CP Prevention by Early Delivery before Fetal Brain Damage in the Loss of

The benign physiologic sinusoidal FHR was synchronized to the periodic fetal respiratory movements and differentiated from the true sinusoidal FHR in ACG (Figure 1) [1]. Since movement spike amplitudes on ACG precisely reflect fetal movement amplitudes [2], the FHR changed along with fetal movements, i.e. large LTV changes along with moderate fetal movements, and small fetal movements provoked common LTV [3].


Introduction
Although it is usually recommended to perform Cesarean section (C-section), when the FHR baseline LTV disappears, an obstetrician experienced unexpected CPdeveloped after C-section due to severe variable decelerations accompanied by the loss of LTV. In addition, to fetal brain damage.

Fetal movements evoked FHR variability and acceleration
The benign physiologic sinusoidal FHR was synchronized to the periodic fetal respiratory movements and differentiated from the true sinusoidal FHR in ACG ( Figure 1) [1]. Since movement spike amplitudes on ACG precisely reflect fetal movement amplitudes [2], the FHR changed along with fetal movements, i.e. large LTV changes along with moderate fetal movements, and small fetal movements provoked common LTV [3].
Triangular FHR accelerations were synchronized to large fetal movement bursts [3]. The electronic simulation confirmed that square shaped 10-Hz wave clusters were converted to single triangular wave after passing through the integral circuit with a 7-sec time constant [3], because the correlation of FHR and movement curves was largest when the movement signal was delayed for 7 sec [4]. In addition, continuous leg motion for 1 min induced a triangular heart rate curve in the adult exercise [3]. The acceleration center seems to be outside the brain cortex, because the exercised person did not recognize the own heart rate change [3], and the center of acceleration was reported to be in the mid-brain [5].
Electric signal group changed to single triangular wave after passing through a integral circuit with 7 sec time constant, and triangle heart rate was produced during adult exercise [3]. Thus, FHR to fetal movements, i.e. large acceleration is provoked by large fetal movements, and LTV derives from small movements [3]. Fetal brain paralysis and damage could be exhibited by the loss of FHR acceleration and LTV, i.e. the acceleration and LTV disappeared in the hypoxic fetal brain paralysis and damage, because both phenomena are produced in the mid-brain, a part of brain. Hypoxic brain damage started by the loss of acceleration in the non-reactive FHR, where acceleration does not appear against fetal movement bursts, but LTV is preserved. Some days later, due to further progress of hypoxia,the bradycardia, severe deceleration and the loss of FHR variability appear. Neonatal states who delivered by the C-section due to the severe NRFS after non-reactive FHR were worse than normal FHR cases. The loss of acceleration against fetal movement bursts and the loss of LTV are found in anencephalic fetus, which loses most parts of the brain. The same FHR changes as anencephalic fetus, found in a severe fetal asphyxia in severe late decelerations, loss of acceleration and LTV but the mother refused C-section, showed severe neonatal asphyxia and the brain damage, of which Apgar score was 3. Such severe asphyxia is rare in the fetus, whereas neuronal cell deaths may accompany to produce cerebral palsy.

Experimental hypoxic bradycardia developed by PaO 2 lower than 50 mmHg
Bradycardia appeared in hypoxic rabbits when the PaO 2 dropped below 50 mmHg, where the heart rate decreased parallel to PaO 2 lowering (Figure 2), while the rabbit showed no hypoxic bradycardia after urethane anesthesia [6]. In addition, anencephalic neonates without brain but preserved medulla oblongata, showed severe bradycardia in the postnatal apnea, where the heart rate recovered to normal by an oxygenated blood infusion [7]. These findings indicate that the parasympathetic center of medulla oblongata was excited by hypoxia to produce bradycardia. The PaO 2 level in hypoxia could be determined by fetal bradycardia or deep deceleration (Figure 2). A human fetus undergoes bradycardia in response to hypoxia, because the fetal umbilical blood PaO 2 is lower than 50 mmHg [8]. The medulla oblongata is stimulated, while other parts of the fetal brain are paralyzed or damaged by hypoxia, i.e. the severity of hypoxia could be determined by FHR in the labor and the possible damage of fetal brain is estimated by the fetal bradycardia.

Possible prevention of cerebral palsy in severe fetal asphyxia
The loss of FHR variability indicates no response of fetal brain to fetal movements in hypoxia. The sign will show that it is a partial sign of general brain damage, and it can be possible to produce neuronal cell deaths, which causes cerebral palsy (CP) after the birth. Therefore the CP will be prevented, if the hypoxic fetus is delivered (LTV). The non-reactive FHR is the loss of FHR acceleration against fetal movements preceding severe hypoxic signs including the loss of variability, severe bradycardia and deceleration some days after the loss of FHR acceleration [9]. Thus, the C-section in non-reactive FHR will be a case to deliver the fetus before the loss of variability. Another way to predict the loss of variability is to estimate fetal PaO 2 in the labor, and the threshold of PaO 2 level will be determined to cause the loss of variability. However, it is very difficult to determine fetal PaO 2 during the labor. Since the rabbit PaO 2 was indicated by the heart rate ( Figure  2), the PaO 2 will be estimated by FHR in the human fetus. An index to determine the threshold to cause the loss of FHR variability will be the Hypoxia Index (HI) to estimate the hypoxic impact on the fetal brain. The HI is shown by the following equation;

Hypoxia Index=Duration (min) of bradycardia (D)×100/the lowest FHR (R)
A HI of V-shaped deceleration is half of U-shaped one, because the area of V-shaped deceleration is half of U-shaped one.

The Hypoxia indices of various FHR samples
duration 15 min.

Rabbits heart rate (bpm)
Rabbits PaO2 (mmHg) Figure 2: The heart rate and PaO 2 of a rabbit were closely correlated in hypoxia [6]. Therefore, the hypoxic index was determined by the lowest FHR instead of fetal PaO 2 . Since the actocardiographic non-reactive FHR, where FHR differentiated from fetal resting state, which shows disappeared acceleration but also no fetal movement, will follow severe NRFS including the loss of LTV within some days, it will be reasonable to perform a C-section before the loss of LTV.
Another way to perform C-section before the loss of LTV is to know the PaO 2 level to produce the loss of LTV and fetal brain damage. The hypoxic index (HI) is proposed in this article to know the PaO 2 threshold, where the lowest FHR is used instead of PaO 2 , a critical HI will indicate the time to perform C-section before the loss of LTV.
Non-hypoxic FHR changes were reported [10,11], but the abnormality would indicate the brain damage, the principle would be the same as hypoxic change, i.e. the fetus of abnormal FHR should be delivered before the loss of LTV in the FHR.

Conclusion
Since the loss of LTV (long term variability of FHR) is the sign of fetal brain damage, the fetus of abnormal FHR should be delivered before the loss of LTV to reduce the CP. A C-section will be indicated in the case of actocardiographic non-reactive FHR or in the case of severely abnormal FHR could indicate the fetal brain damage also in non-hypoxic fetal insults, C-section could be indicated before the loss of LTV in the FHR.