In vivo evaluation of acceleration and deceleration capacity of fetal heart rate in worsening hypoxic acidemia

INTRODUCTION: Fetal heart variability (fHRV) reflects the homeostasis of autonomous nervous system (ANS). The conventional frequency domain analysis is inadequate for a non-stationary signal such as fHR. Phase Rectified Signal Averaging (PRSA) is a novel method able to extract the quasi-periodic components out of non-stationary, noisy time series. The aim of the study was to determine the average acceleration and deceleration capacity (AAC and ADC), computed by PRSA method, in worsening acute hypoxic-acidemic insult as it may occur during labor. METHODS: In near-term fetal sheep (n=9) repetitive umbilical cord occlusions (UCO) were induced for 1 min every 2.5 min as follows: mild partial UCO for 1 h; moderate partial UCO for 1h; and complete UCO x 1-2 h, until arterial pH<7.00. Arterial blood samples were collected at baseline, every 20 min during the UCO series, and at 1 h of recovery. Fetal ECG was recorded. AAC/ADC were computed from ECG for each phase of the stimulation protocol. RESULTS: AAC and ADC increased (in absolute value) across the phases of increasing UCO severity. BASELINE MILD MODERATE SEVERE ADC 3.00(2.28,4.42) 3.16(2.72,4.27) 6.19(5.07,7.19) 9.15(5.97,9.87) AAC -2.77(-3.66,-2.13) -2.98(-3.94,-2.32) -5.39(-6.77,-5.14) -7.62(-9.97,-5.29) pH 7.34(7.34, 7.37) 7.33(7.31, 7.34) 7.28(7.24, 7.30) 6.98(6.96, 7.06) CONCLUSIONS: Our findings show that during an acute hypoxicasphyxic insult, with activation of ANS, there is an increase in AAC and ADC of fHR. These results differ from those obtained in IUGR fetuses, where decreased ACC and ADC are reported (data presented in a separate abstract). We hypothesize that the fetal metabolic reserves are differentially impacted by acute (i.e., UCO insult) versus chronic (i.e., IUGR) hypoxia, which results in a different ANS response as detected by PRSA method.