Introduction: Intrauterine growth restriction is a significant cause of neonatal mortality. The uterine artery Doppler waveform becomes transformed into a high flow with low resistance at 22-24 weeks. The  apt  way  to  reduce  intrauterine  growth  restriction  is  to  identify  the  antenatal  factors,  which ascertain the uterine milieu and nutrient bioavailability. This chapter highlights the relation between abnormal uterine artery flow and resultant fetal growth restriction in a tertiary care center. Presence of high pulsatility is a significant risk factor for early onset IUGR as compared to late onset IUGR. Abnormal Doppler waveforms within the uterine arteries are indicative of elevated resistance. The  perfusion  at  the  trophoblast-maternal interphase is  high  velocity,  low  volume  and  intermittent, resulting  in  intrauterine  growth retardation.  This subsequently  leads  to  the  damage  of  fetal tertiary stem villi floating in the intervillous space. The sensitivity is better for early onset IUGR. This chapter concludes that high pulsatility index in uterine arteries can lead to intrauterine growth restriction .The plausible explanation is reduced Vascular Endothelial Growth Factor (VEGF) from maternal decidual natural killer cells. This study concludes that high pulsatility index in uterine arteries is associated with intrauterine growth restriction. This occurs due to inadequate VEGF secretion from maternal decidua resulting inhigh velocity, low volume diastolic flow in the uterine artery supplying the spiral arterioles, that subsequently leads to the damage of fetal tertiary stem villi floating in the intervillous space. As resistance increases in uterine arteries, the velocity of blood flowing also increases from 10 cm/sec to 1-2 m/s. The uterine artery supplies both the trophoblast maternal interphase and the uterine arterial venous  circulation.  Most  blood  increases  uterine  arterial  venous  circulation  and  helps  in  the development of uterine musculature and local milieu of gestation and protects against post partum hemorrhage. Only a partial amount of blood flowing through uterine arteries is pumped into the dilated spiral arteries and sprinkled (cf shot) over tertiary fetal stem villi in the intervillous space. The damage to placental bed may be ischemic, hemodynamic, oxidative or immunological. The high velocity, low volume, intermittent perfusion by the uterine artery supplying the intervillous space at the trophoblast-maternal interphase can cause hemodynamic and oxidative damage resulting in intrauterine growth retardation. The sensitivity and negative predictive value are better for early onset IUGR.

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