Acceleration of the fetal heart rate CARL






ROBERT Melbourne,


YARDLEY, Victoria,

F.R.C.S., M.Sc.,







Acceleration of the fetal heart rate during contractions was usually followed by deceleration, and evidence is presented to show that it results from increased sympathetic drive and may be associated with fetal tissue hypoxia. However, the presence of accelerations are not serious and merely warn the obstetrician of the possibility of the occurrence of subsequent decelerations. The mechanism thought most likely to produce accelerations is uterine compression of the umbilical vein during contractions. (AM. J. OBSTET. GYNECOL. 134:523, 1979.)

ACCELERATION of the fetal heart rate (FHR) during contractions is stated to be “not an adverse pattern,” indicating good reflex responsiveness of the fetal circulation, the mean fetal pH in association with this change being normal (7.34 k 0.03)’ However, Paul’ states that the clinical significance of acceleration during contractions is unclear, that the change is mediated through the sympathetic division of the autonomic resources system, and that it may be an early response to the stresses of labor. Accelerations may also occur before labor in the absence of contractions and these have been described by Schifrin4 as a reactive pattern. Their appearance has been used as a positive indicator of good health of the fetus, over 700 fetuses with a reactive pattern having no serious problem in subsequent labor. The mechanism producing acceleration before and during labor may be different so that evidence of good health in one group may not be applicable to the

From the Department Monash Univenity, Hospitul.

of Obstetrics and Gynecology, The Queen Victoria Memorial


for publication




18, 1978.

21, 1978.

Rep-int reqwsts: and Gynecology. Australia 3000. 0002-9378/79/130523+05$00.50/O

Dr. Carl Wood, Department of Obstetrics Monash University, Melbourne,


1979 The

C. V. Mosby


xE 1A. FHR uterine pressure recordings from two Patients showing transition from transient accelerations or biphasic change to decelerations.


other, but with the exception of Paul’s” slight uncert,inty, opinions favor the view that accelerations are not important clinically. We wish to present some data associated with accelerations in the human fetus and to discuss this in the light of other evidence, including study of the sheep fetus. 523






Fig. 1B. FHR, uterine pressure, and scalp tissue pH (measured by the height 01 the vertical lines on the pressure trace) recording from patient showing transition from accelerations to biphasic change and decelerations. The scalp tissue pH has declirled from 7.20 to ‘7.10 during the time of change in FHR pattern.

Volume Number


134 5








Fig. 2. Prolonged fall in fetal scalp Pq accompanied by marked rises in fetal heart rate with uterine contractions. As the magnitude of the accelerations diminshes, fetal tissue PO, returns to the basal level. (From Walker, A., Maddern, L., Day, E., Renou, P., Talbot, J,, and Wood, C.: Fetal scalp tissue oxygen tension measurements in relation to maternal dermal oxygen tension and fetal heart rate, Br. J. Obstet. Gynaecol. 78: 1, 1979, published by Headley Bros.)

Material and methods The records of 100 consecutive patients whose FHR was monitored by the fetal intensive care unit were examined for the appearance of accelerations. These were defined as an increase in FHR of more than 20 beats per minute in relation to a uterine contraction. All were patients whose fetuses were at increased risk because of the presence of obstetric complications such as hypertension, proteinuria, antepartum hemorrhage, fetal growth retardation, and low urinary estriol excretion. Patients received intramuscular Demerol, 100 to 150 mg, as an analgesic during the first stage of labor and nitrous oxide and oxygen mixtures during the second stage.

Results FHR accelerations were present in 14 of the patients. In only three were accelerations not accompanied by other changes. The FHR traces of the remaining 11 patients showed both accelerations and decelerations. The accelerations always preceded the development of decelerations and in some instances the trace showed a gradual progression from accelerations, to acceleration and deceleration (biphasic change), to decelerations alone (Figs. 1A and IB). In the same 100 patients there were 11 with decelerations alone, nine beginning in the early-mid phase of the contraction cycle, and three in the late phase of the contraction cycle (one had both early-mid and late decelerations).

The occurrence of accelerations in association with decelerations was highly significant (Table I). Overall comparison of two groups, accelerations + decelerations, and decelerations alone showed no difference in terms of age, parity, gestational length, length of labor, type of delivery, Apgar score, and fetal weight (Table II). The three patients with accelerations alone were not different from the remaining 11 of this group who had both accelerations and decelerations.

Comment The reason for the association between accelerations and decelerations is very unlikely to be due to chance (P < 0.001) and the most likely explanation is that a single process causes both. As accelerations precede decelerations it is also likely that the acceleration represents an early stage of a physiologic or physiopathologic process which would support Paul’? view that it may be an early response to some stress. Three pieces of evidence may throw light on the significance of the accelerations. Maternal injection of a beta-blocking drug abolished accelerations in relation to the contraction cycle in all of the eight fetuses3 This shows that the acceleration is proabably related to increased sympathetic drive. Studies of fetal tissue PO, show correlation between FHR accelerations and falls in fetal scalp tissue Pop (Figs. 2 and 3).5 When the heart rate change is biphasic, the tissue PO, begins to fall at the time of the acceleration, suggesting that the acceleration represents an early stage of a hypoxic process.




and Yardley

Fig. 3. Large

fall in fetal scalp tissue PO, associated with a spontaneous biphasic change ill tetal he,:l: rate. The patient, who suffered from rhe supine Ir) potensive syndrome, ~\as turned fl on) ~hr supine to the right lateral posirion at the 10 minute ma1 k of this record. Kotc that the fall ill ribsue Poll began at the time of the acceleration and became more marked during thr deceleration. I From Walker, ,4.. Maddern. I.., Day, E., Renou. P.. ‘lalbot, j., atld \\‘ood, (:.: Feral scalp tissue oxygen tension me;tsurements in relation to marernal dermal ox~grtl tension and t&,11 hear1 t att’. Kr. ,I. Obstel. Gynaecol. 78: 1, 1979, published by Hradltk Ktr,\.j F8/ 77 GlPOD

Table and

I. Association



decelerdtiolls -


A~c~leration.~ Yes No x2 = 28; p ‘z 0.001.


II ‘4ccelrrution.c + deculwutim.~



, ,2$j

.- -

. ,


TIME !seconds)

Fig. 4. Illustration

of a bidirectional change in heart rare following brief inferior vena caval occlusion (bar) in a near term fetal lamb. Note that heart rate first increases (+‘LO beats/ minute) then decreases (-45 beats/minute) from the haseline level in association with falls in both venous and arterial prrssures. Caval occlusion was effected by inflating a balloon cuf-f which had been implanted al-ound the vessel 30 days prior to the experiment.

a1 1.7 283 8.1

be Parity Gestational length Length of labor Mode of delivery: Spontaneous Forceps Qsarean section Fetal weight (gm) Apgar score (1 minute) Comparison no significant








22 1.4 287 9.6

concerns in



the sheep


2.5 0.3 13 3.4

_f 28.5 7.2

t test showed

hiphasic fetus

(Fig. 4). The during both could

t t 2 It

ti 4 1

by xz test and Student’s

inferior vena caval occlusion and arterial pressure occurs tion

2.1 0.4 tti 2..:

11 2 i Y,J 10 + K’L7 7.2

of groups differences.


t t t L




of brief

fall of venous the acceleta-

be expected

to he as-

Volume 134 Number





sociated with a reduction in cardiac output and, at least A some areas of the body, a fall of fetal tissue PO,. The hypothesis suggested from the observation and evidence cited is that accelerations are most likely a result of a reduction of venous return to the heart, perhaps from cord compression. The acceleration results from sympathetic stimulation as they are abolished by the action of a beta-blocking drug. The transient reduction in fetal scalp tissue PO, which occurs during accelerations cannot be assessed quantitatively, and judging from the case histories, in particular the fetal and neonatal status, the presence of accelerations have no clinical significance except to warn the

REFERENCES 1. Beard, R. W., and Finnegan, T. S.: Fetal Heart Patterns and Their Clinical Application, Sussex, 1974, Chichester Press, p. 18, Sonicaid. 2. Paul, R. H.: Fetal Intensive Care, Los Angeles, 1971, University of Southern California, p. 16. 3. Renou, P., and Wood, C.: Autonomic control of fetal heart rate, AM. J. OBSTET. GYNECOL. 105:949, 1969.


that decelerations

may subsequently


The accelerations, however, are distinct from the transient increase of FHR, and reactive patterns described by Schifrin4 which occur in the antepartum period in the absence of uterine contractions. Other explanations of the data are possible and may involve any circulatory stress which initially would stimulate the sympathetic nervous system and then subsequently stimulate the parasympathetic system when the stress is more severe. However, none seems as likely to occur in utero as restriction of venous return resulting from uterine compression of veins, most likely the umbilical vein.

4. Schifrin, B. S.: Second International Symposium in Perinatal Medicine, Las Vegas, 1977. 5. Walker, A., Maddern, L., Day, E., Renou, P., Talbot, J., and Wood, C.: Fetal scalp tissue oxygen tension measurements in relation to maternal dermal oxygen tension and fetal heart rate, Br. J. Obstet. Gynaecol. 7&l, 1971.

Acceleration of the fetal heart rate.

FETUS, PLACENTA, AND NEWBORN Acceleration of the fetal heart rate CARL WOOD, ADRIAN M.B., B.S., WALKER, ROBERT Melbourne, B.Sc., YARDLEY, Vic...
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