Beruflich Dokumente
Kultur Dokumente
I Introduction
The classification of the fetal heart rate patterns
developed around 1960 lack still a clear and definitive
pathophysiological base. The names given to the several
decelerations suggest however that the pathophysiological
pathways along which they arise are completely clarified.
Therefore we directed our research the last years to
this subject. This paper is restricted to the presentation
of some data concerning the Simulation of variable and late
decelerations in chronically instrumented sheep preparations.
Acute changes in the fetal heart rate pattern can in
general and theoretically be caused by
1. direct hemodynamic changes
2. activitation of the fetal autonomic System by
chemoreceptor mediated hypoxaemia and or direct
fetal adrenal release of catecholamines.
3. direct myocardial depression.
Correct Interpretation of changes in the fetal heart rate
pattern and estimation of the fetal condition requires knowledge
about the activity of each of the three factors mentioned.
II Variable decelerations
Variable decelerations are thought to be due to obstruction
of the umbilical circulation ( 4 ) . Simulation of variable dece-
lerations was performed by placing a special device around
the umbilical cord directly over and fixed to the fetal abdomen
( 3 ) . The device consists of two separated compartments with
inflatable balloons which can be inflated separately or simulta-
neously. Placing both umbilical arteries in one compartment
and the umbilical veins in the other compartment, or one artery
and one vein in each of the compartments each possible impair-
ment of the umbilical flow can be simulated. Following recovery
from anesthesia and surgical procedures the vessels were
occluded during 30 seconds. Fetal femoral artery blood samples
were taken five minutes before and five minutes following the
occlusion äs well äs at the end of the 30 seconds lasting
- occlusion period, With this method a total number of 197
different types of umbilical cord clampings were performed.
Moreover an additional number of 42 clampings were performed
during pharmocological blockäde of the different parts of the
autonomic nervous System.
The fetal arterial pO2 before and at the end of the occlusion
period shows a significant difference in all instances.
Occlusion of both umbilical arteries results in an
immediate rise of th.e systolic and diastolic pressure reaching
a certain steady state and followed in some occlusions by a
second rise especially expressed in the diastolic pressure after
a variable time, however still within the 30 seconds lasting
occlusion period ( f i g . l ) .
The fetal heart frequency decreases immediately within one
or two heart beats to a certain level, followed by a further
decrease simultaneously with the second rise in blood pressure
if present.
In case of occlusion of both umbilical veins a certain delay
0300-5577/81/0091-0002 $ 2.00
Copyright by Walter de Gruyter & Co.
8
^ 600 -
ο
400
-flfl ->
200 _J 1 L.
Ο
MIN
MIN
Fig. l Fetal systolic pressure before, during and following
a 30 seconds lasting occlusion of the umbilical arteries
(upper graph) and umbilical veins (lower graph). The
occlusion period is indicated by the vertical bars.
40-
30-
10-
0-
-10
30sec occlusion
FETflL R R - I N T E R V f l L SH6912
1500
1000
LÜ
00
500
MIN
1000- -
o
Lü
500 -
V -. B -
'-T*^
.. 1 , . ,. , . 1 . ,
MIN
Fig. 3 Fetal R-R interval before, during and following a thirty ||1
seconds lasting occlusion of the total umbilical cord before \
(TT, upper graph) and after cholinergic blockade (T*. '
lower graph). ;
^ 750
-| 500
o
250
0 -i 1 1 1
0
MIN
pH 742 pH
IS b
fetal arterial 1OO η
3.1 kPa
Oa 5.7 kPa
VV30*
f^-J . ^
pressure ...
7δ
(mm Hg)
50- ! ; ? ι
25- ^P' p5^>^4^ ^^^^ ·· ·- '
: ' · . . . ' . .i '-.''. Ί
fetat heart 20O Ί
frequency
(txpm)
.
FECG
... 1. « . . . < . , . . . . . , . . « ^.
pH 7.36
pO2 23 kPa
pC02 52 KPa
B£ -2.6 mmol/l
fetal arterial 100 i
pressure
(mm Hg)
fetal heart
frequency
(b.p.m)
250
1
lüiJ:1-ii---iiiij^^^
•^i^s^**·^*^^
50
:'. ·': ".\'·:\ ' ' i ; : ; h ; : ' : h ! ; ' i i ! ; ; M ; : M l i ^ i i I
intra uterine 0 *
pressure '.
(mm Hg)
25-
4 i H ! i J i i - , r :;.;.i Li.inj-i.yq:·.!:-;.;
,",^. ..
• i i' ·- - · i » > .. 4- i-l ' i 4 4
.|-i~t
? < j ji : ..LH
. ..rfV'rt-'U
i..|4|4
flow uterine 6OO ·
, .J.-.4.. ,. r < r Tt r
•tvid
artery
(ml/min)
FECG
50-
FECG
:
intra uterine
pressure
(mm Hg)
0
2Q
7mm ':'^
flow uterine 5OO -
artery I
(ml/min) QJ
FECG
pH 6.96
pO^ 1.6 kPa
pCO, 7.Θ KPa
ΘΕ 19.7mmot/l
fetal arteriat 1OO
pressure
(mm Hg)
10O'·
intra uterine 0
pressure
(mm Hg)
FEC6
chemoreceptor
sympathetic
itii center
4-
vasoconstriction
- L blockade
—/3 blockade
blood pressure j
l
baro receptor
I
vagal center
\
atropine-
*
fetal heart rate
Fig. 10 Possible pathways producing periodic changes in the fetal
heart rate pattern due to hypoxaemia - hypoxia.
16
REFERENCES
P r o f . D r . J . d e Haan
Rijksuniversiteit Limburg
Zieke'nhuis St.Annadal
Dept.Obstet..* Gynec.
Maastricht/Netherlands