Intrapartum fetal heart rate monitoring

FETUS, PLACENTA, AND NEWBORN

Intrapartum

fetal heart rate monitoring

V. Fetal heart rate patterns H.

B.

KREBS,

in the second stage of labor

M.D.

R. E. PETRES, L. J. DUNN,

M.D. M.D.

Richmond,Virgkia A total of 1,755 fetal heart rate (FHR) tracings of the second stage of labor was analyzed. The FHR patterns were classified according to the behavior of the baseline FHR and are listed in decreasing order of benignity: normocardia, transitory bradycardia, tachycardia, persistent bradycardia, and progressive bradycardia. Each category was further subdivided into four groups on the basis of association or nonassociation with early, variable, or late decelerations. Cord compression patterns were noted in over 50% of the FHR tracings and account for the majority of low Apgar scores and fetal acidosis. FHR abnormalitles occurred in 91% of second-stage labor patterns, and were mild in most cases or of too short duration to influence fetal outcome. An effort was made to establish therapeutic guidelines based on the morphologic features, prognostic grading, and the etiology of the FHR patterns in the second stage of labor. (AM. J. OBSTET. GYNECOL. 140:435, 1981.)

A LTHOLJGH a great deal of information exists in the literature on the evolution of the fetal heart rate (FHR) during the first stage of labor, few reports are limited to discussion of the second stage of labor, also called the stage of expulsion of the fetus. The stage begins with the complete dilation of the cervix and ends with delivery of the infant. During this most critical period of human life, forceful uterine contractions potentiated by bearing-down efforts of the parturient woman induce rapid hemodynamic alterations that result in a variety of FHR changes. From the Department of Obstetrics Medical College of Virginia. Received for publication Revised

December

Accepted January

October

and Gynecology, 7, 1980.

29, 1980. 6, 1981.

Reprint requests: Dr. H. B. Krebs, Department of Obstetrics and Gynecology, Medical College of Virginia, Richmond, Virginia 23298. 0002-9378/81/120435+05$00.50/0

0

1981

The

C. V. Mosby

Co.

The purpose of this study was to classify FHR patterns in the second stage of labor and to investigate their clinical significance, with emphasis placed on bradycardic FHR changes.

Material and methods The study was performed in a retrospective manner and included 1,755 FHR tracings obtained from patients in labor during the time period 1975 to June, 1977. The selected FHR tracings were obtained by internal FHR monitoring and were technically adequate to allow interpretation of the FHR patterns discussed below. Only singleton pregnancies of 34 weeks’ gestation or more were included in the study. All were cephalic presentations, with at least 15 minutes of FHR monitoring in the second stage of labor. The majority of the patients (1,632) had vaginal delivery; 123 had cesarean sections. Following a suggestion of Thiery,’ FHR patterns were classified according to the behavior of the baseline

435

436

Krebs, Petres, and Dunn

persistent in 8.Oyc. The correlation between the l:HR patterns and fetal outcome is demonstrated in Table 1. All bradycardic FHR patterns and tachycardia \vere associated with significantly lower l- and .i-minute Apgar scores and \vith a higher rate of perinatal mortalit? thaII were normocardic patterns (p < O.O:i). -I‘hr most ominous baseline FHR appeared to be progressive brad\ cardia, closely followed by persistent braclycardia. Transitory bradycardia carried a better prognosis than did progressive bradycardia, persistent bradycardia. and tachycardia. but a poor fetal outcome was significantly more often observed than in the normocardic group. The most unfavorable combination oi an abnormal baseline FHR and any type of deceleration in our series was progressive bradycardia and late deceler-ations (Table I). In fact, late decelerations appeared to be ominous irrespective of the baseline FHR. Variable dccelerations with progressive bradycardia, persistent bradycardia, and tachycardia were associated with significantly higher rates of low Apgar scores than variable decelerations in normocardia.

F--------------1 Fig. 1.1, Normocardia.2, Progressive bradycardia. ?, Transitory bradycardia. 4, Persistent bradycardia. 5, Tachycardia. FHR. Normoc-&if FHR: baseline FHR remains in normocardic range ( 120 to 160 bpm). Progrmiw 6m&m&a: baseline FHR falls progressively beneath 120 bpm. Transitory bradycardiu: baseline FHR transiently falls beneath 120 bpm to return to normocardia not before 10 minutes. Bradycardic FHR changes lasting less than 10 but more than 2 minutes are defined as prolonged decelerations.” Prrsistrnt brad~cardia: baseline FHR falls beneath 120 bpm and remains in the bradycardic range. ?hchprardia: Baseline FHR above 160 bpm. These major FHR patterns are graphically represented in Fig. 1. Each category was subdivided into four groups on the basis of association or nonassoc-iation with decelerations of the FHR, tvhich are defined elsewhere.* Pertinent data from the patients’ records were computerized. Analysis for limits of confidence was carried out by chi-square test corrected for continuity.

Results A normocardic FHR was observed in 75% of all FHR tracings during the second stage of labor. Bradycardia occurred in 20.50/c., and tachycardia in 4.5%. Bradycardia was progressive in 6.Y%, transient in 6.2%, and

Comment Careful analysis of FHR patterns in the first stage of labor reveals FHR abnormalities in 43% of the cases if the tracings are scrutinized for baseline FHR, oscillatory amplitude, oscillatory frequency, accelerations and decelerations.” Many of the changes are transient and of no prognostic significance. Truly pathologic tracings occur in only 1% of the cases and may be recognized by a combination of decelerations with low FHR variabilitv and lack of’ accelerations.:’ The clinician may face a therapeutic dilemma when dealing with “suspicious“ FHR tracings, which are observed in almost 7% of FHR patterns in the first stage of labor.” In the second stage of labor, clinical management ot FHR abnormalities is more complex for the following reasons: (1) FHR abnormalities occur very frequently. (2) FHR patterns may be difficult to classify. (5) The pathogenesis of certain FHR changes observed most commonlv in the second stage of labor is still poorly understood. (4) There are no satisfactory guidelines fi)r treatment of bradycardias. ‘4~1 1. Fetal head compression and effects on the umbilical cord, as well as impairment of uteroplacental perfusion, are maximal during the second stage of labor. Thus, a high incidence of deceleration patterns can be anticipated. We observed early decelerations in 14%. late decelerations in 5%. and variable decelerations in 53% of all FHR tracings. \\‘hen baseline FHR changes are included, the incidence of “pathologic” FHR patterns ranges from 50% LO t)Y%.’ We found a normal baseline FHR without tlerelera-

Volume Number

140 4

Table

I. FHR patterns

lntrapartum

score

PeGatal

I min <7 N Normocardia: All No decelerations Early decelerations Variable decelerations Late decelerations Progressive bmdycardia: All No decelerations Early decelerations Variable decelerations Late decelerations Transitory bradycardia: All No decelerations Early decelerations Variable decelerations Late decelerations Persistent brtiycardia: All No decelerations Early decelerations Variable decelerations Late decelerations Tachycardia: All No decelerations Early decelerations Variable decelerations Late decelerations Total are significantly

Yo of Total

n

these

FHR

V

437

changes

% ofN

n

%ofN

75.0 23.7 10.1 38.2 3.0

186 30 14 122 20

14.1 7.2 7.9 18.2 38.5

29 5 1 18 5

2.2 1.2 0.6 2.7 9.6

110 21 12 69 8

6.3 1.2 0.7 3.9 0.5

45 7 4 29 5

40.1* 33.3 33.3 42.0 62.5

13 3

11.8* 14.2 8.3 10.1 25.0

108 23 13 64 8

6.2 1.3 0.7 3.7 0.5

27 3 3 18 3

25.0* 13.0 23.1 28.0 37.5

5 0 0 4

141 32

8.0

45

30.0*

11

1.8 1.8 4.2 0.2

5 28 3

22.6 21.9 38.4 60.0

i 6 1

23 2 2 15 4 326

29.1* 12.5 20.0 32.6 57.1 18.5

5

79

4.5 0.9 0.6 2.6 0.4

16 10 46 7 1,755 different

from

100

those listed

under

as decelerations

or

brady-

cardia. Ad 3. The high incidence of early and variable decelerations in the second stage of labor is readily explained by increasing intrauterine pressure changes and the associated fetal descent that leads to fetal head and umbilical cord compression. The frequent occur-

normal

FHR

mortality

5 min <7

1,317 417 177 671 52

tions in 24% (Table I). Many of these seemingly favorable FHR patterns were associated with lack of accelerations and abnormal FHR variability, which resulted in an overall occurrence of FHR abnormalities in 1,590 of the 1,755 FHR tracings (91%). Ad 2. In the second stage of labor, rapid hemodynamic changes in response to forceful uterine contractions and maternal bearing-down efforts frequently result in bizarre FHR alterations and distortion of deceleration patterns. Combinations of variable and late decelerations or early and late decelerations may be observed. Rapid succession of uterine contractions may result in merging of decelerations: a new contraction induces a new deceleration before the FHR has recovered from the last contraction. It may be impossible to classify

monitoring.

and fetal outcome Apgar

*Figures

FHR

: 2

1

1

0 3 1 63

in the respective

n

% ofN

6 1 1 3 1

0.5

4.5

1.9

4.6* 0.0 2: 12.5 7.8* 6.2 6.5

2.1

6.3* 6.3 0.0 8.7 14.3 3.6

2.5

columns.

1 18 p < 0.05,

1.0 chi-square

test.

rence of late decelerations in the final phase of labor reflects insufficient oxygenation of fetal blood as a consequence of high intervillous space pressures during the time of relative uterine hypertonicity. The pathogenetic mechanism of bradycardia in the second stage of labor is more controversial. Goodlir? reviewed the physiology of FHR responses and concluded that “abrupt and brief bradycardias” depended on vagal reflexes mediated by baroreceptors in response to increased peripheral resistance secondary to various insults, such as hypoxia, fetal cord compression, head compression, fetal grunting, Poseiro effect, and maternal seizures. “Bradycardias of slow onset and prolonged duration” have little or no vagal component and represent decreased cardiac function.” Goodlin and Haesslein,‘j classifying deceleration patterns and bradycardia as “fetal vagal bradycardias,” found that all fetuses demonstrated “terminal and expulsive

bradycardias”

of varying

durations

at the

time

of vaginal delivery and expulsion. They suggested that “fetal vagal bradycardias” often have multiple and complex etiologies. Terminal bradycardias were more

438

Krebs,

Table

Petres,

II. Duration

and Dunn

of bradycardia

and fetal outcome Apgar I-min

score

Perinatal

<7

j-min

mortality

<7

N

%

11

%ofN

n

o/c ofN

n

74%of N

Bradycardia < 15 min Bradycardia z 15 min

162 197

45.1

37 80*

22.8 40.6

7 22*

4.3 11.2

2 8

1.2 4.0

Total

359

117

32.5

29

8.1

10

2.8

54.9 100

*Figures are significantly different from those listed under Bradycardia < 15 min in the respective columns. p < 0.05, chi-square test. severe in primigravid or multigravid women who had a tight perineum in relation to the neonate’s head size. Terminal bradycardias also occurred when the cervix was incompletely dilated, when the mother was bearing down, or when uterine contractions were particularly severe.fi Zilanti and associates’ concluded from their study that fetal bradycardia in the expulsion period was caused by closing of the umbilical placental circulation during the last moments of fetal life, probably secondary to a sharp reduction in umbilical blood flow. In some instances, bradycardia appears to represent a terminal response preceding death of the fetus.+‘” Ad 4. The management of bradycardias poses considerable difficulties, since a third of second-stage bradycardias is associated with neonatal fetal depression and fetal hypoxemia, and two thirds are not. Zilanti and associates7 observed sharp falls in fetal arterial oxygen saturation in most cases of fetal bradycardia in the expulsion period and recommended immediate delivery. Many bradycardias occur in the final moments of the expulsion period. Accelerated delivery by such means as low-forceps extraction is often feasible and successful. Unfortunately, over 50% of secondstage bradycardias in our series occurred at a time when immediate delivery could not be achieved unless by cesarean section. Clearly, guidelines need to be established so as to know when to intervene and when not to. These guidelines should be based upon easily obtainable clinical information and should consider differences in pathogenesis, appearance, and duration of the bradycardia. The duration of the bradycardia is probably of particular importance. In our series, the outcome in fetuses who exhibited bradycardia for not longer than 15 minutes prior to delivery was not significantly different from that in fetuses who exhibited a normocardie FHR (Table II, p > 0.05). The value of Thiery’s classification of bradycardias lies in the fact that it allows prognostic grading of bradycardias on the basis of easily recognizable mor-

phologic features. Progressive bradycardia was associated with fetal hypoxemia and acidosis more frequently than was persistent bradycardia. Transitory bradycardia appeared to be a benign FHR pattern.’ Our figures largely confirm these findings, with the exception of transitory bradycardia, which was also associated with a significantly higher rate of low Apgar scores than was normocardia (Table I). Conclusions with regard to the cause of the bradycardia can often be drawn from the appearance of the tocogram, the preceding FHR pattern, and the type of bradycardia. 1. Uterine hypertonicity secondary to oxytocin hyperstimulation or hyperactive labor results in malperfusion of the intervillous space and fetal hypoxemia. The tocographic pattern is diagnostic. Maternal seizures, supine hypotension, or paracervical blocks may result in bradycardias which have an appearance similar to that of the bradycardias associated with uterine hypertonicity.6 The drop in FHR is more or less abrupt, and, characteristically, the FHR gradually recovers as the underlying cause is eliminated. These bradycardias are of the transitory type and may be found in the first as well as in the second stage of labor. Frequently, the decline in FHR lasts less than 10 minutes and should then be classified as prolonged deceleration. 2. Precipitate falls in FHR are often associated with sudden descent of the fetal head into the true pelvis during the course of vigorous labor. Head compression or umbilical cord compression is likely to be causative.” Preceding early or variable decelerations usually provide clues. The bradycardia is of the persistent or progressive type. Changes in position of the gravida 01 fetal manipulations aimed toward dislodgment of the fetal head from a narrow pelvic cavity or decompression of the umbilical cord may result in return to a normocardic FHR pattern. This type of FHR change is specific for the second stage of labor. 3. Decelerations may deepen and widen in response to the growing vigor and frequency of uterine contractions until, finally, recovery of the FHR does not occur.

Volume Number

lntrapartum FHR monitoring. V

140 4

Thus, the decelerations result in “bradycardia” by merging to establish a new baseline FHR at a lower level. The cause of the “bradycardia” is identical to the cause of the preceding decelerations. These bradycardias are almost exclusively observed in the second stage of labor. They are of the persistent or progressive type unless the uterine contractions are alleviated. 4. Bradycardias persisting from the first into the second stage of labor are usually of moderate severity (FHR, 100 to 119 bpm) and may be associated with congenital heart block. ” More commonly, no underlying cause is apparent. The bradycardia is of the persistent type. 5. Progressive bradycardias without signs of fetal reactivity which often follow preceding phases of late decelerations are indicative of severe anoxia and represent a terminal response preceding the death of the fetus.+‘” It is apparent that all bradycardias are potentially reversible with the exception of the ones listed under Nos. 4 and 5. The FHR recovers spontaneously if the insult responsible for the fall in FHR, such as fetal deprivation of oxygen during uterine hypertonicity, seizures, or supine hypotension, is eliminated. Bradycardias that occur specifically during the second stage of labor may also be alleviated by active intervention. The effect of hyperactive labor on the uteroplacental circu-

439

lation, the umbilical cord, or the fetal head may be halted by the administration of rapidly acting tocolytic drugs, such as beta-sympathicomimetics. Cord or head compression may respond to a change in position of the parturient woman and/or careful fetal manipulations, as mentioned above. In conclusion, bradycardias in the second stage of labor reflect fetal deprivation of oxygen and should be treated by immediate elimination of the underlying cause. The bradycardic hypoxic episode may then be limited so that the FHR can recover. If neither therapy for cause nor expeditious vaginal delivery is feasible, bradycardia and hypoxia will persist and may worsen progressively. The final outcome is then determined by the duration of the hypoxic episode and fetal resistance. Decreasing FHR variability and lack of accelerations associated with bradycardia or decelerations may be observed, signifying decompensation of fetal homeostatic mechanisms.” Bradycardias persisting from the first into the second stage of labor do not require any therapy if they are of moderate severity and associated with good FHR variability and accelerations indicative of satisfactory fetal reserve.2 Therapeutic interventions are usually futile in the case of the rare but prognostically most ominous progressive bradycardia with a flat baseline FHR.“. ”

REFERENCES

Thiery, M., Cited by Fischer, W. M.: Grundlagen und klinische Wertiekeit der Kardiotokoeraohie. in Fischer, W. M., editor: gardiotokographie, Luh;buch und Atlas, Stuttgart, 1976, Georg Thieme Verlag, KG, pp. 206-207. Krebs, H. B., Petres, R. E., Dunn, L. J., Jordaan, H. V. F., and Segreti, A.: Intrapartum fetal heart rate monitoring. I. Classification and prognosis of fetal heart rate patterns, AM. J. OBSTET. GYNECOL. 133:762, 1979. Krebs, H. B., Petres, R. E., Dunn, L. J., Jordaan, H. V. F., and Segreti, A.: Intrapartum fetal heart rate monitoring. II. Multifactorial analysis of intrapartum fetal heart rate tracings, AM. J. OBSTET. GYNECOL. 133:773, 1979. Fischer, W. M.: Gnmdlagen und klinische Wertigkeit der Kardiotokographie, in Fischer, W. M., editor: Kardiotokographie, Lehrbuch und Atlas, Stuttgart, 1976, Georg Thieme Verlag, KG, pp. 142-234. 5. Goodlin, R. C.: Fetal cardiovascular responses to distress. A review, Obstet. Gynecol. 49:371, 1977. 6. Goodlin, R. C., and Haesslein, H. C.: When is it fetal distress? AM. J. OBSTET. GYNECOL. 128:440, 1977.

Zilianti, M., Segura, C. L., Cabello, F., et al.: Studies on fetal bradycardia during birth process. II. Obstet. Gynecol. 42:840, 1973. 8. Carldeyro-Barcia, R., Mendez-Bauer, C., Pose, S., and Poseiro, J.: Fetal monitoring in labor, in Wallace, H. M., Gold, E., and Lis, E., editors: Maternal and Child Health Practices, Springfield, Illinois, 1973, Charles C Thomas. Publisher, p. 356. 9. Goodlin, R. C.: Intrapartum fetal heart rate responses 7.

and plethysmographic 110:210. 1971.

pulse,

AM. J. OBSTET.

GY~ECOL.

10. Hon, E. H., and Lee, S. T.: Electronic evaluation of the fetal heart rate. VIII. Patterns preceding fetal death, further observations. AM. I. OBSTET. GYNECOL. 87:814, 1963. 11. Webster, R. D., Cudmore, D. W., and Gray, J.: Fetal bradycardia without fetal distress. Case presentation and review of the literature, Obstet. Gynecol. 50:505, 1977. 12. Boehm, F.: Prolonged end stage fetal heart rate decelera_I

tions,

Obstet.

Gynecol.

45:579,

1975.