Version May 2024
| Fetal heart rate tracing | Possible etiologies and interpretation | Management |
| Category I | ||
| Baseline 110 to 160 beats per minute with moderate variability and no late or variable decelerations. Accelerations and early decelerations may be present or absent. | This is a normal tracing. | Intermittent or continuous fetal monitoring based on clinical status and underlying risk factors. Review every 30 minutes in the first stage and every 15 minutes in the second stage of labor. |
| Category II | ||
| Intermittent variable decelerations (<50% of contractions) | Common finding usually associated with normal outcome. | No intervention required. |
| Recurrent variable decelerations (>50% of contractions) | Umbilical cord compression. May be associated with impending acidemia, especially if progressive increase in depth, duration, and frequency. Moderate variability and/or accelerations suggest fetus is not currently acidemic. | Reposition mother to left or right lateral. Amnioinfusion is an option. Adjunctive measures to promote fetal oxygenation (intravenous fluid bolus, reduce uterine contraction frequency) may be useful. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic. |
| Delivery is indicated if tracing does not improve and acidemia suspected. | ||
| Recurrent late decelerations | Transient or chronic uteroplacental insufficiency, such as from hypotension, tachystole, or maternal hypoxia. Accelerations and/or moderate variability suggest fetus is not currently acidemic. | Reposition mother to left or right lateral. Adjunctive measures to promote fetal oxygenation include intravenous fluid bolus, reduce uterine contraction frequency. Persistent late decelerations with minimal variability and absent accelerations suggest fetal acidemia; this is even more likely if variability is absent (category III). Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic. |
| Delivery is indicated if tracing does not improve. | ||
| Fetal tachycardia (baseline heart rate greater than 160 beats per minute for at least 10 minutes) | Infection, medication, maternal medical disorders, obstetric complications, fetal tachyarrhythmia (typically rate over 200 beats per minute). Fetal acidemic more likely when associated with minimal or absent variability, absent accelerations, and/or recurrent decelerations. | Treat underlying cause, if known. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic. |
| Delivery is indicated if tracing does not improve and acidemia suspected. | ||
| Bradycardia (baseline heart rate less than 110 beats per minute for at least 10 minutes) | Acute onset may be due to hypotension, umbilical cord occlusion, rapid fetal descent, tachysystole, abruption, uterine rupture. Fetal acidemia more likely when associated with minimal or absent variability and absent accelerations during baseline periods. | Treat underlying cause, if known. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic. Delivery is indicated if tracing does not improve and acidemia suspected. |
| Prolonged decelerations (15 beats per minute drop below baseline for more than 2 and less than 10 minutes) | ||
| Minimal variability | Fetal sleep, medication, fetal acidemia. If due to fetal sleep, should recover in 20 to 60 minutes. If due to maternal medication, should recover as medication wears off. | If decreased fetal oxygenation suspected, reposition mother to left or right lateral. Adjunctive measures to promote fetal oxygenation include intravenous fluid bolus, reduce uterine contraction frequency. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic. |
| If no improvement and no accelerations, delivery is indicated if acidemia suspected or confirmed by scalp pH. | ||
| Tachysystole (more than 5 contractions in 10 minutes, averaged over 30 minutes) with fetal heart rate changes. Tachysystole that is spontaneous and associated with a normal fetal heart rate pattern does not require treatment, but the possibility of placental abruption as the underlying etiology should be considered. | Spontaneous labor: Tachysystole may be associated with fetal acidemia if accompanied by recurrent fetal heart rate decelerations. | Reposition mother to left or right lateral, intravenous fluid bolus. If ineffective, reduce uterine contraction frequency with a tocolytic. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic. |
| Induction or augmentation. | Decrease or stop uterotonic medications. Reposition mother to left or right lateral, intravenous fluid bolus. If ineffective, reduce uterine contraction frequency with a tocolytic. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic. | |
| Category III | ||
| Absent baseline variability and recurrent late decelerations, recurrent variable decelerations, or bradycardia | Increased risk of fetal acidemia. | Prepare for delivery and reposition mother to left or right lateral, intravenous fluid bolus. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic. If no improvement after conservative measures and scalp stimulation does not result in acceleration, delivery is advisable. |
| Sinusoidal | Increased risk of hypoxemia. Risk of acidemia increased if prolonged or amplitude of 15 beats per minute or more. | Prepare for delivery and reposition mother to left or right lateral, intravenous fluid bolus. Initiate scalp stimulation to provoke fetal heart rate acceleration, which is a sign that the fetus is not acidotic. If no improvement after conservative measures and scalp stimulation does not result in acceleration, delivery is advisable. |
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