Giorn. It. Ost. Gin. Giornale Italiano di Ostetricia e Ginecologia CIC Edizioni Internazionali 2013 November-December; 35(6): 717–721. ISSN: 0391-9013
Published online 2014 March 19.

The clinical significance of bradycardia in the second stage of labor


1Maternal and Child Health Department, “Ospedali Riuniti” University Hospital of Ancona, Ancona, Italy
2Department of Odontostomatologic and Specialized Clinical Sciences, Polytechnic University Marche, Ancona, Italy


Understanding the Fetal Heart Rate (FHR) in the second stage of labor is of great importance to understand some critical clinical outcomes observed even in “low-risk” deliveries.

During the second stage of labor fetuses are subject to head compressions that can activate baroreceptor reflexes which cause FHR decelerations. “Early decelerations” have been considered as benign for a long time; then it has been shown that is the entity of the bradycardia, in terms of duration and length, best correlates with critical fetal outcomes.

Our studies significantly correlated a bradycardia of 80 bpm prolonged for 24 minutes, or 70 bpm for 12 minutes or 60 bpm for 8 minutes or 50 bpm for 6 minutes with neonatal acidosis and they showed that when there is a predisposed fetus this bradycardia can cause a cerebral damage.

Whatever the causes of the bradycardia are (more frequently they are fetal head compression, umbilical cord knots, cord loops around fetal neck or body, cord entanglement), the dramatic reality is that the time for intervention is often so short that any maneuver can result ineffective to prevent the cerebral damage. It is clear, therefore, that every delivery carries a risk in the second stage of labor, but this risk is often unpredictable and the Obstetrician cannot always successfully prevent the acidemia.

Keywords: Cardiotocography, Neonatal outcome, Electronic fetal monitoring, Bradycardia, Fetal acidemia

Keywords: Cardiotocografia, Outcome neonatale, Bradicardia, Acidemia fetale

Bradycardia in the second stage of labor

Observational skills are fundamental to new discoveries, together with the ability to link data.

To prove that, the auscultation of the Fetal Heart Rate (FHR), already practiced in the XVII century, gained the status of scientific evidence through the intuition of Le Jumeau (1) and Von Wickel (2) who associated FHR variations to fetal wellbeing.

Those scientists became the pioneers of what became the modern cardiotocography; since then FHR has been considered a fetal wellbeing parameter.

Years went by and FHR analysis became an irreplaceable method in the clinical practice and a deeper knowledge of the cardiotocographic patterns began.

One of the most interesting applications of FHR is the second stage of labor. Melchior and Bernard before (3) and then Piquard (4) studied the different patterns during the second stage of labor. They correlated the deceleration shape and length to contractions and found out that basal FHR, its variability, deceleration’s depth and length are parameters predictive of fetal outcomes. They proposed a grading system for FHR patterns.

Attention has been always paid to the evidence of late decelerations, so called because they begin after the beginning of uterine contraction; those decelerations are clearly associated with fetal pathological processes that can easily turn into fetal distress (5).

On the contrary early decelerations, synchronous to the maternal uterine contractions, have always been considered as a physiological response of the fetus to the head compressions due to uterine contractions during labor.

The hypothesis that early decelerations can cause a significant fetal oxygen reduction and produce severe cerebral damages was first hypothesized by Hon (6).

The pathological mechanisms of the fetal heart rate decelerations are based on the fetal incapacity to compensate the hypoxia.

During labor there is a progressive increase of both frequency and intensity of maternal uterine contractions that can reach 80–100 mmHg. This pressure, higher than the pressure of the uterine arterioles sac (40–60 mmHg) and of the venules (20 mmHg), occludes those vessels and both the blood afflux and efflux are impeded.

Generally, the uterine muscle relax after 30–60 seconds and the reperfusion in the intervillous space is enabled again. The venous reperfusion is possible only with a complete resolution of the uterine contraction, when basal tone is lower than 20 mmHg.

In addition to uterine contractions there are voluntary contractions of the abdominal muscles as well, that are associated with head compressions during the descent of the fetus into the pelvis. These mechanisms can further reduce the cerebral perfusion.

Usually, this mechanisms are physiologic so that a well oxygenated fetus can perfectly compensate the temporary oxygen reduction without damages, although if contractions are prolonged the fetus can exhaust all the oxygen reserves. This reduction of fetal oxygenation can cause a severe hypoxia (7) that triggers a baro-receptorial response which induces bradycardia (8).

It becomes clear the importance of studying not only the entity, but also the duration of the decelerations: a prolonged deceleration, in fact, can cause a severe fetal hypoxia that the fetus cannot overcome.

After the evidence that fetal distress begins at a FHR lower than 90 bpm (3, 4) the FHR study and its variability (9, 10) must be correlated with its length in time.

During the past years the studies on the cardiotocography in the second stage of labor have been further expanded and it has been shown that the most relevant reading parameters are FHR reductions in terms of duration and depth (1113).

Experimental aspects and clinical outcomes

In this experience, we digitally analyzed CTG patterns to quantify fetal bradycardia, then we compared the deceleration areas calculated as the product of FHR in bpm per fetal pH as index of insufficient fetal compensation to hypoxia (14, 15) to validate the hypothesis that increasing bradycardia area is correlated with significant pH decrease (9, 16).

The threshold value of the area, then, has been studied to determine the value of the area that correlates with fetal hypoxia and to distinguish between the physiological response and a pathological distress.

In a recent retrospective study (17) we analyzed the last 60 minutes of 500 CTG patterns with normal FHR, according to ACOG (18) standards. All women had singleton pregnancy and were in the second stage of labor. From this patterns we extracted 33 CTG which in the second stage of labor presented a bradycardia nadir lower than 90 bpm, then we analyzed the area of the bradycardia and we studied the prognostic value.

The 90 bpm upper limit comes from Melchior-Bernard and Piquard classification (types III and IV) (3, 4); areas have been digitalized and saved as files, then studied with the pc program Autocad®.

Autocad® is a computer-aided design (CAD) software available for personal computers. It allows to obtain the area of two-dimensional object by selecting a sequence of spots which form the image.

There’s no limit to the number of point to be selected.

With Autocad® it is possible to scale the image to make it fit perfectly to the original draw.

We correlated the bradycardia areas to the umbilical blood pH at birth considering a pH ≤ 7.10 as representative of acidemia.

We found a linear correlation between the bradycardia area and the fetal pH: increasing this area, the pH decreases.

We have identified as about 12 cm2 the threshold value of the area that correlates with fetal acidemia (neonatal umbilical cord blood pH ≤ 7,10). With such threshold the positive predictive value (PPV) is 78.5%, the negative predictive value (PNV) 68.4% and the accuracy of the test 73%.

We then translated the area in terms of FHR and time.

Cardiotocograms record the frequencies on a paper roll that runs in the printer at a speed of 1cm/min and the FHR vertical scale is 20 bpm/cm so that every cm in width represents a minute and every 0,5 cm in height is 10 bpm (Figure 1).

Figure 1Figure 1
How to transform area in FHR and bpm.

Once the area has been calculated it is possible to translate it in minutes per bpms.

For example an area of 12 cm2 can correspond to 24 minutes per 10 bpm (24cm × 0,5cm = 12 cm2), but also to 6 minutes per 40 bpm [6cm × (0,5cm × 4) = 6cm × 2cm = 12 cm2].

It is clear that area can be the expression of different products and then it can be calculated in function of time for different FHR.

If the threshold value of the area is about 12 cm2, the timing of the onset of acidemia can be calculated as 25 minutes for a bradycardia of 80bpm, 13 minutes for a FHR of 70 bpm, 8 minutes for a FHR of 60 bpm, 6 minutes for a FHR of 50 bpm, and only 5 minutes for a FHR of 40 bpm (Figure 2).

Figure 2Figure 2
Timing of neonatal acidemia for different FHR.

The entity of the bradycardia and possibility of action

Labor is a stress test for the fetus and the second stage of labor is considered the most critical, because there is a progressive increase of both frequency and intensity of maternal uterine contractions which can reach 80–100 mmHg and last even 30–60 seconds.

With such pression in the intervillouse space neither the efflux nor the influx of the blood is allowed: the arterial flux is restored only whether the uterin muscolature relaxes when the pressure reaches 60–40 mmHg.

At the same time with the descent of the fetal head in the pelvis the pushing can activate a baro receptorial answer which causes a reduction of the fetal cerebral flux. This fisiologic mechanism, if temporary and not excessive, is generally well tolerated in a fetus with a good compensation ability.

A severe and prolonged bradycardia, nevertheless, due to an extremely long compression, can easily lead to fetal distress and cause an hypoxic acidemia which correlates with severe and permanent neonatal cerebral damages.

We have studied the threshold value suggestive for fetal hypoxia giving a timing to the acidemia at birth: if acidemia can arise in 25 minutes for FHR of 80 bpm, then in case the frequency decreases the time is shorter and there are less possibilities of a saving intervention.

For FHR lower than 60 bpm the time to intervene is so short that it may not be possible to prevent hypoxia.

Those values are a further diagnostic tool for the obstetrician-gynecologist and they bear the monitoring of the fetal hypoxic state.

This study and the primary role of the CTG in the definition of the medical responsibility in Court are at the base of another reflection: whatever the cause of the deceleration, (fetal head compression, cord loops around fetal neck or body, umbilical cord knots or cord entanglement) the dramatic reality is that the time for intervention is often so short that any maneuver can result ineffective to prevent a cerebral damage. This consciousness can be very important for the interpretation of the timing of medical actions in emergency during the second stage of labor for a evidence-of-effectiveness based judgment.

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