Fetal circulation in utero [link]
Physiological changes to fetal circulation at delivery [link]
Assessment of fetal well-being during pregnancy [link]
Assessment of fetal well-being during labour [link]
The cardiotocograph [link]
Fetal acid–base [link]
Effect of analgesia and anaesthesia on the fetus [link]
Fetal circulation in utero
Oxygen and nutrients are brought to the placenta by the maternal uteroplacental circulation, with delivery to the fetus by the separate fetoplacental circulation.
• Maternal CO together with the spiral arteries within the uterine myometrium and decidua determine blood flow to the intervillous space and fetus.
• Physiological adaptations in pregnancy increase the maternal CO by 40%.
• Oxygen-carrying capacity is increased up to 28% by an increase in the red cell mass.
• Spiral arteries become more tortuous and lose elasticity through placental trophoblast invasion to adapt to the increasing demand of blood supply to the placenta.
• Trophoblast erosion of the spiral arteries occurs in two phases to produce a low pressure, high blood flow system within the placenta.
• Phase 1 occurs in the first trimester and involves trophoblast erosion of the decidual portions of the spiral arteries.
• Phase 2 in the second trimester involves trophoblast erosion into the myometrial portion of the spiral arteries.
• The loss of elasticity within the spiral arteries removes vasoregulation. Therefore, blood flow to the placenta is directly proportional to the maternal CO.
• Oxygenated blood enters the intervillous space from the spiral arteries as jets of blood directed towards the chorionic plate of the placenta.
• Transplacental gas exchange occurs by simple diffusion.
• Blood then flows towards the basal placental plate, aided by uterine contractions and movement of the chorionic villi.
• Deoxygenated blood drains into the uterine veins.
• In the fetus, the placenta performs the functions of the lungs and kidneys.
• Two umbilical arteries (UAs) carry 50% of the fetal CO to the placenta.
• One UA arises from each fetal internal iliac artery and leaves the fetus through the umbilical cord to the placenta.
• In the placenta, the arteries divide into small branches, which enter the chorionic villi where further subdivision into arterioles and capillaries and transplacental gas exchange occur.
• Fetal blood then flows through corresponding venous systems, which drain into a single umbilical vein carrying oxygenated blood back to the fetus through the umbilical cord.
• Approximately 50% of the blood from the umbilical vein passes into the ductus venosus, which enters the IVC, bypassing the fetal liver.
• On reaching the heart, a large proportion of blood within the IVC is directed by the crista dividens through the foramen ovale into the left atrium, avoiding entry into the right heart channel.
• This oxygenated blood passes into the left ventricle from where it is pumped into the aorta.
• From the aorta, two large carotid arteries distribute a large share of the oxygenated blood to the cerebral circulation.
• The smaller portion of blood in the IVC that does not pass through the foramen ovale mixes in the right atrium with deoxygenated blood carried by the superior vena cava (SVC) and the coronary sinus.
• This blood passes to the right ventricle from where it is pumped into the pulmonary circulation.
• Pressure within the pulmonary circulation is much higher than in the aorta, resulting in most of the blood being diverted along the ductus arteriosus, which joins the aorta below the origins of the carotid arteries.
• Less than 10% of the fetal CO enters the pulmonary circulation.
• The blood which passes down the fetal aorta to supply the viscera contains mainly blood that has circulated through the head and arms together with a lesser amount from the LV.
• Two-thirds of the blood from the aorta is pumped along the umbilical arteries to the placenta, with a small amount entering the femoral arteries to the legs.
Physiological changes to fetal circulation at delivery
At birth, a rapid sequence of cardiovascular and respiratory events occur to enable the newborn to switch from placenta to lungs for effective gaseous exchange. This sequence results in the transition from a fetal to an adult pattern of circulation.
• Labour-induced stresses stimulate catecholamine and steroid responses within the fetus, which prepare the lungs for air breathing by reducing the amount of lung fluid secretion and increasing the release of lung surfactant.
• Uterine contractions reduce the flow of blood into the intervillous space, resulting in deterioration in the fetal blood gas status.
• Compression of the fetal thorax as it descends through the birth canal at delivery helps expel some of the fetal lung fluid. Fluid within the alveolar spaces and tracheobronchial tree is absorbed into pulmonary lymphatics.
• Expansion of the fetal thorax as it emerges from the vagina at delivery enables the proximal airways to fill with air.
• Clamping of the umbilical cord results in a deterioration of blood gases and low arterial pO2.
• This change is detected by the carotid and aortic body chemoreceptors and provides a very powerful stimulus to initiate breathing.
• Exposure to other sensory stimuli with delivery (temperature, pain, pressure, tactile stimuli) helps to initiate breathing.
• Entry of air into the lungs raises the interstitial pO2, resulting in a reduction in PVR, an increase in pulmonary blood flow, a rise in the pO2 and increased filling of the left atria.
• Clamping of the cord removes the low resistance placental circulation, with a resulting increase in SVR and reduced VR to the right atrium.
• The pressure gradient within the atrial chambers reverses with the increased pressure in the left atrium, resulting in a functional closure of the foramen ovale.
• This separates the circulatory system into two halves—the right and left.
• The fall in the PVR causes a reversal of blood flow within the ductus arteriosus shunt.
• The perfusion of the ductus arteriosus with oxygen-rich blood together with locally produced vasoactive substances results in its closure.
Physiological remnants of the fetal circulation
• The foramen ovale becomes the adult fosse ovalis.
• The ductus arteriosus becomes the adult ligamentum arteriosum.
• The extrahepatic portion of the umbilical vein becomes the adult ligamentum teres hepatis.
• The ductus venosus becomes the adult ligamentum venosum.
• The proximal portions of the fetal right and left umbilical arteries become the adult umbilical branches of the internal iliac arteries.
• The distal portions of the umbilical arteries become the adult medial umbilical ligaments.
The partial pressure of oxygen within the umbilical vein at term is between 30 and 40mmHg. To meet its tissue oxygen requirements at this relatively low pO2, the fetus has made adaptations to hypoxia.
• At term, the fetal haemoglobin concentration is high, between 16 and 18g/dL, which increases the oxygen-carrying capacity of the blood.
• Fetal haemoglobin is predominantly (60–80%) HbF, which has a higher affinity for O2 than adult haemoglobin (HbA).
• This enables fetal blood to take up oxygen more readily from maternal blood.
• The O2 dissociation curve for HbF is steeper than that for HbA over the range of pO2 found in fetal tissues, allowing better delivery of oxygen to these tissues.
• The anatomy of the fetal circulation ensures that the pO2 within the ascending aorta is 30% higher than in the descending portion, providing more oxygenated blood to the developing brain and heart muscle than to the other fetal organs.
Assessment of fetal well-being during pregnancy
Obstetric patients are risk stratified at booking into two main groups:
• Low risk: no identifiable risk factors. They will have the majority of their care in community-based midwifery-led antenatal clinics.
• High risk: identified by either their past obstetric or medical history. Their care in pregnancy will be co-ordinated through hospital obstetrician-run antenatal clinics.
• All obstetric patients require antenatal fetal assessment, but the frequency and forms of assessment will vary according to risk.
• Patients who initially start as low risk may, during the course of either their pregnancy or labour, develop obstetric complications necessitating additional fetal assessment.
• Normal fetal growth is dependent on an adequate supply of oxygen and nutrients to and across the placenta with sufficient fetal uptake, together with overall regulation of the growth process.
• Any factor which interferes with these processes can result in IUGR.
• The severity of the IUGR will depend on the gestational age at onset, the magnitude of the injury and the success of adaptive mechanisms.
• Factors affecting fetal growth can be broadly subdivided into maternal, uterine, placental and fetal categories.
• Maternal factors include:
• any chronic medical condition.
• alcohol and drug addiction.
• maternal age <16 and >35 years.
• low BMI.
• Uterine abnormalities include:
• congenital uterine malformation.
• uterine fibroids
• Placental factors include:
• impaired trophoblast invasion as seen with pre-eclampsia.
• placental abruption.
• placental infarction.
• placenta praevia.
• Fetal factors include:
• chromosomal abnormalities.
• structural abnormalities.
• congenital infection.
• inborn errors of metabolism.
• multiple pregnancy.
• All obstetric patients require assessment of fetal growth.
• Any method employed to assess fetal growth requires an accurate knowledge of gestational age.
• Most of the tests currently used detect the small for gestational age (SFG) fetus rather than the fetus with IUGR.
• The IUGR fetus is one who has failed to reach its own growth potential. Not all SFG fetuses will be suffering from IUGR, as many will be healthy constitutionally small babies.
• Differentiating the pathological IUGR fetus from the healthy SFG fetus is clinically important as IUGR is associated with an increased risk of:
• intrapartum fetal distress.
• perinatal morbidity.
• Tests used to assess fetal growth are more sensitive and specific when applied to high risk pregnancies compared to the low risk population.
Symphyseal fundal height
• A useful screening test for all obstetric patients.
• The measurement is taken from the top of the maternal symphisis pubis to the top of the uterine fundus and is measured in centimetres.
• Between 20 and 35 weeks gestation, the normal symphyseal fundal height (SFH) should approximate the number of weeks of gestation with an acceptable variation of ±2cm.
• After 35 weeks gestation, the margin of error is ±3cm.
• It does not differentiate between SFG and IUGR and is subject to significant intra- and interobserver error.
• Serial SFH measurements increase its sensitivity as a screening test.
• Sensitivity is further limited by factors including:
• Maternal obesity.
• Uterine fibroids.
• Abnormal amniotic fluid volume.
• Abnormal fetal lie.
• Multiple pregnancies.
• Customized charts which adjust for maternal factors, including BMI, parity and ethnicity, improve the sensitivity and increase the antenatal detection of SFG babies.
• Further investigation, in the form of an ultrasound examination, is required if the SFH measurement differs by more than the expected for gestation.
• Ultrasound is the best available method for detecting a SFG fetus and in monitoring growth.
• Any fetus thought to be at risk of IUGR, from either the maternal obstetric or medical history, should be assessed with serial ultrasound biometry.
• The fetal biparietal diameter, head circumference (HC), abdominal circumference (AC) and femur length are the measurements obtained at ultrasound examinations.
• Growth charts are available for each of these measurements, and most are based on cross-sectional rather than longitudinal population studies.
• On most charts, the 5th, 50th and 95th centiles are plotted.
• The AC, which includes the fetal liver, the size of which is dependent on stored glycogen and hence fetal nutrition, is the best measurement for detecting IUGR.
Two patterns of growth restriction exist
• Symmetric IUGR where both head size and AC are simultaneously reduced, with a HC/AC within normal limits.
• Constitutionally small babies at the lower end of the normal range.
• Pathological due to an insult early in pregnancy at the time of general organ growth. This includes congenital abnormalities, chromosomal abnormalities and congenital infections.
• Asymmetric IUGR is the result of fetal adaptation to an inadequate supply of nutrition in order to protect the developing brain.
• AC is reduced more than the head measurements, giving an increased HC/AC ratio.
• Usually seen in conditions with a later pathological onset, e.g. pre-eclampsia, placental abruption or infarction.
• Ultrasound scanning also enables assessment of the amniotic fluid volume (AFV) and the UA Doppler status, which are both useful in distinguishing the healthy SFG fetus from the one with IUGR.
Amniotic fluid volume
• After 16 weeks gestation, the fetal kidneys produce most of the AFV.
• If the supply of oxygen and nutrients to the growing fetus is insufficient, adaptations occur, with redistribution of fetal blood away from the kidneys in favour of the brain and the myocardium.
• The reduced blood flow to the kidneys results in an overall reduction in the AFV.
• Ultrasound provides the most reliable method of assessment of AFV, which is expressed as the amniotic fluid index (AFI).
• Oligohyramnios is defined as either an AFI of <5cm or a single maximum pocket of <2cm.
• The perinatal mortality is increased in pregnancies with reduced AFV on ultrasound scanning compared with those where the AFV is normal.
Umbilical artery Doppler
• Assessment of the UA Doppler waveform is widely used in the antenatal surveillance of pregnancies with IUGR.
• The UA Doppler waveform is affected by the resistance of blood flow within the placenta and the degree of villous formation.
• Normal placental villous formation produces a low resistance system facilitating forward flow of blood within the UA throughout the fetal cardiac cycle, described as positive end-diastolic flow (EDF) (Fig. 20.2a).
• Various parameters including the resistance index can be calculated from the UA Doppler waveform and are used to assess the degree of resistance within the UA (Fig. 20.2a).
• Conditions such as IUGR and pre-eclampsia are associated with an inadequate maternal vascular response to placentation and result in increased resistance in the placental circulation.
• With increasing placental resistance, the EDF decreases (Fig. 20.2b).
• By this stage, ∼60–70% of the villous vascular tree is damaged.
• Abnormal UA Doppler flow patterns indicate an increased risk of fetal hypoxia and acidaemia.
• Both perinatal mortality and morbidity rates increase with the degree of abnormality within the UA Doppler recording.
Management of IUGR
Once fetal IUGR has been confirmed by serial scanning, the subsequent management will depend on the gestation.
• With early-onset IUGR before 32 weeks gestation or symmetric IUGR, consider chromosomal abnormalities, congenital anomalies and congenital infection.
• Detailed anomaly scan to look for structural abnormalities.
• Consider fetal karyotyping.
• Maternal viral screen (TORCH screen for toxoplasmosis, rubella, cytomegalovirus and herpes simplex).
• Maternal corticosteroid administration, in case preterm delivery <36 weeks is required, to help fetal lung maturation.
• Intensive fetal monitoring as for late-onset IUGR.
• Late-onset IUGR after 32 weeks gestation.
• Regular fetal monitoring using ultrasound scanning assessment of the AFV, the UA Doppler status, serial biometry and CTG.
• Consider maternal steroid administration if delivery before 36 weeks is necessary.
• If the UA Doppler waveform and other tests remain normal, continue twice-weekly fetal monitoring. Some obstetricians may consider delivery at ∼36 weeks whilst others may continue monitoring until term.
• If the UA Doppler shows absent EDF but other tests are normal, consider delivery if an adequate gestation has been reached. Otherwise, careful frequent monitoring at least twice weekly.
• If the UA Doppler shows reversed EDF or the CTG or other biophysical parameters suggest hypoxia, proceed to immediate delivery.
Assessment of fetal well-being during labour
• Clear amniotic fluid drainage is a reassuring feature in labour.
• Meconium-stained liquor (MSL) is present in ∼15% of all labours.
• The main factors influencing the passage of meconium are gestational age and possible fetal compromise. Therefore, the presence of MSL must be interpreted accordingly.
• Meconium is produced in the fetal gut from 10 weeks, but is rarely passed by the fetus before 34 weeks gestation. By term, MSL is present in ∼30% of cases, increasing to 50% by 42 weeks.
• In preterm infants, MSL is very uncommon and is associated with infections such as listeriosis, which produce a fetal gut enteritis.
• Maternal obstetric cholestasis is associated with increased risk of MSL.
• Fresh thick meconium is frequently passed with a fetal breech. presentation in the late first and second stage due to mechanical forces on the presenting part in labour.
• Acute and subacute fetal compromise can lead to the passage of meconium.
• In very acute situations such as cord prolapse or placental abruption, this may not occur.
Grading of meconium
• Meconium is often graded according to its appearance, which will be affected by the volume of amniotic fluid around the fetus and the temporal relationship between its passage and the timing of membrane rupture.
• Meconium consistency will be determined by the diluting influence of the AFV. With decreasing amounts of amniotic fluid, the thickness of meconium will increase.
• Meconium passed several days before rupture of the membranes is often brown and described as old.
• Recently passed meconium is green and often referred to as new or fresh.
Management of meconium-stained liquor in labour
• Continuous fetal monitoring is recommended.
• If the FHR is normal, no other specific action is required in labour.
• If the FHR is abnormal, consideration should be given either to performing a fetal blood sample or immediate delivery depending on the clinical setting.
Meconium aspiration syndrome
• Aspiration of meconium into the fetal or neonatal lungs can lead to meconium aspiration syndrome (MAS).
• Meconium aspiration, defined as the presence of meconium below the vocal cords, occurs in ∼35% of fetuses with MSL.
• Clinically MAS can range from a mild transitory condition to severe respiratory compromise.
• Meconium aspiration can occur in utero, at delivery or after birth.
• In utero meconium aspiration is thought to occur as a result of fetal breathing movements.
• In an infant who has not been exposed to intrauterine hypoxia, meconium aspiration usually results in mild MAS, which is asymptomatic in 90% of cases.
• In severe cases, neonatal mortality can be as high as 40%.
• Meconium causes physical airway obstruction, displaces surfactant, resulting in atelectasis, and produces a local chemical pneumonitis.
Intrapartum prevention of MAS
• Intrapartum saline amnioinfusion is a relatively new technique shown in small studies to reduce the incidence of MAS with MSL.
• Normal saline 1L is instilled into the uterine cavity through an indwelling intrauterine pressure catheter over a 30min period, and repeated after 4–6h in prolonged labour.
• In addition to diluting the meconium concentration, it may reduce cord compression and consequently fetal hypoxia.
• The technique may not be clinically feasible in up to 50% of cases.
Management at delivery
• A paediatrician should be present for delivery in all labours where there is MSL.
• If the baby is vigorous and active following delivery, irrespective of grade of meconium, no further action should be taken.
• With a non-vigorous baby, the vocal cords should be visualized. If meconium is present on or below the cords, direct tracheal suction is required.
• Saline lavage is not recommended as it carries the risk of removing surfactant and it may facilitate further spread of meconium within the lung.
• There is no evidence to support the technique of clamping the chest to delay the first breath, nor is gastric suctioning recommended.
The CTG is a continuous simultaneous recording of the FHR and uterine contractions, known as continuous electronic fetal monitoring (EFM).
• EFM can be performed with external transducers using Doppler ultrasound scanning to assess the FHR and a tocodynamometer, a strain gauge attached to a belt, to assess uterine contractions.
• Alternatively, internal devices such as an electrode applied directly to the presenting fetal part and a calibrated intrauterine pressure catheter can be used.
• External tocography assesses frequency and duration of contractions.
• An intrauterine pressure catheter is required to assess the intensity of contraction.
Fetal monitoring in labour
• In labour, uterine contractions restrict maternal blood supply to the placental bed, which is further compounded by the effects of pushing in the second stage.
• Each fetus has a different capacity to withstand the stress of labour.
• On admission in labour, an assessment is made to identify risk factors that may affect the fetal reserve.
• Maternal factors.
• Medical problems: essential hypertension, IDDM (insulin-dependent diabetes mellitus).
• Antenatal events: antepartum haemorrhage, pre-eclampsia.
• Induced labour.
• Prolonged pregnancy.
• Past obstetric history: previous CS, previous stillbirth.
• Fetal factors.
• Abnormal UA Doppler studies.
• Multiple pregnancy.
• Breech presentation.
• Intrapartum risk factors.
• Augmentation with IV oxytocin.
• Epidural anaesthesia.
• Intrapartum bleeding.
• Maternal pyrexia.
• Development of fresh meconium in labour.
• Abnormal FHR on intermittent auscultation.
Two options exist for fetal monitoring in labour
• For low risk cases, intermittent FHR auscultation is acceptable.
• For high risk cases, continuous EFM is recommended.
External fetal monitoring
• EFM was introduced to try and reduce perinatal mortality and cerebral palsy (CP) rates.
• Only 10% of CP cases are thought to result from intrapartum events, the remainder being due to antenatal factors.
• EFM has failed to reduce CP rates but has led to an increase in instrumental-assisted vaginal delivery.
• EFM is very sensitive in detecting fetal hypoxia but lacks specificity.
• Fetal blood sampling has helped to improve overall specificity.
CTG interpretation in labour
A systematic approach is required to ensure correct CTG interpretation.
• Any existing obstetric risk factors need to be considered.
• Assessment of uterine contractions is required to allow their effect on the FHR to be established.
Features of the FHR to be considered
• The mean FHR when it is stable, over a 5–10min period with both accelerations and decelerations excluded.
• Normal baseline rate in labour is between 110 and 150bpm (Fig. 20.3).
• A tachycardia is a baseline FHR of >150bpm. Between 150 and 170bpm is termed moderate baseline tachycardia and, provided other features are reassuring, is not indicative of hypoxia.
• A bradycardia is a baseline FHR of <110bpm. Between 100 and 110bpm is termed moderate baseline bradycardia, but provided all other features are reassuring is not suggestive of hypoxia.
• A change in baseline may indicate gradually developing hypoxia.
• The degree to which the baseline varies, i.e. the width of the baseline, excluding accelerations and decelerations.
• Normal variability is between 10 and 25 beats (Fig. 20.3).
• A baseline variability of 0–5bpm is classified as silent, 5–10bpm as reduced and >25bpm as saltatory.
• Normal baseline variability is an indicator of adequate oxygenation of the autonomic system.
Presence or absence of accelerations
• Acceleration is a transient increase in the FHR of ≥15bpm lasting ≥15s.
• Two or more accelerations per 20min is termed reactive and is indicative of fetal well-being (Fig. 20.3).
Presence and type of decelerations
• A deceleration is a transient decrease in the FHR of ≥15bpm lasting ≥15s.
• Early decelerations
• These are due to compression of the fetal head causing stimulation of the vagus nerve producing a bradycardia.
• Tend to appear in the late first and second stage of labour with descent of the head.
• They are synchronous with contractions and tend to be uniform in shape (Fig 20.4).
• If isolated and other CTG parameters normal, they are usually benign.
• Late decelerations
• These decelerations are late with respect to the uterine contractions and are associated with uteroplacental insufficiency.
• The retroplacental space provides a variable-sized reservoir of oxygenated blood. In a fetus with IUGR, this reservoir will be small. At the start of a contraction, the fetus uses its reservoir of oxygen.
• Due to restriction of uteroplacental blood supply during a contraction, a hypoxic deceleration begins and continues throughout the contraction.
• Recovery occurs some time after the contraction when full oxygenation has been restored.
• Variable decelerations
• Most common type of FHR decelerations are a consequence of umbilical cord compression with contractions.
• As the cord can be compressed in a different way with each contraction, their appearance can vary in shape, size and timing.
• In the cord, the umbilical vein is thinner and is compressed first before the arteries.
• This results in loss of some of the fetal circulating volume, and autonomic responses result in an increased FHR to compensate, which is seen as an acceleration.
• Further compression of the cord then occludes the thicker umbilical arteries with a relative restoration of the fetal circulation.
• Stimulation of fetal baroreceptors leads to a precipitous fall in the FHR. The nadir of the deceleration occurs when both the umbilical vein and artery are compressed.
• A normal well-grown fetus can tolerate cord compression for a considerable length of time before developing hypoxia. Small IUGR fetuses have less reserve.
• Variable decelerations can be subclassified as typical and atypical.
• Suspicious features associated with atypical variable decelerations include reduced baseline variability, a rising baseline, late recovery, a combined variable and a late deceleration component, and a duration of >60s with a loss of >60 beats from the baseline.
• The presence of atypical variables makes progressive hypoxia more likely.
The CTG is classified as normal, suspicious or pathological.
• Normal. All four features are reassuring.
• Suspicious. No more than one non-reassuring feature.
• Pathological. Two or more non-reassuring features or one or more abnormal features.
Reassuring features on CTG
• Baseline FHR between 110 and 150bpm.
• Baseline variability between 5 and 25bpm.
• Two accelerations per 20min.
• No decelerations.
Non-reassuring or suspicious features on CTG
• Baseline FHR between 100 and 109 bpm or 151 and 170bpm.
• Baseline variability between 5 and 10bpm for >40min.
• Increased baseline variability of >25bpm.
• Variable decelerations.
Action with a non-reassuring CTG
When non-reassuring or pathological features appear on the CTG, a search and treatment of correctable causes should be made, e.g.
• Uterine hyperstimulation.
• Maternal hypotension from aortovenal compression or epidural top-up.
• Maternal dehydration.
• Maternal pyrexia.
• Maternal need for analgesia.
If no underlying cause is identified or the CTG does not improve despite corrective procedures, a fetal blood sample (FBS) to assess fetal acid–base balance should be considered.
• Suspicious and pathological CTG traces are not always associated with acidosis.
• Special attention should be paid to fetuses susceptible to developing acidosis more quickly, including those with IUGR, preterm, post-term, infected, where there is grade 3 meconium or minimal amniotic fluid draining.
• In addition, other factors in labour that have a significant influence on the rate of decline of the fetal pH need to be considered, e.g. use of oxytocin, difficult instrumental delivery as well as acute events such as cord prolapse, uterine scar dehiscence and placental abruption.
• With these acute events, there may not be enough time to perform an FBS and delivery should be expedited.
• FBS is only technically possible once the cervix is 3cm or more dilated.
• Occasionally, it may not be possible to obtain an adequate blood sample and, if the CTG abnormality is persistent, delivery is then necessary.
Fetal blood sample
• An explanation should be given to the mother about the indication for the procedure and the planned action following the FBS.
• Verbal consent should be obtained.
• Midwifery and anaesthetic staff should be aware that the test is taking place in case urgent delivery is necessary.
• Ideally, the mother should be in either the left or right lateral position.
• The lithotomy position should be avoided because of the risk of maternal hypotension from aorto-caval compression. This can produce an iatrogenic fetal hypoxia and acidosis, leading to an unnecessary operative delivery.
• An aseptic technique is used and an amnioscope is passed through the vagina to reach the fetal scalp.
• The fetal scalp is dried using a dental swab and then sprayed with ethyl chloride to produce a hyperaemia, which aids bleeding.
• The fetal scalp is then smeared lightly with a water-repellant gel to help the blood form into a round drop.
• Under direct vision the fetal scalp is stabbed with a 2mm blade.
• The blood droplet is allowed to form and is then drawn up by capillary action into a preheparinized thin glass tube.
• When there is a sufficiently sized sample, it is taken immediately to the blood gas analyser.
• It is essential to inform the anaesthetic team when an FBS is being performed as the result may necessitate immediate delivery.
• Any FBS result should be interpreted taking into account the clinical features of both the mother and baby, any previous FBS results and the progress of the labour.
• As a general guide, Table 20.1 illustrates the subsequent action required following an FBS result according to published guidelines from the Royal College of Obstetricians and Gynaecologists and NICE.
Table 20.1 Fetal blood sample
Fetal blood sample result
Repeat FBS if the FHR abnormality persists
Repeat FBS within 30min or consider delivery if rapid fall since last FBS sample
CTG plus ST analysis of the fetal ECG (STAN)
• Although the use of intrapartum EFM has been shown to reduce the incidence of neonatal seizures, it has had little impact on long-term neonatal outcome. In addition, there is concern that its use has resulted in an increase in the CS rate.
• Whilst the use of FBS can help with CTG interpretation, there are situations where this may not be technically possible, e.g. in the early stages of labour.
• In an attempt to overcome some of these issues, newer methods of intrapartum fetal monitoring have been explored. These methods include CTG in conjunction with STAN, the use of which is becoming more widespread.
• As part of the physiological response to in utero hypoxia, depression of the ST-segment of the fetal ECG has been observed and interpretation of such events with the CTG forms the basis of the STAN analysis.
• Application of a fetal scalp electrode (FSE) is necessary and therefore STAN can only be used in situations where this is technically possible, acceptable to the patient and where no contraindications to the use of FSE exist (e.g. risk of bleeding disorder in the fetus; maternal HIV).
• Interpretation of any ST-segment abnormalities, also know as STAN events, must be made in conjunction with the CTG findings and the overall clinical picture. In the first stage of labour, a significant STAN event will necessitate additional intervention in the form of either a FBS or delivery, depending on the overall clinical picture.
• In the second stage of labour, immediate delivery may be necessary and the anaesthetist must be kept fully informed of the situation to ensure the safest most appropriate method of anaesthesia is employed.
Normal functioning of the fetal enzyme systems depends on stability of the pH within the tissues. Derangements in pH may be primary due to respiratory or metabolic dysfunction, but the clinical picture is often mixed.
Normal gaseous exchange
• The placenta functions as the lung whilst the fetus is in utero.
• Free gaseous exchange depends upon normal flow of both maternal and fetal blood through the placental bed.
• High HbF concentration together with the higher affinity of HbF for O2 ensures adequate amounts of O2 are transferred to the fetus.
• Under normal conditions the fetus obtains the majority of energy by aerobic metabolism of glucose.
• Some of the waste product—CO2—is carried in simple solution, but the vast majority is carried as dissociated hydrogen (H+) and bicarbonate (HCO3–) ions. The H+ ions are mainly buffered by Hb, and the HCO3– ions pass out into the extracellular fluid.
• At the placenta, the CO2 in solution diffuses across to the maternal circulation. The CO2 carried as H+ and HCO3– ions is also released and transferred. Elimination of the CO2 means the concentration of H+ ions in the fetal blood is reduced.
• UA blood (from the fetus to the placenta) has a low pO2, high CO2 and a low pH (opposite of adult circulation).
• Umbilical venous blood (from the placenta to the fetus) has a high pO2, low pCO2 and a low pH (opposite of adult circulation).
Disturbance of normal gaseous exchange
Various factors can disturb normal gaseous exchange at the placenta.
• Maternal factors. Hypotension from aorto-caval compression, regional analgesia or anaesthesia. Uterine contractions may produce high pressure, reducing uterine blood flow. Chronic impairment of uteroplaental blood flow, e.g. pre-eclampsia.
• Placental factors. Placental abruption and abnormal placental circulation, e.g. pre-eclampsia.
• Fetal factors Umbilical cord compression, fetal anaemia and fetal arrhythmia.
Reduction of perfusion of the placenta from fetal vessels is manifest as variable decelerations, whilst a reduction in perfusion from the maternal circulation is manifest as late decelerations.
Impaired gaseous exchange at the placenta has several consequences:
• Respiratory acidosis. During the early stages of reduced placental perfusion, CO2 transfer across the placenta is reduced, leading to a high pCO2 and a low pH. This may be transitory. If corrective measures are taken and the FHR improves, it may be treated conservatively. A degree of respiratory acidosis occurs in most uncomplicated labours.
• Further reduction in placental perfusion affects O2 transfer, resulting in a low pO2. Fetal adaptation occurs. Increased O2 extraction with centralization of blood flow to brain and myocardium at the expense of other organs occurs. Physiological reserve of the fetus will determine how long this can be sustained, but will be reduced in high risk situations.
• Metabolic acidosis. If aerobic metabolism cannot be maintained because of reduced O2 supply, anaerobic metabolism may supplement energy supplies, resulting in lactic acid formation. Lactic acid forms lactate and H+ ions, some of which will be buffered by Hb and HCO3– ions. H+ ions are not easily eliminated at the placenta and buffers have an infinite capacity, and eventually the pH and bicarbonate levels will fall, producing a metabolic acidosis with a low pO2, low pH and low HCO3–. Metabolic acidosis is damaging to fetal tissues.
• Base deficit enables the physician to differentiate between a respiratory and a metabolic acidosis.
• Respiratory acidosis does not use up buffering capacity, whereas metabolic acidosis does.
• Base deficit measures how much available buffer has been used up, and is actually the amount of base (alkali) needed to add to the blood in order to restore the pH to normal.
• Base deficit is defined as the mmol/L of base required to titrate the blood back to a normal pH.
• A base deficit is negative and is calculated from the pH and the pCO2.
Cord gas analysis
• Following delivery, cord gas analysis is a useful adjunct in assessing the overall condition of the newborn and deciding subsequent neonatal management.
• The UA cord blood result better reflects the condition of the fetus.
• Sampling the smaller UA can be technically difficult in comparison with the vein. It is good practice to sample both the UA and umilical vein and compare the two results to ensure that the UA has indeed been analysed.
• The mean difference in pH between the artery and vein is ∼0.08 units.
• Table 20.2 shows the mean blood gas results from both the UA and umbilical vein.
Table 20.2 Mean blood gas results from umbilical artery and vein at delivery
Effect of analgesia and anaesthesia on the fetus
• The pain of labour causes hyperventilation, leading to respiratory alkalosis with resulting vasoconstriction and reduced placental blood flow and oxygen availability to the fetus.
• Many women request pharmacological methods of pain relief in labour, which may confer advantages to the fetus, but may also pose certain risks.
• Most systemic drugs given to the mother are transferred to the fetus. However, the amount transferred will depend on both maternal and fetal factors, as well as the characteristics of the drugs themselves.
• Blood levels of any transmitted drug are disproportionately higher in the fetal brain compared with other tissues.
• This is partly due to the high cerebral blood flow and relatively poor development of the blood–brain barrier in the fetus.
• Chronic fetal hypoxia further increases the levels in the fetal brain as a consequence of the redistribution of blood in favour of the cranial circulation.
Nitrous oxide, in a 50:50 mixture with oxygen known as Entonox, is the most widely available inhalational analgesic for labour.
• Entonox rapidly crosses the placenta but is cleared quickly, resulting in minimal effect on the fetus or neonate.
• Neurobehavioural scores on babies exposed to in utero Entonox have shown little effect at 2 and 24h.
• Maternal hyperventilation, to achieve adequate analgesia, can lead to respiratory alkalosis in the mother, displacing the oxygen dissociation curve to the left, resulting in reduced oxygen availability to the fetus.
• Prolonged use may cause vasoconstriction within the placental bed and reduce uteroplacental blood flow, reducing fetal oxygenation.
• Entonox may reduce maternal respiratory drive, leading to periods of hypoventilation between contractions, with resulting hypoxia.
The opioids pethidine, diamorphine and, to a lesser extent morphine, are widely used to provide analgesia in labour.
• Rapidly crosses the placenta by passive diffusion, causing intrauterine sedation in the fetus.
• The effects are dependent on dose and timing, with maximal effects seen 2–3h after IM administration and with repeated doses. Fetal exposure can result in respiratory depression at birth, leading to lower Apgar scores, reduced oxygen saturations and increased CO2 tensions.
• If given within 1h of delivery, neonatal effects are minimal.
• Fetal sedation can result in CTG alterations.
• Reduction in baseline variability and accelerations are seen 25min after IV and 40min after IM administration.
• Reduced variability can last longer than the 40min normally associated with the quiet or sleep phase.
• CTG interpretation can be more difficult after administration, so it is important that the preceding CTG is normal and reactive.
• A reduction in fetal movements, altered fetal EEG activity and reduced fetal scalp oxygen tensions have been observed, but these effects are of unknown clinical significance.
• Pethidine is a weak base, resulting in increased ionization and accumulation in the relatively more acidic fetal circulation.
• With fetal acidosis, this effect is further increased, making the pethidine less able to cross back into the maternal circulation (ion trapping).
• Norpethidine, the active metabolite of pethidine, compounds the neonatal effects and has proconvulsant properties.
• Neurobehavioural patterns are altered, with babies exposed to intrauterine pethidine tending to be sleepier, less attentive and slower to establish breastfeeding.
• Administration of naloxone to the neonate can reverse the effects of opiates although it is increasingly controversial. The painful stimulus of an IM injection is thought to be largely responsible for ‘waking the baby up’. The opioid effect outlasts the short-acting effect of naloxone.
Morphine and diamorphine
• The fetal side effects of morphine and diamorphine are very similar to those of pethidine.
• Equianalgesic doses of pethidine cause less neonatal respiratory depression than either morphine or diamorphine.
• The metabolite, morphine-3-glucuronide, does not have the side effects of norpethidine.
Regional analgesia and anaesthesia
• Maternal hypotension can occur as a result of either sympathetic blockade or aorto-caval compression, which can be detrimental to the fetus.
• If left untreated, this will cause fetal hypoxia with a fall in fetal pH.
• Continuous fetal monitoring is therefore mandatory following regional techniques.
• However, provided maternal hypotension is avoided and uteroplacental perfusion maintained, regional techniques are well tolerated by the fetus.
• Regional techniques do not influence the resistance in uterine vessels, intervillous blood flow or flow velocity in the UA.
• Relief of pain achieved with regional techniques, by reducing circulating maternal levels of catecholamines, increases placental blood flow.
• Maternal body temperature increases after epidural analgesia. The mechanism is unclear, but marked hyperthermia may result in a fetal tachycardia not associated with significant fetal hypoxia and fetal pH is not affected. This can give rise to an erroneous diagnosis of fetal distress or to a false diagnosis of intrauterine infection, increasing the number of newborns investigated and treated with antibiotics.
• Placental transfer of opioids occurs rapidly after epidural administration and should be considered when delivery is imminent.
• Epidural or intrathecal fentanyl doses >100 micrograms may cause neonatal respiratory depression and have an effect on establishing breastfeeding.
• Approximately 20% of CSs are performed using GA.
• The ideal induction to delivery time is between 5 and 15min.
• Prolonged induction to delivery time increases the risk of fetal acidosis but can be minimized if both aorto-caval compression and hypotension are avoided.
• Lipid-soluble anaesthetic agents rapidly cross the placenta and a prolonged induction to delivery time allows progressive uptake by the fetus, resulting in neonatal sedation with low Apgar scores.
IV induction agents
• Thiopental: this is the most commonly used induction agent and at 4mg/kg the baby is protected from excessive sedation because of the fetal circulation through the liver. At 8mg/kg neonatal depression will occur.
• Propofol: doses >2.5mg/kg can cause neonatal depression. Although associated with rapid wakening in the adult, this advantage has not been observed in the neonate.
• Ketamine: at doses of 1mg/kg, the neonatal condition is comparable with thiopental. At 2mg/kg, neonatal depression and low Apgar scores will result.
• Etomidate: this is rapidly metabolized by a cholinesterase in the placenta and at 0.3mg/kg will cause minimal depression in the neonate. It significantly reduces neonatal plasma cortisol levels at 1h of age, which may be detrimental to an already compromised baby.
• Benzodiazepines: compared with thiopental induction doses, benzodiazepines double the time to sustained neonatal respiration. They can cause neonatal respiratory depression, lethargy, poor feeding, hypothermia, hypotonia and jaundice; should be avoided.
• These agents are ionized compounds at normal physiological pH. Under normal circumstances, placental transfer is minimal with no effect on the fetus or neonate.
• There are case reports of suxamethonium apnoea in an affected neonate after suxamethonium was administered to an affected mother.
• Nitrous oxide: it freely crosses the placenta and if >50% is used, may cause neonatal depression with low Apgar scores. High concentrations of nitrous oxide can cause diffusion hypoxia and fetal acidosis. A 50:50 mixture with oxygen should be administered prior to delivery of the baby.
• Volatile anaesthetic agents: isoflurane, enflurane, desflurane and sevoflurane are widely used for CS.
• These lipid-soluble drugs cross the placenta causing a dose- and time-dependent neonatal depression.
• Using a 1 MAC equivalent with nitrous oxide and an induction–delivery interval of <11min, excessive neonatal depression is avoided.
• Sevoflurane and desflurane are safe but have no benefits over isoflurane.
• Sevoflurane metabolism is associated with fluoride ion production, causing an increase in neonatal serum fluoride 24h after delivery, the consequences of which are unknown.