Acid accumulation during end‐stage bradycardia in term fetuses: how long is too long?

Abstract

Objective To estimate the existence and degree of fetal accumulation of acid during end‐stage bradycardia as reflected by the base deficit. This may set a criterion for proper intervention during labour. Setting Maternity unit of the Tel Aviv Medical Centre. Subjects Forty‐three consecutively born term infants whose mothers were delivered by vacuum extraction were analysed 27 because of end‐stage bradycardia and 16 controls whose mothers were delivered electively because of maternal indications. Main outcome measures Analysis of umbilical arterial cord blood for pH, Pco2, and base deficit. The base deficit was compared between the groups using the two‐tailed Student's t test, and was correlated with variables of fetal heart rate monitoring using the Pearson correlation coefficient. Results The base deficit was greater in newborns who had end‐stage bradycardia than in controls (11.02 vs 5.01, P < 0.0001). The duration of loss of short term variability in fetal heart rate during end‐stage bradycardia correlated positively with the base deficit (r= 0.8, P < 0.0005). Conversely, the time until the loss of short term variability during end‐stage bradycardia correlated negatively with the base deficit. The length and the depth of the bradycardia and their product, had a weaker correlation with the base deficit. Conclusions End‐stage bradycardia, which presumably reflects fetal hypoxia, is associated with acidaemia in the umbilical artery at birth in some fetuses. The fetuses who are predisposed to acidaemia, as reflected by an increased base deficit, are those who lost their fetal heart rate variability during end‐stage bradycardia for more than 4 min or started to lose this in less than 3 min from the beginning of the end‐stage bradycardia. Operative vaginal delivery should be reserved for these indications.

Fetal acidemia and electronic fetal heart rate patterns: Is there evidence of an association?

“…The relationship between minimal or undetectable FHR variability in the presence of late decelerations or variable decelerations, and the presence of acidemia and/or a depressed neonate Eight papers were identified which included a total of 588 appropriate patients, all of which had at most minimal FHR variability and decelerations [7][8][9][10][15][16][17][18]]. We were not always able to distinguish between undetectable or minimal variability in the published data because they were sometimes grouped together.…”

Continuous cardiotocography during labour: Analysis, classification and management

“…Note the presence of 'atypical' variable and late decelerations. deceleration, repetitive late decelerations before the onset of the prolonged deceleration or a drop in the heart rate to >60 bpm are associated with a poor outcome [18], and the '3-, 6-, 9-, 12-and 15-minute' rule should not be applied. Measures should be undertaken to accomplish immediate delivery if this is the case (Fig.…”

Fetal Heart Rate Monitoring: Interpretation and Collaborative Management

“…Given this apparent cause-effect relationship between events known to contribute to fetal hypoxia and acidemia and the incidence of decelerations in the FHR, clinicians perceived many commonly occurring FHR decelerations as "ominous." However, two aspects of FHR physiology not consistently acknowledged and factored into early clinical practice were the importance of FHR variability and pattern evolution over time (7,12,(22)(23)(24)(25)(26)(27)(28)(29)(30)(31).…”

“…Studies examining the relationship between FHR patterns, acidemia, and neonatal morbidity have shown the presence of FHR decelerations, as an independent variable, to be poorly predictive of significant fetal acidemia, except in cases of extreme and persistent severe fetal bradycardia (sustained FHR of less than 60 bpm for 10 minutes) (15, 23,25,26,30 -36). Rather, the preponderance of evidence supports the premise that the degree of baseline FHR variability that accompanies the decelerations is the most sensitive predictor of neonatal outcome (6,22,23,(25)(26)(27)(28)(29)(30). The finding of a relationship between significant acidemia and FHR variability is consistent with the theory that FHR variability is the product of a functioning (ie, adequately oxygenated) neurologic pathway in which numerous impulses from the cerebral cortex, the midbrain, the vagus nerve, and the cardiac conduction system are transmitted.…”

“…In contrast, a FHR tracing with persistent absent or minimal variability (amplitude range 5 bpm or less), with recurrent decelerations or bradycardia, holds the strongest association with fetal acidemia and/or the absence of fetal vigor at birth (27,(43)(44)(45). Subgroups of the following FHR patterns warrant a presumptive diagnosis of significant fetal acidemia: 1) absent variability with recurrent late decelerations; 2) absent variability with recurrent variable decelerations; 3) absent variability with sustained fetal bradycardia 60 bpm or less (in the absence of congenital heart block); and 4) in clinical practice, a persistent bradycardia with a FHR of 80 bpm or less, which occurs remote from delivery, is often treated in a similar fashion (22)(23)(24)27,29,30,38,46). Because these patterns are presumed to be associated with moderate to severe intrapartum asphyxia, there is little likelihood they will be reversed with conservative treatment (maternal position change, fluid bolus, amnioinfusion, etc) Conservative treatment should be carried out only if doing so does not interfere with the move toward rapid delivery.…”