The effect of umbilical vein occlusion on fetal oxygenation, cardiovascular parameters, and fetal electroencephalogram

The effect of umbilical vein occlusion on fetal oxygenation, cardiovascular parameters, and fetal electroencephalogram WOLFGANG KUNZEL, M.D. LEON I. MANN, M.D. AMRUTHA BHAKTHAVATHSALAN, M.D. JAHAGIR AIROMLOOI, M.D. MAIDA LIL', B.S. East Meadow and Stony Brook, New York In 11 fetal sheep experiments, the blood pressure in the fetal a,orta (FA) and in the umbilical vein (UV) was measured following umbilical vein occlusion (UVO), as was the fetal heart rate (FHA), pH, Pco 2, and oxygen saturation (So:J in both fetal vessels, and umbilical blood flow (Qumb) of the common UV. The fetal electroencephalogram was recorded continuously throughout the experiment. The results (No. = 17) were grouped according to the response of FA So 2 into moderate (So2 > 40 per cent, mean 49.8, S.D. 6.3, and severe So2 < 40 per cent, mean 20.4, S.D. 9.2). After 8 to 10 seconds, the fetal blood pressure in FA increased. Umbilical vein blood pressure increased to 25 mm. Hg (S.D. 8) and 35 mm. Hg (S.D. 9) in the moderate and severe groups, respectively. As a result of the decreased perfusion pressure (FA-UV blood pressure) across the fetal side of the placenta, the Qumb fell from 147 mi. per kilogram per minute (S.D. 57) and 120 mi. per kilogram per minute (S.D. 55) to 84 mi. per kilogram per minute (S.D. 48) and 30 mi. per kilogram per minute (S.D. 22), respectively. The fall in FA So2 was related to the decrease in Qumb: FA So 2 = 37.6 x log Qumb - 22.8 (2a < 0.001). There was a mild decrease in So 2 from 70 to 55 per cent When Qumb fell from 250 to 120 mi. per kilogram per minute. Below 80 to 120 mi. per kilogram per minute, the fall in FA S0 2 was almost linear. The So 2 in the UV remained constant so that arteriovenous difference for oxygen (AV Do:J increased. Oxygen consumption decreased almost linearly when Qumb fell below 80 to 120 mi. per kilogram per minute. The fetal electroencephalogram showed no significant change in voltage and the faster activities. From these observations, it is concluded that a decrease in Qumb following UVO jeopardizes the fetus only if a critical Qumb of 80 to 120 mi. per kilogram per minute and fetal artery So 2 of 50 to 60 per cent is achieved. (AM. J. OBSTET. GYNECOL. 128: 201, 1977.)

PARTIAL CORD OCCLUSION where the umbilical vein is preferentially constricted has been suggested as the cause of the variable type of heart rate deceleration pattern during labor. 2 • 5 • 9 The influence of umbilical

From the Department of Obstetrics and Gynecology, Nassau County Medical Center, East Meadow, and the Health Sciences Center, State University of New York at Stony Brook. Supported in part by a grant from the United Cerebral Palsy Research and EducatWn Foundation 237-7 I, the Meadowbrook Medical Research and Education Foundation, Inc., and the Deutsche Forschungsgemeinschaft, Germany.

Accepted for publication December 10, 1976. Reprint requests for the United States: Dr. Leon I. Mann, Professor and Chainnan, Department of Obstetrics and Gynecology, Patrick 541, MFU-MCHV, Burlington, Vermont 0540l.

An abstract of this study was accepted for presentation at the annual meeting of the Society for Gynecologic Investigation, Philadelphia, March, 1976.

Reprint requests for Europe: Prof Dr. Med. W oifgang Universitiits-Fra'Ul!nklinik, JosefSchneider-Str.4, 8700 Wunburg, Germany.

Received for publicatWn june 17, 1976.

Kunu~

Revised for publication November 29, 1976.

201

202 Kunze! et al.

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PLACENTA

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May 15. 1977 Obstet. Gynecol.

and Mott 3 on fetal oxygenation during UVO. However, some discrepancies in the cardiovascular response are revealed, and these will be discussed. The fetal electroencephalogram did not reveal any consistent change.

TISSUE

Material and methods

I

UMBILICAL ARTERY

TISSUE

INFLATABLE

CUFF

UMBILICAL VEIN

FLOWPROBE

Fig. 1. Experimental model for UVO, representing the placenta and the fetus. An inflatable cuff was placed around the umbilical cord. Solid UVO was proved by measuring the pulse pressure in the UA. A decrease of UA pulse pressure would indicate that inflation of the cuff also occludes the umbilical artery. OXYGEN SATURATION

(•J,J 100

UMBILICAL VEIN 9

so

•

so

0

UMBILICAL

40

20

.•

•

ARTERY

r ~ 0,875

2... < 0,001

o CONTROl

• u.v.o. 200 100 1 UMBILICAL BLOOD FLOW ( ml· miii ·kf I

300

Fig. 2. The relationship between the oxygen saturation in the UV and UA, respectively, and umbilical blood flow. The open circles (o) represent values before UVO, the dosed circles (e) represent values following UVO. There is no significant relationship between the UBF and the UV oxygen saturation. The UV oxygen saturation is about 85 per cent. A logarithmic regression line was adapted to the values of the UA: S02 = 37.6 x log UBF- 22.8; 2a < 0.001.

vein occlusion (UVO) on fetal oxygenation and on the cardiovascular system in the mature and premature 3 sheep fetus has been investigated by Dawes and Mott. However, knowledge of fetal brain functions during UVO is still lacking. Therefore, this article includes fetal oxygenation and cardiovascular effects and their relationship to the fetal electroencephalogram following UVO. The present experiments confirm the findings of Dawes

Animal preparation. The experiments were performed on I I ewes with dated gestations from 126 to 137 days. The ewes received no food for 24 hours and no water for 12 hours prior to operation. Progesterone in oil (Proluton, Schering), 150 mg., was given intramuscularly two days prior to operation, as well as on the morning of the experiment. Anesthesia was induced with 3 to 4 per cent fluothane (Halothane, Ayerst Labs.) and maintained by ventilating the ewe with a mixture of 0.5 to 1.5 per cent fluothane and 40 to 60 per cent oxygen in nitrogen through intubation with a cuffed endotracheal tube. The ewe was relaxed with succinylcholine (lnectin), and the respiratory rate was controlled with the Bird respirator. The ewe was placed in a supine position. A polyethylene catheter was placed into the maternal dorsal aorta via a branch of the femoral artery. The abdomen was opened by a midline incision, and the uterine horn containing the fetus was exposed. An incision was then made through an avascular area of myometrium. In some cases the fetus was completely exteriorized and in some cases, it was only partially exteriorized. Tributaries of the umbilical artery (U A) and umbilical vein (lJV) were identified. and polyethylene catheters were passed into the main cord vessels by the technique described by Meschia and associates. 12 An additional catheter was passed into the descending fetal aorta (FA). A right paraumbilical incision was made in the fetal abdomen, and the common UV )NaS exposed. An electromagnetic flow probe with an inner diameter of 5, 6, and 7 mm., respectively. was placed around the vessel. In two animals, the flow probe was fitted to a U A. An inflatable cuff was used for compressing the UV. The cuff was placed around the umbilical cord and in two cases around the abdominal part of the UV. An incision was made in the fetal head, and bipolar electrodes were screwed into the pretapped burr holes placed into the frontolparietal hemisphere. Measurements and calculations. The blood withdrawn from the various vessels was analyzed for pH and Pco2 with an IL-gas analyzer. The percentage of oxygen saturation (per cent So2) and the hemoglobin concentration (CHb) was estimated with an IL-CoOxymeter (Model 182). Umbilical blood flow (UBF) was measured with an electromagnetic flow meter

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203

ARTERIO-VENOUS 02- DIFFERENCE ( ml/100ml l

14

_:5~~~~!_ l~ -----.------------~~~~-~ \

__________ _

UMBILICAL VEIN

12

10

t• :•\ •

8

6

AVDo2 = Vo2 I QUMB Vo2 = 6.1 ml·mirilkg1

,.

••

• ••• •I

·-&,.: •• • • •• • • ••

4

40

• I

120 160 80 200 UMBILICAL BLOOD FLOW

.

21.0

.

280 .

_,.

• _,.

320

: 360

1 ml· mrn-: kg · J

Fig. 3. The relationship between the arteriovenous difference for oxygen (02) and UBF. All measured data were used where the UV oxygen saturation was not less than -75 per cent. The solid line is the theoretical relationship between AV - 02 and UBF for a constant fetal oxygen consumption: 6.1 mi. per kilogram per minute, S.D. 1.1, N = 15. The broken line represents the mean UV oxygen content: 13.4 mg. per 100 mi., S.D. 1.5, No. = 52. The measured data deviate from the theoretical relationship if a critical UBF of about 80 to 120 mi. per kilogram per minute is reached. (Statham SP 2202), and the blood pressure in the various vessels was estimated with strain gauge transducers (Statham P 23A). Fetal heart rate (FHR) was measured with a cardiotachometer (Beckman Type 9857 B) which was triggered by the pulse pressure. Umbilical blood flow, UV blood pressure, FA blood pressure, fetal UA blood pressure, and FHR were monitored continuously throughout each experiment with an eight-channel dynograph recorder (Beckman). From the CHb• the fetal artery and UV So2, and the umbilical blood flow, the oxygen content (Co2) (milligrams per 100 ml.) of the fetal ~lood and the oxygen comsumption of the fetus (Vo 2F) were calculated according to the simple Fick equation. Fetal electroencephalogram was recorded on a second Beckman dynograph with, a paper speed of 2.5 em. per second. A semiquantitative analysis of the electroencephalogram was achieved by measuring the amplitude (microvolts) and counting the over-all fast frequencies. The fast frequencies are given as cycles per second. Experimental procedure. Umbilical vein occlusion (UVO) of varying degrees was achieved by inflating the cuff around the umbilical cord (Fig. I). Isolated UVO could be examined by measuring the U A blood

pressure simultaneously with the UV blood pressure. However, partial UA occlusion could not be completely ruled out. In seven experiments in two sheep, the abdominal part of the common UV was occluded to clarify the mechanism of UVO. In 17 experiments, blood samples were drawn from the UV and the FA before the UVO was released. In serial analysis in 10 experiments, FA So2 reached a steady state 30 to 60 seconds after UVO had started, depending on the degree of occlusion. In addition, 20 control samples were drawn at different times.

Results Fetal oxygenation and UBF following UVO. UV and UA oxygen saturation and UBF. The effect of UVO on UV and UA So 2 related to umbilical blood flow is shown in Fig. 2. The open circles indicate the values before UVO, and the closed circles indicated values following varying degrees of UVO. A logarithmic regression line was adapted to the values of the umbilical artery. Oxygen saturation in the UA is related to UBF. The FA So2 was about 70 per cent if UBF was 250 mi. per kilogram per minute or more. The FA So2 decreased about 15 per cent if UBF fell from 300 to 120 ml. per kilogram per minute. How-

Kunzel et al.

204

Am.

OXYGEN UPTAKE 1 1 lml·min" kg ) 10

e

l

1

•

•

•

20

60

100

140

180

220

260

300

1

340

UMBILICAL BLOOD FLOW ( ml· mn·~ kg" l

Fig. 4. The correlation between the fetal oxygen uptake and UBF. A logarithmic regression line is adapted to the respective date: Vo 2 F = 3.59 · log UBF- 2.36; 2a < 0.001. Fetal oxygen consumption changes less if UBF is more than 150 mi. per kilogram per minute. However, the fall is nearly proportional if the UBF decreases to below 100 mi. per kilogram per minute.

ever, the reduction in So 2 was almost linear if UBF fell below 80 ml. per kilogram per minute. The UV Soz remained unchanged during UVO, remaining at about 85 per cent. Arteriovenous oxygen difference and fetal oxygen comsumption. In Fig. 3, the difference in oxygen concentration between fetal artery and UV blood is plotted to the UBF. All experimental samples were used where UV Soz was not less than 75 per cent. The solid line is a theoretical relationship of the arteriovenous difference for Co 2 and UBF if the oxygen consumption is 6.1 ml. per kilogram per minute (S.D. 1.1; No. = 15) and constant. The oxygen consumption was calculated from the measurements at control, where UBF was 150 ml. per kilogram per minute and more. The broken horizontal line is the mean oxygen concentration in the UV. It was 13.4 mg. per 100 ml. (S.D. 1.5; No. = 52). The measured data and the theoretical relationship of arteriovenous oxygen difference and UBF are in agreement with each other if UBF is 150 ml. per kilogram per minute and more. It deviates from the theoretical line if UBF falls below 80 to 120 ml. per kilogram per minute. The deviation from the theoretical relationship in this range expresses the fact that the oxygen consumption of the fetus decreases if UBF falls below a critical level. The relationship between fetal oxygen consumption and UBF demonstrates this fact (Fig. 4). At flow rates of 150 to 360 ml. per kilogram per minute, the oxygen consumption of the fetus decreased only slightly if blood flow fell. However, below a critical level of 80 to

J

Ma~ 15, 1977 Obstet. Gynecol.

120 ml. per kilogram per minute, the decrease in oxygen consumption was almost linear in its relationship to falling blood flo\\. Fetal cardiovascular alterations following UVO. In order to compare the results of fetal cardiovascular alterations as a response to UVO, the results were grouped (Table I) according to the fall ofF A So 2 (see "Comment"). In the first group (.4 = moderate UVO), where the FA So 2 remained greater than 40 per cent (49.8 per cent; S.D. 6.3). the oxygen consumption decreased from 5.2 to 4.2 mi. per kilogram per minute. In the second group (B =severe UVO), where the So 2 during UVO was iess than 40 per cent (20.4 per cent; S.D. 9.2) the oxygen consumption decreased from 4.9 to 2.6 ml. per kilogram per minute. The fetal arterial pH and Pcoz remained unchanged in the first group and changed significantly in the second group, by about 0.06 and 5 mm. Hg. respectively. The So 2 , pH, and Pco 2 of the UV blood remained essentially unchanged in both groups. In both groups. changes in FA So2 and oxygen consumption were related to cardiovascular alterations of the fetus. The systolic, diastolic and UV blood pressure. Fig. 5 shows the alterations in the systolic, diastolic, and lTV blood pressure as a result of UVO in both groups with moderate (open circles) and severe (closed circles) reduction of FA So 2 . Moderate UVO produced a small but significant fall in systolic blood pressure (2P < 0.01). The fall in diastolic blood pressure was not significant statistically. During the first I 0 seconds, the systolic and diastolic blood pressure fell to 55 and 49 mm. Hg, respectively. UV blood pressure rose from 12 (S.D. 3) to 25 mm. Hg (S.D. 8) within l 0 seconds. During the further time course, the systolic and diastolic blood pressure showed a siight rise. However, this increase was not significant statistically. In severe L'VO. the systolic and diastolic blood pressure increased to 65 and 50 n1n1. 1:-Ig~ respectively. beginning l 0 to 15 seconds after L:vo. The UV blood pressure rose to 35 mm. Hg. Frtal Heart Rate. Accompanying the increase in blood pressure, the FHR fell (Fig. 6). In moderate LTVO, the decrease in FHR was not significant. In some cases there was even a risP of FHR. However, in severe UVO, FHR fell in every case. It fell from 190 to 130 heats per minute. The time to the onset of deceleration was related to the time of systolic blood pressure (FHR1 = 0.8 + 0.99 · BPt. 2a < 0.01). UBF and perfusion pressure. To clarify the mechanism of UVO on UBF, an inflatable cuff was placed around the abdominal part of the UV and blood flow of one UA was measured in seven additional experiments. Foiiowing L_;y compression, the l_'V blood

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Effects of umbilical vein occlusion

205

Table I. The So2 , pH, and Pco2 of FA and UV, UBF, and fetal oxygen consumption before and after UVO Group A: FA So 2 following UVO >40% (mean ± S.D.; No. = 9)

FA

So2 (%) pH Pco2 (mm. Hg)

uv

So2 (%) pH

Pco2 (mm. Hg) UBF (mi./Kg./ min.}

Fetal oxygen consumption (mi./Kg./ min.)

Follo·wing

Following

Before

61.6 ±5.3 7.35 ±0.05 39 ±5

49.8 ±6.3 7.34 ±0.05 40 ±6

54.2 ±8.7 7.32 ±0.06 40 ±7

20.4 ±9.2 7.25 ±0.09 45 ±II

85.5 ±3.9 7.39 ±0.05 32 ±5

85.3 ±4.2 7.39 ±0.05 31 ±6

83.6 ±3.4 7.37 ±0.06 31 ±5

81.3 ±7.0 7.35 ±0.07 33 ±6

147 ±57

84 ±48

120 ±55

30 ±22

5.2 ±1.1

4.2 ±l.O

4.9 ±0.8

2.5 ±1.5

Before Parameter

GroupB: FA SOzfollowing UVO < 40% (mean ±S.D.; No. = 8)

uvo

pressure increased immediately while arterial blood pressure was unchanged. This expresses the fact that the perfusion pressure decreased and umbilical blood flow fell as a result (Fig. 7). There was no increase in umbilical arterial resistance, and there was even a slight decrease during the first seconds of UVO. Fetal electroencephalogram. The relationship between the amplitude (microvolts) of the fetal electroencephalogram and the over-all fast frequencies before and after UVO is shown in Fig. 8. There is a significant relationship between these two parameters. The fast frequencies increase if the amplitude of the fetal electroencephalogram falls, and the reverse of this (open circles) is also true. No significant alteration of the fetal electroencephalogram could be seen if UBF was reduced. In the group with severe reduction of So2 (triangles), there was a fall in amplitude and an increase of the fast frequencies in four of five cases. Comment

Abnormal cord position in human subjects is associated with a mixed cord compression pattern and variable decelerations of FHR in 8.37 per cent of all cases. 4 Animal experiments have shown that these patterns occur in both total ocdusion2 and partial occlusion6· 14 of the umbilical cord. However, the relationship between these patterns and fetal oxygenation is still contradictory. 3 In the following paragraphs, the influence of UVO on cardiovascular alterations and

I

uvo

uvo

1

uvo

fetal oxygenation will be discussed, separately. Fetal oxygenation and cardiovascular alterations. In Table I, the results of the 17 occlusion experiments are grouped according to the fall of the fetal So2 following UVO. For grouping the results, a critical limit for fetal So2 of 40 per cent following UVO was assumed. According to Acheson and associates, 1 Dawes and Mott, 3 and Kunzel and Moll/ fetal oxygen uptake fell to a rather proportional extend, if FA So2 was lower than 40 per cent. Therefore, it is most likely that the alterations of FHR and blood pressure are related to the decrease of fetal So2 • The mean values at control in Table I (especially in Group B) differ somewhat, in FA So2, UBF, and fetal oxygen consumption from those values considered as physiologic. Umbilical blood flow is 120 ml. per kilogram per minme and oxygen consumption is 4.9 mi. per kilogram per minute compared to 147 and 5.2 ml. per kilogram per minute, respectively, in Group A. Despite this fact, the systolic and diastolic blood pressure at control showed no significant difference in either group. However, depending on the degree of UVO, systolic blood pressure in Group A showed a small but significant fall during the initial 10 seconds; there was no significant alteration in the further time course. However, reduction of UBF to 30 ml. per kilogram per minute in Group B produced a significant rise in systolic and diastolic blood pressure after 15 seconds. FHR was not significantly altered in Group A. However, it fell from 170 to 130 beats per minute in Group B.

206 Ki.inzel et al.

Mav 15, 1977 Am. J. Obstet. Gynecol.

BLOOD PRESSLRE

BLOOD PRESSURE

(rrmHg)

( rrmHg)

70

~

60~

i

10

DIASTOLIC BP

MEAN!SE

t

UM81UCAL VEIN OCCLUSION

CONTRQ 20

40

60

80

t (sec) -

CONTROL 20

40

60

80

t (sec)-

Fig. 5. The systolic and diastolic FA blood pressure, as well as UV blood pressure, before and after UVO in 16 experiments. The values are given as means± S.E. The open circles (o) represent the cases where the FA So2 following UVO remained greater than 40 per cent, and the solid circles (•) represent values where the FA So2 was less than 40 per cent.

At first sight, these cardiovascular effects seem to contradict the results reported by Dawes and Mott. 3 They found a fall in fetal blood pressure and an increase in FHR during UVO. Some cases in Group A showed tachycardia following UVO, but tachycardia never occurred if UBF was reduced to 30 mi. per kilogram per minute, that is, if FA So2 and oxygen consumption fell to 20.4 per cent and 2.6 mi. per kilogram per minute, respectiveiy. As previousiy shown; 8 the faii in heart rate is related to the increase in systolic blood pressure not only in UVO but also in reduction of UBF. However, the increase in systolic blood pressure is correlated to the FA So 2 which is achieved after occlusion. Therefore, we believe that the different results are probably due to the degree of flow reduction. S~, oxygen consumption, and UBF. A better insight into the relationship between fetal So2 and oxygen consumption (Vo2 F) following UVO is achieved if these parameters first are correlated to UBF and then arranged in two groups. In every case, UVO was accompanied by a fall in UBF, simply because the perfusion pressure across the placenta fell (Fig. 7). For clinical purposes, it is important to emphasize that a definite fall in the perfusion pressure will not jeopardize fetal oxygenation if control UBF is high. However, it wiii affect FA So2 and Vo2 F if

control UBF is low (Fig. 2). In the present results, FA So 2 was reduced only by 15 per cent if UBF fell from 300 to 150 mi. per kilogram per minute. However, FA So2 fell a proportional extent if UBF was reduced below a critical level of about 80 to 120 mi. per kilogram per minute. These results are in agreement with those of Dawes and Mott. 3 However, a slight difference exists in the oxygen comsumption in the term fetus, whereas in the present experiments the Vo2 F was 6. i mi. per kilogram per minute, if UBF was 150 ml. per kilogram per minute or more, compared with our value of 4.6 mi. per kilogram per minute (S.E. 0.3). In the cited paper, the relationship between Vo 2 and UBF was not reported. This may be one explanation for this discrepancy. In moderate UVO the acid-base parameters did not change significantly; however, in severe UVO, there was a significant fall in the FA pH and a slight rise in the FA Pco 2 • The fall of FA pH will depend on the time and degree of UVO because anaerobic glycolysis takes place if there is a lack of oxygen-in severe cases of UVO, 20.4 per cent (S.D. 9.2)-and a reduced oxygen uptake-in severe UVO, 2.6 ml. per kilogram per minute (S.D. 1.5). It is of ciinicai significance that the acid-base parame-

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Effects of umbilical vein occlusion

FETAL HEART RATE I b/rnin I 220

207

UMBILICAL BLOOD FLOW ( "to OF CONTROL l 100

zoo 80

180

160

c

• ..

60

•

•* ++ +

..6 >.,

/

+ ••

o/ •

/

140

40 120

t

100 it!

I

20

UMBILICAL VEIN OCCWSION

6 MEANtSE

!

0

zo

40

60

80

100

20

TIME I sec I

Fig. 6. FHR before and following UVO. There is a significa,nt fall in FHR following UVO in the group where the FA So2 feU below 40 per cent (dosed circles). In lhe group where the FA So2 remained greater lhan 40 per cent, FHR w'as not severely affected.

ters and So2 in the UV did not change significandy during occlusion. Observations on the UV are not reliable indices of fetal condition. Fetal elec:troencephalogram. Spectral analysis of fetal sheep electroencephalograms, as done previously by Symmes and associates, 13 could not be performed in the present series of experiments. To discover the effect of hypoxia on the fetal electroencephalogram in the present paper, the over-all fast frequencies and the amplitude of the fetal electroencephalogram were measured, although this method of quantifying the electroencephalogram is not free of errors. the measurements do show a significant relationship between the amplitude and the fast frequencies at control, as already described by Mann. 11 This relationship is not significantly affected by the present setup of experiments. That there was no detectable significant change in the fetal electroencephalogram during UVO is probably related to the degree of deoxygenation. Former studies showed that fetal oxygen consumption had decreased by 85 per cent at the onset of the isoelectric stage of the electroencephalogram. 11 In the present experiments, the oxygen consumption of the fetus was lowered only by about 50 per cent of the control level. The lack of fetal electroencephalogram alterations, should not lead to the conclusion that the fetal electroencephalogram is never compromised during UVO. It is conceivable that the UV can also be occluded to such an extent that oxygen-consumption is reduced to zero.

40

60

80

PERFUSION PRESSURE I % OF CONTROL )

Fig. 7. The relationship between UBF (percentage of control) and the perfusion pressure (percentage of control) that is lhe difference of mean aortic blood pressure and UV blood pressure. The broken line is the identity line for the relationship between pressure and flow if the vascular resistance is constant. Each symbol indicates one experiment. The measured data during the first seconds are located on the left of the broken line, indicating that during UVO a slight decrease in umbilical vascular resistance occurred.

AMPLITUDE (}J

v)

240

o CONTROL

e S02,FA > 40°io 200

l

S02,FA < 40"1.

160 120

80 40

' 8 12 16 20 TOTAL FAST FREQUENCIES I sec

Fig. 8. The relationship between the amplitude of the fetal electroencephalogram (microvolts) and lhe over-all fast frequencies during the control period (open circles) and following moderate UVO (solid circles) and severe UVO (triangles}. The arrows indicate the changes by UVO in amplitude and frequency.

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Ki.lnzel et al.

REFERENCES I. Acheson, G. H., Dawes, G. S., and Mott,

2. 3. 4.

5. 6.

7. 8.

J.

C.: Oxygen consumption and the arterial oxygen saturation in foetal and newborn lambs, J. Physiol. 135: 623. I 975. Barcroft, J.: Researches on Prenatal Life, Springfield, Illinois, 194 7, Charles C Thomas, Publisher. Dawes, G. S., and Mott, J. C.: Changes in 0 2 distribution and consumption in foetal lambs with variations in umbilical blood fl~w, J. Physiol. 170: 524, 1964. Goldkrand, J. W., and Speichinger, J. P.: "Mixed cord compression," fetal heart rate pattern, and its relation to abnormal cord position, AM. J. 0BSTET. GYNECOL. 122: 144, 1975. Hon, E. H.: Observations on "pathologic" fetal bradycardia, AM. J. OBSTET. GYNECOL. 77: 1084, 1959. James, L. S., Weisbrot, I. M. Prince, C. E., Holaday, D. A., and Apgar, V.: The acid-base status of human infants in relation to birth asphyxia and the onset of respiration, J. Pediatr. 52: 379, 1958. Kunze!, W .. and Moll, W.: Uterine 02 consumption and blood flow of the pregnant uterus, Z. Geburtshilfe Perinatal. 176: 108, 1972. Kunze!, W., Mann, L. I., Bhakthavathsalan, A., and Ayromlooi, J.: Cardiovascular and fetal brain function observation following total cord occlusion (TCO), umbili-

9. 10. 11. 12.

13. 14.

cal vein occlusion IUVO) and reduction of utei·inc blood flow, Presented at the Forty-first Meeting of the Dutsche Gesellschaft fur Gynakologie und Geburtshilfe. Hamburg. 1976. Arch. Gynaekol. In press. Lee, S. T .. and Hon, E. H.: Fetal Hemodynamic response to umbilical cord compression, Obstet. Gyneml. 22: 553. 1963. Mann, L. l., Prichard, J. W., and Symmes, D.: EEG, ECG, and acid-base observations during acute fetal hypoxia, AM. J. 0BSTET. GYNECOL. 106: 39, 1970. Mann, L I.: Effects of hypoxia on umbilical