Fetal Heart Rate Monitoring

Intrapartum Fetal Monitoring
By Mark Curran, MD
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Early in gestation the fetal heart rate is predominately under the control of the sympathetic nervous system and arterial chemoreceptors [1]. As the fetus develops its heart rate decreases in response to parasympathetic ( vagal stimulation) nervous system maturation and variability becomes more pronounced [2]. Standardized guidelines for the interpretation of the fetal heart rate have been suggested by the National Institute of Child Health and Human Development [3]and are adopted in the following discussion.

Dr. Curran is a perinatologist on staff at the Pomona Valley Hospital Medical Center in Pomona , CA.

The interpretation of the fetal heart rate tracing should follow a systematic approach with a full qualitative and quantitative description of the following:

Baseline rate
Baseline fetal heart rate (FHR) variability
Presence of accelerations
Periodic or episodic decelerations
Changes or trends of FHR patterns over time
Frequency and intensity of uterine contractions

Baseline Fetal Heart Rate (FHR):

The baseline FHR is the heart rate during a 10 minute segment rounded to the nearest 5 beat per minute increment excluding periods of marked FHR variability, periodic or episodic changes, and segments of baseline that differ by more than 25 beats per minute.

The minimum baseline duration must be at least 2 minutes. If minimum baseline duration is < 2 minutes then the baseline is indeterminate.

Bradycardia :Mean FHR < 110 BPM

A rate of 100-119 BPM in the absence of other non reassuring patterns is not usually a sign of compromise[ 4]
Etiologies: Heart block (little or no variability), occiput posterior or transverse position, serious fetal compromise.

Tachycardia: Mean FHR>160 BPM

In the presence of good variability tachycardia is not a sign of fetal distress [4]
Etiologies: Maternal fever, fetal hypoxia, fetal anemia, amnionitis, fetal tachyarrhythmia (usually > 200 BPM with abrupt onset little to no variability) SVT (200-240 BPM) [5] , fetal heart failure, drugs (beta sympathomimetics, vistaril, phenothiazines) , rebound ( transient tachycardia following a deceleration accompanied by decreased variability) [4]

Baseline change: The decrease or increase in heart rate lasts for longer than 10 minutes.

Baseline FHR Variability

Baseline variability is defined as fluctuations in the fetal heart rate of more than 2 cycles per minute. No distinction is made between short-term variability (or beat-to-beat variability or R-R wave period differences in the electrocardiogram) and long-term variability.

Grades of fluctuation are based on amplitude range (peak to trough):

Absent variability = Amplitude range undetectable

Minimal = < 5 BPM

Moderate = 6 to 25 BPM

Marked = > 25 BPM

The tracing to the right shows an amplitude range of ~ 10 BPM (moderate variability ).

A sinusoidal pattern has regular amplitude and frequency and is excluded in the definition of variability. A sinusoidal pattern has a smooth, undulating pattern, lasting at least 10 minutes with a fixed period of three to five cycles per minute and an amplitude of 5-15 bpm. Short-term variability is usually absent. [6]

Persistently minimal or absent FHR variability appears to be the most significant intrapartum sign of fetal compromise [32]. On the other hand the presence of good FHR variability may not always be predictive of a good outcome.[33].

Etiologies of decreased variability: Fetal metabolic acidosis [7], CNS depressants[8,9], fetal sleep cycles[10], congenital anomalies, prematurity [11,12], fetal tachycardia, preexisting neurologic abnormality [13], normal [14], betamethasone[15].

Accelerations

An acceleration is an abrupt increase in FHR above baseline with onset to peak of the acceleration less than < 30 seconds and less than 2 minutes in duration. The duration of the acceleration is defined as the time from the initial change in heart rate from the baseline to the time of return to the FHR to baseline.

Adequate accelerations are defined as:

<32 weeks' : >10 BPM above baseline for >10 seconds [3]
>32 weeks' : >15 BPM above baseline for > 15 seconds[3].

Prolonged acceleration: Increase in heart rate lasts for 2 to 10 minutes.

The absence of accelerations for more than 80 minutes correlates with increased neonatal morbidity [38,39].

Fetal scalp stimulation can be used to induce accelerations. There is about a 50% chance of acidosis in the fetus who fails to respond to stimulation in the presence of a nonreassuring pattern. [17]

REACTIVITY[16]*

An increase of 15 BPM above baseline for 15 second duration (from baseline to baseline) twice in a 20 minute period.

Since the amplitude of accelerations is inversely proportional to the rate premature fetuses often do not meet criteria for reactivity.

Only 65% of fetuses at 28 weeks are reactive by this criteria.

By 34 weeks 95% of fetuses are reactive.

*Reactivity ( a term used in antenatal testing) is not defined by the NIHCD guidelines.

Periodic or episodic decelerations

Episodic patterns are those not associated with uterine contractions .

Periodic patterns are those associated with uterine contractions.

Early and late decelerations (with some exceptions-i.e., supine hypotension) are periodic.
Variables can also be periodic.

Quantitated by the depth of the nadir in BPM below the baseline.The duration is quantitated in minutes and seconds from the beginning to the end of the deceleration. (Accelerations are quantitated similarly.)

The type of the deceleration is distinguished on the basis of its waveform.

Gradual decrease and return to baseline with time from onset of the deceleration to nadir >30 seconds.

Further subclassified based on their relation to the contraction.

Abrupt decrease in FHR of > 15 beats per minute with onset of deceleration to nadir < 30 seconds.

Early deceleration: Gradual decrease in FHR with onset of deceleration to nadir >30 seconds. The nadir occurs with the peak of a contraction.
Late Deceleration: Gradual decrease in FHR with onset of deceleration to nadir >30 seconds. Onset of the decleration occurs after the beginning of the contraction, and the nadir of the contraction occurs after the peak of the contraction.
Variable: Abrupt decrease in FHR of > 15 beats per minute measured from the most recently determined baseline rate. The onset of deceleration to nadir is less than 30 seconds. The deceleration lasts > 15 seconds and less than 2 minutes. A shoulder, if present, is not included as part of the deceleration.

Recurrent decelerations ( variable, early, or late ): Decelerations occur with > 50% of uterine contractions in any 20 minute segment.

Prolonged deceleration : A decrease in FHR of > 15 beats per minute measured from the most recently determined baseline rate. The deceleration lasts >= 2 minutes but less than 10 minutes.

Etiologies: Maternal hypotension [18] , uterine hyperactivity, cord prolapse, cord compression, abruption, artifact (maternal heart rate) , maternal seizure [19]

Although umbilical cord compression is often responsible for a prolonged deceleration a pelvic examination should be performed to rule out umbilical cord prolapse or rapid descent of the fetal head.[4]

Late Decelerations

Late decelerations associated with preservation of beat-to beat variability

These decelerations appear to be mediated by arterial chemo receptors in mild hypoxia.

When the level of oxygen in the fetal blood is below a pO2 of 15-20 mm Hg chemoreceptors are triggered causing reflex alpha adrenergic stimulation which constricts peripheral blood vessels and shunts blood to vital organs. Constriction of peripheral blood vessels leads to hypertension.

The hypertension stimulates a baroreceptor mediated vagal response that slows the heart rate. [20] .

The onset of reflex late decelerations typically precedes the loss of accelerations [21]

Late decelerations associated with no variability (where loss of variability has not been caused by drug administration)

With progressing hypoxia, the decelerations become deeper.

As acidosis develops the brain stem reflexes become blunted and direct myocardial depression causes shallow decelerations [20,22].

If myocardial depression is severe enough, lates may be absent all together [22].

Etiologies

Excessive uterine contractions (hyperstimulation), maternal hypotension, or maternal hypoxemia.
Reduced placental exchange as in hypertensive disorders, diabetes, IUGR, abruption.

Management of late decelerations

These maneuvers are primarily intended to alleviate "reflex" lates.

Place patient on side [23,24]

Administer O2 by tight face mask [25, 40]

Discontinue oxytocin.

Correct any hypotension

IV hydration.

If hyperstimulation is present consider terbutaline 0.25 mg SC [26,27]

If late decelerations persist for more than 30 minutes despite the above maneuvers, fetal scalp pH is indicated.

Scalp pH > 7.25 is reassuring, pH 7.2-7.25 may be repeated in 30 minutes.

Deliver for pH < 7.2 or minimal baseline variability with late or prolonged decelerations and inability to obtain fetal scalp pH [28,29]

Variable Decelerations

Vagally mediated through chemoreceptors or baroreceptors.

Accelerations "shoulders" before and after a variable deceleration are thought to be caused by partial cord occlusion .Decreased venous return causes a baroreceptor-mediated acceleration.

Hypertension and decreased arterial oxygen tension secondary to complete cord occlusion results in deceleration.

Variables occur with head compression secondary to vagal nerve activation, and with movement in the premature fetus[30]

The timing of the deceleration may occur periodically after the contraction [31].

Pure variables are uncommonly associated with adverse fetal outcome. Whereas atypical variables are more often associated with fetal acidosis and low Apgar scores [32]

Management of Variables

Change position to where FHR pattern is most improved. Trendelenburg may be helpful.

Discontinue oxytocin.

Check for cord prolapse or imminent delivery by vaginal exam.

Consider amnioinfusion[35-37]

Administer 100% O2 by tight face mask [4].