Intrapartum Fetal Heart Rate (FHR) Monitoring

Standardized guidelines for the interpretation of the fetal heart rate as suggested by the National Institute of Child Health and Human Development are adopted in the following discussion unless noted otherwise.[2]

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

• 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

Early in gestation the fetal heart rate is predominantly under the control of the sympathetic nervous system and arterial chemoreceptors.

As the fetus develops its heart rate decreases in response to parasympathetic (vagal stimulation) nervous system maturation and variability becomes more pronounced [3,4]. Small brief variable decelerations, associated with fetal movement, are common in the fetal heart tracings of premature fetuses [82].

Baseline 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.”

There must be at least 2 minutes of identifiable baseline segments (not necessarily contiguous) in any 10-minute window, or the baseline for that period is indeterminate. If minimum baseline duration is less than 2 minutes then the baseline is indeterminate. In such cases, it may be necessary to refer to the previous 10-minute window for determination of the baseline. The presence of FHR accelerations (either spontaneous or stimulated) reliably predicts the absence of fetal metabolic acidemia [2].

Bradycardia

Mean FHR < 110 BPM

• A rate of 100–119 BPM when accompanied by normal variability and accelerations is not usually a sign of fetal distress.
• Etiologies:
  • Heart block (< 70 BPM with little or no variability) caused by structural heart defects (e.g. fetal heterotaxy (left atrial isomerism , L-transposition of the great arteries, complete AV canal)or anti-Ro/SSA and anti-La/SSB antibodies
  • Hypothermia, maternal heart rate (signal ambiguity), sinus bradycardia, cytomegalovirus and parvovirus infection, uterine rupture [5,6,45,51,77]

Tachycardia

Mean FHR > 160 BPM

• Etiologies:
  • Sinus tachycardia (<200 BPM) Maternal fever, fetal anemia, chorioamnionitis, maternal hyperthyroidism ,terbutaline, hydroxyzine, IV diphenhydramine , compensatory sympathetic response to hypoxia caused by stimulation of catecholamine production by the adrenal gland [50, 52] maternal heart rate (signal ambiguity)
  • Tachyarrhythmias (usually ≥ 200 BPM with abrupt onset, little to no variability) (34,35):
    • Supraventricular tachycardia (200-240 BPM) accounts for the cause of 70 to 80% tachyarrhythmias and is typically diagnosed at 28 -32 weeks
    • Atrial flutter ( atrial rate of 300–600 BPM accompanied by variable degrees of atrioventricular conduction block) the second most common tachyarrhythmia and accounts for 25% of tachyarrhythmias and may be associated with congenital heart disease. typically diagnosed at 32 weeks , but may be noted at delivery

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

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 and long-term variability.

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

“…in most cases, normal FHR variability provides reassurance about fetal status and the absence of metabolic acidemia.” [33]

Etiologies of decreased variability: Fetal metabolic acidosis (decompensated state) CNS depressants (narcotics) , fetal sleep cycles, congenital anomalies, prematurity , fetal tachycardia, preexisting neurologic abnormality, magnesium, betamethasone, cocaine[9-17, 33].

A SHR pattern is "Visually apparent, smooth, sine wave-like undulating pattern in FHR baseline with a cycle frequency of 3-5 per minute which persists for 20 minutes or more.” A SHR has a regular amplitude and frequency and is excluded in the definition of variability .

This pattern may be generated by fetal sucking movements , central nervous system depressants,Butorphanol, fetal asphyxia/hypoxia, fetal infection, fetal cardiac anomalies, fetal sleep cycles, and severe fetal anemia.

Modanlou and Freeman proposed that an ominous or "true SHR" , such as that associate with severe fetal anemia, should have no areas of normal FHR variability or reactivity.

Murata et al. were able to obtain a SHR pattern in fetal sheep using chemical or surgical vagotomy, and arginine vasopressin infusion (a hormone released during acute blood loss). Power spectral analysis of R-R interval variability suggests the SHR pattern may represent a very low-frequency component inherent in fetal heart rate variability that appears as a result of strongly suppressed autonomic nervous activity. [18–21]

Accelerations are evoked by the sympathetic nervous system Sporadic non episodic accelerations are typically associated with fetal movement. Whereas episodic accelerations are thought to be caused by partial cord occlusion. [23, 32] "The presence of FHR accelerations generally ensures that the fetus is not acidemic"[24, 33]

Reactivity :("FHR accelerations that peak (but do not necessarily remain) at least 15 beats per minute above the baseline and last 15 seconds from baseline to baseline." ) [53] is not defined by the NIHCD guidelines.

 

Prolonged acceleration: lasts 2 to 10 minutes.

Periodic or episodic decelerations

Episodic patterns are those not associated with uterine contractions .

Variable decelerations and accelerations

Periodic patterns are those associated with uterine contractions.

Early and late decelerations
Variable decelerations and accelerations

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 > or equal to 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.

Recurrent decelerations: Variable, early or late occur with >50% of contractions in any 20-minute segment.

Prolonged deceleration:

Defined by NICHD as a decrease in FHR of > 15 beats per minute (BPM) measured from the most recently determined baseline rate The deceleration lasts >= 2 minutes but less than 10 minutes. The International Federation of Gynecology and Obstetrics (FIGO), defines a prolonged deceleration as a FHR decrease of at least 15 BPM that lasts more than 3 minutes; a prolonged deceleration longer than 5 minutes is considered a pathologic feature [72].

Etiologies:

• Oxytocin or prostaglandins, maternal hypotension secondary to supine hypotension or epidural analgesia, umbilical cord compression secondary to maternal position, rapid descent of the fetal head, [28] artifact (maternal heart rate) " maternal seizure [26]
• "Sentinel Hypoxic or Ischemic Event "such as uterine rupture, severe abruptio placentae, umbilical cord prolapse, amniotic fluid embolus with coincident severe and prolonged maternal hypotension and hypoxemia, maternal cardiovascular collapse, and fetal exsanguination from either vasa previa or massive fetomaternal hemorrhage [29]

Acidemia has been found to develop after only 2 minutes of a prolonged deceleration [30,54]. Continuation of a prolonged deceleration for 10 minutes or more is defined by NIHCD guidelines as a baseline change . Unresolved bradycardia following a prolonged deceleration before delivery (also known as terminal bradycardia [28] ) has been associated with a higher risk of acidemia. Despite its association, Cahill AG et. al. found that the presence of unresolved bradycardia prior to delivery was poorly predictive of acidemia with positive predictive value of only 12.9% in their retrospective study [30]. Williams and Galerneau found decreased variability before FHR bradycardia to be significantly correlated with low umbilical artery pH [55].

Contractions are quantified as number in a 10-minute window, averaged over 30 minutes.

Normal: 5 or less contractions in 10 minutes (averaged over 30 minutes).

Tachysystole: More than 5 contractions in 10 minutes (averaged over 30 minutes). Applies to both spontaneous or stimulated labor. Tachysystole should always be qualified as to the presence or absence of associated FHR decelerations.

Etiologies:Tachysytole may occur spontaneously, but has been associated with abruption, preeclampsia, epidural , and the use of oxytocin and / or misoprostol [63, 68]

McNamara and Johnson observed that fetal oxygen saturation (FSpO2) drops during contractions in the course of normal labor. FSpO2 reaches its lowest level 92 seconds after the contraction peaks and takes around 90 seconds to return to its initial level. With oxytocin-induced tachysystole, they observed a nearly thirty percent drop in oxygen saturation. Simpson and James noted a similar decrease in oxygen saturation as well (see graph below). They also observed more periods of absent and minimal variability, less accelerations, more late and recurrent decelerations during oxytocin induced tachysystole [64-66]

The terms hypertonus, hypercontractility, and hyperstimulation [69,70] are not defined by NIHCD guidelines.

Early decelerations appear to be a vagally mediated response to improve cerebral perfusion triggered by an intracranial baroreflex [58, 62].

Late decelerations are brought about by the periodic reduction in perfusion of the intervillous space by uterine contractions. In the normally oxygenated fetus the decelerations appear to be a vagally mediated reflex to chemoreceptor stimulation (reflex lates) [47]. The lag time to the deceleration after the contraction onset reflects the time for the partial pressure of oxygen (pO2) in the fetal blood to fall to the partial pressure of oxygen (pO2) required to activate the aortic chemoreceptors. In chronically hypoxic fetuses with decreased variability (decompensated state) late decelerations are probably secondary to hypoxic myocardial depression (non reflex lates). [48, 49].

Variable decelerations are an adaptive response to acute decreases in oxygen levels during contractions(compression of utero- placental vessels) or cord compression. When the level of oxygen in the fetal blood is low (hypoxia) chemoreceptors are triggered causing reflex vagally mediated slowing of the fetal heart rate that is believed to reduce the myocardial workload, conserving cardiac glycogen levels, and avoiding the onset of anaerobic metabolism with the production of lactic acid. In addition the sympathetic system (including both neural and adrenal components) acts to constrict blood vessels in nonvital peripheral areas such as the arms and legs to divert more blood flow to vital organs such as the heart and brain[27]. In the case of a prolonged deceleration if hypoxia persists the deceleration may be maintained by direct myocardial depression. [28].

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Severe, prolonged, and frequent variables, prolonged uterine contractions, or prolonged decelerations may not allow enough reperfusion time to adequately eliminate CO2 or restore fetal biochemical status and oxygenation. Persistent hypoxia leads to the onset of anaerobic metabolism with the generation of lactic acid . The acid is neutralized primarily by the bicarbonate buffer system and to a lesser extent by hemoglobin. Without oxygen the lactate is not metabolized, production of energy (ATP) is minimal, and the buffer base is consumed by the accumulating acid [30,31,36].

Compromised fetuses may exhibit a sequence of FHR pattern deterioration characterized by the development of FHR decelerations, followed by loss of accelerations, then deeper and wider decelerations, followed by a rise of FHR baseline with frequent episodes of tachycardia or continuous tachycardia, then minimal baseline variability, and ultimately prolonged decelerations or terminal bradycardia [43]. Matsuda Y , et. al . observed that "... premature fetuses can quickly develop abnormal heart rate patterns and that these patterns tend to progress in severity much more rapidly than in term fetuses. " [44]

Recommendations have been developed by the American Congress of Obstetricians and Gynecologists (ACOG) for the interpretation and management of fetal heart rate tracing based on the NICHD Three-Tier Fetal Heart Rate Interpretation System

Algorithms for the Intrapartum Management of Fetal Heart Rate Tracings

Clark et al. algorithm (Category II)
• "This algorithm is not intended as guide to management of fetus with extreme prematurity*."
• "This algorithm does not address the issue of prolonged deceleration, as defined by the NICHD. This definition is too broad to be clinically useful in isolation." *Less than 28 week gestational age.
• CMQCC example algorithm

  “A category II fetal heart rate pattern lasting 60 minutes or more that was identified on initial presentation with persistently minimal or absent variability and lacking accelerations, even in the absence of decelerations, is suggestive of a previously compromised or injured fetus."[75]

Prolonged  deceleration

Perform vaginal exam for impending delivery or cord prolapse if not contraindicated [46, 72]

• If cord prolapse is present:[71]

-Manual elevation with Trendelenburg (15 degrees),

-Tocolysis if contractions are present.

-If the umbilical cord is outside of the vagina, warm and moist wrapping should be used to protect the cord If possible knee-chest position.

-Fill maternal bladder 500 mL if long-distance transportation or a delay in delivery is expected

-Clear obstacles to rapid delivery

• If an irreversible cause of the deceleration is suspected such as abruption or uterine rupture, or the cause is not identified and the deceleration persists after 5 or more minutes ,despite corrective measures, then clear obstacles to rapid delivery

Tachysystole [7, 78]

Spontaneous labor

Category I FHR tracing

-No intervention

Category II or III FHR tracing

-Turn patient to left (preferable) or right lateral position.

-Administer 500 cc LR IV bolus. Consider any fluid restrictions the patient may have.

-If no resolution, consider tocolytic (terbutaline 0.25 mg SC)

Induction or Augmentation [78]

Category I FHR tracing

-Turn patient to left (preferable) or right lateral position.

-Administer 500 cc LR IV bolus. Consider any fluid restrictions the patient may have.

-If uterine activity does not return to normal after 10 minutes, decrease the oxytocin rate by at least half; if uterine activity has not returned to normal after 10 more minutes, discontinue the oxytocin until uterine activity is less than five contractions in 10 minutes

Category II or III FHR tracing

-Discontinue oxytocin/remove dinoprostone insert/ hold next dose of misoprostol

-Turn patient to left (preferable) or right lateral position.

-Administer 500 cc LR IV bolus. Consider any fluid restrictions the patient may have.

-Administer Oxygen at 10 L/min via nonrebreather mask if the first interventions do not resolve the abnormal FHR pattern. Discontinue oxygen as soon as possible.

-If no resolution, consider tocolytic (terbutaline 0.25 mg SC)

"Resumption of oxytocin after discontinuation [78]

-If oxytocin has been discontinued for less than 30 minute and the FHR is normal and contraction frequency, intensity, and duration are normal, resume oxytocin at no more than half the rate that caused the tachysystole, and gradually increase the rate as appropriate based on unit protocol and maternal-fetal status.

-If oxytocin was discontinued for more than 30 minutes, and the FHR is normal and contraction frequency, intensity, and duration are normal, resume oxytocin at 1 to 2mU/min."

Assess the oxygen pathway and consider other causes of FHR changes [60].

Maternal Check maternal 02 sat, Check maternal vitals (fever, tachycardia) infection , check history of pneumonia, asthma, diabetic ketoacidosis, hyperthyroidism, maternal blood antibodies, sepsis, and preeclampsia History of drug use (e.g. cocaine, amphetamine) uterine surgery (e.g. cesarean section, myomectomy); Check current medications : terbutaline , oxytocin , misoprostol, narcotics, epidural.

Uterus Check for tachysystole or tetanic contractions, infection, abruption or uterine rupture

 Fetus Cord prolapse , fetal anemia, arrhythmia, heart block, congenital anomaly preexisting neurologic injury , extreme prematurity, growth restriction .

Corrective measures / Intrauterine resuscitation[7,60, 75, 80].

-Move mother to a lateral position (left or right) to reduce compression of the vena cava and improve uteroplacental blood flow

-IV fluid bolus of at least 500 mL lactated Ringer’s solution (if not contraindicated)

-Reduce or discontinue oxytocin

-Modification of pushing efforts (second stage)

-Administer Oxygen at 10 L/min via nonrebreather mask

-Pressors (ephedrine 5 to 10 mg IV) if hypotension is present and no response to fluid bolus .

-Antibiotic if infection is suspected

-Consider amnioinfusion for moderate variable decelerations during first stage of labor.

Clear obstacles to rapid Delivery [7, 60]

-Evaluate the patient's location and transit time for the operative delivery.

-Prepare the OR or LDR and put the surgical team (surgeon, scrub technician, and anesthesia personnel) together.

-Obtain informed consent.

-Verify the mother's preparedness (e.g. IV access , Foley).

-Review labs and assess need for availability of blood products

-Verify the fetal variables (presentation, EGA, and EFW).

-Gather neonatal resuscitation staff.

• AHRQ: Monitoring for Perinatal Safety — Electronic Fetal Monitoring
• AHRQ: Safe Medication Administration — Oxytocin

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