Intrapartum Fetal Assessment
Delivery of oxygen to the intervillous space:
The uterine & arcuate arteries give rise to radial & uteroplacental arteries which penetrate the myometrium to reach the decidua & uterine cavity. Vessels supplying the placental bed open directly into the intervillous space of the fetal placenta.
The blood volume of the intervillous space is maintained, or even increased, during uterine contractions as a result of the closure of uterine veins.
Flow of oxygenated blood into the intervillous space falls during contractions but the effect on fetal oxygenation will depend upon the total level of oxygen in the blood of the intervillous space.
Fetal response to hypoxia:
Chemoreceptors: approximately half of the venous return is from the umbilical vein containing oxygenated blood from the placenta. This blood passes from the right side to the left side of the heart and enters the ascending aorta and carotid arteries. The carotid chemoreceptors are in an ideal position to sense the oxygen status of the blood supply to the brain.In hypoxaemia, an acute stimulation of autonomic nervous system occurs via the carotid sinus nerve. An increase in vagal tone (parasympathetic) results in an FHR bradycardia. Sympathetic stimulation initiates a peripheral vasoconstriction which results in a redistribution of the fetal cardiac output favouring the brain, heart and adrenal glands.
Hormonal response: increase secretion of catecholamines from the adrenal gland in proportion to the severity of the hypoxaemia results in an increase in blood pressure & stimulation of the fetal heart which, if prolonged, overcomes the vagal bradycardia.
Intrapartum hypoxia:
The presence of any of the following risk factors at the onset of labour would label a fetus as being at “high risk” of intrapartum hypoxia:1.Hypertension/ pre- eclampsia.
2.Diabetes.
3.APH.
4.Significant maternal medical disease.
5.IUGR.
6.Preterm gestation.
7.Isoimmunization.
8.Multiple pregnancy.
9.Breech presentation.
10.Previous C/S.
11.Significant meconium staining of the amniotic fluid.
12.Post-term pregnancy.
13.Epidural analgesia.
14.Induced or augmented labour.
15.Cord prolapse.
16.Supine hypotension.
17.Ruptured uterus.
Cardiotocography (CTG):
Two signals are obtained, the fetal heart beat, converted to a rate in beats per minute, and a representation of uterine contractions. Both signals are plotted continuously on a paper record in order for the effect of uterine contractions on the fetal heart rate to be clearly visualized. (the chart recorder in a rate of 1cm/min.)
Abnormal CTG:
Baseline: the only FHR pattern that indicates fetal hypoxia is a continuous and progressive bradycardia.Fetal bradycardia (<110bpm) can arise with any acute reduction in fetal oxygenation such as: 1.cord compression. 2.abruption. 3.uterine hyperstimulation.
If bradycardia is moderate to severe or associated with other CTG abnormalities and the cause cannot be corrected, abdominal delivery (C/S) will be necessary.
Fetal tachycardia (>180bpm) is rarely, if ever, associated with fetal compromise. It may occur with 1.maternal tachycardia in thyrotoxicosis, or in response to pain. 2.maternal pyrexia (esp. secondary to chorioamnionitis).
Variability: a prolonged period of reduced variability, is clearly abnormal. The most common cause of decreased variability is fetal hypoxaemia, usually chronic, that has depressed central nervous system function. The other causes are pre-existing neurological problems, maternal drugs, congenital heart block.
Accelerations: rarely seen in the presence of a compromised fetus.
Decelerations: these are divided into 3 types, but this can only be determined after observing a pattern repeating overtime.
1.Early decelerations: these decelerations begin with the onset of a contraction. They arise from vagal n.stimulaton secondary to cord compression. They are rarely associated with fetal compromise.
2.Variable decelerations: these are just that-variable. Each deceleration has a different shape and their timing with regard to contractions is unpredictable. They are the most common type of decelerations. They arise from chemoreceptor stimulation secondary to cord compression. They may also result from head compression. Severe variable decelerations (rate drops by >60bpm or decelerations lasts longer than 60 seconds) can be associated with fetal acidosis.
3.Late decelerations: they begin 20-30 seconds after the contraction and the baseline does not return to normal limit until after the contraction has finished. They result from direct fetal myocardial depression secondary to hypoxaemia.
Secondary tests of fetal wellbeing:
1.U/S assessment of amniotic fluid volume.2.Umbilical artery Doppler.
3.Vibroacoustic stimulation (stimulation applied to the maternal abdomen causing acceleration of FHR).
4.Scalp stimulation. Causing acceleration of FHR.
5.Fetal blood sampling (measuring fetal scalp PH. Normal fetal blood PH 7.28-7.34).
6.Fetal electrocardiogram (ECG).
7.Fetal pulse oximetry.
Fetal monitoring in the 1st stage of labour:
In low-risk pregnancies, intermittent auscultation of FHR, either by Pinnard stethoscope or by Sonic aid ,is performed every 15 minutes in the active phase of the 1st stage of labour. This should be for 60 seconds following a contraction, in order to detect significant decelerations.
In high-risk pregnancy, continuous monitoring by CTG should be performed during the 1st stage of labour.
Note: risk can change as labour progresses (like in developing vaginal bleeding, meconium, slow progress).
Fetal monitoring in the 2nd stage of labour:
In low-risk pregnancies, intermittent auscultation of FHR every 5 minutes in the 2nd stage of labour is performed, usually for 60 seconds following a contraction, in order to detect significant decelerations.
In high-risk group, continuous auscultation of FHR.