Fetal reacting bradycardia ROBERT
C. GOODLIN,
HANNS
C.
HAESSLEIN,
Snrmmrnto,
California
M.D. M.D.
Acute and abrupt fetal bradycardias are considered to be vagal in origin. In addition to head compression and funis compression bradycardias, we will report on those acute fetal bradycardias occurring during maternal seizures and maternal voiding, during aortocaval compression, during terminal labor, and during the immediate postpartum period. While certain mechanisms are known which can explain some or parts of these bradycardias, we conclude that in the clinical setting information is insufficient to determine their etiology with precision. Instead of labeling abrupt fetal heart rate pattern as resulting from either head or funis compression, it is suggested that the patterns be described according to their severity and duration. Such acute fetal bradycardias can be detrimental in terms of reduced umbilical flow. Administration of atropine may be indicated in the otherwise healthy fetus with acute bradycardia. (AM. J. OBSTET. GYNECOL. 129: 845, 1977.)
&’ E c ON SI DE R acute reacting fetal bradycardias to be evoked by two different mechanisms. The most common is usually innocuous and vagal in origin while the rare mechanisms reflect cardiovascular dysfunction and are worrisome (Fig. 1). The subject of this article is the vagal fetal bradycardias that are characterized by abrupt beginnings and endings. According to current concepts, vagal bradycardias have only two different etiologies-fetal head compression or funis compression.‘. ’ The latter initially produces a vagal type of bradycardia, which may change to the cardiovascular dysfunctional type if the funis compression is not relieved. In the laboratory, it is possible to demonstrate that many acute fetal responses can lead to vagal activity such as fetal seizures, fetal grunting, or any condition (e.g., hypoxia) giving rise to abrupt rises in fetal vascular resistance and the baroreflex.’ In this report, selected types of fetal heart rate (FHR) responses (from approximately 3,000 deliveries) are analyzed using supplemental information obtained by recordings of fetal scalp pH, systolic time intervals, and maternal blood volume pulse.* Two recordings from a long-term experiment in fetal sheep done in another laboratory are also presented. These data, to
be reported, suggest that fetal vagal bradycardias often have multiple and complex etiologies and that the simplistic view of considering them to be the result of either funis or head compression is inaccurate. We also suggest an alternate interpretation of such FHR patterns and recommend the prophylactic use of atropine. Methods The FHR recordings were obtained with a variety of commercial FHR monitors, including Corometrics. Hewlett-Packard, and Berkeley as well as the Beckman Research Unit and the Berkeley RSR (systolic time) recorders.3 Systolic time intervals were determined with simultaneous recordings of fetal electrocardiograms, Doppler or microphone heart sounds, and Doppler placental pulse. The maternal pulse (photoelectric plethysmographic pulse or blood volume pulse) was obtained with a Beckman pulse monitor.“ Unless otherwise noted, the parturients labored in the lateral recumbent position and were delivered of their infants in the dorsal lithotomy position. One hundred fifty newborn infants were studied immediately after vaginal delivery using a combination of a spiral scalp electrode and a second needle electrode applied to either the extremity or funis of the neonate. During the 15 nonelective deliveries by cesarean section, a spiral scalp electrode was used until the fetal head was disengaged from the pelvis. A Doppler transducer was then applied as soon as possible to the neonate’s chest. Initially, the umbilical cord was clamped in a random fashion before or after the neonate’s first breath, but so many made early breathing efforts that a randomized
From the Department of Obstetrics and Gynecolo~, University of California, Davis, Sacramento Me&al Center. Presented .4mericnn .4prili3-16,
at the One Hundredth Annual Meeting Gyrlecological Society, Litchfield Park, 1977.
of the
.4rizona,
R&int requests: Dr. Robert C. Goodlin, Department of Obstetrics &d Gynecology, University of California, lh~ic. Sacramento Medical Center, 2315 Stockton Blvd.. Sacramento, California 95817.
845
846
Goodlin and Haesslein
Ikcetnher Am. J. Obster.
iFi!?!* piq Uterine
I
Drugs ~sedatives, PC02 levels Vasomotor Tone
Contraction
normal or increased
Worrisome if repetitive
opiates)
1 catecholamine
Benign if not severe
Fig. I. Proposed mechanism of reacting FHR patterns, head compression produce vagal bradycardia directly or after fetal hypertension? Any vagal asphyxia involves both right and left sides of the chart. A-C = Aortocaval.
Table
15. I!477 (Gynecol.
or mild bradycardia
hypoxia can leading to
I Event
Maternal seizure Maternal voiding Independent Poseiro effect (aortocaval compression) Terminal Expulsion Nuchal cord Uterine contraction (fetal sheep)
No. of cases 5 12 A: 150 150 100 1
Fig. No.
Characteristics
2 3 4 5, 8 6, 7 697 8 9, 10
Prolonged, neonate in good condition Inconsistent, prolonged, neonate in good condition Prolonged, after meconium staining, fetal acidemia Brief, related to maternal supine condition and uterine contraction Probably represents both head compression and Poseiro effect Relieved only by ventilation 62% correlation with typical FHR pattern “Bradycardia with localized uterine contraction”
study could not be completed. Differences in 2Y neonates delivered in cold and warm environments were studied. Twelve were delivered into an immediate environment of 40” to 41” C. controlled by an infrared heater and 17 were studied when the defivery room temperature fell below 18” C. The long-term experiment in fetal sheep followed that previously described by Berman and associates.5 In addition to catheters in the amniotic space, fetal aorta, and umbilical vein and a Clark electromagnetic flow transducer around the common umbilical artery, a catheter was also “wedged” in an umbilical vein toward
the cotyledon metrium.
and in a maternal
vein toward
the endo-
Results Unless otherwise noted, all of the neonates described had cord artery pH values that were higher than 7.20. We observed fetal bradycardia in many situations. apparently related to many different causes. Descriptions of some of these (Table I) follow. Maternal
seizure
bradycardia.
We
have
recorded
FHR during five maternal seizures (three were induced by epidural drugs and two were due to eclampsia) and
Volume Number
129 R
Fetal reacting bradycardia
Fig. 2. A 16-year-old mother with severe edema-proteinuria-hypertension
gestosis who had a seizure
despite a serum magnesium level of 4.9 mg. per 100 ml. The patient was given diazepam atropine (0.4 mg.), and additional MagSO, (4.0 Gm.) intravenously. An infant with Apgar and 9 was delivered with low forceps 25 minutes after seizure.
noted that the fetal bradycardia began simultaneously with the start of the maternal convulsion (Fig. 2). The fetal bradycardia often continued into the postictal state but was at least partially relieved by atropine. In two newborn infants delivered within 15 minutes of the maternal drug seizure, the umbilical artery pH was higher rhan 7.25 and in neither case could the anesthetic agent be found in the umbilical blood. Maternal voiding bradycardia. Twelve FHR recordings which demonstrated profound fetal bradycardias during maternal voiding were studied. Neither did measurements of intravesicle pressure correlate with the FHR changes nor did the fetuses demonstrate acidemia. In seven cases, the parturients had just been turned to the supine position. There was an increase in uterine tension in five (as recorded with the external tocograph) and a decrease in four. Eight women were restudied during a second voiding and only five of the eight demonstrated a similar episode of fetal bradycardia. Membranes had been ruptured in nine and in only
847
(5.0 mg.). scol-es of 7
two were the vertices not engaged. In other words, voiding fetal bradycardia could not be absolutely correlated with rupture of membranes, station of the fetal head, rise in intrauterine tension, or intravesicle pressure; also, it was not always reproducible. Fig. 3 is a FHR recording of a parturient who voided three times during a seven-hour labor. During the first voiding, there was a minimal rise in uterine tension with an associated fetal bradycardia. The parturient was given 16 mg. of morphine sulfate, and during a similar voiding episode that occurred two hours after the first, the fetal bradycardia did not recur although there was a similar rise in uterine tension. However, during maternal voiding two and one half hours after the second episode, a severe fetal bradycardia occurred this last bradycardia, there was no again. During significant change in maternal toe pulse height. Independent fetaI bradycardia. Fetal vagal bradycardia independent of uterine contraction is fre-. quently assumed to reflect “grunting” and the fetal
848
Goodlin
and Haesslein
December Am. J. Obscet.
15. 1977 (hvxol.
Fig. 3. FHR recording of a parturient voiding (between arrows) on three different occasions. There was a slight rise in uterine tension when the parturient was placed on a bedpan. See text for details. Valsalva maneuver, which presumably includes the passage of meconium. 2,6 There were cases in which the fetal bradycardia was followed shortly by fresh meconium observed within the amniotic fluid. This type of fetal bradycardia (Fig. 4) is also relieved by atropine, and in two of the four cases in which scalp pH was monitored, there were values of less than 7.15. The subsequently delivered newborn infants appeared to have marked vagal activity with accompanying frequent bradycardias. Poseiro effect bradycardia. Intrapartum fetal bradycardia associated with aortocaval compression (Poseiro effect) during uterine contractions in supine parturients is common in association with epidural anesthesia and is characterized by loss of the maternal toe pulse (Fig. 5), which is relieved by turning the parturient on her side.4r 7 Maternal toe pulses were re-
corded with a standard pulse monitor oscilloscope in more than 300 parturients, and the Poseiro effect is presumed to have occurred during the uterine contraction when the height of the toe pulse was reduced by one third. The Poseiro effect was present in 32 percent of all supine parturients in whom effective epidural anesthesia was obtained, but it occurred in only- 2 1 per cent of laboring women who did not receive this anesthetic. Consistent, abrupt, and brief fetal bradpcardia occurred in 56 per cent of all parturients showing the Poseiro effect. Turning the parturient to the lateral position (the rule on our service) relieved 86 per cent of’ the loss of toe pulse with uterine contractions and 91 per cent of the abrupt fetal bradycardias were similarly relieved. Terminal and expulsive bradycardia. All fetuses demonstrate spectacular “terminal” bradvcardias of
Volume Number
Fetal reacting bradycardia
129 8
849
Fig. 4. FHR recording of profound fetal bradycardia after only a vaginal examination. The parturient was placed in the knee-chest position because of suspected funis prolapse, which was not verified. Fresh meconium was later noted in the amniotic fluid. No more bradycardias occurred; the umbilical artery pH at birth was 7.13.
Fig. 5. FHR recording of a supine The maternal hallux pulse (big-toe the parturient “pushes.” varying expulsion.
durations This
(expulsion
after
abruptly time
of
delivery,
sparse
those
recorded
during
early
rupture
of
seven
neonates
corded 100 b.p.m. In 150
and
with
the
after
until the neonates vaginally delivered
in
had
delivery ventilated. newborn
no
delivery 140 b.p.m.
until
the
Of
had
rel-
section,
FHR’s
were
like
which
there
was
tern tion.
was
the
cord group.
heart were infants
In rates
less
all re-
received
were
who
20
either
drug,
than
130 b.p.m. depressed
until
not
after
intact
three
of each
had
atropine-like
neonates
nuchal
membranes,
mothers an
6). In seven
fetuses
other
A
infant
intact
generally
Doppler,
deliveries
membranes.
infant
rate (Fig.
the the
The
forewaters
immediately
of
with
newborn
newborn
remained
four
atively
delivery and after delivery
heart
or higher
rupture.
one
the
membranes
of membrane
in
the
time
as recorded
present
of vaginal continues
until
which
whose
bradycardia, time
time rate
to 160 b.p.m.
parturients the
at the heart
bradycardia)
ventilates, rises
low
parturient given an epidural anesthetic while in terminal labor. blood volume pulse) decreases with each uterine contraction as
fetal
either
This
group
to attain
at two minutes and apneic and
anesthetic
rates
less than
latter
failed
a general heart
110 b.p.m. had
heart
neonates
delivered the same
rates
gravid perineum
whose
premature
than
by
nonelective
“expulsive”
cesarean
heart
nontraumatic
rate
pat-
to ventilato deliver
conditions
and
no
occurred.
Terminal
than
under
Eight
of more
at rates of less than 110 b.p.m. prior In the other four cases, it was possible infants
or more
ventilated.
after birth were uniformly required resuscitation.
16 showed
bradycardias
or
immediately
bradycardias or
multigravid in relation infants
are
more
severe
in
primi-
women who have a tight to the neonates head size and in with
mobile
skulls.
Atropine
(0.4
850
Goodlin
and Haesslein
Fig. 6. Fetal and newborn heart rate tracing from a multigravida woman: labor, D is delivery, B is first breath, and H is heat applied to neonate.
2 refers
to second
stage of
Fig. 7. FHR and newborn heart rate tracing from a prim&avid woman. Terminal bradycardia continued until delivery of the neonate’s head when the nasopharynx was gently aspirated. Brief break of bradvcardia .occurred until the infant ventilated. Bradycardia occurred again \\ith esophageal &ion. mg.)
administered
prior
to
to
delivery
the
mother
completely
sive bradycardia
and
Terminal
minutes
were
tery
pH
the
or
if uterine
is
rolled
on
lateral
Sims
return creases FHR
also when
her
position,
or
then
but
A number
neonate posure when
the
seems
to
fetal
of
anesexpul-
the cervix is bearing the
of the
20 Ter-
does
The
mother
not
is in the
represent
a variety
head
compression
performed
on the
and fetuses
amounts
an infrared heater or to a stream
of time
were
taken
of
ar-tifacts fetus.
(Fig.
7).
of. movements
hypertension)
as well
time
of inter-
terminal
recordings
and contain
of both
it was determined relatively increased
tpisodc
systolic during
These
remained suggesting
(fetal
a br-ief’
fetal
the SLICC
to delivery
was
in 43 cases
because
However-.
time intervals bradycardia,
that
mother
the ejection
constant during the fetal cardiac aftetr as decreased
cardiac
performance. Nuchal 100
cord
newborn
deliver\ moderately
im-
than
the
the
upon gentle
prior
there
recorder,
in a dark-
in which
nasopharynx
bradycardias.
the
upon exof C12, or to clamp
many
load
necessarily
toe pulse inthe terminal
RSR
place effect
cases
to baseline
determined
expulsive and
to the shoulders,
the
were
took
no appreciable In two
returning
With
delivery
was
applied
infant’s
FHR
vals
is indovvn,
infant
was
the
ar-
severe.
maternal level. Thus,
tion
or when
there bradycardia.
of the
than cases.
cords, room,
neonates
after birth to see if their bradycardias could prior to the time of ventilation. When the
was warmed with to a cold environment varying
of nine
when
the FHR
of tests were
type
ened
umbilical
particularly
reduced
mechanisms, including Poseiro effect. mediately be relieved
out
is delivered
to baseline when to its precontraction pattern
longer
occur when the mother are
often side
umbilical
a tachycardia
a decreased
in five
contractions
bradycardia
lasting
with
lower)
minal bradycardias completely dilated, or
displays
bradycardias
(7.15
this
minutes
cent. At times general markedly alters this
neonate
associated
20
relieved
bradycardia in only 37 per thesia (especially ketamine) instead.
10 to
were
four
bradycardia. infants
with
The nuchal
FHK
recordings
cords
at the
analyzed. Sixty-two had severe (variable) bradycardias
occasions.
Twenty-four
showed
tachycardias with uterine contractions which changed to decelerations in late other
infants
bradyc,ardias per cent.
with
no
nuchal
occurred before The dut-ation of
cords, terminal terminal
of
time
of
abrupt on
and more
initial
FHR
in ear-Iv labor labor. Of 100 similar labor and
fetal
in only 38 espulsivc
Fetal
Volume 129 Number
reacting
bradycardia
851
8
Fig. 8. Simultaneous recordings of fetal heart rate (FHR), uterine tension (UT), fetal placenta ultrasound (PUS), and hallux pulse (HP) of two different supine parturients. On the left, the uterine (hallux) “pulse” decreases with contraction and bradycardia, while on the right, the funis (placental) pulse decreases with contraction and bradycardia. Both fetal bradycardias were diminished by turning the parturient to a lateral position. bradycardias was unrelated of a nuchal cord.
to the presence
or absence
Comparison of Poseiro effect with funis effect bradycardia Recordings of acute fetal bradycardia with simultaneous recordings of uterine tension, maternal toe pulse, and fetal placenta Doppler flow are presented in Fig. 8. While the fetal heart rate responses are similar, in one case FHR appears to be related to a decreased pulse height (Poseiro effect) and in the other to decreased placental flow (funis effect).
Fetal sheep studies Fig. 9 is from a long-term experiment in fetal sheep at 130 days’ gestation and two days after operation. Catheters had been placed in the amniotic fluid and fetal aorta (FNI ,4)-t) and “wedged” in the maternal uterine vein toward the myometrium (UT vrin) and in the umbilical vein toward the uterus (Urn ruin ulrdgpi. The umbilical flow was determined from a Clark electromagnetic flow transducer with pulsatile flow (Urn @ and mean umbilical flow (ihn 0) recorded. FHR is recorded in beats per minute, pressure in torrs, and flow in milliliters per minute. A spontaneous rise in maternal uterine vein wedge pressure occured which is assumed to represent a IocaIized uterine contraction as
no pressure rise was noted in the amniotic fluid. This “localized uterine contraction” is associated with fetal bradycardia and decreased umbilical flow. Fig. 10 is from the results of the same experiment obtained on the fourth postoperative day. On this occasion, a prolonged rise occurred in umbilical vein wedge pressure which was associated with fetal bradycardia. fetal hypertension, and decreased umbilical flow.
Comment The
heart rate of the fetus in utero obviously for many reasons, some due to changes of fetal arousal or levels of metabolites and some associated with movement or stress. This article is concerned only with those abrupt intrapartum fetal bradycardias which appear to be mediated by the vagus nerve and which are sometimes associated with stress, the mechanisms of which are at best only superficially understood. As Sureau’ has noted, there is often a lack of correlation with the occurrence of Hon’s definition of an umbilical cord compression FHR pattern and act.ual funis compression. Unfortunately, we have not clarified the problem. Even when the placental Doppler pulse9 diminished during a uterine contraction, we did not at the time of delivery find the funis consistently in a position of possible compression. A fatse positive “placental changes
Fig. 9. RCCOI dings from a long-term experiment in fetal sheep done in another laboratory strate a significant rise of maternal uterine vein wedge (CJl zvin) pressur-e assoc-iatcd bradycartlia without apparent rise of amniotic fluid pressure. See text for details.
pulse”
test
may
minished occurs Our cent
indicate
in all types more
often
own
analysis
of
fetuses
deceleration
than with
On
the with
other
by
an equally
which
in
turn
positive
60 per
cent
occasional
FHR
include termittent
many other recovery,
patterns
Based cord
increase
abrupt the of
and
rate
umbilical
and ef-
The flects
of the
presumably
and
severe
baroreflex. umbilical
funis occurs
since 40 per obstructed;
cent this
cord
in
of the is fol-
hypertension However,
the
compression
responses such as tachycardia. inand marked increases in beat-toon in both
previous exteriorized
studies
of’ prolapse sheep
tetuses
and
can
such
major
return
compression inf’ants noted
were of all types the area of FHR nate’s
condition
occlusion in observed
degree
of decrease
in
the
variability ac tivitv
two
in
studies.
probabl! fetal
and
found
celerations
with
have
FHR
(early. late, deceleration the
that
recat-
previously
and also correlated
had
‘I‘ipton
either
of and
patterns
of
I’ipton
and
fetal bradycardia O’Gureck and
SO per
assumed
depressed
vari&le). Onlv with the neo-
the incidence than
subject
in
cords,
experience
when
the
deceleration
onset of the By contrast.
fetuses
for
nuchal
prior
in
f)n
patterns.
tight
that
was greater
all of the
of opinion
FHR
and not the contraction).
leagues”’
a severe
cord
levels.’ is no uniformity
Chang. uterine
described
dif’ferent-es
achieved
tachycar-
compression.“’
venous
to the
increase in heat-to-hear the excessive vagal
newborn Chang”
N’c
these
venous
have
with
be related
the early
vein
Paul, ” however,
Perhaps
echolamine
tions, cord.
that
umbilical
associated
rates
There
of‘ the
suggested
partial
bradycardia heart
“cord-
complete
it has been
reflects
in sheep.
FHK
is supine (the Poseiro
even
acute
resistance, has been
initiates
clinical
umbilical
Reynolds 63 per
of possible
false
man,
I.
the mechanisms
with
A marked
lowed
of the
about
have
to understand
peripheral vascular fetal cardiac output
variability.
this
and dia
funis-type
parturient obtained
only
cords
bradycardia
compression.
beat
if the has been
be di-
probably
about
in a position
below,
hand,
by Fig. in only
severe
found
can
and
funis
like” bradycardias. It appears easy vagal-type
that
a typical
nuchal
flow
is suggested
As discussed
is increased markedly epidurat anesthesia fetuses
umbilical bradycardia
suggests
is the cord
compression.
fect).
that
of vagat
demonwith fetal
of variable cent
with
a short that
“head
(to colde-
contrar-
or a nuchal compres-
Volume Number
129 8
represents Cushing’s sion” type of fetal bradycardia i.e., increased intracranial pressure acPh enomenon. companied by systemic hypertension. However, work in adult animals has shown that the elicitation of a bradvcardia response to increased intracranial pressure requires the integrity of the connections between the brain stem and the spinal cord. Furthermore, the response is not completely blocked by atrapine or by P adrenergic agents, but it is abolished by cy adrenergic agents. Unlike clinical “head compression” bradycardia. the vagal reflex is not a critical factor in the bradycardia of Cushing’s phenomenon.‘” The mechanism is further confused for in long-term experiments in fetal sheep. fetal head compression elicited a severe acute bradycardia zojlh~z~t a preceding fetal hypertension or the baroreflex. Such fetal bradycardias are prevented and abolished by atropine. Determinations of human fetal systolic time interval during terminal bradycardia usually demonstrate unchanging ejection times, an observation which strongly suggests an associated hypertensiom2 Since head compression is considered an important component of rerminal bradycardias, it may be that there are at least two types of “head compression bradycardia,” one with and one without fetal hypertension. It is the Poseiro effect which appears to be common” and is perhaps the most baffling to understand. These bradycardias are correlated directly with uterine contractions which implies a pressure relationship, but instead the effect is apparently one of reduced uterine blood flow. Further confusion occurs since uterine blood flolv is reduced during all uterine contractions,‘” and yet most uterine contractions are not associated with fetal bradycardia. Both Berman and associates,‘6 lvho did a long-term experiment in fetal sheep, and Kiinzel and co-workers,” in a short-term experiment. have noted a fetal vagal type of bradycardia following reduction of uterine blood flow achieved by occlusion of the maternal vena cava. However, both groups described a significant latent interval between the decline of uterine blood flow and the occurrence of fetal bradycardia and both attributed this to time required for development of fetal hypoxia. Walker and associates” likewise found in the human fetus a significant lag time for low-tension maternal oxygen to be expressed. The apparent association between the Poseiro effect and rupture of the membranes, occiput-posterior positions, intensity of uterine contractions, maternal hypotension, and epidural anesthesia suggests that there may be a common denominator of all vagal fetal bradycardias which could be reduced uterine blood flolv. Before the sluice theory was disproved,16 it offered pressure concepts which could explain the im-
Fetal
reacting
bradycardia
853
Fig. 10. Same fetal experiment as in Fig. 9, two days later there was a spontaneous rise of umbilical wedge pressure associated with fetal hypertension and bradycardia. See text for details.
mediate onset of fetal bradycardia with the beginning of the Poseiro effect. ” Until more data become available, it appears prudent to observe that through unknown mechanisms an acute decrease in uterine blood flow is able to evoke an equally acute fetal bradycardia?O Bustos and colleagues21 like many other investigators, have described the neonate as having a tachycardia immediately post partum. Others have noted bradycardia in neonates but have ascribed it to clamping of the umbilical cord.ZZ As we have observed, Zilianti and colleaguesz3 reported that the bradycardia in newborn infants was relieved by the infant’s first respiratory movement. These South American observers ascribed the expulsion bradycardia to the reduction in placental vascular bed and subsequent increase in umbilical vascular resistance and hypertension. Our systolic time interval measurements likewise suggest fetal hypertension at this time. Zilanti and co-workers found, as we did, that cord clamping made no difference in the bradycardia, which it should aggravate if hypertension were the etiology. In addition, we found no less expulsive bradycardias in fetuses whose mothers had atonic uteri. Independent fetal vagal activity (grunting) may be the source of unexplained increases in fetal peripheral resistance, hypertension, and bradycardia. Its occur-
854
Goodlin
and Haesslein
rence is fairly well documented in fetal sheep,24 but the same is not true for human fetuses. Certainly a human infant’s grunting as part of the Valsalva maneuver has an associated profound bradycardia.25 We suggest that these cases of fetal bradycardia followed by fresh meconium staining described herein represent similar fetal events in utero. Such fetal grunting may be deleterious because of the associated decreased cardiac outpUt.2 Fetal bradycardias associated with maternal seizures (those related either to epidural drugs or to eclampsia) begin with the onset of the maternal convulsion and often last much longer. The absence of anesthetic drugs in the fetal blood, a latent period, or fetal acidemia would suggest that the rise in intrauterine evokes the fetal bradycardia. Why the pressure bradycardia has such a delayed recovery is unknown. A similar fetal bradycardia pattern occurs with maternal vomiting, but in our experience, it is not associated with such a prolonged delayed recovery as that which occurs with maternal seizures. We have no explanation for the voiding bradycardia except to note that it occurs repeatedly with some fetuses and not at all with others and that it is not necessarily associated with fetal acidemia. It seemingly occurs with or without a rising intrauterine pressure and with or without the Poseiro effect. Manipulation of the fetal vertex can evoke either fetal tachycardia or bradycardia. We previously described the different fetal responses to the various fetal arousal levels.26 Others have suggested that minimal fetal manipulation could result in increased uterine tension.27 The recordings (Figs. 9 and 10) of the sheep fetus suggest that local areas of uterine tension insufficient to elevate amniotic fluid pressure can be associated with fetal bradycardia perhaps secondary to fetal hypertension. Whether such cardiovascular relationships occur in human fetuses is unknown, but similar episodes of unexplained (without apparent contractions) bradycardia do occur. Laboratory recordings of sheep during uterine contractions often suggest a greater rise in fetal blood pressure than amniotic fluid pressure. The clinical implications of the fetal sheep studies are that fetal hypertension responses related to increased umbilical vascular resistance and the baroreflex may explain many of the so-called “head compression” or “independent” fetal bradycardias.
REFERENCES
1. Schwartz, R. L., Althabe, O., Belitzky, R., et al.: Fetal heart rate patterns in labor with intact and with ruptured membranes, J. Perinat. Med. 1: 153. 1973.
December Am. J, Obstet.
13, 1977 Gynecol.
This article has been an anecdotal account c)f man! different apparent etiologies of fetal bradycardias. The common theme has been that the information at hand is insufficient to explain their occurrences. It is doubtful that any acute fetal bradycardia is ever “physiologic” in the sense that it is completely innocuous. Furthermore, it serves no useful purpose to label fetal bradycardias according to their theoretical mechanisms. Others disagree, believing that certain FHR patterns are diagnostic of umbilical cord c.omprt&m, and recommend immediate cesarean section C’VCII I\ hen failing to find the prolapsed umbilical cord.*s Still others suggest that head compression is the basis of nearly all fetal bradycardias and that the amniotic membrane should be protected.’ We have- suggested that the maternal supine position always bc avoided.’ Given this relative lack of knowledge and disagreement over etiology, it is proposed that all abrupt fetal bradycardias simply be referred to as “vagal bradycat-dias” and that they be described and treated according to their severity. Prolapse of the funis and t&al asphyxia should always be ruled out, but other-u&t, the bradycardia treatment should be considered tier its own possible detrimental effects upon the irtus. Rudolph 2g has demonstrated that fetal cardiac output in fetal sheep is often dependent on heart rate. Our own systolic interval measurements in human fetuses also suggest that ejection times do not uni. formly increase during fetal hradycardia. indicating that the fetuses’cardiac outputs decrease during severe and prolonged vagal bradycardia. Under rhcst, [I, :r, .,t iI pl o found deceleration or bradccardia after ~lci ~~litl~ TO 1 f feet an immediate delivw z 1 would like to ask the authors: (1) if Tltc,t.c- \v;L\ LC.;Lson to depart from the act-eptcd defimtiow 3)f Ffl K decelerations and FHR brad){-archas. (2) if rhc, \hapc, c J the deceleration or brad)carclias lvas ~orrc-Ltrctl WI rh rlinical outcome, and (3) if the use of to111 tliffcrctll types of FHR monitors might have affected Ihc. rc,sulrs? DR. G~ODLIN (Closing). I do not have an! ,irgumcnl with \\,hat Dr. Queenan has said. for it is the standard American vie!+. My basic concern is that v hen we use the (crm “ter,tl heart rate deceleration” \\e immediately thinh of either head or cord compression. And \ce do arg\zv i11 this articlc that there are many other events that c\ ol\v Iltl same sort of response on the part of the fetus; thwcfore, I think the term “fetal heart rate decclewtion” is no longer an appropriate term. As far as the use of the atropine is concerned. this argument has been going on for years. Basicall\, I contend that fetal bradycardia is never of benefit to rhc fetus: that if one makes ccl-tain that there is no umbilical cord prolapse or no fetal acidemia and that if the bradycardia or. if you vcish, severe deceleration COILtinues and if the fetus is not to be delivered immediately, it is appropriate to use atropine. I believe the risks of a markedly reduced fetal cardiac output are thus avoided.
C. GOODLIN,
HANNS
C.
HAESSLEIN,
Snrmmrnto,
California
M.D. M.D.
Acute and abrupt fetal bradycardias are considered to be vagal in origin. In addition to head compression and funis compression bradycardias, we will report on those acute fetal bradycardias occurring during maternal seizures and maternal voiding, during aortocaval compression, during terminal labor, and during the immediate postpartum period. While certain mechanisms are known which can explain some or parts of these bradycardias, we conclude that in the clinical setting information is insufficient to determine their etiology with precision. Instead of labeling abrupt fetal heart rate pattern as resulting from either head or funis compression, it is suggested that the patterns be described according to their severity and duration. Such acute fetal bradycardias can be detrimental in terms of reduced umbilical flow. Administration of atropine may be indicated in the otherwise healthy fetus with acute bradycardia. (AM. J. OBSTET. GYNECOL. 129: 845, 1977.)
&’ E c ON SI DE R acute reacting fetal bradycardias to be evoked by two different mechanisms. The most common is usually innocuous and vagal in origin while the rare mechanisms reflect cardiovascular dysfunction and are worrisome (Fig. 1). The subject of this article is the vagal fetal bradycardias that are characterized by abrupt beginnings and endings. According to current concepts, vagal bradycardias have only two different etiologies-fetal head compression or funis compression.‘. ’ The latter initially produces a vagal type of bradycardia, which may change to the cardiovascular dysfunctional type if the funis compression is not relieved. In the laboratory, it is possible to demonstrate that many acute fetal responses can lead to vagal activity such as fetal seizures, fetal grunting, or any condition (e.g., hypoxia) giving rise to abrupt rises in fetal vascular resistance and the baroreflex.’ In this report, selected types of fetal heart rate (FHR) responses (from approximately 3,000 deliveries) are analyzed using supplemental information obtained by recordings of fetal scalp pH, systolic time intervals, and maternal blood volume pulse.* Two recordings from a long-term experiment in fetal sheep done in another laboratory are also presented. These data, to
be reported, suggest that fetal vagal bradycardias often have multiple and complex etiologies and that the simplistic view of considering them to be the result of either funis or head compression is inaccurate. We also suggest an alternate interpretation of such FHR patterns and recommend the prophylactic use of atropine. Methods The FHR recordings were obtained with a variety of commercial FHR monitors, including Corometrics. Hewlett-Packard, and Berkeley as well as the Beckman Research Unit and the Berkeley RSR (systolic time) recorders.3 Systolic time intervals were determined with simultaneous recordings of fetal electrocardiograms, Doppler or microphone heart sounds, and Doppler placental pulse. The maternal pulse (photoelectric plethysmographic pulse or blood volume pulse) was obtained with a Beckman pulse monitor.“ Unless otherwise noted, the parturients labored in the lateral recumbent position and were delivered of their infants in the dorsal lithotomy position. One hundred fifty newborn infants were studied immediately after vaginal delivery using a combination of a spiral scalp electrode and a second needle electrode applied to either the extremity or funis of the neonate. During the 15 nonelective deliveries by cesarean section, a spiral scalp electrode was used until the fetal head was disengaged from the pelvis. A Doppler transducer was then applied as soon as possible to the neonate’s chest. Initially, the umbilical cord was clamped in a random fashion before or after the neonate’s first breath, but so many made early breathing efforts that a randomized
From the Department of Obstetrics and Gynecolo~, University of California, Davis, Sacramento Me&al Center. Presented .4mericnn .4prili3-16,
at the One Hundredth Annual Meeting Gyrlecological Society, Litchfield Park, 1977.
of the
.4rizona,
R&int requests: Dr. Robert C. Goodlin, Department of Obstetrics &d Gynecology, University of California, lh~ic. Sacramento Medical Center, 2315 Stockton Blvd.. Sacramento, California 95817.
845
846
Goodlin and Haesslein
Ikcetnher Am. J. Obster.
iFi!?!* piq Uterine
I
Drugs ~sedatives, PC02 levels Vasomotor Tone
Contraction
normal or increased
Worrisome if repetitive
opiates)
1 catecholamine
Benign if not severe
Fig. I. Proposed mechanism of reacting FHR patterns, head compression produce vagal bradycardia directly or after fetal hypertension? Any vagal asphyxia involves both right and left sides of the chart. A-C = Aortocaval.
Table
15. I!477 (Gynecol.
or mild bradycardia
hypoxia can leading to
I Event
Maternal seizure Maternal voiding Independent Poseiro effect (aortocaval compression) Terminal Expulsion Nuchal cord Uterine contraction (fetal sheep)
No. of cases 5 12 A: 150 150 100 1
Fig. No.
Characteristics
2 3 4 5, 8 6, 7 697 8 9, 10
Prolonged, neonate in good condition Inconsistent, prolonged, neonate in good condition Prolonged, after meconium staining, fetal acidemia Brief, related to maternal supine condition and uterine contraction Probably represents both head compression and Poseiro effect Relieved only by ventilation 62% correlation with typical FHR pattern “Bradycardia with localized uterine contraction”
study could not be completed. Differences in 2Y neonates delivered in cold and warm environments were studied. Twelve were delivered into an immediate environment of 40” to 41” C. controlled by an infrared heater and 17 were studied when the defivery room temperature fell below 18” C. The long-term experiment in fetal sheep followed that previously described by Berman and associates.5 In addition to catheters in the amniotic space, fetal aorta, and umbilical vein and a Clark electromagnetic flow transducer around the common umbilical artery, a catheter was also “wedged” in an umbilical vein toward
the cotyledon metrium.
and in a maternal
vein toward
the endo-
Results Unless otherwise noted, all of the neonates described had cord artery pH values that were higher than 7.20. We observed fetal bradycardia in many situations. apparently related to many different causes. Descriptions of some of these (Table I) follow. Maternal
seizure
bradycardia.
We
have
recorded
FHR during five maternal seizures (three were induced by epidural drugs and two were due to eclampsia) and
Volume Number
129 R
Fetal reacting bradycardia
Fig. 2. A 16-year-old mother with severe edema-proteinuria-hypertension
gestosis who had a seizure
despite a serum magnesium level of 4.9 mg. per 100 ml. The patient was given diazepam atropine (0.4 mg.), and additional MagSO, (4.0 Gm.) intravenously. An infant with Apgar and 9 was delivered with low forceps 25 minutes after seizure.
noted that the fetal bradycardia began simultaneously with the start of the maternal convulsion (Fig. 2). The fetal bradycardia often continued into the postictal state but was at least partially relieved by atropine. In two newborn infants delivered within 15 minutes of the maternal drug seizure, the umbilical artery pH was higher rhan 7.25 and in neither case could the anesthetic agent be found in the umbilical blood. Maternal voiding bradycardia. Twelve FHR recordings which demonstrated profound fetal bradycardias during maternal voiding were studied. Neither did measurements of intravesicle pressure correlate with the FHR changes nor did the fetuses demonstrate acidemia. In seven cases, the parturients had just been turned to the supine position. There was an increase in uterine tension in five (as recorded with the external tocograph) and a decrease in four. Eight women were restudied during a second voiding and only five of the eight demonstrated a similar episode of fetal bradycardia. Membranes had been ruptured in nine and in only
847
(5.0 mg.). scol-es of 7
two were the vertices not engaged. In other words, voiding fetal bradycardia could not be absolutely correlated with rupture of membranes, station of the fetal head, rise in intrauterine tension, or intravesicle pressure; also, it was not always reproducible. Fig. 3 is a FHR recording of a parturient who voided three times during a seven-hour labor. During the first voiding, there was a minimal rise in uterine tension with an associated fetal bradycardia. The parturient was given 16 mg. of morphine sulfate, and during a similar voiding episode that occurred two hours after the first, the fetal bradycardia did not recur although there was a similar rise in uterine tension. However, during maternal voiding two and one half hours after the second episode, a severe fetal bradycardia occurred this last bradycardia, there was no again. During significant change in maternal toe pulse height. Independent fetaI bradycardia. Fetal vagal bradycardia independent of uterine contraction is fre-. quently assumed to reflect “grunting” and the fetal
848
Goodlin
and Haesslein
December Am. J. Obscet.
15. 1977 (hvxol.
Fig. 3. FHR recording of a parturient voiding (between arrows) on three different occasions. There was a slight rise in uterine tension when the parturient was placed on a bedpan. See text for details. Valsalva maneuver, which presumably includes the passage of meconium. 2,6 There were cases in which the fetal bradycardia was followed shortly by fresh meconium observed within the amniotic fluid. This type of fetal bradycardia (Fig. 4) is also relieved by atropine, and in two of the four cases in which scalp pH was monitored, there were values of less than 7.15. The subsequently delivered newborn infants appeared to have marked vagal activity with accompanying frequent bradycardias. Poseiro effect bradycardia. Intrapartum fetal bradycardia associated with aortocaval compression (Poseiro effect) during uterine contractions in supine parturients is common in association with epidural anesthesia and is characterized by loss of the maternal toe pulse (Fig. 5), which is relieved by turning the parturient on her side.4r 7 Maternal toe pulses were re-
corded with a standard pulse monitor oscilloscope in more than 300 parturients, and the Poseiro effect is presumed to have occurred during the uterine contraction when the height of the toe pulse was reduced by one third. The Poseiro effect was present in 32 percent of all supine parturients in whom effective epidural anesthesia was obtained, but it occurred in only- 2 1 per cent of laboring women who did not receive this anesthetic. Consistent, abrupt, and brief fetal bradpcardia occurred in 56 per cent of all parturients showing the Poseiro effect. Turning the parturient to the lateral position (the rule on our service) relieved 86 per cent of’ the loss of toe pulse with uterine contractions and 91 per cent of the abrupt fetal bradycardias were similarly relieved. Terminal and expulsive bradycardia. All fetuses demonstrate spectacular “terminal” bradvcardias of
Volume Number
Fetal reacting bradycardia
129 8
849
Fig. 4. FHR recording of profound fetal bradycardia after only a vaginal examination. The parturient was placed in the knee-chest position because of suspected funis prolapse, which was not verified. Fresh meconium was later noted in the amniotic fluid. No more bradycardias occurred; the umbilical artery pH at birth was 7.13.
Fig. 5. FHR recording of a supine The maternal hallux pulse (big-toe the parturient “pushes.” varying expulsion.
durations This
(expulsion
after
abruptly time
of
delivery,
sparse
those
recorded
during
early
rupture
of
seven
neonates
corded 100 b.p.m. In 150
and
with
the
after
until the neonates vaginally delivered
in
had
delivery ventilated. newborn
no
delivery 140 b.p.m.
until
the
Of
had
rel-
section,
FHR’s
were
like
which
there
was
tern tion.
was
the
cord group.
heart were infants
In rates
less
all re-
received
were
who
20
either
drug,
than
130 b.p.m. depressed
until
not
after
intact
three
of each
had
atropine-like
neonates
nuchal
membranes,
mothers an
6). In seven
fetuses
other
A
infant
intact
generally
Doppler,
deliveries
membranes.
infant
rate (Fig.
the the
The
forewaters
immediately
of
with
newborn
newborn
remained
four
atively
delivery and after delivery
heart
or higher
rupture.
one
the
membranes
of membrane
in
the
time
as recorded
present
of vaginal continues
until
which
whose
bradycardia, time
time rate
to 160 b.p.m.
parturients the
at the heart
bradycardia)
ventilates, rises
low
parturient given an epidural anesthetic while in terminal labor. blood volume pulse) decreases with each uterine contraction as
fetal
either
This
group
to attain
at two minutes and apneic and
anesthetic
rates
less than
latter
failed
a general heart
110 b.p.m. had
heart
neonates
delivered the same
rates
gravid perineum
whose
premature
than
by
nonelective
“expulsive”
cesarean
heart
nontraumatic
rate
pat-
to ventilato deliver
conditions
and
no
occurred.
Terminal
than
under
Eight
of more
at rates of less than 110 b.p.m. prior In the other four cases, it was possible infants
or more
ventilated.
after birth were uniformly required resuscitation.
16 showed
bradycardias
or
immediately
bradycardias or
multigravid in relation infants
are
more
severe
in
primi-
women who have a tight to the neonates head size and in with
mobile
skulls.
Atropine
(0.4
850
Goodlin
and Haesslein
Fig. 6. Fetal and newborn heart rate tracing from a multigravida woman: labor, D is delivery, B is first breath, and H is heat applied to neonate.
2 refers
to second
stage of
Fig. 7. FHR and newborn heart rate tracing from a prim&avid woman. Terminal bradycardia continued until delivery of the neonate’s head when the nasopharynx was gently aspirated. Brief break of bradvcardia .occurred until the infant ventilated. Bradycardia occurred again \\ith esophageal &ion. mg.)
administered
prior
to
to
delivery
the
mother
completely
sive bradycardia
and
Terminal
minutes
were
tery
pH
the
or
if uterine
is
rolled
on
lateral
Sims
return creases FHR
also when
her
position,
or
then
but
A number
neonate posure when
the
seems
to
fetal
of
anesexpul-
the cervix is bearing the
of the
20 Ter-
does
The
mother
not
is in the
represent
a variety
head
compression
performed
on the
and fetuses
amounts
an infrared heater or to a stream
of time
were
taken
of
ar-tifacts fetus.
(Fig.
7).
of. movements
hypertension)
as well
time
of inter-
terminal
recordings
and contain
of both
it was determined relatively increased
tpisodc
systolic during
These
remained suggesting
(fetal
a br-ief’
fetal
the SLICC
to delivery
was
in 43 cases
because
However-.
time intervals bradycardia,
that
mother
the ejection
constant during the fetal cardiac aftetr as decreased
cardiac
performance. Nuchal 100
cord
newborn
deliver\ moderately
im-
than
the
the
upon gentle
prior
there
recorder,
in a dark-
in which
nasopharynx
bradycardias.
the
upon exof C12, or to clamp
many
load
necessarily
toe pulse inthe terminal
RSR
place effect
cases
to baseline
determined
expulsive and
to the shoulders,
the
were
took
no appreciable In two
returning
With
delivery
was
applied
infant’s
FHR
vals
is indovvn,
infant
was
the
ar-
severe.
maternal level. Thus,
tion
or when
there bradycardia.
of the
than cases.
cords, room,
neonates
after birth to see if their bradycardias could prior to the time of ventilation. When the
was warmed with to a cold environment varying
of nine
when
the FHR
of tests were
type
ened
umbilical
particularly
reduced
mechanisms, including Poseiro effect. mediately be relieved
out
is delivered
to baseline when to its precontraction pattern
longer
occur when the mother are
often side
umbilical
a tachycardia
a decreased
in five
contractions
bradycardia
lasting
with
lower)
minal bradycardias completely dilated, or
displays
bradycardias
(7.15
this
minutes
cent. At times general markedly alters this
neonate
associated
20
relieved
bradycardia in only 37 per thesia (especially ketamine) instead.
10 to
were
four
bradycardia. infants
with
The nuchal
FHK
recordings
cords
at the
analyzed. Sixty-two had severe (variable) bradycardias
occasions.
Twenty-four
showed
tachycardias with uterine contractions which changed to decelerations in late other
infants
bradyc,ardias per cent.
with
no
nuchal
occurred before The dut-ation of
cords, terminal terminal
of
time
of
abrupt on
and more
initial
FHR
in ear-Iv labor labor. Of 100 similar labor and
fetal
in only 38 espulsivc
Fetal
Volume 129 Number
reacting
bradycardia
851
8
Fig. 8. Simultaneous recordings of fetal heart rate (FHR), uterine tension (UT), fetal placenta ultrasound (PUS), and hallux pulse (HP) of two different supine parturients. On the left, the uterine (hallux) “pulse” decreases with contraction and bradycardia, while on the right, the funis (placental) pulse decreases with contraction and bradycardia. Both fetal bradycardias were diminished by turning the parturient to a lateral position. bradycardias was unrelated of a nuchal cord.
to the presence
or absence
Comparison of Poseiro effect with funis effect bradycardia Recordings of acute fetal bradycardia with simultaneous recordings of uterine tension, maternal toe pulse, and fetal placenta Doppler flow are presented in Fig. 8. While the fetal heart rate responses are similar, in one case FHR appears to be related to a decreased pulse height (Poseiro effect) and in the other to decreased placental flow (funis effect).
Fetal sheep studies Fig. 9 is from a long-term experiment in fetal sheep at 130 days’ gestation and two days after operation. Catheters had been placed in the amniotic fluid and fetal aorta (FNI ,4)-t) and “wedged” in the maternal uterine vein toward the myometrium (UT vrin) and in the umbilical vein toward the uterus (Urn ruin ulrdgpi. The umbilical flow was determined from a Clark electromagnetic flow transducer with pulsatile flow (Urn @ and mean umbilical flow (ihn 0) recorded. FHR is recorded in beats per minute, pressure in torrs, and flow in milliliters per minute. A spontaneous rise in maternal uterine vein wedge pressure occured which is assumed to represent a IocaIized uterine contraction as
no pressure rise was noted in the amniotic fluid. This “localized uterine contraction” is associated with fetal bradycardia and decreased umbilical flow. Fig. 10 is from the results of the same experiment obtained on the fourth postoperative day. On this occasion, a prolonged rise occurred in umbilical vein wedge pressure which was associated with fetal bradycardia. fetal hypertension, and decreased umbilical flow.
Comment The
heart rate of the fetus in utero obviously for many reasons, some due to changes of fetal arousal or levels of metabolites and some associated with movement or stress. This article is concerned only with those abrupt intrapartum fetal bradycardias which appear to be mediated by the vagus nerve and which are sometimes associated with stress, the mechanisms of which are at best only superficially understood. As Sureau’ has noted, there is often a lack of correlation with the occurrence of Hon’s definition of an umbilical cord compression FHR pattern and act.ual funis compression. Unfortunately, we have not clarified the problem. Even when the placental Doppler pulse9 diminished during a uterine contraction, we did not at the time of delivery find the funis consistently in a position of possible compression. A fatse positive “placental changes
Fig. 9. RCCOI dings from a long-term experiment in fetal sheep done in another laboratory strate a significant rise of maternal uterine vein wedge (CJl zvin) pressur-e assoc-iatcd bradycartlia without apparent rise of amniotic fluid pressure. See text for details.
pulse”
test
may
minished occurs Our cent
indicate
in all types more
often
own
analysis
of
fetuses
deceleration
than with
On
the with
other
by
an equally
which
in
turn
positive
60 per
cent
occasional
FHR
include termittent
many other recovery,
patterns
Based cord
increase
abrupt the of
and
rate
umbilical
and ef-
The flects
of the
presumably
and
severe
baroreflex. umbilical
funis occurs
since 40 per obstructed;
cent this
cord
in
of the is fol-
hypertension However,
the
compression
responses such as tachycardia. inand marked increases in beat-toon in both
previous exteriorized
studies
of’ prolapse sheep
tetuses
and
can
such
major
return
compression inf’ants noted
were of all types the area of FHR nate’s
condition
occlusion in observed
degree
of decrease
in
the
variability ac tivitv
two
in
studies.
probabl! fetal
and
found
celerations
with
have
FHR
(early. late, deceleration the
that
recat-
previously
and also correlated
had
‘I‘ipton
either
of and
patterns
of
I’ipton
and
fetal bradycardia O’Gureck and
SO per
assumed
depressed
vari&le). Onlv with the neo-
the incidence than
subject
in
cords,
experience
when
the
deceleration
onset of the By contrast.
fetuses
for
nuchal
prior
in
f)n
patterns.
tight
that
was greater
all of the
of opinion
FHR
and not the contraction).
leagues”’
a severe
cord
levels.’ is no uniformity
Chang. uterine
described
dif’ferent-es
achieved
tachycar-
compression.“’
venous
to the
increase in heat-to-hear the excessive vagal
newborn Chang”
N’c
these
venous
have
with
be related
the early
vein
Paul, ” however,
Perhaps
echolamine
tions, cord.
that
umbilical
associated
rates
There
of‘ the
suggested
partial
bradycardia heart
“cord-
complete
it has been
reflects
in sheep.
FHK
is supine (the Poseiro
even
acute
resistance, has been
initiates
clinical
umbilical
Reynolds 63 per
of possible
false
man,
I.
the mechanisms
with
A marked
lowed
of the
about
have
to understand
peripheral vascular fetal cardiac output
variability.
this
and dia
funis-type
parturient obtained
only
cords
bradycardia
compression.
beat
if the has been
be di-
probably
about
in a position
below,
hand,
by Fig. in only
severe
found
can
and
funis
like” bradycardias. It appears easy vagal-type
that
a typical
nuchal
flow
is suggested
As discussed
is increased markedly epidurat anesthesia fetuses
umbilical bradycardia
suggests
is the cord
compression.
fect).
that
of vagat
demonwith fetal
of variable cent
with
a short that
“head
(to colde-
contrar-
or a nuchal compres-
Volume Number
129 8
represents Cushing’s sion” type of fetal bradycardia i.e., increased intracranial pressure acPh enomenon. companied by systemic hypertension. However, work in adult animals has shown that the elicitation of a bradvcardia response to increased intracranial pressure requires the integrity of the connections between the brain stem and the spinal cord. Furthermore, the response is not completely blocked by atrapine or by P adrenergic agents, but it is abolished by cy adrenergic agents. Unlike clinical “head compression” bradycardia. the vagal reflex is not a critical factor in the bradycardia of Cushing’s phenomenon.‘” The mechanism is further confused for in long-term experiments in fetal sheep. fetal head compression elicited a severe acute bradycardia zojlh~z~t a preceding fetal hypertension or the baroreflex. Such fetal bradycardias are prevented and abolished by atropine. Determinations of human fetal systolic time interval during terminal bradycardia usually demonstrate unchanging ejection times, an observation which strongly suggests an associated hypertensiom2 Since head compression is considered an important component of rerminal bradycardias, it may be that there are at least two types of “head compression bradycardia,” one with and one without fetal hypertension. It is the Poseiro effect which appears to be common” and is perhaps the most baffling to understand. These bradycardias are correlated directly with uterine contractions which implies a pressure relationship, but instead the effect is apparently one of reduced uterine blood flow. Further confusion occurs since uterine blood flolv is reduced during all uterine contractions,‘” and yet most uterine contractions are not associated with fetal bradycardia. Both Berman and associates,‘6 lvho did a long-term experiment in fetal sheep, and Kiinzel and co-workers,” in a short-term experiment. have noted a fetal vagal type of bradycardia following reduction of uterine blood flow achieved by occlusion of the maternal vena cava. However, both groups described a significant latent interval between the decline of uterine blood flow and the occurrence of fetal bradycardia and both attributed this to time required for development of fetal hypoxia. Walker and associates” likewise found in the human fetus a significant lag time for low-tension maternal oxygen to be expressed. The apparent association between the Poseiro effect and rupture of the membranes, occiput-posterior positions, intensity of uterine contractions, maternal hypotension, and epidural anesthesia suggests that there may be a common denominator of all vagal fetal bradycardias which could be reduced uterine blood flolv. Before the sluice theory was disproved,16 it offered pressure concepts which could explain the im-
Fetal
reacting
bradycardia
853
Fig. 10. Same fetal experiment as in Fig. 9, two days later there was a spontaneous rise of umbilical wedge pressure associated with fetal hypertension and bradycardia. See text for details.
mediate onset of fetal bradycardia with the beginning of the Poseiro effect. ” Until more data become available, it appears prudent to observe that through unknown mechanisms an acute decrease in uterine blood flow is able to evoke an equally acute fetal bradycardia?O Bustos and colleagues21 like many other investigators, have described the neonate as having a tachycardia immediately post partum. Others have noted bradycardia in neonates but have ascribed it to clamping of the umbilical cord.ZZ As we have observed, Zilianti and colleaguesz3 reported that the bradycardia in newborn infants was relieved by the infant’s first respiratory movement. These South American observers ascribed the expulsion bradycardia to the reduction in placental vascular bed and subsequent increase in umbilical vascular resistance and hypertension. Our systolic time interval measurements likewise suggest fetal hypertension at this time. Zilanti and co-workers found, as we did, that cord clamping made no difference in the bradycardia, which it should aggravate if hypertension were the etiology. In addition, we found no less expulsive bradycardias in fetuses whose mothers had atonic uteri. Independent fetal vagal activity (grunting) may be the source of unexplained increases in fetal peripheral resistance, hypertension, and bradycardia. Its occur-
854
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and Haesslein
rence is fairly well documented in fetal sheep,24 but the same is not true for human fetuses. Certainly a human infant’s grunting as part of the Valsalva maneuver has an associated profound bradycardia.25 We suggest that these cases of fetal bradycardia followed by fresh meconium staining described herein represent similar fetal events in utero. Such fetal grunting may be deleterious because of the associated decreased cardiac outpUt.2 Fetal bradycardias associated with maternal seizures (those related either to epidural drugs or to eclampsia) begin with the onset of the maternal convulsion and often last much longer. The absence of anesthetic drugs in the fetal blood, a latent period, or fetal acidemia would suggest that the rise in intrauterine evokes the fetal bradycardia. Why the pressure bradycardia has such a delayed recovery is unknown. A similar fetal bradycardia pattern occurs with maternal vomiting, but in our experience, it is not associated with such a prolonged delayed recovery as that which occurs with maternal seizures. We have no explanation for the voiding bradycardia except to note that it occurs repeatedly with some fetuses and not at all with others and that it is not necessarily associated with fetal acidemia. It seemingly occurs with or without a rising intrauterine pressure and with or without the Poseiro effect. Manipulation of the fetal vertex can evoke either fetal tachycardia or bradycardia. We previously described the different fetal responses to the various fetal arousal levels.26 Others have suggested that minimal fetal manipulation could result in increased uterine tension.27 The recordings (Figs. 9 and 10) of the sheep fetus suggest that local areas of uterine tension insufficient to elevate amniotic fluid pressure can be associated with fetal bradycardia perhaps secondary to fetal hypertension. Whether such cardiovascular relationships occur in human fetuses is unknown, but similar episodes of unexplained (without apparent contractions) bradycardia do occur. Laboratory recordings of sheep during uterine contractions often suggest a greater rise in fetal blood pressure than amniotic fluid pressure. The clinical implications of the fetal sheep studies are that fetal hypertension responses related to increased umbilical vascular resistance and the baroreflex may explain many of the so-called “head compression” or “independent” fetal bradycardias.
REFERENCES
1. Schwartz, R. L., Althabe, O., Belitzky, R., et al.: Fetal heart rate patterns in labor with intact and with ruptured membranes, J. Perinat. Med. 1: 153. 1973.
December Am. J, Obstet.
13, 1977 Gynecol.
This article has been an anecdotal account c)f man! different apparent etiologies of fetal bradycardias. The common theme has been that the information at hand is insufficient to explain their occurrences. It is doubtful that any acute fetal bradycardia is ever “physiologic” in the sense that it is completely innocuous. Furthermore, it serves no useful purpose to label fetal bradycardias according to their theoretical mechanisms. Others disagree, believing that certain FHR patterns are diagnostic of umbilical cord c.omprt&m, and recommend immediate cesarean section C’VCII I\ hen failing to find the prolapsed umbilical cord.*s Still others suggest that head compression is the basis of nearly all fetal bradycardias and that the amniotic membrane should be protected.’ We have- suggested that the maternal supine position always bc avoided.’ Given this relative lack of knowledge and disagreement over etiology, it is proposed that all abrupt fetal bradycardias simply be referred to as “vagal bradycat-dias” and that they be described and treated according to their severity. Prolapse of the funis and t&al asphyxia should always be ruled out, but other-u&t, the bradycardia treatment should be considered tier its own possible detrimental effects upon the irtus. Rudolph 2g has demonstrated that fetal cardiac output in fetal sheep is often dependent on heart rate. Our own systolic interval measurements in human fetuses also suggest that ejection times do not uni. formly increase during fetal hradycardia. indicating that the fetuses’cardiac outputs decrease during severe and prolonged vagal bradycardia. Under rhcst, [I, :r, .,t iI pl o found deceleration or bradccardia after ~lci ~~litl~ TO 1 f feet an immediate delivw z 1 would like to ask the authors: (1) if Tltc,t.c- \v;L\ LC.;Lson to depart from the act-eptcd defimtiow 3)f Ffl K decelerations and FHR brad){-archas. (2) if rhc, \hapc, c J the deceleration or brad)carclias lvas ~orrc-Ltrctl WI rh rlinical outcome, and (3) if the use of to111 tliffcrctll types of FHR monitors might have affected Ihc. rc,sulrs? DR. G~ODLIN (Closing). I do not have an! ,irgumcnl with \\,hat Dr. Queenan has said. for it is the standard American vie!+. My basic concern is that v hen we use the (crm “ter,tl heart rate deceleration” \\e immediately thinh of either head or cord compression. And \ce do arg\zv i11 this articlc that there are many other events that c\ ol\v Iltl same sort of response on the part of the fetus; thwcfore, I think the term “fetal heart rate decclewtion” is no longer an appropriate term. As far as the use of the atropine is concerned. this argument has been going on for years. Basicall\, I contend that fetal bradycardia is never of benefit to rhc fetus: that if one makes ccl-tain that there is no umbilical cord prolapse or no fetal acidemia and that if the bradycardia or. if you vcish, severe deceleration COILtinues and if the fetus is not to be delivered immediately, it is appropriate to use atropine. I believe the risks of a markedly reduced fetal cardiac output are thus avoided.
