Is It Time to Redefine Fetal Decelerations in Cardiotocography?

Abstract

Historically, fetal heart rate (FHR) decelerations were classified into "early", "late", and "variable" based on their relationship with uterine contractions. So far, three different putative etiologies were taken for granted. Recently, this belief, passed down through generations of birth attendants, has been questioned by physiologists. This narrative review aimed to assess the evidence on pathophysiology behind intrapartum FHR decelerations. This narrative review is based on information sourced from online peer-reviewed articles databases and recommendations from the major scientific societies in the field of obstetrics. Searches were performed in MEDLINE/PubMed, EMBASE, and Scopus and selection criteria included studies in animals and humans, where the physiology behind FHR decelerations was explored. The greater affinity for oxygen of fetal hemoglobin than the maternal, the unicity of fetal circulation, and the high anaerobic reserve of the myocardium, ensure adequate oxygenation to the fetus, under basal conditions. During acute hypoxic stress the efficiency of these mechanisms are increased because of the peripheral chemoreflex. This reflex, activated at each uterine contraction, is characterized by the simultaneous activation of two neural arms: the parasympathetic arm, which reduces the myocardial consumption of oxygen by decreasing the FHR and the sympathetic component, which promotes an intense peripheric vasoconstriction, thus centralizing the fetal blood volume. This review summarizes the evidence supporting the hypoxic origin of FHR decelerations, therefore archiving the historical belief that FHR decelerations have different etiologies, according to their shape and relationship with uterine contractions. The present review suggests that it is time to welcome the new scientific evidence and to update the CTG classification systems.

Keywords: FHR decelerations; bradycardia; cardiotocography; fetal physiology; labor; myocardial hypoxia; peripheral chemoreflex.

Figure 1

Pathophysiology of fetal decelerations. Each contraction decreases the blood flow of the intervillous space, thus leading to transient fetal hypoxemia. The peripheral chemoreflex, which is characterized by two neural arms, is activated at each contraction. The parasympathetic arm reduces the myocardial consumption of oxygen by decreasing the FHR. The sympathetic component promotes an intense peripheric vasoconstriction, thus centralizing the fetal blood volume. The combined effect of these two actions increases the fetal systemic pressure, guaranteeing the blood supply to central organs such as the heart, the brain, and the adrenal glands. The greater the hypoxic insult, the more intense is the activation of the peripheral chemoreflex. When the hypoxic insult is prolonged the deceleration is maintained by the myocardial hypoxia.