Yoshiyuki Shintaku

The slope of fetal heart rate deceleration is predictive of fetal condition during repeated umbilical cord compression in sheep

The relationship between components of fetal heart rate deceleration and fetal arterial blood gas values or plasma catecholamine concentrations was investigated by repeated complete umbilical cord compression in chronically instrumented fetal lamb. Fetal arterial pH and bicarbonate levels decreased, while plasma norepinephrine and epinephrine concentrations increased more than tenfold. The slope of the descending limb of the fetal heart rate deceleration curve decreased and correlated strongly with fetal arterial pH, bicarbonate, and logarithmic plasma norepinephrine and epinephrine concentrations. Fetal arterial pH and bicarbonate levels were significantly lower in the group with lower fetal heart rate deceleration slope, and a greater plasma catecholamine concentration in this group suggested a redistribution of blood flow to vital organs. Therefore, during repeated umbilical cord compression, the fetal acid-base and hormonal state was predicted by the fetal heart rate deceleration slope. This relationship may be applicable to human fetuses in the diagnosis of fetal distress caused by umbilical cord compression during labor.

Change in electrocardiogram T-wave amplitude during umbilical cord compression is predictive of fetal condition in sheep

OBJECTIVE The purpose of this study is to assess the usefulness of the dynamic change in T/QRS ratio in fetal electrocardiograms in predicting the fetal condition when repetitive variable decelerations are seen in intrapartum cardiotocograms. STUDY DESIGN We investigated the relationship, using linear regression and Wilcoxons test, between T/QRS and blood gas values, catecholamine concentrations, and blood pressure during repetitive cord compression in five chronically instrumented lamb fetuses. RESULTS T/QRS during cord compression correlated significantly (p less than 0.01) with fetal arterial pH (r = -0.7711), norepinephrine concentration (r = 0.7551), and duration of elevated blood pressure during compression (r = -0.8619). Fetal arterial pH and base excess were lower, the duration of elevated blood pressure during compression was shorter, and carbon dioxide partial pressure and catecholamine concentrations were higher in the stage with higher (greater than 0.50) T/QRS during compression (p less than 0.005). CONCLUSION We can estimate the severity of fetal distress by measuring T/QRS near the bottom of the decelerations.

Biochemical evaluation of fetus with hypoxia caused by severe preeclampsia using cordocentesis

Biochemical evaluation of the fetus using cordocentesis was performed in sixteen pregnant women with severe preeclampsia. In addition, FHR monitoring and Doppler flow velocimetry of the umbilical artery were examined in these cases before the cordocentesis. Other than blood gas and routine hematologic and biochemical examinations, catecholamine and hypoxanthine concentrations were also evaluated in some cases. According to the results it is obvious that the fetus of mother with severe preeclampsia is exposed to hypoxemia with the delta pO2, the difference from the mean in each gestation, of -22 mmHg. Especially, the prognosis of the severely growth-retarded babies with pO2 below 10 mmHg, or delta pO2 30 mmHg lower than the mean standard value, is poor. Among 16 babies, 4 with severe hypoxia or acidosis and growth retardation died perinatally. In contrast, severely growth-retarded babies without hypoxia or acidosis were alive. Since neither FHR monitoring nor Doppler velocimetry always reflect biochemical values of the fetus of a severe preeclamptic mother, hence the precise evaluation of fetal condition using cordocentesis is indispensable to determine the timing of the delivery and to prevent the neurological sequelae caused by hypoxia, especially when the fetal growth is retarded.

Alteration of FHR pattern and cerebral metabolic rate of glucose of the fetus measured by positron emission tomography during progress of acidemia. The significance of overshoot acceleration in FHR

In order to investigate the significance of overshoot acceleration in FHR with acidosis induced by serial cord compression, cerebral glucose metabolic rate (CMRglc) was measured in four chronically instrumented fetuses before cord compression and immediately after appearance of the overshoot acceleration in FHR. The investigation of CMRglc was carried out using positron emission tomography to assess accumulation of cyclotron-produced F18-FDG in the fetal brain. CMRglc in the fetal brain in the nonacidemic condition was 1.73 mg/100 g/min. In acidemia, with fetal arterial pH near 7.15 in which FHR showed the characteristic pattern with overshoot acceleration, CMRglc was significantly decreased to 0.73 mg/100 g/min. We concluded that, to avoid neuronal damage, it is necessary to intervene when the fetal condition deteriorates to the extent that overshoot acceleration in FHR occurs.

Femoral artery blood flow monitoring has distinct advantages for examining redistribution of blood flow in fetal acidosis

Changes of blood flow in umbilical artery, carotid artery and femoral artery were examined during the progression of acidemia in fetal sheep by means of indwelling transit-time ultrasonic blood flow meters. Moreover, catecholamines in fetal blood were measured and its interrelation to the alteration in blood flow was examined. Gradually progressing fetal acidemia was induced by repeated cord compression. Umbilical blood flow showed a initial increase thereafter maintaining a plateau through the experiment, which seemed to be dependent on fetal arterial pressure. Carotid artery flow gradually increased until the arterial pH in fetal blood declined to 7.20 and remained at this level even though the acidemia further progressed. Femoral artery flow markedly decreased around fetal arterial blood pH 7.20 and its change correlated well with the plasma level of catecholamines. This change of femoral artery flow may be evaluated by examination of the flow index as well as flow volume. Redistribution of blood flow in the progression of fetal acidemia may be initiated at around fetal arterial pH 7.20 and can be detected by studying femoral artery flow.