有规律的发作,坚强,和进行性子宫收缩可能导致对人类胎儿的机械(胎儿头部和/或脐带的压迫)和缺氧(脐带的重复和持续的压迫或子宫胎盘氧合的减少)应力。大多数胎儿能够产生有效的代偿反应,以避免缺氧缺血性脑病和继发于心肌内无氧代谢的围产期死亡。最终导致心肌乳酸性酸中毒。此外,胎儿血红蛋白的存在,即使在低氧分压下,对氧的亲和力也高于成人血红蛋白,尤其是胎儿血红蛋白的增加(即,胎儿180-220克/升vs成人110-140克/升),帮助胎儿在分娩过程中承受低氧压力。目前正在使用不同的国家和国际指南来解释产时胎儿心率。这些用于分娩期间胎儿心率解释的传统分类系统基于对胎儿心率的某些特征进行分组(即,基线胎儿心率,基线变异性,加速度,和减速)分为不同的类别(例如,第一类,II,和III追踪,“正常,可疑,和病理“或”正常,中介,和异常\“)。这些指南彼此不同,因为它们包含在不同类别中的特征,以及它们为每个特征规定的任意时间限制,以保证产科干预。这种方法无法个性化护理,因为规定参数的“正常性范围”适用于人类胎儿群体,而不适用于所讨论的个体胎儿。此外,不同的胎儿具有不同的储备和代偿反应以及不同的子宫内环境(羊水的胎粪染色的存在,宫内炎症,和子宫活动的性质)。胎儿心率追踪的病理生理学解释是基于临床实践中胎儿对产时机械和/或低氧应激的反应知识的应用。实验动物研究和观察人类研究都表明,就像成年人进行跑步机锻炼一样,人类胎儿对逐渐演变的产时低氧应激表现出可预测的代偿反应.这些反应包括减速的开始,以减少心肌负荷和保持有氧代谢,消除不必要的躯体运动的加速度损失,和儿茶酚胺介导的基线胎儿心率的增加以及有效的再分配和集中以保护胎儿中央器官(即,心脏,大脑,和肾上腺),这对宫内存活至关重要。此外,纳入临床背景(分娩进展,胎儿大小和储备,羊水的胎粪染色和宫内炎症的存在,和胎儿贫血),并了解暗示胎儿在非缺氧途径中受损的特征(例如,绒毛膜羊膜炎和母胎出血)。重要的是要意识到及时识别产时缺氧的发作速度(即,急性,亚急性,并逐渐发展)和先前存在的子宫胎盘功能不全(即,慢性缺氧)对胎儿心率追踪对改善围产期结局至关重要。
The onset of regular, strong, and progressive uterine contractions may result in both mechanical (compression of the fetal head and/or umbilical cord) and hypoxic (repetitive and sustained compression of the umbilical cord or reduction in uteroplacental oxygenation) stresses to a human fetus. Most fetuses are able to mount effective compensatory responses to avoid hypoxic-ischemic encephalopathy and perinatal death secondary to the onset of anaerobic metabolism within the myocardium, culminating in myocardial lactic acidosis. In addition, the presence of fetal hemoglobin, which has a higher affinity for oxygen even at low partial pressures of oxygen than the adult hemoglobin, especially increased amounts of fetal hemoglobin (ie, 180-220 g/L in fetuses vs 110-140 g/L in adults), helps the fetus to withstand hypoxic stresses during labor. Different national and international guidelines are currently being used for intrapartum fetal heart rate interpretation. These traditional classification systems for fetal heart rate interpretation during labor are based on grouping certain features of fetal heart rate (ie, baseline fetal heart rate, baseline variability, accelerations, and decelerations) into different categories (eg, category I, II, and III tracings, \"normal, suspicious, and pathologic\" or \"normal, intermediary, and abnormal\"). These guidelines differ from each other because of the features included within different categories and because of their arbitrary time limits stipulated for each feature to warrant an obstetrical intervention. This approach fails to individualize care because the \"ranges of normality\" for stipulated parameters apply to the population of human fetuses and not to the individual fetus in question. Moreover, different fetuses have different reserves and compensatory responses and different intrauterine environments (presence of meconium staining of amniotic fluid, intrauterine inflammation, and the nature of uterine activity). Pathophysiological interpretation of fetal heart rate tracing is based on the application of the knowledge of fetal responses to intrapartum mechanical and/or hypoxic stress in clinical practice. Both experimental animal studies and observational human studies suggest that, just like adults undertaking a treadmill exercise, human fetuses show predictable compensatory responses to a progressively evolving intrapartum hypoxic stress. These responses include the onset of decelerations to reduce myocardial workload and preserve aerobic metabolism, loss of accelerations to abolish nonessential somatic body movements, and catecholamine-mediated increases in the baseline fetal heart rate and effective redistribution and centralization to protect the fetal central organs (ie, the heart, brain, and adrenal glands), which are essential for intrauterine survival. Moreover, it is essential to incorporate the clinical context (progress of labor, fetal size and reserves, presence of meconium staining of amniotic fluid and intrauterine inflammation, and fetal anemia) and understand the features suggestive of fetal compromise in nonhypoxic pathways (eg, chorioamnionitis and fetomaternal hemorrhage). It is important to appreciate that the timely recognition of the speed of onset of intrapartum hypoxia (ie, acute, subacute, and gradually evolving) and preexisting uteroplacental insufficiency (ie, chronic hypoxia) on fetal heart rate tracing is crucial to improve perinatal outcomes.