Magister De Hitoria

Ultrasound Obstet Gynecol 1998;11:190–194

Ductus venosus agenesis prevents transmission
of central venous pulsations to the umbilical
vein in fetal sheep
T. Kiserud, C. Crowe and M. Hanson
Fetal and Neonatal Research Group, Department of Obstetrics and Gynaecology, University College London Medical
School, London, UK

Key words:

UMBILICAL VEIN, DUCTUS VENOSUS, CIRCULATION, BLOODFLOW, FETUS, ULTRASOUND, DOPPLER, SHEEP

ABSTRACT
heart disease. In the human fetus, pulsations in the
umbilical vein were first described by Lingman and
colleagues in fetuses with imminent asphyxia2. Typically,
such an umbilical vein pulsation is a short deflection during
atrial contraction in the otherwise even peak velocity
recording of the blood flow. In twin–twin transfusion syndrome,the whole central venous flow velocity during the
heart cycle may be reflected in a corresponding bi- or
triphasic umbilical pulsation3. These pulsations were
shown to be a predictor of poor outcome in hydropic
fetuses with congestive heart failure in the last half of
pregnancy4. In early pregnancy (before 13 weeks), however,
umbilical venous pulsations are regularly found in normalfetuses5. The incidence of pulsations in the cord vein falls
from 30% at 13–14 weeks to 5–8% after 23 weeks6. The
association between the umbilical pulsation and reduced or
reversed blood velocity in the ductus venosus during atrial
contraction, found in fetuses with growth retardation2,7
and cardiac diseases8, supported the assumption made by
Lingman and colleagues2 that the ductus venosus playsan
important role in the transmission of the central venous
pressure pulse into the umbilical vein. It has been questioned, however, whether the small ductus venosus (diameter 0.5–2 mm at the isthmus9) can have any significant
function as a channel for pressure transmission to the umbilical vein.
The aim of the present study was to examine whether
umbilical venous pulsations could beprovoked in a case of
ductus venosus agenesis in the fetal sheep by imposing
stress otherwise known to cause such pulsations.

Velocity pulsations in the umbilical vein are widely used as
a marker for congestive heart failure in the fetus. It has
been suggested that the atrial pressure waves are transmitted to the umbilical vein mainly through the ductus
venosus. In a case of ductus venosusagenesis in a fetal
sheep of 110 days’ gestation, we recorded pressures in the
inferior vena cava and umbilical vein simultaneously with
Doppler velocimetry in the medial hepatic vein and umbilical vein, under general anesthesia. During fetal respiratory
acidosis (pH 7.01) and varying degrees of umbilical clamping, we did not observe the typical pulsations in the umbilical vein (deflections of themaximum velocity during atrial
contraction) in spite of varying degrees of reversed flow in
the hepatic vein (5–16%). The systolic–diastolic pressure
amplitude in the inferior vena cava was 5.5–6.4 mmHg,
sometimes reaching 9.19–11.03 mmHg. Varying degrees of
reversed portocaval pressure gradient during atrial contraction (1.40–9.51 mmHg), periods of reversed portocaval
pressure gradientthroughout the entire cardiac cycle,
tachycardia (240 beats/min) or bradycardia (99 beats/min)
also did not produce the type of pulsation in the umbilical
vein that reflects augmented atrial contractions. The results
support the hypothesis that the ductus venosus is essential
for the transmission of atrial pressure waves to the umbilical vein.

INTRODUCTION
An increased pulsation of bloodflow in the precordial
veins in fetal sheep challenged with hypoxia or after administration of norepinephrine or isoproterenol was described
by Reuss and colleagues1. Pulsations were traced as far out
in the venous system as the umbilical vein after acetylcholine administration. This pattern of venous flow corresponds to the pattern commonly found during congestive

METHODS
A ewe of mule...