Assessing Fetal Wellbeing: A Practical Guide

Preface

Welcome to the second edition of Assessing fetal wellbeing: a practical guide. This handbook has been specifically written to support the RANZCOG Fetal Surveillance Education Program (FSEP) and to be an easy-to-read resource for all midwives, doctors and trainees involved in the care of women in pregnancy and labour.

The book is the result of a partnership between the RANZCOG FSEP and the Maternal Fetal Medicine Unit at Monash Health, Clayton. This is the second edition of the joint handbook, the origins of which can be traced through four previous editions from the Monash Unit first published in 1984.

The authors of Assessing fetal wellbeing: a practical guide have strived to keep the handbook short and clinically focused. As with the FSEP, a solid understanding of fetal physiology underpins the clinical application of knowledge. In this way, it is hoped that clinicians will be better equipped to interpret and manage the diverse fetal heart rate (FHR) patterns that they will encounter in their daily work. As such, the handbook is not meant to be an exhaustive textbook of fetal physiology and heart rate control. Rather, the handbook should find daily use in birth suites and maternity units by midwives, GPs, trainees and specialist obstetricians alike.

For those wishing to extend their reading, there are many other excellent resources, including the online education programs and teaching and assessment tools presented by the RANZCOG FSEP (www.fsep.edu.au).

Acknowledgements

A large number of ‘behind the scenes’ individuals have made this handbook possible. In particular, the authors wish to thank the many midwives and obstetricians who contributed to the previous edition, Fetal Surveillance: a practical guide and RANZCOG administrative staff for their support with the development of this new edition.

CHAPTER ONE

THE PHYSIOLOGY

OF FETAL

SURVEILLANCE

The utero-placental unit

The placenta acts as a link between the fetal and maternal circulations. The transfer of oxygen (O2) and nutrients from the mother to the fetus and the transfer of carbon dioxide (CO2) and waste products from the fetus to the mother are dependent on (i) an adequate maternal circulation (including good uterine perfusion), (ii) a healthy placenta and (iii) an adequate fetal circulation.

This is important because if any of these are interrupted then the delivery of O2 to the fetus or removal of CO2 and metabolic acids from the fetus will be impaired. When assessing a pregnancy the clinician should always consider the mother, the placenta, and the fetus. We will now discuss how maternal blood perfuses the placenta to supply the fetus its needs and in what clinical situations maternal, placental, and/or fetal perfusion may be adversely affected.

Figure 1 Uteroplacental blood flow

Oxygenated maternal blood enters the intervillous space, between the uterus and the placenta, via the uterine spiral arteries. These arteries perforate the uterine muscle and so can be easily occluded by even moderate uterine contractions. Deoxygenated fetal blood enters the placenta via the two umbilical arteries, flowing into the chorionic villi that project into the intervillous space to be bathed in oxygenated maternal blood. It is here that all gaseous, nutrient, and metabolic by-product exchange occurs. In the healthy placenta, while the fetal and maternal circulations are in close contact, they do not actually mix. Oxygenated blood is returned to the fetus via the umbilical vein. In healthy pregnancies, the level of O2 in the maternal blood is higher than in the fetal blood and the level of CO2 in the fetal blood is higher than that in the maternal blood. This allows O2 to diffuse from the mother to the fetus and CO2 to diffuse from the fetus to the mother (Figure 1).

Remembering that an adequate maternal circulation, a healthy placenta, and an adequate fetal circulation are all necessary for satisfactory gaseous exchange, we need to consider each of these when assessing the fetus.

Maternal circulation

If the maternal circulation is impaired then delivery of oxygenated maternal blood into the intervillous space will be compromised. Common clinical situations where this may happen include maternal hypotension and excessive uterine activity. In maternal hypotension (such as occurs with supine hypotension, epidural/spinal anaesthesia, blood loss) the low maternal blood pressure (BP) results in decreased uterine blood flow, reducing O2 delivery to the placenta and fetus. When there are too many uterine contractions (tachysystole) or a lack of uterine rest (uterine hypertonus), the spiral arteries are occluded, preventing maternal blood from entering the intervillous space. This impairs delivery of O2 to the placenta and fetus.

Placenta

Diffusion of O2 and CO2 across the placenta may be impaired as a result of a chronically reduced placental surface area or an acute loss of placental surface area. A chronic reduction in placental surface area, and therefore capacity for O2 exchange, is likely in the setting of preeclampsia and/or fetal growth restriction (FGR). Acute changes in placental surface area such as may occur with a placental abruption may likewise reduce the functional area of the placenta.

Fetal circulation

If the fetal circulation is impaired then the uptake of O2 from the placenta may be reduced. This most commonly occurs with cord compression, particularly where oligohydramnios is present. Cord compression interrupts blood flow to and from the fetus and so impairs oxygenation.

By understanding and appreciating the contributions of the maternal, placental, and fetal circulations to normal fetal oxygenation, and situations when these are likely to be compromised, the skilled clinician can quickly assess and correct likely problems. For example, maternal hypotension may be avoided by ensuring appropriate maternal positioning or by maintaining adequate hydration. Similarly, persistent cord compression may be alleviated by changing maternal position and excessive uterine activity, be it by tachysystole or hypertonus, can be temporarily managed by the administration of tocolytics, such as terbutaline.

Control of the fetal heart rate

The fetal heart rate (FHR) is controlled by a number of inputs including the sinoatrial node, autonomic nervous system (sympathetic and parasympathetic), catecholamines, chemoreceptors, baroreceptors, and the cardioregulatory centre (Figure 2).

The primary pacemaker of the heart is the sinoatrial node (SA node), which is located in the wall of the right atrium. It has an intrinsic rate of between 110 and 160 beats per minute (bpm). The SA node is innervated by the autonomic nervous system, comprising both sympathetic and parasympathetic nerves. Sympathetic input increases the FHR, through the action of the catecholamines, adrenaline, and noradrenaline, while parasympathetic input reduces the FHR through the action of acetylcholine.

Since the sympathetic system matures earlier in pregnancy than the parasympathetic system, the heart rate of a preterm fetus is typically faster than that of a term fetus.

As the parasympathetic system matures with advancing pregnancy it plays an increasing role in the control of the FHR, leading to a lowering of the baseline rate. However, any reduction in parasympathetic ‘tone’ will increase the FHR by allowing the sympathetic ‘tone’ to dominate.

The balance of the sympathetic and parasympathetic input determines the baseline heart rate while the constant balancing between them generates baseline variability. This is important because the presence of normal baseline variability reflects a balanced sympathetic and parasympathetic input and is indicative of a well-oxygenated fetus.

Figure 2 FHR regulation

The FHR is also influenced by signalling from the chemoreceptors and baroreceptors, either directly or via the cardioregulatory centre. Since both chemoreceptors and baroreceptors are involved in the mechanisms underlying FHR changes, such as decelerations, a basic understanding of how they work helps in the interpretation of Cardiotocography (CTG).

Chemoreceptors are found in the carotid arteries, the arch of the aorta, and in the brain stem. They are very sensitive to changes in pO2 and pCO2. They have a high metabolic rate and so require well oxygenated blood. This makes them very sensitive to falling O2 levels and rising CO2 levels.