Andersons pediatric cardiology 174

Fetal Vascular Physiology Arterial Physiology The role of the endothelium in modulating vascular responses is well recognized A series of studies performed in children and young adults with risk factors for later disease have shown that it is possible to detect abnormalities in vascular responses to stimuli both dependent and independent of the endothelium before there are signs of overt disease.181–183 Although it is not yet possible to examine directly the responses of the fetal endothelium in this way, information is available on the pulsations of the vessel wall and the velocity of the pulse wave of the fetal aorta, which have been measured using wall-tracking devices Pulsations of the arterial wall (Fig 6.19) reflect impedance from distal vascular beds along the fetal arterial tree The pulsatile change in cross-sectional area of the fetal aorta during the cardiac cycle at the 20th week of gestation is approximately 22%, falling to 17% at term compared with approximately 9% in the adult aorta.184 This may reflect a reduction in arterial mural compliance with increasing blood pressure in the growing fetus, and with structural changes within the vessel wall, which alter its physical properties Information about the fetal vascular tree may be gained from analysis of the separate parts of the wall as it moves Studies using a feline model have correlated the diameter of the movements of the pulsating wall with invasive measures of ventricular function and afterload185 and found the maximal incremental velocity of the arterial pulse waveform to be the best single variable, reflecting total peripheral resistance and late decremental velocity better to reflect a lower stroke volume and reduced cardiac output The maximum incremental velocity (see Fig 6.19) may provide additional information on ventriculovascular coupling in the fetal circulation Standard arterial Doppler assessment using the ratio of acceleration to ejection periods at the level of the arterial valve is said to reflect the mean arterial pressure in that artery and also to reflect on the ventricular function Unfortunately, this has not proved to be reliable.186 In contrast, the maximum incremental velocity has been shown in animal studies to correlate well with the acceleration in aortic flow and with the rate of rise of left ventricular pressure.185 The rate of increase in the aortic diameter in early systole is dependent on ventricular systolic function but is dependent also on distal impedance If this can be considered to remain relatively constant for a single examination, then maximum incremental velocity may be a better noninvasive indicator of ventriculovascular coupling than currently available Doppler measures FIG 6.19 Arterial pulse waveform, illustrating the maximum incremental velocity (MIV), the relative pulse amplitude (ΔD), and the late decremental velocity (LDV) Ddiast, Diastolic diameter; Tprop, propagation time of the pulse wave measured from foot to foot of the arterial impulse Venous Physiology The venous system is considerably more pulsatile in the fetus than after birth Pulsations of the wall of the inferior caval vein reflect not only the fetal central venous pressure but also the changes in ventricular relaxation and filling The information derived has provided interesting physiologic insights into fetal circulatory development.184–187 In contrast to the arterial system, the relative pulse amplitude of the inferior caval vein increases with gestation.187 The relative gestational increase in venous pulse amplitude may reflect an improvement in the filling and emptying of the right ventricle This is supported by the findings, using Doppler, of a reduction in reversal of flow of blood away from the heart in the inferior caval vein of the healthy fetus.61 That venoventricular coupling is further improved is suggested by the finding of forward diastolic flow in the pulmonary trunk in normally growing fetuses with increased venous mural pulsatility.184 Diastolic flow in the pulmonary trunk has been reported in association with a restrictive right ventricle in children following repair of tetralogy of Fallot,188 but these fetal Doppler indexes suggest that diastolic filling of the right ventricle improves with gestation The Doppler findings suggest that improved filling is a consequence of reduced distal impedance drawing blood into the arterial duct at the end of diastole, before the valve opens fully.189,190 Venous mural pulsations therefore may reflect the falling impedance of the arterial tree distal to the arterial duct, as well as improving cardiac compliance Pulse Wave Velocity Measurement of compliance or elastance of a blood vessel may be determined from the speed of propagation of a pulse traveling in its wall: the faster the velocity, the stiffer the wall Such velocity has been shown to increase by approximately 1 m/s in chick embryos from stage 18 to 29191 and in normal fetuses from 20 weeks to term.184 The velocity depends on the mean distending pressure of the vessel, coupled with changes in the composition of the wall The mean aortic blood pressure increases during gestation, as does the thickness of the aortic wall relative to the lumen and the supporting adventitial tissue The composition of the wall changes with accelerated deposition of elastin during the last weeks of gestation This continues during the first months of life and confers increased distensibility to the aorta.192 The velocity of the pulse wave has been shown to increase with age and is an important determinant of coronary arterial flow and left ventricular function.193 It has also been shown to correlate with atherosclerosis and to be increased in coronary arterial disease.194 Reduced arterial distensibility contributes to the pathogenesis of hypertension A reduction in the arterial characteristic impedance results in increased pulse pressure, and the pulsatile cardiac workload is accentuated Furthermore, the resultant increase in the velocity of the pulse wave results in early return of the reflected wave and further augments the systolic pressure