o_1977r8vv9vk1ts2ms0kd8pksa.pdf

120 J. Itskovitz-Eldor, I. Thaler
Table 9.1. Distribution of blood flow expressed as percent of combined (biventricular) cardiac output
Near-term
fetal lambs
[24]
Human
fetuses [68]
(13±41 weeks)
Human
fetuses [7]
(19±39 weeks)
Human
fetuses [4]
(18±37 weeks)
Right cardiac output, % 60 59 53±60
Left cardiac output, % 40 41 47±40
Ductus arteriosus blood flow, % 54 46 32±40
Pulmonary blood flow, % 6 11 13±25 22 6
Foramen ovale blood flow, % 34 33 34±18 17±31 36
Biventricular output, ml ´ min ±1 ´kg ±1 462 425 470-503
Human
fetuses [39]
(age unknown)
Table 9.2. Combined ventricular output (450±500 ml ´ min ±1
´kg ±1 ) and its distribution in fetal lambs
Anatomic site %
Placenta 40
Carcass a 33
Lungs 7
Gastrointestinal tract 4
Brain 4
Myocardium 3
Kidneys 3
Spleen 1
Liver (hepatic artery) 1
Adrenals 0.1
a Skin, muscle and bone.
Fig. 9.5. Velocity tracings in the pulmonary trunk and ascending
aorta obtained by electromagnetic flow transducer
implantation. Note the rapid rise of velocity in the pulmonary
trunk compared with that in the aorta. There is a
characteristic notch in the descending limb of the velocity
curve. The ascending aortic tracing also shows a sharp incisura
at the end of ejection caused by backflow. The area
under each curve reflects stroke volume; flow in the pulmonary
trunk is about twice that in the aorta. (Reprinted
from [72] with permission)
The factors regulating cardiac output in the fetus
and the mechanisms responsible for the increase in
output after birth have attracted considerable attention.
Cardiac function and the volume of blood
ejected by the heart are, in general, determined by
cardiac and circulatory factors [79]. Early studies
suggested that the normal fetal heart at rest operates
close to the top of its ventricular function curve
(Frank-Starling curve), with little reserve available to
further increase the output [60, 80±82].
In these studies little attention was directed to the
changes in arterial pressure that occur with volume
loading or withdrawal. It is well known that the fetal
heart is sensitive to an increase in afterload, and so
the cardiac output falls dramatically as arterial pressure
increases. In early studies the arterial pressure
(afterload) was not controlled, and therefore left ventricular
stroke volume showed little increase above
the left atrial mean pressures of about 6 mmHg
(slightly higher than normal atrial pressure at rest).
However, when the left ventricular stroke volume was
related to left atrial pressure at the same levels of
mean arterial pressure, the stroke volume continued
to increase above the atrial mean pressure of about
10 mmHg [83], suggesting that the fetal heart rate is
able to increase its output provided the preload is increased
and the afterload is maintained or if the preload
is maintained but the afterload is decreased.
However, because a large proportion of the fetal
blood volume is sequestered in the highly compliant
umbilical-placental circulation, the fetus is unable to
increase venous return readily and therefore has limited
ability to increase its cardiac output acutely [84].
While the plateau observed in the fetal cardiac
function curve was related to arterial pressure and increasing
afterload, it has been demonstrated that the
maximal stroke volume in the fetus is largely determined
by the constraining effect that the pericardium
and the chest wall-lung combination (i.e., extracardiac
constraint) has on ventricular filling [85]. When
ventricular transmural pressure, a more appropriate
measure of ventricular preload than ventricular filling
pressure, is used in ventricular function curve analysis,
stroke volume is linearly related to preload and
the plateau is absent [85]. The major limitation upon
left ventricular function in the near-term fetal lamb
results from extracardiac constraint limiting ventricular
filling while, at the same time, a much smaller