Fetal Heart Rate

 

 

 

 

The FHR tracing should be interpreted only in the context of the clinical scenario, and any therapeutic intervention should consider the maternal condition as well as that of the fetus. For example, fetuses with intrauterine growth restriction are unusually susceptible to the effect of hypoxemia, which tends to progress rapidly.

The normal FHR range is between 120 and 160 beats per minute (bpm).

FHR assessment may be equal or superior to measurement of fetal blood pH in the prediction of both good and bad fetal outcomes

 

Fetuses with a normal pH, i.e., greater than 7.25, respond with an acceleration of the fetal heart rate following fetal scalp stimulation. Fetal scalp sampling for pH is recommended if there is no acceleration with scalp stimulation

 

 

 

Selected High-Risk Indications for Continuous Monitoring of Fetal Heart Rate


Maternal medical illness
Gestational diabetes
Hypertension
Asthma

Obstetric complications
Multiple gestation
Post-date gestation
Previous cesarean section
Intrauterine growth restriction
Premature rupture of the membranes
Congenital malformations
Third-trimester bleeding
Oxytocin induction/augmentation of labor
Preeclampsia

Psychosocial risk factors
No prenatal care
Tobacco use and drug abuse


Adapted with permission from Byrd JE. Intrapartum electronic fetal heart rate monitoring (EFM) and amnioinfusion. Advanced Life Support in Obstetrics Course Syllabus. Kansas City, Mo.: American Academy of Family Physicians 1996:97-106.

A Systematic Approach to Reading Fetal Heart Rate Recordings


1.        Evaluate recording--is it continuous and adequate for interpretation?

2.        Identify type of monitor used--external versus internal, first-generation versus second-generation.

3.        Identify baseline fetal heart rate and presence of variability, both long-term and beat-to-beat (short-term).

4.        Determine whether accelerations or decelerations from the baseline occur.

5.        Identify pattern of uterine contractions, including regularity, rate, intensity, duration and baseline tone between contractions.

6.        Correlate accelerations and decelerations with uterine contractions and identify the pattern.

7.        Identify changes in the FHR recording over time, if possible.

8.        Conclude whether the FHR recording is reassuring, nonreassuring or ominous.

9.        Develop a plan, in the context of the clinical scenario, according to interpretation of the FHR.

10.     Document in detail interpretation of FHR, clinical conclusion and plan of management.


FHR=fetal heart rate.

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Nonreassuring and Ominous Patterns


Nonreassuring patterns

Fetal tachycardia

Fetal bradycardia

Saltatory variability

Variable decelerations associated with a nonreassuring pattern

Late decelerations with preserved beat-to-beat variability

Ominous patterns

Persistent late decelerations with loss of beat-to-beat variability

Nonreassuring variable decelerations associated with loss of beat-to-beat variability

Prolonged severe bradycardia

Sinusoidal pattern

Confirmed loss of beat-to-beat variability not associated with fetal quiescence, medications or severe prematurity

Periodic FHR Changes

Accelerations
Accelerations are transient increases in the FHR (Figure 1). They are usually associated with fetal movement, vaginal examinations, uterine contractions, umbilical vein compression, fetal scalp stimulation or even external acoustic stimulation.
15 The presence of accelerations is considered a reassuring sign of fetal well-being. An acceleration pattern preceding or following a variable deceleration (the "shoulders" of the deceleration) is seen only when the fetus is not hypoxic.15 Accelerations are the basis for the nonstress test (NST). The presence of at least two accelerations, each lasting for 15 or more seconds above baseline and peaking at 15 or more bpm, in a 20-minute period is considered a reactive NST.

Early Decelerations
Early decelerations are caused by fetal head compression during uterine contraction, resulting in vagal stimulation and slowing of the heart rate. This type of deceleration has a uniform shape, with a slow onset that coincides with the start of the contraction and a slow return to the baseline that coincides with the end of the contraction. Thus, it has the characteristic mirror image of the contraction (Figure 5). Although these decelerations are not associated with fetal distress and thus are reassuring, they must be carefully differentiated from the other, nonreassuring decelerations.

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Figure 5

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FIGURE 5. Early deceleration in a patient with an unremarkable course of labor. Notice that the onset and the return of the deceleration coincide with the start and the end of the contraction, giving the characteristic mirror image.

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Figure 6

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FIGURE 6. Nonreassuring pattern of late decelerations with preserved beat-to-beat variability. Note the onset at the peak of the uterine contractions and the return to baseline after the contraction has ended. The second uterine contraction is associated with a shallow and subtle late deceleration.

Late Decelerations
Late decelerations are associated with uteroplacental insufficiency and are provoked by uterine contractions. Any decrease in uterine blood flow or placental dysfunction can cause late decelerations. Maternal hypotension and uterine hyperstimulation may decrease uterine blood flow. Postdate gestation, preeclampsia, chronic hypertension and diabetes mellitus are among the causes of placental dysfunction. Other maternal conditions such as acidosis and hypovolemia associated with diabetic ketoacidosis may lead to a decrease in uterine blood flow, late decelerations and decreased baseline variability.
23

A late deceleration is a symmetric fall in the fetal heart rate, beginning at or after the peak of the uterine contraction and returning to baseline only after the contraction has ended (Figure 6). The descent and return are gradual and smooth. Regardless of the depth of the deceleration, all late decelerations are considered potentially ominous. A pattern of persistent late decelerations is nonreassuring, and further evaluation of the fetal pH is indicated.16 Persistent late decelerations associated with decreased beat-to-beat variability is an ominous pattern19 (Figure 7).

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Figure 7

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FIGURE 7. Late deceleration with loss of variability. This is an ominous pattern, and immediate delivery is indicated.

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Figure 8

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FIGURE 8. Variable deceleration with pre- and post-accelerations ("shoulders"). Fetal heart rate is 150 to 160 beats per minute, and beat-to-beat variability is preserved.

Variable Decelerations
Variable decelerations are shown by an acute fall in the FHR with a rapid downslope and a variable recovery phase. They are characteristically variable in duration, intensity and timing. They resemble the letter "U," "V" or "W" and may not bear a constant relationship to uterine contractions. They are the most commonly encountered patterns during labor and occur frequently in patients who have experienced premature rupture of membranes
17 and decreased amniotic fluid volume.24 Variable decelerations are caused by compression of the umbilical cord. Pressure on the cord initially occludes the umbilical vein, which results in an acceleration (the shoulder of the deceleration) and indicates a healthy response. This is followed by occlusion of the umbilical artery, which results in the sharp downslope. Finally, the recovery phase is due to the relief of the compression and the sharp return to the baseline, which may be followed by another healthy brief acceleration or shoulder (Figure 8).

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Figure 9

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FIGURE 9. Severe variable deceleration with overshoot. However, variability is preserved.

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Figure 10

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FIGURE 10. Late deceleration related to bigeminal contractions. Beat-to-beat variability is preserved. Note the prolonged contraction pattern with elevated uterine tone between the peaks of the contractions, causing hyperstimulation and uteroplacental insufficiency. Management should include treatment of the uterine hyperstimulation. This deceleration pattern also may be interpreted as a variable deceleration with late return to the baseline based on the early onset of the deceleration in relation to the uterine contraction, the presence of an acceleration before the deceleration (the "shoulder") and the relatively sharp descent of the deceleration. However, late decelerations and variable decelerations with late return have the same clinical significance and represent nonreassuring patterns. This tracing probably represents cord compression and uteroplacental insufficiency.

Variable decelerations may be classified according to their depth and duration as mild, when the depth is above 80 bpm and the duration is less than 30 seconds; moderate, when the depth is between 70 and 80 bpm and the duration is between 30 and 60 seconds; and severe, when the depth is below 70 bpm and the duration is longer than 60 seconds.4,11,24 Variable decelerations are generally associated with a favorable outcome.25 However, a persistent variable deceleration pattern, if not corrected, may lead to acidosis and fetal distress24 and therefore is nonreassuring. Table 7 lists signs associated with variable decelerations indicating hypoxemia4,11,26 (Figures 9 and 10). Nonreassuring variable decelerations associated with the loss of beat-to-beat variability correlate substantially with fetal acidosis4 and therefore represent an ominous pattern.

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Figure 11A
A

Figure 11B
B

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FIGURE 11. (A) Pseudosinusoidal pattern. Note the decreased regularity and the preserved beat-to-beat variability, compared with a true sinusoidal pattern (B).

Sinusoidal Pattern
The true sinusoidal pattern is rare but ominous and is associated with high rates of fetal morbidity and mortality.
24 It is a regular, smooth, undulating form typical of a sine wave that occurs with a frequency of two to five cycles per minute and an amplitude range of five to 15 bpm. It is also characterized by a stable baseline heart rate of 120 to 160 bpm and absent beat-to-beat variability. It indicates severe fetal anemia, as occurs in cases of Rh disease or severe hypoxia.24 It should be differentiated from the "pseudosinusoidal" pattern (Figure 11a), which is a benign, uniform long-term variability pattern. A pseudosinusoidal pattern shows less regularity in the shape and amplitude of the variability waves and the presence of beat-to-beat variability, compared with the true sinusoidal pattern (Figure 11b).

 

 

A scalp pH less than 7.25 but greater than 7.20 is considered suspicious or borderline. Results in this range must also be interpreted in light of the FHR pattern and the progress of labor, and generally should be repeated after 15 to 30 minutes. A scalp pH of less than 7.20 is considered abnormal and generally is an indication for intervention, immediate delivery, or both.12 A pH less than 7.20 should also be assumed in the absence of an acceleration following fetal scalp stimulation when fetal scalp pH sampling is not available. Table 4 lists recommended emergency interventions for nonreassuring patterns.4,14 These interventions should also be considered for ominous patterns while preparations for immediate delivery are initiated.

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TABLE 4
Emergency Interventions for Nonreassuring Patterns


Call for assistance

Administer oxygen through a tight-fitting face mask

Change maternal position (lateral or knee-chest)

Administer fluid bolus (lactated Ringer's solution)

Perform a vaginal examination and fetal scalp stimulation

When possible, determine and correct the cause of the pattern

Consider tocolysis (for uterine tetany or hyperstimulation)

Discontinue oxytocin if used

Consider amnioinfusion (for variable decelerations)

Determine whether operative intervention is warranted and, if so, how urgently it is needed


Adapted with permission from Wolkomir MS. Understanding and interpreting intrapartum fetal heart rate monitoring. Milwaukee: Center for Ambulatory Teaching Excellence, Department of Family and Community Medicine, Medical College of Wisconsin, 1995:18.

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TABLE 5
Causes of Fetal Tachycardia


Fetal hypoxia

Maternal fever

Hyperthyroidism

Maternal or fetal anemia

Parasympatholytic drugs

 

Atropine

 

Hydroxyzine (Atarax)

Sympathomimetic drugs

 

Ritodrine (Yutopar)

 

Terbutaline (Bricanyl)

Chorioamnionitis

Fetal tachyarrhythmia

Prematurity

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Causes of Severe Fetal Bradycardia


Prolonged cord compression

Cord prolapse

Tetanic uterine contractions

Paracervical block

Epidural and spinal anesthesia

Maternal seizures

Rapid descent

Vigorous vaginal examination

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TABLE 7
Signs of Nonreassuring Variable Decelerations that Indicate Hypoxemia


Increased severity of the deceleration

Late onset and gradual return phase

Loss of "shoulders" on FHR recording

A blunt acceleration or "overshoot" after severe deceleration26 (Figure 9)

Unexplained tachycardia

Saltatory variability

Late decelerations or late return to baseline (Figure 10)

Decreased variability


FHR=fetal heart rate.

1.      Hon EH. The electronic evaluation of the fetal heart rate. Am J Obstet Gynecol 1958;75:1215.

2.      National Center for Health Statistics. Advance report of maternal and infant health data from the birth certificate, 1991. Monthly vital statistics report; vol. 42, no. 11. Hyattsville, Md.: Public Health Service, 1994.

3.      Boehm FH, Fields LM, Hutchison JM, Bowen AW, Vaughn WK. The indirectly obtained fetal heart rate: Comparison of first- and second-generation electronic fetal monitors. Am J Obstet Gynecol 1986;155:10-4.

4.      Fetal heart rate patterns: monitoring, interpretation, and management. ACOG technical bulletin no. 207. Washington, D.C.: ACOG, 1995.

5.      National Center for Health Statistics. Annual summary of births, marriages, divorces, and deaths: United States, 1993. Monthly vital statistics report; vol. 42, no. 13. Hyattsville, Md.: Public Health Service, 1995.

6.      Shields D. Fetal and maternal monitoring: maternal reactions to fetal monitoring. Am J Nurs 1978; 78:2110-2.

7.      U.S. Preventive Services Task Force. Guide to clinical preventive services. 2d ed. Baltimore: Williams & Wilkins, 1996:433-42.

8.      Vintzileos AM, Nochimson DJ, Guzman ER, Knuppel RA, Lake M, Schifrin BS. Intrapartum electronic fetal heart rate monitoring versus intermittent auscultation: a meta-analysis. Obstet Gynecol 1995; 85:149-55.

9.      Sandmire HF. Whither electronic fetal monitoring? Obstet Gynecol 1990;76:1130-4.

10.  Schifrin BS. Medicolegal ramifications of electronic fetal monitoring during labor. Clin Perinatol 1995; 22:837-54.

11.  Byrd JE. Intrapartum electronic fetal heart rate monitoring (EFM) and amnioinfusion. Advanced Life Support in Obstetrics Course Syllabus. Kansas City, Mo.: American Academy of Family Physicians, 1996:97-106.

12.  Assessment of fetal and newborn acid-base status. ACOG technical bulletin no. 127. Washington, D.C.: ACOG, 1989.

13.  Clark SL, Paul RH. Intrapartum fetal surveillance: the role of fetal scalp blood sampling. Am J Obstet Gynecol 1985;153:717-20.

14.  Wolkomir MS. Understanding and interpreting intrapartum fetal heart rate monitoring. Milwaukee: Center for Ambulatory Teaching Excellence, Department of Family and Community Medicine, Medical College of Wisconsin, 1995:1-19.

15.  Hutson JM, Mueller-Heubach E. Diagnosis and management of intrapartum reflex fetal heart rate changes. Clin Perinatol 1982;9:325-37.

16.  Gimovsky ML, Caritis SN. Diagnosis and management of hypoxic fetal heart rate patterns. Clin Perinatol 1982;9:313-24.

17.  Kurse J. Electronic fetal monitoring during labor. J Fam Pract 1982;15:35-42.

18.  Druzin ML. Antepartum fetal heart rate monitoring. State of the art. Clin Perinatol 1989;16:627-42.

19.  Martin CB Jr. Physiology and clinical use of fetal heart rate variability. Clin Perinatol 1982;9:339-52.

20.  Beard RW, Filshie GM, Knight CA, Roberts GM. The significance of the changes in the continuous fetal heart rate in the first stage of labour. J Obstet Gynaecol Br Commonw 1971;78:865-81.

21.  Krebs HB, Petres RE, Dunn LJ, Jordaan HV, Segreti A. Intrapartum fetal heart rate monitoring. I. Classification and prognosis of fetal heart rate patterns. Am J Obstet Gynecol 1979;133:762-72.

22.  Paul RH, Suidan AK, Yeh S, Schifrin BS, Hon EH. Clinical fetal monitoring. VII. The evaluation and significance of intrapartum baseline FHR variability. Am J Obstet Gynecol 1975;123:206-10.

23.  Hagay ZJ, Weissman A, Lurie S, Insler V. Reversal of fetal distress following intensive treatment of maternal diabetic ketoacidosis. Am J Perinatol 1994;11:430-2.

24.  Schneider EP, Tropper PJ. The variable deceleration, prolonged deceleration, and sinusoidal fetal heart rate. Clin Obstet Gynecol 1986;29:64-72.

25.  Bissonnette JM. Relationship between continuous fetal heart rate patterns and Apgar score in the newborn. Br J Obstet Gynecol 1975;82:24-8.

26.  Goodlin RC, Lowe EW. A functional umbilical cord occlusion heart rate pattern. The significance of overshoot. Obstet Gynecol 1974;43:22-30.

The discriminatory values for hCG and presence of an intrauterine gestation sac are well documented. Below are some for other scan findings you may come across on the Early Pregnancy Assessment Unit.


Normal scan findings

By TVS, a normal intrauterine sac should on average demonstrate the following development from LMP:

yolk sac

33 days (4.7w) (hCG approx. 1000iu/l)

embryonic echoes

38 days (5.4w)

visible heart activity

43 days (6.1w)


Not all women ovulate exactly midcycle, so findings after a single scan should be interpreted with caution.


Missed abortion

The diagnosis of missed abortion is usually made by serial ultrasound scans demonstrating inadequate development. On occasion it may be possible to diagnose missed abortion after one scan, when considering the following well-defined discriminatory findings.

Observation

Measured variable

TAS

TVS

Presence of an embryo
inside gestational sac

Mean sac diameter
(MSD)

25 mm

20 mm

Presence of an
embryonic heartbeat

Embryonic length

9 mm

5 mm


To calculate MSD, add together the dimensions given and divide by the number to give an average (eg. 15mm x 18mm x 12mm = MSD 15.0mm).

A missed or incomplete abortion should not be diagnosed unless the sonographic findings coincide with the measurements above. For example, if ultrasound scan demonstrates an empty sac of MSD 25mm, or a 6mm embryo has no demonstrable heartbeat, a missed abortion may be reliably diagnosed.

If the bleeding is minimal, the measurements are close to the descriminatory values and the pregnancy is desired, it is quite reasonable to repeat the ultrasound in 7-10 days.

Consideration should be given to other factors in the history. It is not uncommon for women who normally have regular menses to ovulate late in a conception cycle, leading to what might seem to be delayed development when considering dates by LMP. The timing of a positive pregnancy test is helpful, for example a positive pregnancy test 3 weeks previously would indicate a gestational age of at least 7 weeks, against which sonographic findings may be interpreted.

[ref's: 1,2,3,4]


Miscarriage rates after confirmed viability by ultrasound

Menstrual age

Pregnancy loss

6 - 7.9w

17%

8 - 9.9w

11.2%

10 - 11.9w

5.6%

12 - 13w

4.3%

overall 6-13w

8.8%



This information is useful for counselling patients after a reassuring scan. Loss rate after a normal scan is similar in symptomatic vs asymptomatic patients, thus a patient who experiences some vaginal bleeding may be reassured that her prognosis is as good as that of an asymptomatic patient if the scan is normal.

[ref: 5]


Fetal bradycardia

Normal heart rate at 6 weeks is 90-113 bpm and at 9 weeks is 144-170 bpm. At 5-8 weeks a bradycardia (<90 bpm) is associated with a high risk of spontaneous abortion.

Heart rate

Embryonic demise

40-69 bpm

100%

70-79 bpm

91%

80-90 bpm

79%

overall <90 bpm

86%


[ref: 6]


Early Oligohydramnios

Between 5.5 - 9w menstrual age, oligohydramnios is present when (MSD-CRL) < 5mm, where MSD is mean sac diameter and CRL is crown-rump length. Early oligohydramnios is associated with a very high risk of spontaneous abortion, and a guarded prognosis should be given when arranging another scan.

[ref: 7]


 



References

1. Nyberg DA, Laing FC, Filly RA. Threatened abortion: sonographic distinction of normal and abnormal gestation sacs. Radiology 1986; 158: 397-400

2. Levi CS, Lyons EA, Lindsay DJ. Early diagnosis of nonviable pregnancy with endovaginal ultrasound. Radiology 1988; 167: 383-5

3. Pennell RG, Needleman L, Pajak T et al. Prospective comparison of vaginal and abdominal sonography in normal early pregnancy. J Ultrasound Med 1991; 10: 63-7

4. Levi CS, Lyons EA, Zheng XH, Lindsay DJ, Holt SC. Endovaginal US: demonstration of cardiac activity in embryos of less than 5.0mm in crown-rump length. Radiology 1990; 176: 71-4

5. Frates MC, Benson CB, Doubilet PM. Pregnancy outcome after a first trimester sonogram demonstrating fetal cardiac activity. J Ultrasound Med 1993; 12: 383-6

6. Benson CB, Doubilet PM. Slow embryonic heart rate in early first trimester: indicator of poor pregnancy outcome. Radiology 1994; 192: 343-4

7. Bromley B, Harlow BL, Laboda LA, Benacerraf BR. Small sac size in the first trimester: a predictor of poor fetal outcome. Radiology 1991; 178: 375-7