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The relationship of fetal heart rate patterns to the fetal transcutaneous Po 2
The relationship of fetal heart rate patterns to the fetal transcutaneous PO, KOBIN
J.
,JEFFRE:Y
C.
LEONARD JOHN Loui.wille,
WILLCOURT, KING, INDYK,
T.
QUEENAN,
Kentucky,
ana! Elk
M.D. M.D.* PH.D. M.D.* Grove,
Illinois
Continuous transcutaneous PO, (tcPo,) monitoring of the human fetus was performed during 46 labors, 30 of which were complicated by abnormal fetal heart rate (FHR) patterns. FHR variability decreased with increases in the fetal tcPo,, and FHR variability increased with decreases in the fetal tcPo,. Analysis of the tcPoz and FHR tracings provided an explanation for this apparent discrepancy. White rising fetal tcPo, values were usually associated with decreased FHR variability, the pattern of late deceleration and decreased variability must still be considered an ominous pattern. The fetal tcPo, declined during the decleration and rose thereafter, with corresponding decreased FHR variability. Incomplete recovery of the fetal tcPo, was associated with progressive acidosis. Repetitive and isolated late deceleration patterns showed markedly dissimilar fetal tcPo, changes, suggesting different mechanisms may be involved in their production. Further studies are required before any definite conclusions can be drawn about the relationship of the FHR and the fetal tcPo,. (AM. J. OBSTET. GYNECOL. 140:760, 1961.)
fetal monitoring (EFM) has attained a role in obstetric practice that, despite some reports to the contrary, would indicate that it may have a beneficial effect on the management of patients in labor. Since its introduction, and following classification of the fetal heart rate (FHR) patterns,’ numerous investigators have found a degree of correlation between the patterns and the Apgar scores’ and in subsequent infBnt development.” In order to understand the FHR further, we used the continuous transcutaneous PO, (tcPo,) technique as originally described by Huch and associates.’ ELECTRONIC
From the Department oj Obstetrics and Gynecology, Univer.siQ Hospital, Louisville, and Litton Medical Ekctronics, Elk Grozw. Revived
for publicatzon
Rezlised FebruaT Accepted Februaq
June 27, 1980.
3, 1981. 13, 1981.
Reprint requests: Robin J. Willcourt, M.D., Department of Obstetrics and Gynecology, Georgetown University Hospital, 3800 Resew&r Road, N. W., Washington, D. C. 20007. *Current Gynecology,
Reservoir
760
&dress: Department oj‘ Obstetrics and Georgetown Unizlersity Hospital, 3800 Road, N.W., Washington, D. C. 20007.
Material and methods A group of 46 women was monitored for 138 hours with monitoring periods of 1 to 6 hours. All fetuses were in the cephalic presentation. Multiple pregnancies were excluded from the study. Thirty patients were selected because of one or more features that distinguished them as high risk, and the fetuses exhibited abnormal FHR patterns during labor.’ For comparison, 16 patients were selected because they had normal pregnancies and entered labor in a low-risk category. The technique of monitoring was similar to that described by Huch and associates,” modified by one of the authors (R. J. W.). The modification consisted of inserting a 15 p thick polyethylene membrane “spacer” (bathed on both sides by electrolyte) under the standard 12 k Teflon cover used by Huch. This doublelayer membrane assembly produced a more rapid response of the electrode to tcPoz changes (onset of’ response was reduced by 6 to 8 seconds in side-by-sidr measurements on mothers). The fetal tcPo, electrode was introduced by means ot an amnioscope after the cervix had reached 3 to 4 cm of dilatation and was placed on a shaved area of the fetal scalp. Another electrode was placed in the supraclavicular region of the mother to record maternal 0002~9378/81/150760+
10$01.00/O
0 1981 '1-k
C. V. Mosby Co
Volume Number
140 7
Relationship
tcPo,. Equilibration of oxygen transport through the skin depended upon achieving adequate thermal vasodilatation, which usually occurred within 10 minutes. The thermal vasodilatation temperatures selected were 44” C for the fetus and 45” C for the mother.” After 1’/2 hours of continuous fetal monitoring, the temperature of the fetal electrode was reduced intermittently to 37” C to ensure fetal skin integrity. All data relating the tcPo, values to the FHR patterns were taken at 44” C after time was allowed for thermal reequilibration. Skin irritation and edema have been reported to lower tcPo, values following continuous monitoring of 3 hours’ duration at the higher temperatures. The electrode was repositioned after 3 hours of monitoring in two cases. The electrodes and Oxymonitors were supplied by Litton Medical Electronics.* The FHR, obtained by a spiral electrode, and the intrauterine pressure (IUP) were recorded on either a Sonicaid FMSR? or a Corometrics lOlB$ fetal monitor. All tcPo, data were recorded on Hewlett-Packard multichannel recorder HP775SAg at a recorder speed of 3 cm/min. Cord blood gas values were analyzed in all instances by means of a Radiometer ABL 2 blood gas analyzer.11 The Oxymonitor monitored both tcPoB and relative heating power (RHP). The RHP is a measure of the amount of energy supplied to the electrode to maintain the selected temperature. It has been demonstrated in external monitoring on the skin that the RHP is significantly affected by environmental influences. We found that the fetal tcPo* electrode was in a relatively stable thermal environment in the vagina. The RHP reading was relatively constant with the only significant changes seen during vaginal examinations and compression of the electrode on the pelvic wall. These data were, therefore, rejected. The electrodes were calibrated directly before use to the PO, of the humidified ambient air and then to zero PO, with the use of the test solution supplied by Litton. The electrode recalibration was checked after removal. The range of drift was found to be 0 to 2% per hour. The data relating FHR changes to fetal tcPo, changes were analyzed with the use of chisquare statistics to test for significance. Thirty-four of the 46 mothers had an epidural catheter placed for continuous lumbar epidural anesthesia. Epidural-related late deceleration? were avoided by meticulous attention to maternal positioning and adequate hydration. Eight patients in the low-risk group *Litton Medical Electronics, Elk Grove, Illinois. TSonicaid, Fredericksburg, Virginia. $Corometrics Medical Systems, Wallingford, §Hewlett-Packard, Waltham, Massachusetts. IlLondon/Radiometer, Cleveland, Ohio.
Connecticut.
of FHR
to trancutaneous
PO,
761
labored
without an epidural anesthetic. No other mediwere used in any of the patients. Oxygen was administered intermittently to some of the mothers, and we observed the effects of oxygenation and positioning on the fetal maternal tcPo,. In many instances oxygen was administered for up to 3 hours. Informed consent was obtained from all patients in accordance with the policy of the University Hospital. cations
Results There were eight cesarean sections, two for fetal distress and six for cephalopelvic disproportion, for a primary cesarean section rate of 17%. Seven outlet forceps deliveries and 31 assisted vaginal deliveries composed the balance of the group. Of the 46 infants, two showed some degree of distress at delivery (Apgar scores of <7 at 1 and 5 minutes). One neonatal death occurred because of severe congenital abnormalities, including pulmonary hypoplasia, in a female fetus who had shown no significant FHR pattern abnormalities during labor and who appeared healthy immediately on delivery. Thus, 44 babies (96%), including the infant with the congenital malformations, had Apgar scores of 8 or greater at 1 minute. In the study group overall, the fetal tcPo, varied from levels of 0 to 34 tort-. Levels of 15 to 30 torr were recorded for most of the time during which FHR decelerations did not occur and oxygen was not administered. Oxygen was administered to some of the mothers as part of the study. Flow rates of 8 to 10 L/min were required, via a face mask, to raise the maternal tcPo, to over 250 torr. During oxygen administration, the fetal tcPo, generally began to rise 60 to 90 seconds after oxygen was initiated, reaching levels of 5 to 10 torr
above
the
baseline
in
5 to
8 minutes.
The skin underlying the electrode was checked post partum in the mothers and neonates. No reaction other than mild erythema was noted in the neonates. Three mothers had small blisters which appeared 2 to 3 hours following removal of the electrode. The tcPo, values did not appear to be affected in these instances. All of the blisters resolved within 24 to 48 hours.
Relationship of the FHR variability to the tcP& There were 126 isolated instances of decreased long-term variability in the total number of tracings. Because an on-line computer system was not used, only changes in long-term variability could be assessed semiquantitatively by means of a method proposed by Hon.’ The FHR record also showed recognizable changes in short-term variability, but these could not be analyzed
quantitatively.
762
Willcourt
et al.
Fig. 1. Decreasing which is indicated
FHR variability by the change
Fig. 2. Maternal hyperoxygenation, ing FHR variability.
as the fetal in scale.
shown
tcPo,
by a change
Intervals of 10 minutes before, during, and after changes in long-term FHR variability were analyzed. FHR variability was classified as increased, decreased, or no change. The levels to which the tcPo, needed to rise before a change occurred were noted. The changes
rises,
caused
by maternal
in scale and a rising
hyperoxygenatwn.
fetal tcPo, with
decreas-
in FHR variability and tcPo, values were then tested for significance by chi-square analysis (Table I). One hundred seventeen instances of decreased variability were associated with rising levels of fetal tcPo, (p < 0.001) (Figs. 1 and 2), and in nine instances there
Volume Number
Relationship of FHR to trancutaneous
140
Pq
763
7
Fig. 3. The marked effect on the fetal tcPo, of changing the mother from the supine to the left lateral position (arrow). Although normal to decreased FHR variability preceded this change of position by 4 minutes, the variability did not increase despite the rising fetal tcPo,. was no change in the tcPo,. The changes in tcPo, ranged from 4 to 12 torr. There were no instances of decreasing tcPo, associated with decreasing variability. In addition, there were six tracings wherein fetal tcPo, levels considered to be in the normal range (15 to 34 torr) were associated with a reduction in both shortterm and long-term variability (Fig. 3). Conversely, when the fetal tcPo, was decreasing, variability was seen to increase in 112 of 146 instances (p < 0.001) (Figs. 4 and 5). Changes of at least +3 torr in fetal tcPo, were required before an obvious alteration (either an increase or a decrease) was seen in FHR variability. The changes in variability persisted for 10 to 50 minutes, and then the FHR pattern would frequently revert to the previous pattern despite the new level of tcPo,. Exaggerated beat-to-beat variability was seen on a number of occasions. The fetal tcPo, response in each instance was clear. During these episodes of exaggerated variability, the fetal tcPo, declined markedly (Fig. 6). The tcPo, values before the decline were all above 13 torr and during the episodes of exaggerated variability the levels fluctuated from 3 to 9 torr.
Relationship of late decelerations to the tcPo, Four fetuses displayed for a total of 12 hours (Cases 5, 27,44, and 46). decelerations were seen
consistent late decelerations, of observation of this pattern Eight instances of isolated late in the other tracings. There
Table I. Results of 275 observations of FHR variability and the accompanying changes in fetal tcPo,* Increased variability
Rising tcP0, Declining tcPo,
2 112
Decreased No change
9 34
V&bil~
117 0
*Chi-square analysis yielded p < 0.00 1. were, in addition, some severe variable decelerations with late components. A decrease in the fetal tcPo, was seen in all cases of late decelerations but the magnitude of the FHR decline did not correlate with the magnitude of the decline in tcPo, which in some instances was great and in others was minimal (Figs. 7 and 8). This is in contrast to the eight fetuses who had isolated late decelerations. In these instances, the FHR drop was greatest when the tcPor was greatest (Fig. 9). However, the tcPo, did not have to decline to low absolute values to be associated with a late deceleration (Fig. 8). The long-term (and short-term) variability of the FHR was not decreased in these isolated instances, in contrast to the persistent group, where reduced variability was the rule rather than the exception. In general, the tcPo, declined 30 to 40 seconds after the beginning of the uterine contractions, with the fall in FHR starting 10 to 15 seconds earlier. This difference
Fig. 4. Increasing FHK variability rvith declining fetal tcPo, levels. following removal of matern:ll c,x):gen administration. Minimal uterine activity as measured by an external tocodynamometcr.
in time hueen the observed change in the tcPon and the FHR ma\’ reflect the lag time in the tcPo, eiec~trode-skin tompIe?;.tcPm and fetal distress One of the two babies with low Apgdr scone ws born to an insulin-dependent diabetic patient (Case 3). This fetus exhibited fate decelerations and poorvariability f’or 2 haul-s, during which the tcPo, remained in the range of‘ 1.3 to 9 I toIT After :! nxJl‘c hours. the tcPo, fell to a range of 8 to IS torr. A decision was made to deliver the baby, but because of’ an unavoidable dela!,, cesarean section was not done f’or arrothel- hour. During this time the tcPo, fell to 3 to 3 torr. Ultimately, a 3.8 kg male infant lvith Apgar scores of 4 (I minute) and 7 (.i minutes) ~vas delivered. (Zord blood gas values indicated marked acidosis (umbilical arterial pH = 7.08). The other infant ((;ase MI) had mild to moderate late decc1erations in the first stage of labor. accompanied 1~~ a progressiveI!falling tcPo,. A level ot‘ 3 torr was reached at the nadir of descent and the level remained below 10 torr f’or 60 minutes. A cesarean section \cas performed and the baby was clearly asphyxiated at delivery with Apgar scores of -I (1 minute) and 6 (3 minutes) with an arterial pH of 7.18.
Comment Acute studies in exteriorized fetal lambs by Dawes and associates’ showed that aortic chemoreceptors are
responsi\ e to oxygen changes and that the effect on the 1;HR may be mediated, at least in part, by the vagus nerve. In mature, chronically catheterized fetal lambs, made hypoxemic by administration of’ a 10% oxygen mixture to the ewes, bradycardia and a rise in systemic btood pressure were seen with a f’afling arterial pressure of oxygen (Pa&. The bradycardia is most likely a barorcceptor response to hypertension. This response did not persist, however. despite continuing hypoxemia, and the heart rate returned to or beyond its original Ic\cI.~ In addition, the myocardium can be stimulatecl hy alpha- and beta-adrenergic receptors which are present and f’unctional in the fetal myocardium after 120 days.” ‘Thus, the FHK is influenced by various factors. one of which is a change in the Pa,,,. ?o study the relationship of’ the FHR to oxygen changes, the transcut;tneous technique was selected. It must be u11derstood that the tcPo, tnay not be representative of the central PO,. although there is strong evidence to support that this may be so’ unless the local circulation is impaired significantly. Variability of’ the baseline heart rate as computed fi-om fetal electrocardiogram signals obtained by direct techniques has been accepted by many obstetricians as a valid measure of fetal health. Hammacher and associates”’ and Hon and Quilligan” have expressed this L ie{v, postulating that decreased variability or fixed baseline heart rate may indicate significant f’etal hypoxia. In a report by Cibils” and one I,)- Cetrulo and Schifrin.‘: late decelerations, tachycardia. and the loss
VoIume Number
140 7
Relationship of FHR to trancutaneous
Fig. 5. Increasing been stopped.
FHR
variability
as the fetal
tcPo,
declines,
after
Fig. 6. The mother had reached 8 to 9 cm of cervical dilatation Exaggerated FHR variability occurred when the fetal tcPo, fell persisted with the lowered tcPo, values. Maternal hyperoxygenation
of
beat-to-beat
variability
preceded
an
unstable
heart
rate pattern prior to fetal death. In our study, decreased variability was associated with a rising tcPo2 in most of the instances that this pattern was observed. Conversely, increased variability was usually associated with a declining fetal tcPo,. Dal-
maternal
hyperoxygenation
Po2 765
has
and was pushing involuntarily. from 13 to 5 torr. This pattern did not improve the fetal tcPo,.
ton and associates’” reported an increase in variability during experimental hypoxemic episodes in fetal lambs and this effect was also noted in the human fetus. Except
for
produced istration
four
patients.
decreasing
when maternal or both
were
used
positioning to increase
FHR
variability
was
or oxygen adminthe fetal
tcPo2.
It
766
Willcourt et al.
Fig. 7. Spontaneous uterine hyperactivity with a late deceleration pattern. the fetal tcPo,. Note the increasing variability during the late deceleration ahilit\J with the rising tcPo,.
should be noted tllat even with low f’etat tcP0, values the FHR did not shop decrcascd variability (Fig. 3). It wn~lct seem. thcwtore, that neither the presence non the absent (~of’FHK variability is a reHection of‘the actual level of’ thy tcPo, bur may indicate an interaction within the fetal sensing and control centers that detect oxygen changes. ~l‘his concept is in keeping with other known ph~siotogic~ control mechanisms where changes rather than absolute levels in the systems elicit a response. E:xaggerated FttR variability is seen in Fig. 6. In all instances where this pattern was seen, there was an associated marked reduction in the f’etal tcPo, Close inspection of’this pattern suggests small variable decelerations and nnav I-epresenr a fetal cardiac response to ~atec~ltolanli~le release caused b) hvpoxemia, as shown experimentall\ In Dalton and associates” and Jones and Robilw)n.” \Vith the exception of the baby whose pattel II is S~CII in b-ig. (5, the other cases of exaggerated variahilit!, were associated \vith babies horn in good condition. II1 this mildly asphyxiated baby, Apgar scores t\ere .? ( I minute) and 8 (3 minutes). This might be attributed to the continuous nature of’the pattern in this example. ivhereas it ~cas intermittent in other f’etuws. ‘I-his is similar to the pattern that was seen bv
Marked falls are sect, in and the decreasing vari-
Dawes and associates’ in tetat lambs as they were rendered hypoxic. Late decelerations have been fi)und to occur up to four times more often in hypoxic fetuses than in normal fetuses.” This implies that the presence ot’ late decelerations may partially predict poor Ma1 outs ome. Late decelerations may he associated lvith either norrnat or reduced heart rate variabitit!. In the examples of normal or even exaggerated variability in our study, either the decelerations were nonrepetitiw (Fig. !)) or the decline in the fetal tcPo, was only .i to 8 torr. as compared to late decelerations with absent variability in which the declines and recovery in tcPo, were greater than 8 torr. The isolated late deceleration pattern seen in Fig. 9 sometimes Mowed the onset of‘ an epidural block. This prolonged deceleration is not smooth but shou.s exaggerated variability. Bursts of‘ vagat ncIvc’ activitv could produce the appearance of sudden small decelerations superimposed on the broad overall dec-eteration. Parer and associates’” recently reported this tvpc of response in hypoxic fetal lambs. This same group also showed that late decelerations could present as two types, one of which was abolished by atropine and one
Volume Number
Relationship of FHR to trancutaneous
140 7
PO, 767
mm
Fig. 8. Subtle late declerations (Case 46) with falls in the fetal tcPo,. This resulted in an overall decline in the fetal tcPo,, leading to fetal acidosis. Note that the decline in fetal tcPo2 follows the changes in the FHR. This may be due to an impaired peripheral circulation.
Fig. 9.
Isolated late deceleration
which was not.‘” Others have suggested that late decelerations may be the result of both vagal stimulation and a direct myocardial response to hypoxemia.6 The tcPo, changes that we have recorded with widely dissimilar FHR responses would support the presence of at least two types of mechanisms. In addition, there may be
with marked declines in the fetal tcPo,. superimposed catecholamine activity,‘l. ” gerated variability on a vagally mediated The repetitive late deceleration pattern, pared to the isolated deceleration pattern, ferences in response to declining fetal Even though fetal tcPo2 changes of 5 to
seen as exagdeceleration. when comshowed diftcPo, values. 13 torr were
768
Willcourt et al.
seen in the repetitive deceleration group, the depth of the deceleration was not as pronounced as in the isolated type and, hence, did not reflect the magnitude of the change. Instead, the variability of the FHR tended to reHect the magnitude of the tcPo, changes. Thus, the decline in the fetal trPo, in the repetitive group was reflected as a late deceleration, accompanied by some FHR variability. \Vith good recovery of the fetal tcPoz there \vas markedly decreased FHR variability (Fig. 7). If the fetal tcPo, rose slowly (this response occurred frequently). the FHR variability would appear to change less than when the tcPo, rose more rapidly (Fig. 8). Therefore, a late deceleration pattern with unchanging or only slightly diminished FHR variability implies that the tcPo, is rising less markedly in the postdeceleration phase than in those instances where the postdeceleration variability is significantly decreased or absent. If the falls in the fetal tcPo, are small but recovery is complete, then the FHR variability will not appear to be significantly diminished and the outcome will be good. If the fttal tc.Po, declines markedly and there is good recover) in the postdeceleration phase, sufficient to prevent a continual decline in the tcPo,, there will be poor FHR variability, but there will also be a good neonatal outcome. It is in those instances where the fetal tcPo, recovery is incomplete and the level continuall!- declines (Fig. 8, Case 46) that the fetus will be compromised. This reasoning Hould reinforce the concept that all patterns of repetitive late decelerations are to be \ie\ved as ominous because FHR variability cannot be used to differentiate clearly the compromised fetus from the nonasphyxiated one. This study strongl) suggests that the many previously recorded examples of intrapartum fetal asphyxia, where loss of FHR variability \vas a characteristic sign, were a demonstration of this pattern as a late event.“. I” The pathophysiology modifying the FHR in these cases is very likely different f.rom the much more commonly encountered loss of FHR variability that occurs with no signs of fetal compromise apparent at delivery. Therefore, it would seem that loss of FHR variability can occur under varied c-onditions. from fetal well-being to an agonal state. The conditions that produce loss of variability but without initial fetal compromise may eventually lead to fetal acidosis with the FHR pattern appearing remarkabi\, sitnilar at these metabolic extremes. As an example. one of the two asphyxiated fetuses in our study demonstrated a pattern of mild to moderate late decel-
REFERENCES
1. Hon. E. H.: The classification of fetal heart rate, Obstet. Gynecol. 22:137. 1963.
erations with slightly diminished FHR variability. 1 hr declines in the fetal tcPo, lvere minimal with each cotitraction. but the overall level declined to \-alues of 3 to X tar-r before delivery could be accomplished. Over rite Icicle range of tcPo, values seen in this cxatnplc (!?I to 3 torr), the FHR pattern remained the same, supporting the concept that the absolute levels of ox! get1 do IUII correlate significantly with the FHR patter” (Fig. Xl. The other tWo fetuses with late decelerations tj cre maintained at higher fetal tcPo, levels and \vert: born it1 good condition. ‘The fact that decreased variability ma! occur with an increasing fetal tcP0, suggests cautious evaluation of the FHR pattern after maternal hvperoxvgenation 1’01. intrauterine resuscitation. It is quite possible, as in this case. that the fetal distress has actually bectt relie\ctl (which could be sholvrt bv measllremenr ot’ the ftital tcPo, or by fetal scalp blood sampling), although tlx FHR tracing might lead one to conclude otherwise. Normal FHR variability was associated with a good perinatal outcome in this study, as has beet1 reported in other studies where larger nutnbers gal c’ statistical significance to this observation.‘-” Inc reasing- FHK variability was associated with a declining fetal tcl’o, and decreasing FHR variability was seen with a rising fetal tcPo,. This apparent conflict with earEel- concepts of the significance of decreased FHR variability is resolved when it is realized that changes in fetal tcPo, rather than absolute values of the fetal tcPo, relate these two parameters. Late decelerations were alwavs associated with a declining fetal tcPo, although the magnitude of the FHR deceleration olten did not refect the extent of the decline in the tetal tcPo, and the presence or absence of FHR variabilitv dicl not reHect the baseline levels of fetal oxygenation. Further studies supporting the validity of the fetal technique of transcutaneous oxygen measurements are necessary before any definite conclusions can be drawn about the precise relationship of the FHR and the fetal tcPo,. Experiments with the method to date would indicate that it has the potential to impro\.r our understanding of the physiology and pathtrph!siolttgy that relate FHR patterns and fetal oxygenation. \Ve acknowledge and M.D., and John Patrick, advice in the preparation residents and nurses who
thank Roget K. Freeman, M.D., for their analysis and of this manusc.ript, and the helped in the study.
2. Schifrin, B., and Dame. L.: Fetal heat-t rate patterns. Prediction of Apgar score. JAMA 219: 1322, 1972. 3. Painter, M. J., Depp. R., and O’Donoghue. P. D.: Fetal
Volume Number
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5.
6. 7.
8.
9.
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heart rate patterns and development in the first year of life, AM. J. OBSTET. GYNECOL. 132:217, 1978. Huch, A., Huch, R., Schneider, H., et al: Continuous transcutaneous monitoring of fetal oxygen tension during labour. Br. J. Obstet. Gynaecol. (Suppl.) 84: 1, 1977. McDonald, J. S., Bjorkman, L., and Reed, E.: Epidural anesthesia for obstetrics, AM. J. OBSTET. GYNECOL. 120: 1055, 1974. Hon. E. H.: An Atlas of Fetal Heart Rate Patterns, New Haven, 1968, Harty Press Inc. Dawes, G. S., Duncan, S. L. B., Lewis, B. V.. et al.: Hypoxaemia and aortic body chemoreceptor function in foeial lambs, J. Physiol. 2011105, 1969. Boddv. K.. Dawes. G. S.. Fisher. R.. et al.: Foetal resoiratory movements and electrocortical and cardiovascular responses to hypoxaemia and hypercapnia in sheep, J. Physiol. 243:599. 1974. Rudolph, A. M., and Heymann, N.: Control of the foetal circulation, in Comline, R. S., Cross, K. W.. Dawes, G. S., and Nathanielsz, P. W., editors: Foetal and Neonatal Physiology. London, 1973, Cambridge University Press, pp. 89-111. I,
of FHR
to trancutaneous
PO,
769
10. Hammacher, K., Huter, K. A., Bokelmann, J., et al.: Foetal heart frequency and perinatal conditions of the foetus and newborn. Gvnaecoloeia 166:349. 1968. 11. Hon. E. H., and Quilligan, E. J.: ?‘he classification of fetal heart rate, Conn. Med. 31:779, 1967. 12. Cibils, L. A.: Clinical significance of fetal heart rate patterns during labor. IV. Agonal patterns, AM. J. OBSTET. GYNECOL. 129:833. 1977. C. L., and Schifrin, B. S.: Fetal heart rate pat13. Cetrulo, terns preceding death in utero. Obstet. Gynecol. 48:521, 1976. 14. Dalton, K. J.. Dawes, G. S., and Patrick. J. E.: Diurnal, respiratory and other rhythms of fetal heart rate in lambs, AM. J. OBSTET. GYNECOL. 127:414, 1977. R. 0.: Plasma catecholamines 15. Jones, C. T., and Robinson. in foetal and adult sheep, J. Physiol. 248:15, 1975. T. R., and Harris, J. L.: Fetal oxy16. Parer, J. T., Krueger, gen consumption and mechanisms of heart rate response during artificially produced late decelerations of fetal heart rate in sheep, AM. J. OBSTET. GYNECOL. 136:478, 1980.
J.
,JEFFRE:Y
C.
LEONARD JOHN Loui.wille,
WILLCOURT, KING, INDYK,
T.
QUEENAN,
Kentucky,
ana! Elk
M.D. M.D.* PH.D. M.D.* Grove,
Illinois
Continuous transcutaneous PO, (tcPo,) monitoring of the human fetus was performed during 46 labors, 30 of which were complicated by abnormal fetal heart rate (FHR) patterns. FHR variability decreased with increases in the fetal tcPo,, and FHR variability increased with decreases in the fetal tcPo,. Analysis of the tcPoz and FHR tracings provided an explanation for this apparent discrepancy. White rising fetal tcPo, values were usually associated with decreased FHR variability, the pattern of late deceleration and decreased variability must still be considered an ominous pattern. The fetal tcPo, declined during the decleration and rose thereafter, with corresponding decreased FHR variability. Incomplete recovery of the fetal tcPo, was associated with progressive acidosis. Repetitive and isolated late deceleration patterns showed markedly dissimilar fetal tcPo, changes, suggesting different mechanisms may be involved in their production. Further studies are required before any definite conclusions can be drawn about the relationship of the FHR and the fetal tcPo,. (AM. J. OBSTET. GYNECOL. 140:760, 1961.)
fetal monitoring (EFM) has attained a role in obstetric practice that, despite some reports to the contrary, would indicate that it may have a beneficial effect on the management of patients in labor. Since its introduction, and following classification of the fetal heart rate (FHR) patterns,’ numerous investigators have found a degree of correlation between the patterns and the Apgar scores’ and in subsequent infBnt development.” In order to understand the FHR further, we used the continuous transcutaneous PO, (tcPo,) technique as originally described by Huch and associates.’ ELECTRONIC
From the Department oj Obstetrics and Gynecology, Univer.siQ Hospital, Louisville, and Litton Medical Ekctronics, Elk Grozw. Revived
for publicatzon
Rezlised FebruaT Accepted Februaq
June 27, 1980.
3, 1981. 13, 1981.
Reprint requests: Robin J. Willcourt, M.D., Department of Obstetrics and Gynecology, Georgetown University Hospital, 3800 Resew&r Road, N. W., Washington, D. C. 20007. *Current Gynecology,
Reservoir
760
&dress: Department oj‘ Obstetrics and Georgetown Unizlersity Hospital, 3800 Road, N.W., Washington, D. C. 20007.
Material and methods A group of 46 women was monitored for 138 hours with monitoring periods of 1 to 6 hours. All fetuses were in the cephalic presentation. Multiple pregnancies were excluded from the study. Thirty patients were selected because of one or more features that distinguished them as high risk, and the fetuses exhibited abnormal FHR patterns during labor.’ For comparison, 16 patients were selected because they had normal pregnancies and entered labor in a low-risk category. The technique of monitoring was similar to that described by Huch and associates,” modified by one of the authors (R. J. W.). The modification consisted of inserting a 15 p thick polyethylene membrane “spacer” (bathed on both sides by electrolyte) under the standard 12 k Teflon cover used by Huch. This doublelayer membrane assembly produced a more rapid response of the electrode to tcPoz changes (onset of’ response was reduced by 6 to 8 seconds in side-by-sidr measurements on mothers). The fetal tcPo, electrode was introduced by means ot an amnioscope after the cervix had reached 3 to 4 cm of dilatation and was placed on a shaved area of the fetal scalp. Another electrode was placed in the supraclavicular region of the mother to record maternal 0002~9378/81/150760+
10$01.00/O
0 1981 '1-k
C. V. Mosby Co
Volume Number
140 7
Relationship
tcPo,. Equilibration of oxygen transport through the skin depended upon achieving adequate thermal vasodilatation, which usually occurred within 10 minutes. The thermal vasodilatation temperatures selected were 44” C for the fetus and 45” C for the mother.” After 1’/2 hours of continuous fetal monitoring, the temperature of the fetal electrode was reduced intermittently to 37” C to ensure fetal skin integrity. All data relating the tcPo, values to the FHR patterns were taken at 44” C after time was allowed for thermal reequilibration. Skin irritation and edema have been reported to lower tcPo, values following continuous monitoring of 3 hours’ duration at the higher temperatures. The electrode was repositioned after 3 hours of monitoring in two cases. The electrodes and Oxymonitors were supplied by Litton Medical Electronics.* The FHR, obtained by a spiral electrode, and the intrauterine pressure (IUP) were recorded on either a Sonicaid FMSR? or a Corometrics lOlB$ fetal monitor. All tcPo, data were recorded on Hewlett-Packard multichannel recorder HP775SAg at a recorder speed of 3 cm/min. Cord blood gas values were analyzed in all instances by means of a Radiometer ABL 2 blood gas analyzer.11 The Oxymonitor monitored both tcPoB and relative heating power (RHP). The RHP is a measure of the amount of energy supplied to the electrode to maintain the selected temperature. It has been demonstrated in external monitoring on the skin that the RHP is significantly affected by environmental influences. We found that the fetal tcPo* electrode was in a relatively stable thermal environment in the vagina. The RHP reading was relatively constant with the only significant changes seen during vaginal examinations and compression of the electrode on the pelvic wall. These data were, therefore, rejected. The electrodes were calibrated directly before use to the PO, of the humidified ambient air and then to zero PO, with the use of the test solution supplied by Litton. The electrode recalibration was checked after removal. The range of drift was found to be 0 to 2% per hour. The data relating FHR changes to fetal tcPo, changes were analyzed with the use of chisquare statistics to test for significance. Thirty-four of the 46 mothers had an epidural catheter placed for continuous lumbar epidural anesthesia. Epidural-related late deceleration? were avoided by meticulous attention to maternal positioning and adequate hydration. Eight patients in the low-risk group *Litton Medical Electronics, Elk Grove, Illinois. TSonicaid, Fredericksburg, Virginia. $Corometrics Medical Systems, Wallingford, §Hewlett-Packard, Waltham, Massachusetts. IlLondon/Radiometer, Cleveland, Ohio.
Connecticut.
of FHR
to trancutaneous
PO,
761
labored
without an epidural anesthetic. No other mediwere used in any of the patients. Oxygen was administered intermittently to some of the mothers, and we observed the effects of oxygenation and positioning on the fetal maternal tcPo,. In many instances oxygen was administered for up to 3 hours. Informed consent was obtained from all patients in accordance with the policy of the University Hospital. cations
Results There were eight cesarean sections, two for fetal distress and six for cephalopelvic disproportion, for a primary cesarean section rate of 17%. Seven outlet forceps deliveries and 31 assisted vaginal deliveries composed the balance of the group. Of the 46 infants, two showed some degree of distress at delivery (Apgar scores of <7 at 1 and 5 minutes). One neonatal death occurred because of severe congenital abnormalities, including pulmonary hypoplasia, in a female fetus who had shown no significant FHR pattern abnormalities during labor and who appeared healthy immediately on delivery. Thus, 44 babies (96%), including the infant with the congenital malformations, had Apgar scores of 8 or greater at 1 minute. In the study group overall, the fetal tcPo, varied from levels of 0 to 34 tort-. Levels of 15 to 30 torr were recorded for most of the time during which FHR decelerations did not occur and oxygen was not administered. Oxygen was administered to some of the mothers as part of the study. Flow rates of 8 to 10 L/min were required, via a face mask, to raise the maternal tcPo, to over 250 torr. During oxygen administration, the fetal tcPo, generally began to rise 60 to 90 seconds after oxygen was initiated, reaching levels of 5 to 10 torr
above
the
baseline
in
5 to
8 minutes.
The skin underlying the electrode was checked post partum in the mothers and neonates. No reaction other than mild erythema was noted in the neonates. Three mothers had small blisters which appeared 2 to 3 hours following removal of the electrode. The tcPo, values did not appear to be affected in these instances. All of the blisters resolved within 24 to 48 hours.
Relationship of the FHR variability to the tcP& There were 126 isolated instances of decreased long-term variability in the total number of tracings. Because an on-line computer system was not used, only changes in long-term variability could be assessed semiquantitatively by means of a method proposed by Hon.’ The FHR record also showed recognizable changes in short-term variability, but these could not be analyzed
quantitatively.
762
Willcourt
et al.
Fig. 1. Decreasing which is indicated
FHR variability by the change
Fig. 2. Maternal hyperoxygenation, ing FHR variability.
as the fetal in scale.
shown
tcPo,
by a change
Intervals of 10 minutes before, during, and after changes in long-term FHR variability were analyzed. FHR variability was classified as increased, decreased, or no change. The levels to which the tcPo, needed to rise before a change occurred were noted. The changes
rises,
caused
by maternal
in scale and a rising
hyperoxygenatwn.
fetal tcPo, with
decreas-
in FHR variability and tcPo, values were then tested for significance by chi-square analysis (Table I). One hundred seventeen instances of decreased variability were associated with rising levels of fetal tcPo, (p < 0.001) (Figs. 1 and 2), and in nine instances there
Volume Number
Relationship of FHR to trancutaneous
140
Pq
763
7
Fig. 3. The marked effect on the fetal tcPo, of changing the mother from the supine to the left lateral position (arrow). Although normal to decreased FHR variability preceded this change of position by 4 minutes, the variability did not increase despite the rising fetal tcPo,. was no change in the tcPo,. The changes in tcPo, ranged from 4 to 12 torr. There were no instances of decreasing tcPo, associated with decreasing variability. In addition, there were six tracings wherein fetal tcPo, levels considered to be in the normal range (15 to 34 torr) were associated with a reduction in both shortterm and long-term variability (Fig. 3). Conversely, when the fetal tcPo, was decreasing, variability was seen to increase in 112 of 146 instances (p < 0.001) (Figs. 4 and 5). Changes of at least +3 torr in fetal tcPo, were required before an obvious alteration (either an increase or a decrease) was seen in FHR variability. The changes in variability persisted for 10 to 50 minutes, and then the FHR pattern would frequently revert to the previous pattern despite the new level of tcPo,. Exaggerated beat-to-beat variability was seen on a number of occasions. The fetal tcPo, response in each instance was clear. During these episodes of exaggerated variability, the fetal tcPo, declined markedly (Fig. 6). The tcPo, values before the decline were all above 13 torr and during the episodes of exaggerated variability the levels fluctuated from 3 to 9 torr.
Relationship of late decelerations to the tcPo, Four fetuses displayed for a total of 12 hours (Cases 5, 27,44, and 46). decelerations were seen
consistent late decelerations, of observation of this pattern Eight instances of isolated late in the other tracings. There
Table I. Results of 275 observations of FHR variability and the accompanying changes in fetal tcPo,* Increased variability
Rising tcP0, Declining tcPo,
2 112
Decreased No change
9 34
V&bil~
117 0
*Chi-square analysis yielded p < 0.00 1. were, in addition, some severe variable decelerations with late components. A decrease in the fetal tcPo, was seen in all cases of late decelerations but the magnitude of the FHR decline did not correlate with the magnitude of the decline in tcPo, which in some instances was great and in others was minimal (Figs. 7 and 8). This is in contrast to the eight fetuses who had isolated late decelerations. In these instances, the FHR drop was greatest when the tcPor was greatest (Fig. 9). However, the tcPo, did not have to decline to low absolute values to be associated with a late deceleration (Fig. 8). The long-term (and short-term) variability of the FHR was not decreased in these isolated instances, in contrast to the persistent group, where reduced variability was the rule rather than the exception. In general, the tcPo, declined 30 to 40 seconds after the beginning of the uterine contractions, with the fall in FHR starting 10 to 15 seconds earlier. This difference
Fig. 4. Increasing FHK variability rvith declining fetal tcPo, levels. following removal of matern:ll c,x):gen administration. Minimal uterine activity as measured by an external tocodynamometcr.
in time hueen the observed change in the tcPon and the FHR ma\’ reflect the lag time in the tcPo, eiec~trode-skin tompIe?;.tcPm and fetal distress One of the two babies with low Apgdr scone ws born to an insulin-dependent diabetic patient (Case 3). This fetus exhibited fate decelerations and poorvariability f’or 2 haul-s, during which the tcPo, remained in the range of‘ 1.3 to 9 I toIT After :! nxJl‘c hours. the tcPo, fell to a range of 8 to IS torr. A decision was made to deliver the baby, but because of’ an unavoidable dela!,, cesarean section was not done f’or arrothel- hour. During this time the tcPo, fell to 3 to 3 torr. Ultimately, a 3.8 kg male infant lvith Apgar scores of 4 (I minute) and 7 (.i minutes) ~vas delivered. (Zord blood gas values indicated marked acidosis (umbilical arterial pH = 7.08). The other infant ((;ase MI) had mild to moderate late decc1erations in the first stage of labor. accompanied 1~~ a progressiveI!falling tcPo,. A level ot‘ 3 torr was reached at the nadir of descent and the level remained below 10 torr f’or 60 minutes. A cesarean section \cas performed and the baby was clearly asphyxiated at delivery with Apgar scores of -I (1 minute) and 6 (3 minutes) with an arterial pH of 7.18.
Comment Acute studies in exteriorized fetal lambs by Dawes and associates’ showed that aortic chemoreceptors are
responsi\ e to oxygen changes and that the effect on the 1;HR may be mediated, at least in part, by the vagus nerve. In mature, chronically catheterized fetal lambs, made hypoxemic by administration of’ a 10% oxygen mixture to the ewes, bradycardia and a rise in systemic btood pressure were seen with a f’afling arterial pressure of oxygen (Pa&. The bradycardia is most likely a barorcceptor response to hypertension. This response did not persist, however. despite continuing hypoxemia, and the heart rate returned to or beyond its original Ic\cI.~ In addition, the myocardium can be stimulatecl hy alpha- and beta-adrenergic receptors which are present and f’unctional in the fetal myocardium after 120 days.” ‘Thus, the FHK is influenced by various factors. one of which is a change in the Pa,,,. ?o study the relationship of’ the FHR to oxygen changes, the transcut;tneous technique was selected. It must be u11derstood that the tcPo, tnay not be representative of the central PO,. although there is strong evidence to support that this may be so’ unless the local circulation is impaired significantly. Variability of’ the baseline heart rate as computed fi-om fetal electrocardiogram signals obtained by direct techniques has been accepted by many obstetricians as a valid measure of fetal health. Hammacher and associates”’ and Hon and Quilligan” have expressed this L ie{v, postulating that decreased variability or fixed baseline heart rate may indicate significant f’etal hypoxia. In a report by Cibils” and one I,)- Cetrulo and Schifrin.‘: late decelerations, tachycardia. and the loss
VoIume Number
140 7
Relationship of FHR to trancutaneous
Fig. 5. Increasing been stopped.
FHR
variability
as the fetal
tcPo,
declines,
after
Fig. 6. The mother had reached 8 to 9 cm of cervical dilatation Exaggerated FHR variability occurred when the fetal tcPo, fell persisted with the lowered tcPo, values. Maternal hyperoxygenation
of
beat-to-beat
variability
preceded
an
unstable
heart
rate pattern prior to fetal death. In our study, decreased variability was associated with a rising tcPo2 in most of the instances that this pattern was observed. Conversely, increased variability was usually associated with a declining fetal tcPo,. Dal-
maternal
hyperoxygenation
Po2 765
has
and was pushing involuntarily. from 13 to 5 torr. This pattern did not improve the fetal tcPo,.
ton and associates’” reported an increase in variability during experimental hypoxemic episodes in fetal lambs and this effect was also noted in the human fetus. Except
for
produced istration
four
patients.
decreasing
when maternal or both
were
used
positioning to increase
FHR
variability
was
or oxygen adminthe fetal
tcPo2.
It
766
Willcourt et al.
Fig. 7. Spontaneous uterine hyperactivity with a late deceleration pattern. the fetal tcPo,. Note the increasing variability during the late deceleration ahilit\J with the rising tcPo,.
should be noted tllat even with low f’etat tcP0, values the FHR did not shop decrcascd variability (Fig. 3). It wn~lct seem. thcwtore, that neither the presence non the absent (~of’FHK variability is a reHection of‘the actual level of’ thy tcPo, bur may indicate an interaction within the fetal sensing and control centers that detect oxygen changes. ~l‘his concept is in keeping with other known ph~siotogic~ control mechanisms where changes rather than absolute levels in the systems elicit a response. E:xaggerated FttR variability is seen in Fig. 6. In all instances where this pattern was seen, there was an associated marked reduction in the f’etal tcPo, Close inspection of’this pattern suggests small variable decelerations and nnav I-epresenr a fetal cardiac response to ~atec~ltolanli~le release caused b) hvpoxemia, as shown experimentall\ In Dalton and associates” and Jones and Robilw)n.” \Vith the exception of the baby whose pattel II is S~CII in b-ig. (5, the other cases of exaggerated variahilit!, were associated \vith babies horn in good condition. II1 this mildly asphyxiated baby, Apgar scores t\ere .? ( I minute) and 8 (3 minutes). This might be attributed to the continuous nature of’the pattern in this example. ivhereas it ~cas intermittent in other f’etuws. ‘I-his is similar to the pattern that was seen bv
Marked falls are sect, in and the decreasing vari-
Dawes and associates’ in tetat lambs as they were rendered hypoxic. Late decelerations have been fi)und to occur up to four times more often in hypoxic fetuses than in normal fetuses.” This implies that the presence ot’ late decelerations may partially predict poor Ma1 outs ome. Late decelerations may he associated lvith either norrnat or reduced heart rate variabitit!. In the examples of normal or even exaggerated variability in our study, either the decelerations were nonrepetitiw (Fig. !)) or the decline in the fetal tcPo, was only .i to 8 torr. as compared to late decelerations with absent variability in which the declines and recovery in tcPo, were greater than 8 torr. The isolated late deceleration pattern seen in Fig. 9 sometimes Mowed the onset of‘ an epidural block. This prolonged deceleration is not smooth but shou.s exaggerated variability. Bursts of‘ vagat ncIvc’ activitv could produce the appearance of sudden small decelerations superimposed on the broad overall dec-eteration. Parer and associates’” recently reported this tvpc of response in hypoxic fetal lambs. This same group also showed that late decelerations could present as two types, one of which was abolished by atropine and one
Volume Number
Relationship of FHR to trancutaneous
140 7
PO, 767
mm
Fig. 8. Subtle late declerations (Case 46) with falls in the fetal tcPo,. This resulted in an overall decline in the fetal tcPo,, leading to fetal acidosis. Note that the decline in fetal tcPo2 follows the changes in the FHR. This may be due to an impaired peripheral circulation.
Fig. 9.
Isolated late deceleration
which was not.‘” Others have suggested that late decelerations may be the result of both vagal stimulation and a direct myocardial response to hypoxemia.6 The tcPo, changes that we have recorded with widely dissimilar FHR responses would support the presence of at least two types of mechanisms. In addition, there may be
with marked declines in the fetal tcPo,. superimposed catecholamine activity,‘l. ” gerated variability on a vagally mediated The repetitive late deceleration pattern, pared to the isolated deceleration pattern, ferences in response to declining fetal Even though fetal tcPo2 changes of 5 to
seen as exagdeceleration. when comshowed diftcPo, values. 13 torr were
768
Willcourt et al.
seen in the repetitive deceleration group, the depth of the deceleration was not as pronounced as in the isolated type and, hence, did not reflect the magnitude of the change. Instead, the variability of the FHR tended to reHect the magnitude of the tcPo, changes. Thus, the decline in the fetal trPo, in the repetitive group was reflected as a late deceleration, accompanied by some FHR variability. \Vith good recovery of the fetal tcPoz there \vas markedly decreased FHR variability (Fig. 7). If the fetal tcPo, rose slowly (this response occurred frequently). the FHR variability would appear to change less than when the tcPo, rose more rapidly (Fig. 8). Therefore, a late deceleration pattern with unchanging or only slightly diminished FHR variability implies that the tcPo, is rising less markedly in the postdeceleration phase than in those instances where the postdeceleration variability is significantly decreased or absent. If the falls in the fetal tcPo, are small but recovery is complete, then the FHR variability will not appear to be significantly diminished and the outcome will be good. If the fttal tc.Po, declines markedly and there is good recover) in the postdeceleration phase, sufficient to prevent a continual decline in the tcPo,, there will be poor FHR variability, but there will also be a good neonatal outcome. It is in those instances where the fetal tcPo, recovery is incomplete and the level continuall!- declines (Fig. 8, Case 46) that the fetus will be compromised. This reasoning Hould reinforce the concept that all patterns of repetitive late decelerations are to be \ie\ved as ominous because FHR variability cannot be used to differentiate clearly the compromised fetus from the nonasphyxiated one. This study strongl) suggests that the many previously recorded examples of intrapartum fetal asphyxia, where loss of FHR variability \vas a characteristic sign, were a demonstration of this pattern as a late event.“. I” The pathophysiology modifying the FHR in these cases is very likely different f.rom the much more commonly encountered loss of FHR variability that occurs with no signs of fetal compromise apparent at delivery. Therefore, it would seem that loss of FHR variability can occur under varied c-onditions. from fetal well-being to an agonal state. The conditions that produce loss of variability but without initial fetal compromise may eventually lead to fetal acidosis with the FHR pattern appearing remarkabi\, sitnilar at these metabolic extremes. As an example. one of the two asphyxiated fetuses in our study demonstrated a pattern of mild to moderate late decel-
REFERENCES
1. Hon. E. H.: The classification of fetal heart rate, Obstet. Gynecol. 22:137. 1963.
erations with slightly diminished FHR variability. 1 hr declines in the fetal tcPo, lvere minimal with each cotitraction. but the overall level declined to \-alues of 3 to X tar-r before delivery could be accomplished. Over rite Icicle range of tcPo, values seen in this cxatnplc (!?I to 3 torr), the FHR pattern remained the same, supporting the concept that the absolute levels of ox! get1 do IUII correlate significantly with the FHR patter” (Fig. Xl. The other tWo fetuses with late decelerations tj cre maintained at higher fetal tcPo, levels and \vert: born it1 good condition. ‘The fact that decreased variability ma! occur with an increasing fetal tcP0, suggests cautious evaluation of the FHR pattern after maternal hvperoxvgenation 1’01. intrauterine resuscitation. It is quite possible, as in this case. that the fetal distress has actually bectt relie\ctl (which could be sholvrt bv measllremenr ot’ the ftital tcPo, or by fetal scalp blood sampling), although tlx FHR tracing might lead one to conclude otherwise. Normal FHR variability was associated with a good perinatal outcome in this study, as has beet1 reported in other studies where larger nutnbers gal c’ statistical significance to this observation.‘-” Inc reasing- FHK variability was associated with a declining fetal tcl’o, and decreasing FHR variability was seen with a rising fetal tcPo,. This apparent conflict with earEel- concepts of the significance of decreased FHR variability is resolved when it is realized that changes in fetal tcPo, rather than absolute values of the fetal tcPo, relate these two parameters. Late decelerations were alwavs associated with a declining fetal tcPo, although the magnitude of the FHR deceleration olten did not refect the extent of the decline in the tetal tcPo, and the presence or absence of FHR variabilitv dicl not reHect the baseline levels of fetal oxygenation. Further studies supporting the validity of the fetal technique of transcutaneous oxygen measurements are necessary before any definite conclusions can be drawn about the precise relationship of the FHR and the fetal tcPo,. Experiments with the method to date would indicate that it has the potential to impro\.r our understanding of the physiology and pathtrph!siolttgy that relate FHR patterns and fetal oxygenation. \Ve acknowledge and M.D., and John Patrick, advice in the preparation residents and nurses who
thank Roget K. Freeman, M.D., for their analysis and of this manusc.ript, and the helped in the study.
2. Schifrin, B., and Dame. L.: Fetal heat-t rate patterns. Prediction of Apgar score. JAMA 219: 1322, 1972. 3. Painter, M. J., Depp. R., and O’Donoghue. P. D.: Fetal
Volume Number
4.
5.
6. 7.
8.
9.
140 7
Relationship
heart rate patterns and development in the first year of life, AM. J. OBSTET. GYNECOL. 132:217, 1978. Huch, A., Huch, R., Schneider, H., et al: Continuous transcutaneous monitoring of fetal oxygen tension during labour. Br. J. Obstet. Gynaecol. (Suppl.) 84: 1, 1977. McDonald, J. S., Bjorkman, L., and Reed, E.: Epidural anesthesia for obstetrics, AM. J. OBSTET. GYNECOL. 120: 1055, 1974. Hon. E. H.: An Atlas of Fetal Heart Rate Patterns, New Haven, 1968, Harty Press Inc. Dawes, G. S., Duncan, S. L. B., Lewis, B. V.. et al.: Hypoxaemia and aortic body chemoreceptor function in foeial lambs, J. Physiol. 2011105, 1969. Boddv. K.. Dawes. G. S.. Fisher. R.. et al.: Foetal resoiratory movements and electrocortical and cardiovascular responses to hypoxaemia and hypercapnia in sheep, J. Physiol. 243:599. 1974. Rudolph, A. M., and Heymann, N.: Control of the foetal circulation, in Comline, R. S., Cross, K. W.. Dawes, G. S., and Nathanielsz, P. W., editors: Foetal and Neonatal Physiology. London, 1973, Cambridge University Press, pp. 89-111. I,
of FHR
to trancutaneous
PO,
769
10. Hammacher, K., Huter, K. A., Bokelmann, J., et al.: Foetal heart frequency and perinatal conditions of the foetus and newborn. Gvnaecoloeia 166:349. 1968. 11. Hon. E. H., and Quilligan, E. J.: ?‘he classification of fetal heart rate, Conn. Med. 31:779, 1967. 12. Cibils, L. A.: Clinical significance of fetal heart rate patterns during labor. IV. Agonal patterns, AM. J. OBSTET. GYNECOL. 129:833. 1977. C. L., and Schifrin, B. S.: Fetal heart rate pat13. Cetrulo, terns preceding death in utero. Obstet. Gynecol. 48:521, 1976. 14. Dalton, K. J.. Dawes, G. S., and Patrick. J. E.: Diurnal, respiratory and other rhythms of fetal heart rate in lambs, AM. J. OBSTET. GYNECOL. 127:414, 1977. R. 0.: Plasma catecholamines 15. Jones, C. T., and Robinson. in foetal and adult sheep, J. Physiol. 248:15, 1975. T. R., and Harris, J. L.: Fetal oxy16. Parer, J. T., Krueger, gen consumption and mechanisms of heart rate response during artificially produced late decelerations of fetal heart rate in sheep, AM. J. OBSTET. GYNECOL. 136:478, 1980.