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Variable FHR decelerations are variable in shape as well as in timing with respect to the uterine contraction pattern. Click here for our latest report at FullHouseTrader.
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This FHR pattern must be present for at least 10 minutes to avoid overdiagnosing this rare pattern, which classically is associated with severe fetal anemia e. When persistent, a true sinusoidal pattern may signify significant fetal compromise, and appropriate diagnostic or therapeutic maneuvers should be initiated. More commonly, however, a sinusoidal-like pattern is not of clinical significance. Fetal Heart Rate Accelerations: Spontaneous and Evoked Periodic intrapartum FHR accelerations more than 14 bpm above baseline lasting more than 14 seconds and less than 2 minutes 14 may be spontaneous, associated with uterine contractions, or related to fetal movements.
As in the setting of antenatal surveillance e. The presence of spontaneous FHR accelerations clearly is a reassuring sign. The converse, however, is not true; the absence of such accelerations is not necessarily worrisome, and other FHR tracing characteristics should be used to evaluate fetal status. Intrapartum FHR accelerations also can be evoked with either scalp stimulation of vibroacoustic stimulation. Clark and associates 20 reported that the presence of FHR accelerations 15 bpm for at least 15 seconds after digital or instrumental fetal scalp stimulation uniformly was associated with a fetal scalp pH greater than 7.
On a practical basis, the fetal scalp stimulation test is useful for evaluation of the fetus showing a nonreassuring FHR pattern, particularly when the cervix is not sufficiently dilated to permit fetal scalp sampling for pH determination.
Smith and associates 21 observed that similar FHR accelerations evoked by transabdominal vibroacoustic stimulation in the setting of nonreassuring FHR data were associated with a fetal scalp pH of greater than 7. The presence of evoked FHR accelerations is an excellent predictor of fetal well-being, although scattered reports have described isolated instances of fetal acidemia in fetuses with a reactive response to intrapartum vibroacoustic stimulation. Despite the myriad of classification systems proposed, we prefer to categorize these decelerations typically, but not always, decreases of at least 10—15 bpm from the baseline value simply as early, variable, or late in character.
Most authentic disagreements about the analysis of FHR decelerations stem from differing assessments of the FHR baseline value. One unifying generalization typifies the discussion: The types of FHR decelerations are described in what most authorities agree is the order of increasing potential concern. Early decelerations display an onset, nadir, and recovery that is synchronous with the onset, peak, and end of the uterine contraction.
In short, early decelerations mirror the uterine contraction pattern. Generally ascribed to fetal head compression with resultant vagal stimulation , early FHR decelerations are the least common variety of intrapartum FHR deceleration observed and usually are of no clinical significance. Variable FHR decelerations are variable in shape as well as in timing with respect to the uterine contraction pattern. Characterized by an abrupt decline defined as onset of deceleration to beginning of nadir less than 30 seconds 14 from the FHR baseline value and an equally abrupt recovery, variable decelerations display a variety of waveforms, such as V, U, W, or combinations Fig.
The decline in FHR below baseline is more than 14 bpm, lasting more than 14 seconds and less than 2 minutes from onset to return to baseline. A severe variant of the variable deceleration is defined by a decline of the FHR to less than 60 bpm or a decrease of the FHR by at least 60 bpm from the baseline value lasting 60 seconds or longer.
Fetal heart rate pattern with variable heart rate decelerations and reassuring variability. The etiology of variable decelerations is likely related to umbilical venous and arterial occlusion. Initially, with occlusion of the thin-walled umbilical vein, venous return to the fetal right atrium is reduced, producing a reflex tachycardia. This pattern often is observed as a shoulder on the FHR monitor strip immediately before the abrupt variable FHR deceleration. Shoulders that precede and follow variable decelerations are indicative of intact fetal central nervous system function and, thus, relative fetal well-being Fig.
When cord occlusion becomes complete including the umbilical artery , the low-resistance placental circulation is no longer in series. Instead, the elevated peripheral resistance that is caused by umbilical artery occlusion predictably leads to fetal hypertension, with subsequent baroreceptor stimulation.
The baroreceptor and resultant vagal responses ultimately produce the parasympathetically mediated FHR deceleration. With relief of the umbilical cord occlusion, the sequence is reversed. Fetal heart rate pattern with repetitive variable fetal heart rate decelerations.
Reassuring shoulders accelerations are obvious before and after each deceleration. In isolation, variable FHR decelerations are not indicative of fetal compromise. If unremitting umbilical cord occlusion results in persistent, deep, variable FHR decelerations, however, the potential exists for the development of a fetal metabolic acidemia that cannot be managed satisfactorily by the fetal buffer system.
Evidence of ensuing acidemia includes late recovery from the deceleration and decreased or absent interdeceleration variability as well as an ensuing bradycardia. The practice of amnioinfusion for the prevention or relief of umbilical cord compression, with resultant variable decelerations, is an accepted method of intrapartum management. Amnioinfusion with normal saline room temperature can be accomplished via either bolus or continuous infusion using an infusion pump or gravity intravenous bag 3—4 feet above the catheter.
A bolus infusion of up to mL may be administered, initially at a rate of 10—20 mL per minute until FHR decelerations resolve, and then up to an additional mL to reach a maximum of mL total.
For a continuous infusion, a rate of 10 mL per minute is administered by infusion pump for 60 minutes, followed by an infusion at 3 mL per minute. Indications for discontinuation of the amnioinfusion include observation of a significant increase in the baseline intrauterine pressure, uterine hyperstimulation, or FHR bradycardia.
Late FHR decelerations are characterized by a decline after the onset of the uterine contraction, a nadir after the peak of the contraction, and a slow recovery to the FHR baseline value after the end of the uterine contraction Fig. Late declarations have been described as being of two distinct etiologies. The first, caused by reflex, is mediated by the fetal central nervous system.
The second, direct myocardial depression, is seen more often in a setting of metabolic acidemia. Classically ascribed to relative uteroplacental insufficiency, occasional or intermittent late decelerations are not at all uncommon during most labors. The presence of persistent late decelerations, however, must be carefully evaluated because they may be secondary to transient fetal hypoxemia in response to decreased placental perfusion associated with uterine contractions.
Late decelerations have been described as being of two distinct etiologies. Fetal heart rate pattern with baseline value of approximately bpm and repetitive late decelerations. These decelerations reach a nadir after the peak of the uterine contraction and then show a slow return to the fetal heart rate baseline value. The potential for fetal compromise in the presence of persistent late FHR decelerations mandates appropriate diagnostic and therapeutic interventions. Therapeutic maneuvers include maternal repositioning in the lateral recumbent position, satisfactory intravenous hydration, maternal oxygen therapy, and relief of uterine hyperstimulation, if present.
If palliative measures are unsuccessful and late FHR decelerations persist, an attempt to evoke a FHR acceleration via either digital examination or vibroacoustic stimulation, or a fetal pH determination via scalp sampling may be considered.
Although isolated late FHR decelerations are not an indication for immediate cesarean section, persistent late FHR decelerations remote from the time of anticipated vaginal delivery often ultimately prompt operative abdominal delivery.
Finally, a prolonged deceleration is a decrease in the FHR from baseline of more than 14 bpm lasting more than 2 minutes and less than 10 minutes from onset to return to original baseline.
A combination of various types of FHR decelerations may occur. For instance, FHR decelerations may show an abrupt decline from the baseline value, with a nadir after the peak of the contraction followed by a slow recovery to the baseline level. These variable decelerations with a late component may appear in labors that are complicated by intermittent umbilical cord occlusion, fetal malposition, or cephalopelvic disproportion.
Persistence of this pattern of FHR deceleration, with progressively longer recovery times to the baseline level, may be associated with an increased potential for fetal compromise.
Clearly, it would be an error to consider only shallow, smooth decelerations with a slow return to the baseline value as late. An important principle of accurate fetal assessment is an appreciation of the timing and depth of any FHR deceleration, regardless of the type of FHR pattern that may have preceded it. The evaluation and treatment of variable FHR decelerations with a late component logically proceed as described above for classic late FHR decelerations.
The FHR decelerations observed with maternal pushing during the second stage of labor are not typically indicative of potential fetal compromise and usually are not an indication for immediate operative delivery.
Despite their depth, which can be significant, these decelerations tend not to persist. Unless complicated by a protracted second stage of labor, development of a late component, loss of previously normal variability, or a prolonged deceleration, these FHR decelerations likely reflect fetal head compression, with resultant vagal stimulation, rather than evidence of uteroplacental dysfunction.
Under ambiguous clinical circumstances, fetal scalp sampling for pH determination may be helpful to assess fetal status more accurately. There is evidence that these types of decelerations are associated with evolving hypoxia, and prompt delivery is indicated if intrauterine resuscitative methods fail to improve the FHR tracing. It is our impression that since the publication of previous editions of this chapter, the practice of scalp pH determination has become much less common on many labor and delivery units.
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