Objective
Recent guidelines classify variable decelerations without detail as to degree of depth. We hypothesized that variable deceleration severity is highly correlated with fetal base deficit accumulation.
Study Design
Seven near-term fetal sheep underwent a series of graded umbilical cord occlusions resulting in mild (30 bpm decrease), moderate (60 bpm decrease), or severe (decrease of 90 bpm to baseline <70 bpm) variable decelerations at 2.5 minute intervals.
Results
Mild, moderate, and severe variable decelerations increased fetal base deficit (0.21 ± 0.03, 0.27 ± 0.03, and 0.54 ± 0.09 mEq/L per minute) in direct proportion to severity. During recovery, fetal base deficit cleared at 0.12 mEq/L per minute.
Conclusion
In this model, ovine fetuses can tolerate repetitive mild and moderate variable decelerations with minimal change in base deficit and lactate. In contrast, repetitive severe variable decelerations may result in significant base deficit increases, dependent on frequency. Modified guideline differentiation of mild/moderate vs severe variable decelerations may aid in the interpretation of fetal heart rate tracings and optimization of clinical management paradigms.
Intrapartum electronic fetal heart rate (FHR) monitoring (EFM) is used for assessment of fetal well-being in the vast majority of laboring patients in industrialized countries. Although debates continue regarding the relative merit of continuous EFM vs intermittent FHR auscultation, the majority of hospitals use continuous monitoring. A major goal of EFM is the reduction or, ideally, the elimination of intrapartum fetal asphyxia. However, despite widespread EFM use there has been little prospective evidence of its benefits. Initially, retrospective reports indicated significant improvements in perinatal mortality and newborn outcomes, although subsequent prospective studies have demonstrated little evidence of the clinical benefit of EFM.
For Editors’ Commentary, see Contents
To achieve the goal of a reduction in perinatal asphyxia and perhaps cerebral palsy, EFM assessment must be directed at prevention of severe metabolic acidosis at birth, defined by the American Congress of Obstetrics and Gynecologists and others as a base deficit (BD) equal to or greater than 12 mEq/L. However, current assessment of EFM heart rate patterns use broad categorizations of fetal well-being (reassuring, indeterminate, nonreassuring: Category 1, 2, 3). In contrast, there has been minimal codification of EFM patterns in regard to the degree of metabolic acidosis, associated with abnormal FHR patterns including that associated with FHR decelerations.
The most common FHR deceleration associated with fetal hypoxia during labor is a variable deceleration, likely a result of umbilical cord occlusion (UCO). In the early years of fetal monitoring, variable FHR deceleration classification was based on duration and depth of the deceleration. As defined by Kubli et al, marked (severe) variable FHR decelerations drop to below 70 beats per minute (bpm) and last at least 60 seconds, although mild/moderate variable decelerations do not achieve these depth/duration parameters. Human fetal acidosis is correlated with severe variable decelerations, though not with mild or moderate variable decelerations. Animal data confirm that severe variable decelerations occurring frequently may be less well tolerated by the fetus, resulting in accumulation of metabolic acids. The NICHD Task Force on EFM in 2008 defined all variable decelerations as a single category, perhaps because of the lack of objective evidence of the impact of subcategories of variable decelerations.
Our research team recently quantified the changes in BD and lactate in response to repetitive complete UCO in the near term ovine fetus, simulating severe variable decelerations. These studies demonstrated that BD increased at a rate of 0.56 mEq/L per minute of severe UCO. During recovery periods, between or after UCO, BD normalized at a rate of approximately 0.1 mEq/L per minute. In view of the frequency of mild and moderate variable decelerations occurring in labor, we sought to examine the changes in fetal BD in association with varying degrees of UCO to better characterize the impact of subcategories of partial UCO induced variable decelerations on the development of metabolic acidosis.
Materials and Methods
Surgical preparation
Seven (7) near-term ovine fetuses (124 ± 1 days gestational age [GA], term = 145 days) of mixed breed were surgically instrumented. The anesthetic and surgical procedures and postoperative care of the animals have been previously described. Briefly, polyvinyl catheters were placed in the right and left brachiocephalic arteries, the cephalic vein, and the amniotic cavity. Stainless steel electrodes were sewn onto the fetal chest to monitor the electrocardiogram (EKG). An inflatable silicon rubber cuff (In Vivo Metric, Healdsburg, CA) was placed around the proximal portion of the umbilical cord and secured to the abdominal skin. Stainless steel electrodes were implanted biparietally on the dura for the recording of electrocortical activity (ECOG). A polyvinyl catheter was also placed in the maternal femoral vein. Postoperatively, animals were allowed 4 days to recover and were 128 ± 1 days GA on the first day of experimental study. Animal care was according to the guidelines of the Canadian Council on Animal Care and was approved by the University of Western Ontario Council on Animal Care.
Experimental procedure
Animals were studied over a 4- to 6-hour period. After a 1- to 2-hour baseline control period (to assure maternal and fetal well-being), mild, moderate, and severe series of repetitive UCOs were performed. UCOs were induced in all series by graduated inflation of the occluder cuff with a saline solution. Preliminary studies were performed to determine the amount of volume necessary to achieve mild, moderate, and severe variable decelerations. During the first hour following baseline, mild variable decelerations were performed with a partial UCO for 1 minute duration every 2.5 minutes, with the goal of decreasing FHR by ∼30 bpm, corresponding to an ∼50% reduction in umbilical blood flow. During the second hour, moderate variable decelerations were performed with an increased partial UCO for 1 minute duration every 2.5 minutes with the goal of decreasing FHR by ∼60 bpm, corresponding to an ∼75% reduction in umbilical blood flow. After the moderate variable decelerations, animals underwent severe variable decelerations with complete UCO for 1 minute duration every 2.5 minutes ( Figure 1 ) until the targeted fetal arterial pH of less than 7.0 was detected, at which point the repetitive UCOs were terminated. All animals were allowed to recover after the last UCO.
Maternal venous blood samples were drawn at baseline and at completion of the UCO protocol. Fetal arterial blood samples were drawn at baseline, at the end of the first UCO of each series (mild, moderate, severe), and at 20-minute intervals (between UCOs) throughout each of the series, as well as at 1, 24, and 48 hours of recovery. For each UCO series blood gas sample, 0.7 mL of fetal blood was withdrawn, and 4 mL of fetal blood was withdrawn at baseline, at pH nadir less than 7.00, and at 1 hour and 48 hours of recovery. The amounts of blood withdrawn were documented for each fetus and replaced with an equivalent volume of maternal blood at the end of day 1.
All blood samples were analyzed for blood gas values, pH, glucose, and lactate with an ABL-725 blood gas analyzer (Radiometer Medical, Copenhagen, Denmark) corrected to 39.0°C.
After the 48-hour recovery blood sample, the ewe and the fetus were killed by an overdose of barbiturate and the location and function of the umbilical occluder was confirmed.
Data acquisition and analysis
Arterial and amniotic pressures were measured continuously through the baseline and repetitive UCO periods and during the first hour of the recovery period using Statham pressure Transducers (Gould Inc, Oxnard, CA). PowerLab system was used for data acquisition and analysis. Pressures, EKG, and ECOG were recorded and digitized at 1000 Hz for further study (results to be reported separately). FHR was triggered and calculated online from arterial pressure systolic peaks. True arterial blood pressure (ABP) was determined as the difference between instantaneous values of arterial blood and amniotic pressures.
Averaged values of FHR and ABP were calculated from artifact-free baseline (a representative 10-minute interval), consecutive variable deceleration series (mild, moderate, severe), and the first hour of recovery. The values of individual consecutive nadirs of the FHR decelerations and corresponding ABP changes were determined for every fetus in each variable deceleration series and average values determined for every variable deceleration series.
BD (mEq per liter) was calculated as follows :
B D = − ( ( 0.02786 × p C O 2 ( 10 [ p H − 6.1 ] ) + 13.77 × p H − 124.58 ) w i t h p C O 2 m e a s u r e d i n m m H g .
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