A. Mori et al., THE FETAL CENTRAL VENOUS-PRESSURE WAVE-FORM IN NORMAL-PREGNANCY AND IN UMBILICAL PLACENTAL INSUFFICIENCY, American journal of obstetrics and gynecology, 172(1), 1995, pp. 51-57
OBJECTIVE: Our purpose was to study the fetal central venous pressure
waveform recorded noninvasively from the inferior vena cava in normal
and complicated pregnancies by means of newly developed equipment to f
ollow the vessel lumen diameter. STUDY DESIGN: A paired ultrasonic pha
se-locked loop echo tracking system with a high sampling frequency (30
00 Hz) was used to follow the movement (point displacement) of diametr
ically opposite points of the vessel wall. The lumen was measured as t
he interval between these points. We studied 70 normal fetuses (20 to
40 weeks) and 54 complicated pregnancies with increased umbilical plac
ental resistance. RESULTS: The four component waves of the central ven
ous pressure waveform (A, X, V, Y) were identified and measured in the
fetal recording. The crests of the A and V waves were of approximatel
y equal height. An increase in the descent of the Y trough was observe
d with advancing gestation. By means of data from the normal group, th
e complicated group was divided into three subgroups. In 10 fetuses th
e waveform was normal. In 31 there was a high pulsatile pattern with d
eep descent from the A crest to X trough so that the pulsatility of th
e waveform appeared increased. In 13 this was shallow and the pulsatil
ity appeared reduced. Clinical outcome (nonreactive fetal heart rate,
percentile birth weight, days in neonatal intensive care unit) was sig
nificantly worse in both these latter two subgroups in comparison with
normal and in the low compared with the high-pulsatile group. CONCLUS
IONS: Human fetal central venous pressure waveforms can be simply reco
rded and represented by the transluminal diameter waveform. In fetal c
ompromise the high pulsatility waveform may result from a reduced vent
ricular ejection and increased end-diastolic pressure in response to t
he increase in ventricular afterload caused by the placental vessel ob
literation. In the most profoundly compromised fetuses the low pulsati
lity waveform may indicate depressed myocardial function and output.