Heart Rate and Blood Flow Velocity Variability in the Human Fetus

Much of what we know about the embryonic circulation Is derived from studies of the chick embryo (Clark and Hu 1982). The similarities between the chick, rat (Nakazawa 1988) and fetal lamb (Kirkpatrick 1976) suggest that, while the details of functional change may vary, common mechanisms are expressed In these animal groups (Nakazawa 1988). Some of the mechanisms that control the cardiovascular system in the mature animal are expressed early In development (Clark 1990). The primary determinants of cardiovascular function in the embryo as in the mature animal are preload, afterload, heart rate and myocardial contractility. These factors regulate cardiac output before the development of the functioning autonomic nervous system. The Frank-Starling relationship Is operative and effective in both the fetal lamb heart (Kirkpatrick 1976) and the chick embryo (Wagman 1990). After maturation of the autonomic nervous system, both the parasympathetic and sympathetic systems control cardiovascular function in the fetal lamb (Nuwayhid 1975)

Assessment of fetal heart rate variability and velocity variability by Doppler velocimetry of the descending aorta at 10-20 weeks of gestation

Objectives: Determination of gestational age-related modulations in fetal heart rate and descending aorta blood flow velocity in the early human fetus and comparison of aortic variability data with data obtained from the umbilical artery. It is hypothesized that these modulations present in the umbilical artery also occur in the descending aorta. Methods: Doppler studies of descending aorta velocity waveforms were performed at 10-20 weeks in 55 normal pregnant women. In 24 of the 55 women, Doppler recordings from both the descending aorta and the umbilical artery were collected. Absolute values and variability of fetal heart rate, peak systolic and time-averaged velocities were determined from flow velocity waveforms of at least 18 s in duration. Results: From 10 to 20 weeks of gestation, the descending aorta peak systolic and time-averaged velocities increased, whereas the fetal heart rate decreased. The descending aorta peak systolic variability also increased. However, the time-averaged velocity variability and the fetal heart rate variability remained constant during the study period. In the subset of 24 women, the fetal heart rate variability and velocity variability data from the descending aorta and umbilical artery were not significantly different. Conclusions: Reproducible fetal heart rate and velocity variability data can be derived from the descending aorta and umblilical artery. The increase in heart rate variability observed in the umbilical artery was not seen in recordings obtained from the descending aorta. Different fetal activity states may be the underlying mechanism for these heart rate variability discrepancies

Acutely altered hemodynamics following venous obstruction in the early chick embryo

In the venous clip model specific cardiac malformations are induced in the chick embryo by obstructing the right lateral vitelline vein with a microclip. Clipping alters venous return and intracardiac laminar blood flow patterns, with secondary effects on the mechanical load of the embryonic myocardium. We investigated the instantaneous effects of clipping the right lateral vitelline vein on hemodynamics in the stage-17 chick embryo. 32 chick embryos HH 17 were subdivided into venous clipped (N=16) and matched control embryos (N=16). Dorsal aortic blood flow velocity was measured with a 20 MHz pulsed Doppler meter. A time series of eight successive measurements per embryo was made starting just before clipping and ending 5h after clipping. Heart rate, peak systolic velocity, time-averaged velocity, peak blood flow, mean blood flow, peak acceleration and stroke volume were determined. All hemodynamic parameters decreased acutely after venous clipping and only three out of seven parameters (heart rate, time-averaged velocity and mean blood flow) showed a recovery to baseline values during the 5h study period. We conclude that the experimental alteration of venous return has major acute effects on hemodynamics in the chick embryo. These effects may be responsible for the observed cardiac malformations after clipping

Ventricular diastolic filling characteristics in stage-24 chick embryos after extra-embryonic venous obstruction

Alteration of extra-embryonic venous blood flow in stage-17 chick embryos results in well-defined cardiovascular malformations. We hypothesize that the decreased dorsal aortic blood volume flow observed after venous obstruction results in altered ventricular diastolic function in stage-24 chick embryos. A microclip was placed at the right lateral vitelline vein in a stage-17 (52-64 h of incubation) chick embryo. At stage 24 (4.5 days of incubation), we measured simultaneously dorsal aortic and atrioventricular blood flow velocities with a 20-MHz pulsed-Doppler velocity meter. The fraction of passive and active filling was integrated and multiplied by dorsal aortic blood flow to obtain the relative passive and active ventricular filling volumes. Data were summarized as means +/- S.E.M. and analyzed by t-test. At similar cycle lengths ranging from 557 ms to 635 ms (P>0.60), dorsal aortic blood flow and stroke volume measured in the dorsal aorta were similar in stage-24 clipped and normal embryos. Passive filling volume (0.07+/-0.01 mm(3)) was decreased, and active filling volume (0.40+/-0.02 mm(3)) was increased in the clipped embryo when compared with the normal embryo (0.15+/-0.01 mm(3), 0.30+/-0.01 mm(3), respectively) (P<0.003). In the clipped embryos, the passive/active ratio was decreased compared with that in normal embryos (P<0.001). Ventricular filling components changed after partially obstructing the extra-embryonic venous circulation. These results suggest that material properties of the embryonic ventricle are modified after temporarily reduced hemodynamic load