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Abnormal fetal heart rate patterns caused by pathophysiologic processes other than fetal acidemia

Journal

AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
Volume 228, Issue 5, Pages S1144-S1157

Publisher

MOSBY-ELSEVIER
DOI: 10.1016/j.ajog.2022.05.002

Keywords

absent or minimal variability; bradyarrhythmia; cerebral palsy; congenital heart or cardiac disease; fetal anemia; fetal arrhythmia; fetal bradycardia; fetal central nervous injury; fetal heart rate decelerations; fetal infection; fetal inflammation; fetal tachycardia; ischemic encephalopathy; late decelerations; sinusoidal; tachyarrhythmia

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Fetal acidemia is a common cause of fetal death and central nervous system injury. However, certain fetal pathophysiological processes can cause significant changes in fetal heart rate patterns even before the development of acidemia. These processes include fetal infection/inflammation, anemia, fetal congenital heart disease, and fetal central nervous system injury. It is important for clinicians to consider these possibilities when significant changes in fetal heart rate patterns are observed. The fetal heart rate patterns may provide more insight into the fetal condition and pathophysiology than the acid-base status at birth.
Fetal acidemia is a common final pathway to fetal death, and in many cases, to fetal central nervous system injury. However, certain fetal pathophysiological processes are associated with significant category II or category III fetal heart rate changes before the development of or in the absence of fetal acidemia. The most frequent of these processes include fetal infection and/or inflammation, anemia, fetal congenital heart disease, and fetal central nervous system injury. In the presence of significant category II or category III fetal heart rate patterns, clinicians should consider the possibility of the aforementioned fetal processes depending on the clinical circumstances. The common characteristic of these pathophysiological processes is that their associated fetal heart rate patterns are linked to increased adverse neonatal outcomes despite the absence of acidemia at birth. Therefore, in these cases, the fetal heart rate patterns may provide more insight about the fetal condition and pathophysiology than the acidebase status at birth. In addition, as successful timing of intrapartum interventions on the basis of evolution of fetal heart rate patterns aims to prevent fetal acidemia, it may not be logical to continue to use the fetal acidebase status at birth as the gold standard outcome to determine the predictive ability of category II or III fetal heart rate patterns. A more reasonable approach may be to use the umbilical cord blood acidebase status at birth as the gold standard for determining the appropriateness of the timing of our interventions.

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