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Sinusoidal fetal heart rate
FETUS, PLACENTA, AND NEWBORN
Sinusoidal fetal heart rate I. Clinical BRUCE
significance
K. YOUNG,
MIRIAM
KATZ,
STEPHEN
M.D.,
F.A.C.O.G.*
M.D.
J. WILSON,
M.D.
New York, New York Sixteen cases of SHR are analyzed with respect to perinatal outcome, fetal scalp and umbilical arterial pH, and characteristics of the FHR pattern. There were no perinatal deaths in this series. The SHR is defined and a plan for management of the patient with SHR is proposed. A theoretical explanation of the pathophysiology of SHR is presented in terms of a fetal COmpenSatOty mechanism for hypoxia, based on these observations as well as a review of the literature. Biochemical data may provide valuable information permitting optimal management of patients with SHR patterns. (AM. J. OBSTET. GYNECOL. 136587, 1980.)
SINUSOIDAL fetal heart rate (SHR) isconsidered indicative of severe fetal jeopardy by most authors. This fetal heart rate (FHR) pattern is thought to appear just prior to fetal death whether seen with intrapartum or antepartum monitoring. The perinatal mortality rate associatedwith SHR has been reported as 50 to 75%.le5The sinusoidalpattern was first recognized by Manseauand associates’in patients with Rh isoimmunization. They describeda regular rhythmicity of variation resembling a sinusoidalwave, with a relatively fixed periodicity of 15 to 30 seconds,and relatively fixed amplitude of 5 to 15 beats per minute THE
From th Division of Maternal-Fetal Medicine, Departme& of Obstetrics and Gynecology, New York University School of Medicine and Bellevue Hospital Center. Received for publication Revised March Accepted March Reprint Center, 10016. *Irma
December
28, 1978.
13, 1979.
Materials and methods The study population consistedof 4,800 patients delivered on the Bellevue Obstetrical Service from 1975 through 1977. More than 90% of these labors were monitored, but only 50% of the patients had internal monitoring. The intrapartum cases reported were diagnosed by internal monitoring with a spiral electrode* and a standard fetal monitor.?
16, 1979.
requests: Bruce K. Young, M.D., N.Y. LT. Medical Suite 2C, 566 First Ave., New York, New York T. Hirsch1
(bpm). They also noted a flattening of the short-term variability associatedwith this pattern. Others have extended these observations to include a frequency of 3 to 5 cycles per minute (cpm), and an amplitude as low as5 bpm3and ashigh as30 bpm.2 In the present study SHR wasdefined asa FHR pattern of regular variability resembling a sine wave, with a relatively fixed periodicity of 3 to 5 cpm, and an amplitude of 5 to 40 bpm from the baselineFHR, lasting at least 10 minutes. This report reviews 16 casesof SHR observed on the Bellevue Obstetrical Service.
Career
Scientist.
0002-9378/80/050587+07$00.70/0 @I 1980 Tbe C. V. Mosby Co.
*CorometricsSpiral FECG electrode,CorometricsInc., Wallingford,Connecticut. tRoche Fetal Monitor lOlB, Roche Medical Electronics, Cranbury, NewJersey. 587
588
Young,
Table
Katz,
1. Clinical
March 1, 1980 Am. J. Obstet. Gynecol.
and Wilson
course and perinatal
outcome Sinusoidal
Pt.
K. c:. I). D. c;. I.. c. M. M. I). S. F. B. G. A. A. s. s. P. C. A. J. P. G. .I. v. .4. H. I.. s. K. 0.
Duration (rain)
Cowbplication5 Post dates, meronium None Post dates, partial abruptio placentae Severe anemia Post dates, toxemia None None
Premature labor (35 wk) Premature labor (36 wk) None None None Occult prolapse of cord Nuchal cord Occult prolapse of cord Post dates, toxemia, partial ahruptio placentae
pattern
Frequency (per min)
York.
Umbilical at-q PH
7.20 7.32 7.18
7.24 7.32 7.20
7.18 7.19
7.21
7.28 7.32
7.26
20-35 IO-15 30-40
Cesarean section Spontaneous Cesarean section
2-5 9-10 8-9
11 14 14 20 17 20 60 35 30 15 25 45 35
3 4 4 3 5 4 4-5 4
IO-15 35-40 5-10 IO-12 IO-14 5-10 IO-20 IO-15 IO-15 15-20 15-20 lo-25 10-15
Low forceps Cesarean section Cesarean section Low forceps Spontaneous Low forceps Low forceps Low forceps Low forceps Low forceps Low forceps Cesarean section Cesarean section
9-10 4-7 4-8 6-8 9-9 8-Y 9-10 Y-10 Y-10 6-8 8-9 9-10 8-9
3 4-5 3-4
Incidence. Sixteen cases, or less than 0.3% of out monitored patients exhibited a SHR. However, only SHR patterns having a duration of 10 minutes or more were considered in this study. Eleven of 16 patients with SHR were primigravidas. One was gravida 4 and the remainder were gravida 2 or 3. The patients ranged in age from 17 to 40 (mean 25.3) years. The average gestational age was 40.1 weeks (range 35 to 43 weeks). Ten of the 16 pregnancies were found to be at high risk. Four had a history of being late for dates (by last menstrual period, first-trimester examination, and/or serial ultrasound examination). Premature labor occurred in two cases. These high-risk cases were also associated with meconium-stained amniotic fluid, mild pre-eclampsia, partial abruptio placentae in two cases, and cord entanglement in three cases (Table I). One patient diagnosed antepartum demonstrated the SHR on an ultrasonic external monitor during an antepartum oxytocin stress test with recurrence of the SHR intrapartum. Another patient demonstrated the New
Scalp PH
3 3 4
Results
165, Corning,
.SCOW
APw
@Pm)
20 12 40
Scalp capillary blood samples were obtained in 11 cases. Specimens of umbilical artery and vein blood were obtained in eight cases. Blood gas analysis was performed on a standard microanalyzer.* Records were analyzed for baseline FHR, variability, associated FHR patterns, and the SHR. The clinical course and perirratal outcome were reviewed for each fetus with SHR (Table I).
*Corning
~4mplitude
pattern
only
on
unstressed
7.28 7.28 7.23 7.26
7.30 7.2 1 7.28
monitoring.
and
not
in
labor. In Patient A. J. the SHR was first seen in the fil.sL stage of labor. disappeared. and then recurred during the second stage. In 11 of the remaining patients the SHR was observed only during the first stage of labor. Two patients exhibited only second-stage SHR. Outcome. There were no perinatal deaths among these 16 cases exhibiting a SHR. Two fetuses were tlelivered by normal spontaneous vaginal delivery, eight by low forceps, and six by primary cesarean section. Of the latter,
three
were
and
three
proportion
performed for
for
fetal
cephalopelvic
dis-
distress.
One-minute Apgar scores of 6 or less were noted in five newborn infants. Of these five, one had a scalp pH of 7.28 and was allowed to labor, with low-forceps delivery,
and
three
were
delivered
by
cesarean
section
after having repeated scalp pH values of 7.20 or less. Only one of these neonates had an Apgar score of less than
6 at 5 minutes,
related
at least
in part
to meco-
nium aspiration. A total of 11 cases of SHR were monitored by fetal scalp blood sampling. Five of these fetuses had preacidosis
or
7.25.
Four
less.
Three
7.20
or
acidosis, of these
less
with were
scalp
pH
acidotic
values
(36%)
of less
with
pH
than
7.20
or
of the four cases having scalp pH values 01 were
associated
with
a SHR
of
15 bpm
amplitude or more. Two of these three had scores of 6 or less at 1 minute. Thus, three of fetuses monitored biochemically during labor SHR pattern had repeated scalp pH values of less, and Apgar scores of 6 or less at 1 minute
for a 7.20 or (27%).
Conversely,
showed
seven
of
these
SHR
cases
(64%)
Apgar the
11
Volume Number
1% 5
Sinusoidal
7.40
FHR.
I
589
7.40
O. 7.30
7.30
m
0 0 ,---------------.-----------------------------
____________________--------------------------NOWYIL
NON 0
0
0
0
0
0 0
% 7.20 4' x
: 0
0
i
7.10 I -
7.10
1
7.M I5
1
10
1
15
MEAN AMPLITUDE
20 (BEATS
I
25
30
35
40
PER MINUTE)
7.00
I 5
I
10
15
MEAN AMPLITUDE
20
25
I
30
1
35
40
(BEATS PER MINUTE)
Fig. 1. Scalp blood pH changes showing an inverse relationship to the amplitude of the sinusoidal pattern.
Fig. 2. Umbilical artery blood pH values, when compared with amplitude of the sinusoidal pattern, show a breakpoint at 15 bpm.
normal scalp blood pH measurements and Apgar scores of 7 or more. When scalp pH is compared with amplitude of the SHR, there is a highly significant relationship with a correlation coefficient of r = -0.73. Thus, low pH is correlated with increased amplitude (Fig. 1). Eight of the 11 cases monitored with fetal scalp blood sampling also were studied with umbilical artery pH. A highly significant inverse relationship with amplitude of SHR was observed as well, with correlation coefficient of -0.69 (Fig. 2). The break point for acidosis appears to be at an amplitude of 15 bpm or above. Associated FHR changes. The baseline FHR preceding the observed SHR in all cases ranged from 120 to 150 bpm. Fetal tachycardia was observed to follow the sinusoidal rhythm in only one case. Three other patients had a baseline moderate bradycardia. A decrease in the baseline FHR was noted to follow the
sinusoidal pattern in nine cases and an increase in four cases; in only three did the baseline return to its original level. Table II summarizes the associated changes in FHR observed prior to and after the sinusoidal pattern. In only one case was variable deceleration noted during the SHR pattern (Fig. 3). However, variable decelerations occurred both before and after the observed sinusoidal FHR in one of the three babies having cord complications. There were no late decelerations. Three patients had recurrent episodes of sinusoidal patterns alternating with other abnormal FHR patterns. These abnormal patterns consisted of variable decelerations with late components and decreased variability with a baseline from 110 to 130 bpm. In these three cases, the amplitudes of the sinusoidal FHR were less than 15 bpm. Repeated scalp sampling showed pH of greater then 7.23. These infants were
590
Young, Katz, and Wilson
March 1, 1980 Am. J. Obstet. Gynecol.
Fq. 3. Fetal monitoring record. Upper trace shows a minor sinusoidal pattern with variable decelerations. Lower trace shows uterine contractions.
Table II. Associated
fetal heart rate changes &fore
P&e?%
Reduced baseline variability Increased baseline variability Variable deceleration Variable deceleration with late component Acceleration Moderate bradycardia Tachycardia
No.
After %
No.
%
53
6 4 5 0
35 24 29 0
9 2 7 2
:: 12
9
53 0 0
6 3 1
35 18 6
8
delivered with Apgar scores of 8 or better. Three additional cases without recurrent sinusoidal patterns were noted irregularly to have unusual FHR patterns consisting of accelerations and variable decelerations alternately or in combination. The fetuses showing this pattern also were delivered with Apgar scores of at least 8. The average frequency of the observed SHR patterns was 3.7 (range 3 to 5), with a mean amplitude of 16.4 bpm (range 5 to 40). Forty-seven minutes on the average (range 12 to 120 minutes) was allowed to elapse between the initial appearance of the SHR pattern and the time of delivery. The average duration of the SHR was 20.1 minutes (range 11 to 40 minutes). -nt Since 1972, when the first reports describing SHR appeared, the pattern often has been interpreted as impending fetal death. The majority of these cases involved severely Rh-isoimmunized fetuses. Table III summarizes the literature. The sinusoidal FHR has
been described as an “ominous” pattern when observed during antepartum and intrapartum monitoring.’ The average perinatal mortality rate in the literature is 63%. We have observed 16 cases, none of which was associated with perinatal death. Eleven of our patients were monitored by repeated scalp and umbilical artery pH assays. To our knowledge, this is the first analysis of SHR with biochemical data as well. Baskett and Koh’ made the first attempt at correlating the severity of the sinusoidal pattern with fetal outcome. They considered a minor pattern to be an episode lasting 1 to 5 minutes with regular oscillations of the fetal heart having an amplitude of 5 to 15 bpm. A pattern having an amplitude of 30 to 70 bpm was considered a marked sinusoidal pattern. Three of our cases had a marked pattern as described by these criteria. Eleven cases had an amplitude of 10 to 25 and two cases had an amplitude of 5 to 10 bpm. However, sinusoidal patterns, regardless of the amplitude, were not diagnosed if their duration was under 10 minutes. Figs. 1 and 2 show the relationship between the amplitude of the SHR oscillations and fetal acidosis. We consider an amplitude of 15 bpm to be the threshold for diagnosis of a marked SHR (Fig. 4). The seven cases of marked sinusoidal pattern were monitored with repeated scalp blood samples during the period of SHR; preacidotic or acidotic levels were noted in four. Cesarean section was performed in these four cases. Two of these four neonates had 1 minute Apgar scores of less than 6, confirming khe serious character of a SHR with amplitude over 15 bpm. However, an acidotic scalp pH was noted in one case exhibiting an amplitude of 5 to 10 bpm, so even the minor
Volume Number
Sinusoidal
136 5
I
-1
FHR.
I
591
MN.
AT JcnrtM1N.
Fig. 4. Fetal monitoring record showing a marked sinusoidal pattern. The amplitude is 20 bpm. The lower trace shows a hypertonic uterine contraction. Table
III. Comparison
of reported
sinusoidal
FHR patterns
Description
Author
of case(s)
Method
of delivery
No. of patients obmved
No. of deaths
Antepatium:
Kubli et al.. 1972 Manseau et al., 1972 Rochard et al., 1976 Moudanlou,
et al., 1977
Mueller-Heubach
et al.. 1978
Multiple high-risk factors including Rh involvement, toxemia anemia, antepartum bleeding Rh involvement Severe Rh isoimmunization, antepartum nonstress testing Chronic hypertension, OCT pos., severe fetal anemia Severe Rh isoimmunization, post-intrauterine fetal transfusion Severe Rh isoimmunization, post-intrauterine transfusion X 3
Not indicated
12
9
Cesarean section
9 20
7 10
Cesarean section
1
0
Cesarean section
1
Cesarean section
0 44
7
Zntrapartum:
Baskett and Koh, 1974 Cetrulo and Schifrin, 1976
Pre-eclampsia, postdates Post dates
Total SHR may be potentially dangerous. Nevertheless, of the 11 cases monitored biochemically, five of the six having scalp pH’s of greater than 7.25 were delivered with 1 minute Apgar scores of at least 8. One-minute Apgar scores of less than 6 were noted in three of the four fetuses having acidotic scalp blood samples, illustrating the usefulness of scalp sampling in assessing fetal condition in cases of SHR. In comparing the interval between the onset of the sinusoidal pattern and the time of delivery, no correla-
Cesarean section Cesarean section
1
1
r
-l
2 --
-2
46
29
tion could be made with the 1 minute Apgar score. The duration of the sinusoidal FHR also showed no statistitally significant relationship with the Apgar score. All fetuses having patterns lasting less than 14 minutes were delivered with nonacidotic umbilical artery samples. Scalp pH samples from these same fetuses were not acidotic. Patterns lasting 14 minutes or longer were associated with preacidotic or acidotic scalp and/or umbilical artery samples in only two of eight such cases. The pathophysiology of the SHR is not understood.
592
Young,
Katz,
lMarch 1, 1980 Am. J. Obstet. Gynecol.
and Wilson
I PH NERVOUS
PO,
SVSTEM
PC02
r MEDULLARY CARDlOkESPlRATORV CENTER
Fig. 5. Diagram I ‘11e pattern.
The
I FETAL
MYOCARDI;M
illustrating the feedback mechanism arrows represent pathways which
Haskett speculated that the sinusoidal pattern was due to deranged nervous control of the fetal heart caused I)! h\poxia. Severe anemia due to Rh disease OI fetomaternal transfusion (and thus possibly highoutput heart failure) has been associated with the sinusoidal pattern.” 3 In only two of our cases could severe fetal anemia due to partial abruptio placentae be considered as a cause of the SHR. The majorit) of. investigators agree that the SHR represents fetal hypoxia, but there is no demonstrable relationship to fetal asphyxia or degree of hypoxic inFult in the litcxrature. Our study presents biochemical data which suggest that acidosis may follow the SHR but is not intrmsic to this FHR pattern. In fact, we have shown that the SHR may begin without acidosis being present, and persist in a normal or preacidotic state for long periods.* Thus, fetal acidosis ma) exert some influence on the pathophysiologp of the SHR, but is not essential. Thc~ SHR can O~CLIT without acidosis and, in general, is associated with a low Apgar score only in the presence of fetal acidosis in our experience. The physiology of the SHR remains unresolved. The sinusoidal pattern has been observed in the premature newborn infhnt without perinatal death, accompanied by a pattern r~f’ periodic breathing.’ This association of cardiac and respiratory periodicity suggests that the fetal autonomic nervous systrm is the likely cxplanation tar the SHR. The occurrence of SHR in Rh isoimmunization, abruptio placentae, cord entanglement or prolapse, postdates, toxemia, and maternal anemia points toward fetal hypoxia as the common denominator. The effects of tissue hypoxia on the medullary centers in the fetal brain which regulate heart rate might account for this unusual FHR pattern. Baskett and Koh suggested that hypoxia “completely deranged” the autonomic nervous control of the FHR. We would offer an alternative hypothesis. We suggest
responsible for the control influence fetal heart t-ate.
of the fetal
heart
that the fetal heart rate is regulated b! ;I flerlhac-kcontrolled system in which the sensitivit\ is increased by hypoxia. The system control is most likely mothulated by the medullary cardioregulator! center ill the fetal brain. The feedback loops probably are the peripheral sensors of cardiorespiratory function, most importantly the carotid and aortic bodies sensitive. to PO, and Pco,. Under conditions of mild hypoxia. the initial FHR response is acceleration in the human subject, probably mediated by sympathetic nervous discharge. I” With increasing or decreasing hypoxia, parasympathetically mediated deceleration follows. It is the interaction of these two nervous discharges which regulates FHR.7 Under conditions where cardioregulator) center sensitivity is high (hypoxia). and feedback signals are undamped (abruptio placentae, fetal anemia, placental insufficiency, cord compression), SLICK a feedback-controlled system can be caused to oscillate, producing a sinusoidal pattern in the FHR recording (Fig. 5). ‘Therefore, the autonomic nervous control is not deranged, but discharging alternately, struggling to maintain homeostasis in a strong compensatory effect under conditions of hypoxia. If the hypoxia abates, the SHR may disappear. If conditions worsrn. the FHR pattern may deteriorate to bradycardia and acidosis may develop as well. Support for this theory is found in the demonstration that the response to progres.sivr hypoxia down to a PO, of 10 mm is an increased index of beat-to-beat variability in the absence of acidosis in the fetal sheep. I’ This represents activation of the autonomic nervous control of heart rate, rather than derangement. Since the human long-term FHR variability is the arithmetic sum of the beat-to-beat changes, a sinusoidal pattern might easily result from relatively mild hypoxia in the absence of acidosis or shock.” Further supporting evidence is the estimated time of
Volume 136 Number5
10 to 20 seconds for fetal blood flow from the placental villous capillaries to the fetal carotid receptors in the human subject.“~ Similarly, after alteration of maternal oxygenation, it takes 20 to 30 seconds for the fetal monkey to show changes in tissue oxygenation in the neck.‘l These time intervals closely approximate the 3 to 5 cpm of the sinusoidal pattern, confirming the chemoreceptor-autonomic nervous system interaction in the genesis of the SHR. Thus, the SHR could be the result of an actively functioning autonomic nervous system in the presence of mild to moderate fetal hypoxia, and the absence of fetal hypotension or acidosis. When the fetus is unable to compensate for the hypoxic insult, or the hypoxia produces sufficient acidosis, the SHR may progress to typical fetal distress patterns. The metabolic deterioration then might lead to the combination of hypoxia and acidosis, which is most deleterious and predisposes to unwanted perinatal outcome. The over-all incidence of the SHR pattern is very low. The occurrence is not predictably related to preexisting high-risk factors. Of the fetuses showing a sinusoidal pattern, 31% had preacidotic or acidotic
Sinusoidal
FHR.
I
593
scalp pH values. There was a 31% incidence of fetal distress as determined by fetuses having low Apgar scores as well, but there were no perinatal deaths. At least in the non-Rh-isoimmunized pregnancy, the appearance of a SHR does not necessarily imply impending fetal death, or necessitate an emergency delivery. It probably indicates hypoxia of mild to moderate degree. and maternal oxygen administration is advisable. Sinusoidal patterns having amplitudes of greater than 15 bpm have a greater risk of fetal acidosis. The decision to intervene should be based on careful biochemical monitoring. Labor and vaginal delivery of patients exhibiting a SHR is indicated as long as reliable biochemical data confirm a nonacidotic fetus despite the presence of a SHR. When the SHR appears in antepartum monitoring in a non-Rh-isoimmunized patient, further evaluation by other means, such as stress testing, estriols, and amniocentesis for meconium should be performed. In such cases the decision to deliver should be based on complete clinical evaluation of each patient rather than the SHR alone. Close observation of the fetal status, combined with disappearance of the SHR, permit conservative management of these patients.
REFERENCES
1. Manseau, P., Vaquier, J., et al.: Le rhythme cardiaque foetal “sinusoidal,” J. Obstet. Gynecol. Biol. Reprod. 1:343, 1972. 2. Baskett, T. F., and Koh, K. S.: Sinusoidal fetal heart rate pattern. A sign of fetal hypoxia, Obstet. Gynecol. 44:379, 1974. 3. Rochard, F., Schifrin, B. S., Goupil, F., et al.: Nonstressed fetal heart rate monitoring in the antepartum period, AM. J. OBSTET. GYNECOL. 126y699, 1976.’ . 4. Kubli. F.. Ruttcrers. H.. Haller. U.. et al.: Die antenartale fetale’ herz fre&enz. II. Verholten von Grundfre’quenz, Fluktuation und Dezerationen bei antepartalem Fruchttod, Z. Geburtshilfe Perinatol. 176:309, 1972. 5. Modanlou, H. D., Freedman, R. K., Ortiz, O., et al.: Sinusoidal fetal heart rate pattern and severe fetal anemia, Obstet. Gynecol. 49:537, 1977. 6. Mueller-Heubach, E., Caritis, S. N., and Edelson, D. I.: Sinusoidal fetal heart rate pattern following intrauterine fetal transfusion. Obstet. Gynecol. 52(Suppl. 1):43, 1977. 7. Cetrulo, C. L., and Schifrin, B. S.: Fe&l-heart rate patterns nreceding death in utero, Obstet. Gvnecol. 48:52 1. 1976.’ v 8. Katz, M., Wilson, S., and Young, B. K.: Sinusoidal fetal
heart rate. II. Evaluation by continuous tissue pH, AM. J. OBSTET.
GYNECOL.
In press.
9. Messer, J., Schick, A. R., Willard, D., et al.: Le cardiorespirogramme de nouveau-&, J. Obstet. Gynecol. Biol. Reprod. 4:815, 1975. 10. Cohn, H. E., Sacks, E. J., Heymann, M. A. et al.: Cardiovascular responses to hypoxemia and acidemia in fetal lambs, AM.J. ~BSTET. GY~OL. 120:817, 1974. 11. Stanee. L.. Rosen. K. G.. Hokegarde, K. H .. et al.: Ouantifi&on of fetal heart rate va;iability in relation tooxygenation in the sheep fetus, Acta Obstet. Gynecol. Stand. 56:205, 1977. 12. Young, B. K., Weinstein, H. N., Hochberg, H. M., et al.: observations in perinatal heart rate monitoring. I. A quantitative method of describing baseline variability in t’he fetal heart rate, J. Reprod. Mid. 20:205, 1978. 13. Mvers. R. E.. Mueller-Heubach, E., and Adamsons, K.: Predictabilitv of the state of fetaloxygenation from a quantitative analysis of the components-of late deceleration. AM. I.OBSTET.GYNECOL. 115:1083. 1973. 14. Mvers, R.-E., Stange, L., loelson, I., et al.: Effects upon the fetus of oxyg& adm&istration to the mother, Acta Obstet. Gynecol. Stand. 56: 195, 1977.
Sinusoidal fetal heart rate I. Clinical BRUCE
significance
K. YOUNG,
MIRIAM
KATZ,
STEPHEN
M.D.,
F.A.C.O.G.*
M.D.
J. WILSON,
M.D.
New York, New York Sixteen cases of SHR are analyzed with respect to perinatal outcome, fetal scalp and umbilical arterial pH, and characteristics of the FHR pattern. There were no perinatal deaths in this series. The SHR is defined and a plan for management of the patient with SHR is proposed. A theoretical explanation of the pathophysiology of SHR is presented in terms of a fetal COmpenSatOty mechanism for hypoxia, based on these observations as well as a review of the literature. Biochemical data may provide valuable information permitting optimal management of patients with SHR patterns. (AM. J. OBSTET. GYNECOL. 136587, 1980.)
SINUSOIDAL fetal heart rate (SHR) isconsidered indicative of severe fetal jeopardy by most authors. This fetal heart rate (FHR) pattern is thought to appear just prior to fetal death whether seen with intrapartum or antepartum monitoring. The perinatal mortality rate associatedwith SHR has been reported as 50 to 75%.le5The sinusoidalpattern was first recognized by Manseauand associates’in patients with Rh isoimmunization. They describeda regular rhythmicity of variation resembling a sinusoidalwave, with a relatively fixed periodicity of 15 to 30 seconds,and relatively fixed amplitude of 5 to 15 beats per minute THE
From th Division of Maternal-Fetal Medicine, Departme& of Obstetrics and Gynecology, New York University School of Medicine and Bellevue Hospital Center. Received for publication Revised March Accepted March Reprint Center, 10016. *Irma
December
28, 1978.
13, 1979.
Materials and methods The study population consistedof 4,800 patients delivered on the Bellevue Obstetrical Service from 1975 through 1977. More than 90% of these labors were monitored, but only 50% of the patients had internal monitoring. The intrapartum cases reported were diagnosed by internal monitoring with a spiral electrode* and a standard fetal monitor.?
16, 1979.
requests: Bruce K. Young, M.D., N.Y. LT. Medical Suite 2C, 566 First Ave., New York, New York T. Hirsch1
(bpm). They also noted a flattening of the short-term variability associatedwith this pattern. Others have extended these observations to include a frequency of 3 to 5 cycles per minute (cpm), and an amplitude as low as5 bpm3and ashigh as30 bpm.2 In the present study SHR wasdefined asa FHR pattern of regular variability resembling a sine wave, with a relatively fixed periodicity of 3 to 5 cpm, and an amplitude of 5 to 40 bpm from the baselineFHR, lasting at least 10 minutes. This report reviews 16 casesof SHR observed on the Bellevue Obstetrical Service.
Career
Scientist.
0002-9378/80/050587+07$00.70/0 @I 1980 Tbe C. V. Mosby Co.
*CorometricsSpiral FECG electrode,CorometricsInc., Wallingford,Connecticut. tRoche Fetal Monitor lOlB, Roche Medical Electronics, Cranbury, NewJersey. 587
588
Young,
Table
Katz,
1. Clinical
March 1, 1980 Am. J. Obstet. Gynecol.
and Wilson
course and perinatal
outcome Sinusoidal
Pt.
K. c:. I). D. c;. I.. c. M. M. I). S. F. B. G. A. A. s. s. P. C. A. J. P. G. .I. v. .4. H. I.. s. K. 0.
Duration (rain)
Cowbplication5 Post dates, meronium None Post dates, partial abruptio placentae Severe anemia Post dates, toxemia None None
Premature labor (35 wk) Premature labor (36 wk) None None None Occult prolapse of cord Nuchal cord Occult prolapse of cord Post dates, toxemia, partial ahruptio placentae
pattern
Frequency (per min)
York.
Umbilical at-q PH
7.20 7.32 7.18
7.24 7.32 7.20
7.18 7.19
7.21
7.28 7.32
7.26
20-35 IO-15 30-40
Cesarean section Spontaneous Cesarean section
2-5 9-10 8-9
11 14 14 20 17 20 60 35 30 15 25 45 35
3 4 4 3 5 4 4-5 4
IO-15 35-40 5-10 IO-12 IO-14 5-10 IO-20 IO-15 IO-15 15-20 15-20 lo-25 10-15
Low forceps Cesarean section Cesarean section Low forceps Spontaneous Low forceps Low forceps Low forceps Low forceps Low forceps Low forceps Cesarean section Cesarean section
9-10 4-7 4-8 6-8 9-9 8-Y 9-10 Y-10 Y-10 6-8 8-9 9-10 8-9
3 4-5 3-4
Incidence. Sixteen cases, or less than 0.3% of out monitored patients exhibited a SHR. However, only SHR patterns having a duration of 10 minutes or more were considered in this study. Eleven of 16 patients with SHR were primigravidas. One was gravida 4 and the remainder were gravida 2 or 3. The patients ranged in age from 17 to 40 (mean 25.3) years. The average gestational age was 40.1 weeks (range 35 to 43 weeks). Ten of the 16 pregnancies were found to be at high risk. Four had a history of being late for dates (by last menstrual period, first-trimester examination, and/or serial ultrasound examination). Premature labor occurred in two cases. These high-risk cases were also associated with meconium-stained amniotic fluid, mild pre-eclampsia, partial abruptio placentae in two cases, and cord entanglement in three cases (Table I). One patient diagnosed antepartum demonstrated the SHR on an ultrasonic external monitor during an antepartum oxytocin stress test with recurrence of the SHR intrapartum. Another patient demonstrated the New
Scalp PH
3 3 4
Results
165, Corning,
.SCOW
APw
@Pm)
20 12 40
Scalp capillary blood samples were obtained in 11 cases. Specimens of umbilical artery and vein blood were obtained in eight cases. Blood gas analysis was performed on a standard microanalyzer.* Records were analyzed for baseline FHR, variability, associated FHR patterns, and the SHR. The clinical course and perirratal outcome were reviewed for each fetus with SHR (Table I).
*Corning
~4mplitude
pattern
only
on
unstressed
7.28 7.28 7.23 7.26
7.30 7.2 1 7.28
monitoring.
and
not
in
labor. In Patient A. J. the SHR was first seen in the fil.sL stage of labor. disappeared. and then recurred during the second stage. In 11 of the remaining patients the SHR was observed only during the first stage of labor. Two patients exhibited only second-stage SHR. Outcome. There were no perinatal deaths among these 16 cases exhibiting a SHR. Two fetuses were tlelivered by normal spontaneous vaginal delivery, eight by low forceps, and six by primary cesarean section. Of the latter,
three
were
and
three
proportion
performed for
for
fetal
cephalopelvic
dis-
distress.
One-minute Apgar scores of 6 or less were noted in five newborn infants. Of these five, one had a scalp pH of 7.28 and was allowed to labor, with low-forceps delivery,
and
three
were
delivered
by
cesarean
section
after having repeated scalp pH values of 7.20 or less. Only one of these neonates had an Apgar score of less than
6 at 5 minutes,
related
at least
in part
to meco-
nium aspiration. A total of 11 cases of SHR were monitored by fetal scalp blood sampling. Five of these fetuses had preacidosis
or
7.25.
Four
less.
Three
7.20
or
acidosis, of these
less
with were
scalp
pH
acidotic
values
(36%)
of less
with
pH
than
7.20
or
of the four cases having scalp pH values 01 were
associated
with
a SHR
of
15 bpm
amplitude or more. Two of these three had scores of 6 or less at 1 minute. Thus, three of fetuses monitored biochemically during labor SHR pattern had repeated scalp pH values of less, and Apgar scores of 6 or less at 1 minute
for a 7.20 or (27%).
Conversely,
showed
seven
of
these
SHR
cases
(64%)
Apgar the
11
Volume Number
1% 5
Sinusoidal
7.40
FHR.
I
589
7.40
O. 7.30
7.30
m
0 0 ,---------------.-----------------------------
____________________--------------------------NOWYIL
NON 0
0
0
0
0
0 0
% 7.20 4' x
: 0
0
i
7.10 I -
7.10
1
7.M I5
1
10
1
15
MEAN AMPLITUDE
20 (BEATS
I
25
30
35
40
PER MINUTE)
7.00
I 5
I
10
15
MEAN AMPLITUDE
20
25
I
30
1
35
40
(BEATS PER MINUTE)
Fig. 1. Scalp blood pH changes showing an inverse relationship to the amplitude of the sinusoidal pattern.
Fig. 2. Umbilical artery blood pH values, when compared with amplitude of the sinusoidal pattern, show a breakpoint at 15 bpm.
normal scalp blood pH measurements and Apgar scores of 7 or more. When scalp pH is compared with amplitude of the SHR, there is a highly significant relationship with a correlation coefficient of r = -0.73. Thus, low pH is correlated with increased amplitude (Fig. 1). Eight of the 11 cases monitored with fetal scalp blood sampling also were studied with umbilical artery pH. A highly significant inverse relationship with amplitude of SHR was observed as well, with correlation coefficient of -0.69 (Fig. 2). The break point for acidosis appears to be at an amplitude of 15 bpm or above. Associated FHR changes. The baseline FHR preceding the observed SHR in all cases ranged from 120 to 150 bpm. Fetal tachycardia was observed to follow the sinusoidal rhythm in only one case. Three other patients had a baseline moderate bradycardia. A decrease in the baseline FHR was noted to follow the
sinusoidal pattern in nine cases and an increase in four cases; in only three did the baseline return to its original level. Table II summarizes the associated changes in FHR observed prior to and after the sinusoidal pattern. In only one case was variable deceleration noted during the SHR pattern (Fig. 3). However, variable decelerations occurred both before and after the observed sinusoidal FHR in one of the three babies having cord complications. There were no late decelerations. Three patients had recurrent episodes of sinusoidal patterns alternating with other abnormal FHR patterns. These abnormal patterns consisted of variable decelerations with late components and decreased variability with a baseline from 110 to 130 bpm. In these three cases, the amplitudes of the sinusoidal FHR were less than 15 bpm. Repeated scalp sampling showed pH of greater then 7.23. These infants were
590
Young, Katz, and Wilson
March 1, 1980 Am. J. Obstet. Gynecol.
Fq. 3. Fetal monitoring record. Upper trace shows a minor sinusoidal pattern with variable decelerations. Lower trace shows uterine contractions.
Table II. Associated
fetal heart rate changes &fore
P&e?%
Reduced baseline variability Increased baseline variability Variable deceleration Variable deceleration with late component Acceleration Moderate bradycardia Tachycardia
No.
After %
No.
%
53
6 4 5 0
35 24 29 0
9 2 7 2
:: 12
9
53 0 0
6 3 1
35 18 6
8
delivered with Apgar scores of 8 or better. Three additional cases without recurrent sinusoidal patterns were noted irregularly to have unusual FHR patterns consisting of accelerations and variable decelerations alternately or in combination. The fetuses showing this pattern also were delivered with Apgar scores of at least 8. The average frequency of the observed SHR patterns was 3.7 (range 3 to 5), with a mean amplitude of 16.4 bpm (range 5 to 40). Forty-seven minutes on the average (range 12 to 120 minutes) was allowed to elapse between the initial appearance of the SHR pattern and the time of delivery. The average duration of the SHR was 20.1 minutes (range 11 to 40 minutes). -nt Since 1972, when the first reports describing SHR appeared, the pattern often has been interpreted as impending fetal death. The majority of these cases involved severely Rh-isoimmunized fetuses. Table III summarizes the literature. The sinusoidal FHR has
been described as an “ominous” pattern when observed during antepartum and intrapartum monitoring.’ The average perinatal mortality rate in the literature is 63%. We have observed 16 cases, none of which was associated with perinatal death. Eleven of our patients were monitored by repeated scalp and umbilical artery pH assays. To our knowledge, this is the first analysis of SHR with biochemical data as well. Baskett and Koh’ made the first attempt at correlating the severity of the sinusoidal pattern with fetal outcome. They considered a minor pattern to be an episode lasting 1 to 5 minutes with regular oscillations of the fetal heart having an amplitude of 5 to 15 bpm. A pattern having an amplitude of 30 to 70 bpm was considered a marked sinusoidal pattern. Three of our cases had a marked pattern as described by these criteria. Eleven cases had an amplitude of 10 to 25 and two cases had an amplitude of 5 to 10 bpm. However, sinusoidal patterns, regardless of the amplitude, were not diagnosed if their duration was under 10 minutes. Figs. 1 and 2 show the relationship between the amplitude of the SHR oscillations and fetal acidosis. We consider an amplitude of 15 bpm to be the threshold for diagnosis of a marked SHR (Fig. 4). The seven cases of marked sinusoidal pattern were monitored with repeated scalp blood samples during the period of SHR; preacidotic or acidotic levels were noted in four. Cesarean section was performed in these four cases. Two of these four neonates had 1 minute Apgar scores of less than 6, confirming khe serious character of a SHR with amplitude over 15 bpm. However, an acidotic scalp pH was noted in one case exhibiting an amplitude of 5 to 10 bpm, so even the minor
Volume Number
Sinusoidal
136 5
I
-1
FHR.
I
591
MN.
AT JcnrtM1N.
Fig. 4. Fetal monitoring record showing a marked sinusoidal pattern. The amplitude is 20 bpm. The lower trace shows a hypertonic uterine contraction. Table
III. Comparison
of reported
sinusoidal
FHR patterns
Description
Author
of case(s)
Method
of delivery
No. of patients obmved
No. of deaths
Antepatium:
Kubli et al.. 1972 Manseau et al., 1972 Rochard et al., 1976 Moudanlou,
et al., 1977
Mueller-Heubach
et al.. 1978
Multiple high-risk factors including Rh involvement, toxemia anemia, antepartum bleeding Rh involvement Severe Rh isoimmunization, antepartum nonstress testing Chronic hypertension, OCT pos., severe fetal anemia Severe Rh isoimmunization, post-intrauterine fetal transfusion Severe Rh isoimmunization, post-intrauterine transfusion X 3
Not indicated
12
9
Cesarean section
9 20
7 10
Cesarean section
1
0
Cesarean section
1
Cesarean section
0 44
7
Zntrapartum:
Baskett and Koh, 1974 Cetrulo and Schifrin, 1976
Pre-eclampsia, postdates Post dates
Total SHR may be potentially dangerous. Nevertheless, of the 11 cases monitored biochemically, five of the six having scalp pH’s of greater than 7.25 were delivered with 1 minute Apgar scores of at least 8. One-minute Apgar scores of less than 6 were noted in three of the four fetuses having acidotic scalp blood samples, illustrating the usefulness of scalp sampling in assessing fetal condition in cases of SHR. In comparing the interval between the onset of the sinusoidal pattern and the time of delivery, no correla-
Cesarean section Cesarean section
1
1
r
-l
2 --
-2
46
29
tion could be made with the 1 minute Apgar score. The duration of the sinusoidal FHR also showed no statistitally significant relationship with the Apgar score. All fetuses having patterns lasting less than 14 minutes were delivered with nonacidotic umbilical artery samples. Scalp pH samples from these same fetuses were not acidotic. Patterns lasting 14 minutes or longer were associated with preacidotic or acidotic scalp and/or umbilical artery samples in only two of eight such cases. The pathophysiology of the SHR is not understood.
592
Young,
Katz,
lMarch 1, 1980 Am. J. Obstet. Gynecol.
and Wilson
I PH NERVOUS
PO,
SVSTEM
PC02
r MEDULLARY CARDlOkESPlRATORV CENTER
Fig. 5. Diagram I ‘11e pattern.
The
I FETAL
MYOCARDI;M
illustrating the feedback mechanism arrows represent pathways which
Haskett speculated that the sinusoidal pattern was due to deranged nervous control of the fetal heart caused I)! h\poxia. Severe anemia due to Rh disease OI fetomaternal transfusion (and thus possibly highoutput heart failure) has been associated with the sinusoidal pattern.” 3 In only two of our cases could severe fetal anemia due to partial abruptio placentae be considered as a cause of the SHR. The majorit) of. investigators agree that the SHR represents fetal hypoxia, but there is no demonstrable relationship to fetal asphyxia or degree of hypoxic inFult in the litcxrature. Our study presents biochemical data which suggest that acidosis may follow the SHR but is not intrmsic to this FHR pattern. In fact, we have shown that the SHR may begin without acidosis being present, and persist in a normal or preacidotic state for long periods.* Thus, fetal acidosis ma) exert some influence on the pathophysiologp of the SHR, but is not essential. Thc~ SHR can O~CLIT without acidosis and, in general, is associated with a low Apgar score only in the presence of fetal acidosis in our experience. The physiology of the SHR remains unresolved. The sinusoidal pattern has been observed in the premature newborn infhnt without perinatal death, accompanied by a pattern r~f’ periodic breathing.’ This association of cardiac and respiratory periodicity suggests that the fetal autonomic nervous systrm is the likely cxplanation tar the SHR. The occurrence of SHR in Rh isoimmunization, abruptio placentae, cord entanglement or prolapse, postdates, toxemia, and maternal anemia points toward fetal hypoxia as the common denominator. The effects of tissue hypoxia on the medullary centers in the fetal brain which regulate heart rate might account for this unusual FHR pattern. Baskett and Koh suggested that hypoxia “completely deranged” the autonomic nervous control of the FHR. We would offer an alternative hypothesis. We suggest
responsible for the control influence fetal heart t-ate.
of the fetal
heart
that the fetal heart rate is regulated b! ;I flerlhac-kcontrolled system in which the sensitivit\ is increased by hypoxia. The system control is most likely mothulated by the medullary cardioregulator! center ill the fetal brain. The feedback loops probably are the peripheral sensors of cardiorespiratory function, most importantly the carotid and aortic bodies sensitive. to PO, and Pco,. Under conditions of mild hypoxia. the initial FHR response is acceleration in the human subject, probably mediated by sympathetic nervous discharge. I” With increasing or decreasing hypoxia, parasympathetically mediated deceleration follows. It is the interaction of these two nervous discharges which regulates FHR.7 Under conditions where cardioregulator) center sensitivity is high (hypoxia). and feedback signals are undamped (abruptio placentae, fetal anemia, placental insufficiency, cord compression), SLICK a feedback-controlled system can be caused to oscillate, producing a sinusoidal pattern in the FHR recording (Fig. 5). ‘Therefore, the autonomic nervous control is not deranged, but discharging alternately, struggling to maintain homeostasis in a strong compensatory effect under conditions of hypoxia. If the hypoxia abates, the SHR may disappear. If conditions worsrn. the FHR pattern may deteriorate to bradycardia and acidosis may develop as well. Support for this theory is found in the demonstration that the response to progres.sivr hypoxia down to a PO, of 10 mm is an increased index of beat-to-beat variability in the absence of acidosis in the fetal sheep. I’ This represents activation of the autonomic nervous control of heart rate, rather than derangement. Since the human long-term FHR variability is the arithmetic sum of the beat-to-beat changes, a sinusoidal pattern might easily result from relatively mild hypoxia in the absence of acidosis or shock.” Further supporting evidence is the estimated time of
Volume 136 Number5
10 to 20 seconds for fetal blood flow from the placental villous capillaries to the fetal carotid receptors in the human subject.“~ Similarly, after alteration of maternal oxygenation, it takes 20 to 30 seconds for the fetal monkey to show changes in tissue oxygenation in the neck.‘l These time intervals closely approximate the 3 to 5 cpm of the sinusoidal pattern, confirming the chemoreceptor-autonomic nervous system interaction in the genesis of the SHR. Thus, the SHR could be the result of an actively functioning autonomic nervous system in the presence of mild to moderate fetal hypoxia, and the absence of fetal hypotension or acidosis. When the fetus is unable to compensate for the hypoxic insult, or the hypoxia produces sufficient acidosis, the SHR may progress to typical fetal distress patterns. The metabolic deterioration then might lead to the combination of hypoxia and acidosis, which is most deleterious and predisposes to unwanted perinatal outcome. The over-all incidence of the SHR pattern is very low. The occurrence is not predictably related to preexisting high-risk factors. Of the fetuses showing a sinusoidal pattern, 31% had preacidotic or acidotic
Sinusoidal
FHR.
I
593
scalp pH values. There was a 31% incidence of fetal distress as determined by fetuses having low Apgar scores as well, but there were no perinatal deaths. At least in the non-Rh-isoimmunized pregnancy, the appearance of a SHR does not necessarily imply impending fetal death, or necessitate an emergency delivery. It probably indicates hypoxia of mild to moderate degree. and maternal oxygen administration is advisable. Sinusoidal patterns having amplitudes of greater than 15 bpm have a greater risk of fetal acidosis. The decision to intervene should be based on careful biochemical monitoring. Labor and vaginal delivery of patients exhibiting a SHR is indicated as long as reliable biochemical data confirm a nonacidotic fetus despite the presence of a SHR. When the SHR appears in antepartum monitoring in a non-Rh-isoimmunized patient, further evaluation by other means, such as stress testing, estriols, and amniocentesis for meconium should be performed. In such cases the decision to deliver should be based on complete clinical evaluation of each patient rather than the SHR alone. Close observation of the fetal status, combined with disappearance of the SHR, permit conservative management of these patients.
REFERENCES
1. Manseau, P., Vaquier, J., et al.: Le rhythme cardiaque foetal “sinusoidal,” J. Obstet. Gynecol. Biol. Reprod. 1:343, 1972. 2. Baskett, T. F., and Koh, K. S.: Sinusoidal fetal heart rate pattern. A sign of fetal hypoxia, Obstet. Gynecol. 44:379, 1974. 3. Rochard, F., Schifrin, B. S., Goupil, F., et al.: Nonstressed fetal heart rate monitoring in the antepartum period, AM. J. OBSTET. GYNECOL. 126y699, 1976.’ . 4. Kubli. F.. Ruttcrers. H.. Haller. U.. et al.: Die antenartale fetale’ herz fre&enz. II. Verholten von Grundfre’quenz, Fluktuation und Dezerationen bei antepartalem Fruchttod, Z. Geburtshilfe Perinatol. 176:309, 1972. 5. Modanlou, H. D., Freedman, R. K., Ortiz, O., et al.: Sinusoidal fetal heart rate pattern and severe fetal anemia, Obstet. Gynecol. 49:537, 1977. 6. Mueller-Heubach, E., Caritis, S. N., and Edelson, D. I.: Sinusoidal fetal heart rate pattern following intrauterine fetal transfusion. Obstet. Gynecol. 52(Suppl. 1):43, 1977. 7. Cetrulo, C. L., and Schifrin, B. S.: Fe&l-heart rate patterns nreceding death in utero, Obstet. Gvnecol. 48:52 1. 1976.’ v 8. Katz, M., Wilson, S., and Young, B. K.: Sinusoidal fetal
heart rate. II. Evaluation by continuous tissue pH, AM. J. OBSTET.
GYNECOL.
In press.
9. Messer, J., Schick, A. R., Willard, D., et al.: Le cardiorespirogramme de nouveau-&, J. Obstet. Gynecol. Biol. Reprod. 4:815, 1975. 10. Cohn, H. E., Sacks, E. J., Heymann, M. A. et al.: Cardiovascular responses to hypoxemia and acidemia in fetal lambs, AM.J. ~BSTET. GY~OL. 120:817, 1974. 11. Stanee. L.. Rosen. K. G.. Hokegarde, K. H .. et al.: Ouantifi&on of fetal heart rate va;iability in relation tooxygenation in the sheep fetus, Acta Obstet. Gynecol. Stand. 56:205, 1977. 12. Young, B. K., Weinstein, H. N., Hochberg, H. M., et al.: observations in perinatal heart rate monitoring. I. A quantitative method of describing baseline variability in t’he fetal heart rate, J. Reprod. Mid. 20:205, 1978. 13. Mvers. R. E.. Mueller-Heubach, E., and Adamsons, K.: Predictabilitv of the state of fetaloxygenation from a quantitative analysis of the components-of late deceleration. AM. I.OBSTET.GYNECOL. 115:1083. 1973. 14. Mvers, R.-E., Stange, L., loelson, I., et al.: Effects upon the fetus of oxyg& adm&istration to the mother, Acta Obstet. Gynecol. Stand. 56: 195, 1977.