnson, RN
Years in Practice:
15
Clinical Setting:
Hospital
Geographic Location:
Southeast United States
I was caring for a laboring person whose partner was very excited to be a part of the birth. They had planned for the partner to help cut the umbilical cord. It was an important part of their birth plan. Unfortunately, a Category II tracing was noted with minimal variability that occurred over 30 minutes. I repositioned the person to the left side, stopped the oxytocin infusion, started an IV bolus of lactated Ringer’s solution, and took the blood pressure. The blood pressure was normal. I explained that I would watch the FHR tracing to see if an improvement in the variability occurred. About 15 minutes later, repetitive late decelerations began occurring. I called the health-care provider to report a Category III tracing and prepared the laboring person for a cesarean birth. I spoke with the health-care provider and explained the importance of the partner cutting the umbilical cord. At the birth of the baby, the partner was able to cut the cord as I took their picture. It was a beautiful moment to witness. Their newborn was healthy with Apgar scores of 7 and 9. They were so thankful their birth plan was followed even in an emergency.
FHR Response
The FHR response to uteroplacental insufficiency can be seen in the baseline variability and periodic changes . Baseline FHR variability decreases from moderate to minimal to absent in the presence of uteroplacental insufficiency. Late FHR decelerations occur because of the decrease in oxygen perfusion. Prolonged decelerations are extended signs of decreased perfusion. These FHR tracings are pathologic and need intervention.
Fetal Nervous System
The fetal nervous system influences the fetal circulatory system and in turn the baseline FHR. The autonomic nervous system controls and regulates body functions such as breathing, blood pressure, and heart rate. In early fetal development, the FHR may be higher than 160 bpm. As the fetus grows, the nervous system matures, and the FHR baseline slows to a rate of 110 to 160 bpm. In cases of fetal hypoxia , the FHR slows and causes bradycardia .
Fetal Cardiovascular System
Uteroplacental insufficiency causes decreased perfusion to the fetal circulatory system. The fetus is unable to circulate oxygenated blood, and fetal bradycardia occurs. Alterations in the fetal cardiovascular system can also occur due to congenital heart disease . Fetal bradycardia can be caused by heart block, and tachycardia can be caused by fetal cardiac arrhythmias.
Fetal Reserve
The fetus’s capacity to tolerate the normal intermittent interruptions in oxygenation during labor and recover back to full oxygenation is called fetal reserve (Evans et al., 2022). The fetus should recover from these interruptions if they are separated by periods of oxygenation and recovery. The fetus can initially compensate during an event that causes asphyxia, but if the event progresses, fetal reserve will be depleted, and severe acidosis, cardiovascular decompensation, and brain damage will occur (Arnold & Gawrys, 2020). Fetal reserve may last several hours if the event is not severe or is short in duration. However, some fetuses have less reserve than others. Complications causing uteroplacental insufficiency also cause decreases in the fetal reserve. In cases of chronic uteroplacental insufficiency such as preeclampsia, the placenta no longer functions at the optimal level. The fetus can become growth restricted and will decompensate faster due to the lower level of fetal reserve. An FHR tracing of minimal to absent variability , late decelerations , or prolonged decelerations signals the minimal amount or lack of fetal reserve.