Case Report Fetal Circulatory Variation in an Acute Incident Causing Bradycardia Safak Olgan, 1 Mehmet Sakinci, 1 Murat Ozekinci, 1 Nasuh Utku Dogan, 1 Erkan Cagliyan, 2 and Sabahattin Altunyurt 2 1 Department of Obstetrics and Gynecology, Akdeniz University Faculty of Medicine, 07059 Antalya, Turkey 2 Department of Obstetrics and Gynecology, Dokuz Eylul University Faculty of Medicine, 35340 Izmir, Turkey Correspondence should be addressed to Safak Olgan; safakolgan@gmail.com Received 11 November 2014; Revised 22 November 2014; Accepted 4 December 2014; Published 18 December 2014 Academic Editor: Svein Rasmussen Copyright © 2014 Safak Olgan et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Umbilical artery\vein, middle cerebral artery, and ductus venosus Doppler velocimetry were performed at 33 weeks of gestation in the settings of an intrauterine growth restricted fetus during a heart rate deceleration. Interestingly, we recorded a sudden onset redistribution of fetal blood low with fetal bradycardia. Spontaneous normalization of waveforms was observed once fetal heart rate returned to normal. Our case provides evidence to circulatory variation of a human fetus resulting from an acute incident causing bradycardia. 1. Introduction Hypoxemia was known to alter fetal cardiac functions. he major alterations can be summarized as the decrease in cardiac output, increase in arterial pressure and associated aterload, and major redistribution of the blood low by selective peripheral vasoconstriction [1]. Doppler velocime- try relects the hypoxemic status of the fetus, and decrease in oxygen saturation subsequently results in changes of fetal blood low waveforms [2]. However, we neither know the circulatory changes that occur with an acute insult such as fetal bradycardia nor if there is a chance of spontaneous normalization as the primary insult ceases in an intrauterine growth restricted human fetus. 2. Case Presentation A 38-year-old multiparous woman at 33 weeks of gestation was referred to Dokuz Eylul University Hospital for evalua- tion of fetal intrauterine growth restriction (IUGR). Maternal vital signs were within normal limits at the time of admission. Cardiotocographic (CTG) monitoring revealed nonreassur- ing fetal heart rate tracing and few fetal movements. here were mild uterine contractions 20 minutes apart. A Voluson V730 Expert (GE Healthcare, Milwaukee, WI, USA) ultra- sound machine was used for ultrasound examination. Fetal biometry was below 5th percentile, but amniotic luid index was consistent with normal amniotic luid volume (85 mm). Early in Doppler ultrasonography, we manually determined a uterine contraction and then coincidentally recorded the fetal Doppler velocimetry during a heart rate deceleration (70 beats/minute, 4 minutes). During this period, fetal umbilical artery blood low diminished progressively till diastolic blood low disappeared (Figure 1(a)). Umbilical vein was in single pulsating pattern (Figure 1(b)). Middle cerebral artery (MCA) consistent with brain sparing turned into high resistance pattern (Figure 1(c)). Interestingly, character- istic ductus venosus (DV) tracing, demonstrating marked prolongation of ventricular diastole with delayed onset of reversed A-wave, was recorded (Figure 1(d)). Spontaneous reversion of these waveforms to predeceleration phase was observed once fetal heart rate returned to normal (Figures 1(e), 1(f), 1(g), and 1(h)). he patient was hospitalized and initially monitored with continuous CTG. Shortly ater the fetal monitoring, we detected a late type of deceleration for a second time (Figure 2). She was recommended bed rest and hydrated with 1000 mL of lactated Ringer solution. Additionally, maternal corticosteroid was given (two doses Hindawi Publishing Corporation Case Reports in Obstetrics and Gynecology Volume 2014, Article ID 820318, 4 pages http://dx.doi.org/10.1155/2014/820318