Monitoring a fetus’s heart rate is standard practice during pregnancy and labor, providing insight into the baby’s overall health. This surveillance helps providers detect changes, such as fetal tachycardia, which is defined as an abnormally high heart rate sustained over a specific period. While an elevated rate can be a temporary, benign response, determining the underlying cause is important for assessing well-being and identifying potential risks.
What Fetal Tachycardia Means
Fetal heart rate (FHR) is measured in beats per minute (bpm). The normal range during pregnancy is typically 110 to 160 bpm. Fetal tachycardia is defined as a sustained baseline FHR greater than 160 bpm for at least ten minutes, though some definitions use 170 bpm. This rapid rate is the body’s attempt to compensate for changes in the fetal environment.
Tachycardia must be distinguished from a transient acceleration, which is a normal, temporary increase associated with fetal movement. FHR is primarily monitored using external Doppler ultrasound devices during routine visits or continuous electronic fetal monitoring (EFM) during labor. If an abnormality is detected, specialized tests like fetal echocardiography may be used to examine the heart’s structure and electrical system, especially if the rate exceeds 200 bpm.
Common Causes of Elevated Fetal Heart Rate
The triggers for fetal tachycardia are grouped into maternal factors or those stemming from the fetus itself.
Maternal Factors
Maternal conditions influencing the fetal heart include fever, often accompanying infection or inflammation (chorioamnionitis). An elevated maternal temperature directly increases the fetal metabolic rate, leading to a compensatory rise in heart rate.
Other factors include severe dehydration, which reduces blood flow to the placenta, or the administration of certain medications. Drugs like terbutaline (used to inhibit contractions) or atropine are known to have a stimulating effect that increases the FHR. Maternal hyperthyroidism, characterized by excessive thyroid hormone, can also cross the placenta and directly stimulate the fetal heart.
Fetal Factors
Fetal-specific causes often involve maintaining oxygen delivery or a primary electrical issue. A lack of sufficient oxygen (fetal hypoxia) triggers tachycardia as a compensatory mechanism to pump oxygenated blood more quickly. Fetal anemia, where the blood’s oxygen-carrying capacity is reduced, also causes a compensatory heart rate increase.
A different category involves primary fetal tachyarrhythmias, which are electrical rhythm disturbances. The most common is Supraventricular Tachycardia (SVT), where the rate can exceed 200 bpm. These arrhythmias are less common than compensatory responses but require specialized management.
When Fetal Tachycardia Signals Danger
Fetal tachycardia alone is often classified as a Category II (indeterminate) finding on a heart rate tracing, requiring continued surveillance. The danger arises not from the high rate itself, but from the presence of other non-reassuring signs indicating progression toward metabolic acidosis and distress. The rapid heart rate increases the heart’s oxygen consumption, making the fetus vulnerable to oxygen debt.
A concerning sign is when tachycardia is accompanied by a loss of beat-to-beat variability (the subtle, normal fluctuation in heart rate). Moderate variability indicates a well-oxygenated fetal brain; its loss suggests the central nervous system is suppressed by lack of oxygen. The presence of recurrent late decelerations (drops in FHR starting after the peak of a contraction) combined with tachycardia signals uteroplacental insufficiency.
When these patterns are present, the fetus risks developing fetal acidemia (low blood pH due to acid buildup). Sustained, very rapid rates, especially those from primary arrhythmias like SVT, can strain the developing heart muscle. This strain can lead to decreased heart function, heart failure, and hydrops fetalis (fluid accumulation in multiple fetal body compartments). The combination of absent variability, recurrent decelerations, and tachycardia places the tracing in the most concerning Category III, requiring immediate intervention.
Medical Management and Next Steps
The initial response to fetal tachycardia is to promptly address any reversible underlying causes through intrauterine resuscitation. This process involves several steps:
- Changing the mother’s position, typically to the left or right side, to relieve compression on major blood vessels and improve placental blood flow.
- Discontinuing medications used to stimulate labor, such as oxytocin, to reduce uterine activity and allow for fetal reoxygenation.
- Administering an intravenous fluid bolus to correct maternal hypotension or dehydration, enhancing placental perfusion.
- Treating maternal fever with antipyretic medication to lower the mother’s core temperature, which often resolves compensatory tachycardia.
Supplemental oxygen may also be given to the mother, though its effectiveness is debated unless the mother is hypoxic.
If the tachycardia is due to a primary fetal arrhythmia, a fetal cardiologist may recommend transplacental treatment, where antiarrhythmic medications are given to the mother to treat the fetus. If tachycardia persists despite intrauterine resuscitation, or if the tracing deteriorates into a Category III pattern, the decision is made to expedite delivery. This may involve an assisted vaginal delivery or an emergency Cesarean section, depending on the urgency and stage of labor.