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This study was designed to determine (1) the value of Doppler echocardiography in depicting the presence of a fetal pulmonary stenosis, (2) its reliability in the assessment of the severity of the lesion, and (3) the usefulness of additional markers from the left side of the heart as criteria of severity. Fourteen pregnant ewes were included in this study (gestational age, 90 to 120 days). Banding of the fetal main pulmonary artery created mild (n = 3), moderate (n = 3), and severe (n = 5) stenosis. Three lambs were sham operated. Intrauterine fetal Doppler echocardiographic data obtained 15 days after surgery were compared with preoperative values. Peak velocities recorded through the band increased linearly from baseline in the groups with mild and moderate stenosis but did not show any further increase in the group with severe stenosis. Compared with the sham-operated group, right ventricular output in the group with stenosis was either similar or reduced significantly. The increase in right ventricular free wall thickness was significantly greater in the groups with stenosis compared with that of the sham-operated group; the correlation with the degree of severity was r = 0.65 and p < 0.05. A A stronger positive correlation was found between the severity of stenosis and aortic valve diameters: r = 0.82 and p < 0.01. The strongest correlation was found for right ventricular/left ventricular outputs (r = 0.92; p < 0.001). Thus Doppler peak velocities through the obstruction can help detect pulmonic stenosis but are not reliable for the assessment of its severity during fetal life. Other ultrasound measurements such as the size of the aortic anulus and especially the ratio of right ventricular/left ventricular output could be used as sensitive markers of the severity of stenosis.

A fetal lamb model was used to investigate whether the effects of maternal O2 administration on fetal blood gases and hemodynamics were modified when the fetoplacental circulation was compromised by stepwise compression of both umbilical veins. At basal state, O2 administration increased O2 saturation (Sao2) and the pulsatility index (PI) of the carotid artery Doppler wave form (p < 0.01). The first compression decreased left ventricular output (–21 ± 16%, mean ± 1 SD, p < 0.01) and umbilical mean velocity (–22 ± 28%, p < 0.01) but did not modify carotid pH, Sao2, or the PI in any of the arteries studied. At this level of compression, O2 administration increased carotid Sao2 (p < 0.01) but did not affect carotid PI. After a second compression, left ventricular output and umbilical mean velocity were even more reduced [–39 ± 21% (p < 0.01) and –53 ± 23% (p < 0.01), respectively]. With this compression, carotid pH, Sao2, and PI decreased, whereas umbilical and descending aorta PI increased. O2 administration at this level of compression increased carotid Sao2 (p < 0.01) but did not modify carotid PI. Throughout the three stages of the experiment, O2 administration did not affect umbilical PI, descending aorta PI, or umbilical mean velocity. A good linear relationship (r = 0.77, p < 0.001) was demonstrated between left ventricular O2 delivery and carotid PI. Thus, at basal state, O2 administration induced velocity changes compatible with an increase in cerebral vascular resistance. With an increase in umbilical vein resistance, this response was no longer demonstrated, even at a level of vein compression not significantly affecting carotid, umbilical, or descending aorta PI. These results support future use of fetal Doppler velocimetry during maternal hyperoxygenation as a method to evaluate fetal O2 reserve and fetoplacental hemodynamic function.

Eleven preterm newborn infants had a Doppler echocardiographic examination of their ventricular filling patterns during intermittent positive pressure ventilation. Peak velocity during early ventricular filling (VE) and during atrial systole (VA) and diastolic velocity-time integral of early (IE) and late (IA) ventricular filling caused by atrial contraction were measured. The ratios of VE/VA and IE/IA were also calculated. Diastolic peak velocities, as well as the diastolic velocity-time integral of early and late ventricular filling measured through the mitral valve were significantly higher during inspiration. The peak of the wave representing the velocity during atrial systole (A) was always higher than the peak of the wave representing the velocity of early ventricular filling (E). As a result, the ratio of these two variables (E/A) was always less than 1, showing no significant variation from inspiration to expiration. The flow patterns into the right ventricle were the opposite of those observed through the mitral valve. During inspiration, a significant decrease (p less than 0.001) in peak and time integral velocities of both the early ventricular filling and atrial systole waves was observed. Heart rate did not vary with respiration. It is concluded that during positive pressure ventilation, inspiration decreases right ventricular filling and enhances left ventricular filling. Opposite changes are recorded during expiration. Early and late phases of diastolic filling are equally affected. These changes are different from those observed during spontaneous breathing and should be taken into account in the assessment of diastolic ventricular function in preterm infants requiring assisted ventilation.

Aim: To evaluate foetal left ventricular performance when its preload was increased by banding the pulmonary artery, a study design where a simultaneous change in left ventricular afterload is unlikely. Methods: Nine ovine foetuses were studied with real-time images and Doppler echocardiography before, 3–4 and 6–8 d after surgery. Seven of these foetuses were also studied during the surgical intervention, immediately before and within 2 min after banding. Results: The immediate effects of a 90-95% reduction of the pulmonary artery cross-sectional area were: a 53 ±; 20% (mean ±; SD) decrease and a 38 ±; 10% increase of right (RvQ) and left ventricular output (LvQ), respectively. Comparing measurements before and 3–4 d after operation, there was a 64 ±; 16% decrease of RvQ and a 64 ±; 25% increase of LvQ. The increase in LvQ was due to an increase in both heart rate (19 ±; 10%) and stroke volume (38 ±; 18%). After an additional 3–4 postoperative days, heart rate remained increased to the same extent, but there was a more pronounced increase of LvQ (93 ±; 19%) and stroke volume (59 ±; 22%). Conclusion: The parallel foetal circulation has a capacity to handle a severely increased afterload for the right ventricle by immediately improving and maintaining an increased left ventricular performance. This improvement was in part accomplished by an increase in stroke volume.

Fetuses with pulmonary stenosis and constriction of the ductus arteriosus or the recipient twin in the context of a twin-to-twin transfusion syndrome may present with severe right ventricular myocardial dysfunction. Free O2 radicals are known to be increased in hypertrophied adult myocardium secondary to an increase in endocavitary pressure. This study investigates whether products of reactive O2 species generation are abnormally elevated in the myocardium of fetuses with increased right ventricular pressure. Banding of the main pulmonary artery was performed in five fetal lambs at 90 to 100 days of gestation. Three other animals had a sham intervention and were used as controls. Postoperative observation lasted on average 42 days (range 33-49 days). The levels of hydroperoxides were found to be significantly higher in the right ventricle of the stenosed lambs (6.6 +/- 3.5 nmol/mg protein) compared to the left ventricle of the same lambs (0.7 +/- 0.7 nmol/mg protein), and compared to the right (0.12 +/- 0.1 nmol/mg protein) and the left (0.5 +/- 0.8 nmol/mg protein) ventricles of the controls. It is concluded that during fetal life, an increase in right ventricular pressure is associated with a marked accumulation of products of reactive O2 species generation in the right ventricular myocardium.

AIM—To verify whether extra uterine changes in total peripheral vascular resistance and cardiac output, caused by raised haematocrit, occur in fetal life and if they can be documented using conventional ultrasound techniques. METHODS—An exchange transfusion with packed red cells was performed on five fetal lambs at 140 days of gestation (weight 3.44, SD 0.48 kg); three others were used as controls. The haematocrit was raised from 44 ± 3 to 64 (SD2)%. RESULTS—Body temperature, blood gas, and pH remained within normal limits. Blood viscosity increased from 5.3 ( 0.3) to 9.6 (1.6) cps. Combined cardiac output fell to 30% of its initial value. The pulsatility index (PI) remained unchanged in the umbilical artery (0.66, SD 0.1) and descending aorta (1.3, SD 0.3). A significant positive correlation was found between haematocrit and PI only in the carotid artery (r=0.67, p

Eleven fetal sheep were studied to investigate if Doppler echocardiography could document redistribution of blood flow during maternal oxygen administration. Velocities through the pulmonary valve, aortic valve, common brachiocephalic trunk, aortic arch, descending aorta, umbilical and carotid artery were recorded before, during and after oxygen was delivered to the ewe by face mask. Indices of cardiac performance (shortening fraction, velocity of fiber shortening and systolic time intervals) were also obtained. The aortic arch was the only recording site where significant changes in mean velocity related to oxygen administration and withdrawal were demonstrated (p < 0.01). Changes in the velocity waveform suggesting an increase in cerebral vascular resistance during oxygen administration were found in the carotid artery. Thus, using Doppler velocimetry, the carotid artery and the aortic arch (equivalent to the human aortic isthmus) appear to be suitable sites to document changes induced by maternal oxygen administration.

BACKGROUND This study investigated the effects of impairment to placental flow on flow patterns through the aortic isthmus because in the fetus, this vascular segment is the link between the parallel vascular systems perfused by the left and right ventricles. METHODS AND RESULTS A progressive increase in resistance to blood flow through the placenta was created in seven exteriorized fetal lambs by mechanical umbilical vein compression. Blood flows were measured in the ascending aorta, pulmonary artery, aortic isthmus, and umbilical artery at baseline and at each compression level. The severity of the levels of compression was determined by changes in the flow profile through the umbilical artery. An increase in placental resistance causing a fall in umbilical blood flow of approximately 50% was associated with a retrograde diastolic flow through the aortic isthmus even though the diastolic flow through the umbilical artery remained forward. Because of the systolic predominance, however, the net flow in the isthmus was forward. With a more severe increase in placental resistance corresponding to a decrease of 75% in umbilical blood flow, the net flow through the isthmus approached zero. A strong positive correlation was found between the umbilical blood flow and the net flow through the aortic isthmus (r = .89). CONCLUSIONS Variations in Doppler blood flow velocity waveforms and integrals of the aortic isthmus can be used as a sensitive indicator of the state of the umbilical circulation.

Blood flow velocimetry studies in animal fetuses with reverse diastolic flow in the umbilical artery have shown marked changes in the fetal central circulation characterized by a retrograde diastolic flow in the descending aorta, and as far as the aortic arch, along with a significant forward diastolic flow in the arteries going to the brain. Documentation and the implications of this phenomenon in human fetuses, to date, have not been reported. Doppler echographic evaluations of the diastolic patterns in the umbilical artery, descending aorta, the aortic arch, and the common carotid artery were performed on 5 fetuses in whom reverse diastolic flow was observed in the umbilical artery. In all five cases reverse diastolic flow was observed not only in the umbilical artery but also in the aortic arch. In the carotid artery, however, a forward diastolic flow was always recorded. It can be concluded, by inference, that in these fetuses, the area of lowest resistance was no longer the placenta, as seen in normal conditions, but the cerebral circulation. Furthermore, in four fetuses the retrograde component of the flow profiles was more prominent in the aortic arch compared with the descending aorta, suggesting that, in diastole, blood was coming from the pulmonary artery through the ductus arteriosus.

We speculated that a relationship may exist between transient peripheral pulmonary stenosis and the closure of the ductus arteriosus. Fifty preterm infants had pulmonary artery and ductal color doppler flow velocity assessments performed before and after closure of the ductus arteriosus. No flow turbulence or increase in velocity was observed immediately after birth, although a significant discrepancy in size was observed between the main pulmonary artery and its two branches. After closure of the ductus, 15 infants has signs of transient peripheral pulmonary stenosis of the left pulmonary artery in association with a significant decrease of diameter at the origin of the same artery. In all 50 infants, no significant gradient was observed in the right pulmonary artery. We conclude that, at least in the preterm infant, transient peripheral pulmonary stenosis is not present at birth but is an acquired phenomenon closely related to closure of the ductus arteriosus.

To evaluate the effects of elevated placental resistance on the diastolic blood flow in the main arteries of the fetus, placental resistance was mechanically increased in six exteriorized lambs. A string was inserted into the exposed section of the umbilical cord and placed around the veins isolating them from the arteries. Doppler flow velocities waveforms were measured by placing a lightweight acoustic bag on the umbilical cord. Placental resistance was increased by tightening the string until retrograde diastolic flow was observed in the umbilical artery. All measurements were obtained within 10 minutes. Heart rate, PO2, PCO2, and pH before umbilical vein compression were 177 +/- 24 beats/min, 16.4 +/- 1.8 mm Hg, 42.5 +/- 4 mm Hg, and 7.3 +/- 0.05, respectively, and 112 +/- 38 beats/min, 5.9 +/- 1.5 mm Hg, 56.6 +/- 7.0 mm Hg, and 7.2 +/- 0.05, respectively, after umbilical vein compression. The patterns of diastolic flow observed after compression were descending aorta, retrograde; aortic arch, retrograde; ascending aorta, bidirectional; cephalic aorta, forward, which were quite different from their respective baseline patterns. It is concluded that the appearance of reverse diastolic flow in the umbilical artery indicates that (1) the lowest vascular resistance in the fetal circulatory network is no longer at the placental but at the cerebral level, and (2) preplacental blood with low oxygen content from the descending aorta and pulmonary artery is being shifted toward the brain.