A new assessment of what late and variable decelerations mean.
This fifth article in the Electronic Fetal Monitoring Mythbusters series reviews the scientific evidence behind the notion that late decelerations are more ominous than variable decelerations.
In this series, we have reviewed standard electronic fetal monitoring (EFM) nomenclature, explored various systems of classifying fetal heart rate (FHR) decelerations, and refuted an obscure myth concerning the consequences of intrapartum fetal head compression.
This column will examine the evidence underlying the common misconception that late decelerations are "ominous," while variable decelerations are "benign."
As early as the 19th century, investigators using intermittent auscultation described episodes of slowing FHR that later became known as decelerations.1 The advent of EFM permitted visual analysis and objective quantitation of decelerations. Hon, Kubli, and others classified decelerations as early, late, variable, or prolonged, based upon visual appearance and temporal relationship to uterine contractions.2,3 Early decelerations were ascribed to fetal head compression, and were considered innocuous.3 Variable decelerations were attributed to umbilical cord compression, and late decelerations were thought to be indicative of interference with maternal-fetal gas exchange during uterine contractions (ie, "uteroplacental insufficiency").
In 1969, Kubli, et al reported that late decelerations were associated with lower fetal scalp pH values than were mild or moderate variable decelerations.3 This study did not attempt to distinguish between benign respiratory acidemia, caused by elevated pCO2, and potentially significant metabolic acidemia, caused by tissue hypoxia, anaerobic metabolism, and accumulation of lactic acid. In addition, the study did not address neonatal outcome and did not control for such confounding factors as baseline rate, variability, accelerations, or frequency of decelerations. Nevertheless, the authors stated that late deceleration of the FHR is "more ominous than moderate or mild variable deceleration" and that "the mere presence of late deceleration is ominous."3 this line of reasoning set the stage for one of the most pervasive myths in contemporary fetal monitoring: the misconception that "late decelerations are ominous, and variable decelerations are benign."
Defining late decelerations
In 1997 and 2008, the National Institute of Child Health and Human Development published standardized definitions of FHR patterns, including late and variable decelerations.4,5 A late deceleration is defined as a gradual (onset to nadir ≥30 seconds) decrease in FHR, with the onset, nadir, and recovery of the deceleration occurring after the beginning, peak, and ending of the contraction, respectively.
In 1979, Martin, et al used autonomic blocking agents to demonstrate the physiologic mechanism of late deceleration in fetal lambs.6 Transient interruption of fetal oxygenation resulted in a biphasic autonomic reflex response. Fetal hypoxemia, detected by chemoreceptors, triggered sympathetic outflow and fetal hypertension, which was prevented by alpha-adrenergic blockade. Transient fetal hypertension resulted in baroreceptor stimulation and re-flex parasympathetic slowing of the heart rate, which was blocked by atropine.
Subsequent studies in animals have demonstrated that fetal hypoxemia results in increased vascular resistance and decreased blood flow to nonvital vascular beds of the intestine, limbs, and kidneys, while blood flow to the vital vascular beds of the brain, heart, and adrenal glands is preserved or increased.7,8 When oxygen deprivation is sufficient to result in metabolic acidemia, a late deceleration can reflect transient hypoxic myocardial depression.6
In humans, Low, et al reported a 45% incidence of metabolic acidemia when late decelerations accompanied at least 10% of uterine contractions in a 2-hour period. However, even in the absence of decelerations, metabolic acidemia was observed in 10% of newborns.9