Intrapartum fetal heart rate monitoring: Clinical sciences

Intrapartum monitoring of the fetal heart rate, or FHR, is performed to evaluate FHR patterns, assess fetal well-being, and guide interventions during labor.

The basis for monitoring is that the fetal brain modulates cardiac activity through sympathetic and parasympathetic effects which are influenced by oxygenation status and acid-base balance.

The FHR demonstrates predictable patterns in response to intrapartum events, such as fetal sleep, maternal medications, compression of the umbilical cord, hypoxia, and acidemia.

Two methods of FHR monitoring are electronic fetal monitoring, or EFM, and intermittent auscultation. EFM can be performed externally or internally, while intermittent auscultation involves periodic listening to the FHR using a Doppler device or fetal stethoscope on the maternal abdomen.

Now, when a patient presents for evaluation and intrapartum fetal heart rate monitoring, your first step is to obtain a focused history and physical examination. Factors to consider in your patient’s history include gestational age; amniotic membrane status; and medications the patient is receiving such as oxytocin, IV opioids like butorphanol, or an epidural. On physical exam, note your patient’s vital signs, and keep in mind that abnormalities in maternal blood pressure, temperature, and oxygenation can cause significant FHR changes. Also, perform a sterile vaginal exam to check cervical dilation.

Your next step is to assess for high-risk conditions, including hypertension or diabetes. If there are no high-risk conditions, you can monitor with either intermittent fetal auscultation or with continuous EFM. However, if a high-risk condition is present or if continuous monitoring is preferred by your patient, perform continuous EFM.

Next, apply the monitors to the patient and assess the FHR and uterine contraction patterns. The fetal heart rate pattern is described by the baseline, variability, and presence of accelerations or decelerations. Additionally, a sinusoidal pattern is an uncommon but important finding.

Now, the baseline is the average FHR rounded to increments of 5 beats per minute during a 10-minute segment. A normal baseline is between 110 and 160 beats per minute. Tachycardia is above 160 and bradycardia is below 110.

Next is variability, or the normal fluctuation of the baseline FHR. It’s a result of the FHR modulation by the parasympathetic and sympathetic nervous systems, and is irregular in both amplitude and frequency.

Variability can be absent with no fluctuation; minimal, with detectable fluctuations 5 beats in amplitude or less; moderate, with fluctuations between 6 and 25 beats in amplitude; and marked, with an amplitude greater than 25 beats in amplitude from baseline.

Persistently absent variability is concerning for fetal acidemia but can be normal in fetuses less than 28 weeks of gestation; minimal variability can occur with the fetal sleep cycle, or with medications like intravenous opioids or magnesium sulfate; moderate variability usually indicates a well-oxygenated fetus; and marked variability is usually a benign finding which could be associated with an increase in alpha-adrenergic activity.

Next, accelerations are abrupt, transient increases in the FHR above the baseline for at least 15 beats per minute with a duration of at least 15 seconds. Accelerations are a reassuring sign and reflect normal fetal acid-base status, and are usually associated with fetal movement.

Decelerations are decreases in the FHR, and are categorized by their relationship with uterine contractions. Early decelerations have a gradual, symmetric decrease and return to baseline that mirror the timing of a contraction. They start at the onset of a contraction, nadir at the peak of the contraction, and recover at the end of the contraction. Early decelerations represent a fetal vagal response to head compression during descent in the pelvis. They are benign and do not reflect abnormal fetal acid-base status.

In contrast, late decelerations are a gradual, symmetric decrease and return from the baseline, also associated with contractions, but delayed in timing compared to early decelerations. The onset, nadir, and recovery of a late deceleration start after the beginning, peak, and end of a contraction, respectively. Late decelerations represent uteroplacental insufficiency, leading to reduced fetal oxygenation and an increased risk of fetal acidemia.

Now, there are also variable decelerations, which are an abrupt decrease in FHR below the baseline. They often resemble the letter “U,” “V,” or “W” and are called “variable” because their timing, duration, and amplitude fall and rise abruptly. Variable decelerations may or may not be associated with uterine contractions and represent the FHR response to umbilical cord compression which often occurs after membrane rupture when less amniotic fluid is present to cushion the cord. Deeper and more frequent variable decelerations increase the risk for fetal hypoxemia and acidemia because the flow of oxygenated blood from the placenta to the fetus is reduced while the cord is compressed.

Next up are prolonged decelerations, or a decrease in the FHR lasting between 2 and 10 minutes that may or may not be associated with a uterine contraction. Deeper and more prolonged decelerations are more likely to have adverse effects on fetal oxygenation.

Here’s a high-yield fact! If a prolonged deceleration or an acceleration lasts more than 10 minutes, it's considered a change in the baseline FHR!

Lastly, a sinusoidal pattern is a smooth, sine wave-like undulating change in the baseline with a cyclic frequency of 3 to 5 per minute. It can be associated with severe fetal anemia or the recent use of butorphanol.