Whereas in the majority of high-risk pregnancies there are either no or minimal noxious fetal consequences, in a small percentage, estimated to be in the range of 2% to 3% based on our large clinical trials of more than 82,000 referrals, the fetus will be exposed to potentially damaging or even lethal interruptions in placental respiratory function. Unable to extricate itself from this hostile environment the mammalian fetus has evolved remarkable protective compensatory mechanisms. It is these adaptations to hypoxemia and acidemia (asphyxia) that result in the deviation from normal of the components of the BPS. In response to acute hypoxemia, for example, as may occur with fulminant preeclampsia or abruption, the fetus ceases all acute biophysical activities nonessential to immediate survival: the fetus will stop moving and breathing and will lose flexor tone. In the fetal lamb, abolition of all skeletal muscle activity, as induced by pharmacologic footplate blockade (eg, gallamine), produces an immediate reduction in oxygen consumption by up to 17% and yields a rise in fetal Po2.11 In the human fetus, we have observed a similar effect: In alloimmune anemic fetuses undergoing intravascular transfusion, the measured Po2 in venous blood increases after pancuronium blockade.12 This adaptive response is mediated by acute tissue hypoxia in central nervous system neurons that initiate the discrete biophysical activities (Figure 23-1). Evidence of this adaptive response in high-risk human fetuses is demonstrated by antenatal venous cord blood analysis. For each of the individual acute biophysical variables, the mean pH was always significantly higher when the activity was observed than when the activity was absent (Figure 23-2).13 Further, there appears to be a differential sensitivity between these acute variables: The NST and fetal breathing movements were absent with the least decline in pH, whereas larger falls were observed before fetal body movement and tone became abnormal. The animal fetus with mild to moderate sustained stable nonacidemic hypoxemia may exhibit the return of acute biophysical activities, albeit at a lower frequency.14 The physiologic basis for this partial recovery is complex and involves such factors as increased oxygen-carrying capacity, improved oxygen extraction, resetting of receptor thresholds, and increased cerebral blood flow. Thus, the BPS is a reflection of tissue hypoxemia but may not predict circulating Po2. The statistically significant but clinically poor correlation between the fetal BPS and antenatal venous Po2 confirms this explanation.14 It is of clinical importance to note that progressive hypoxemia, acidemic hypoxemia (asphyxia), or both have not been associated with reemergence of acute biophysical variables in either animal or human fetuses.
A schematic of the factors, both normal and pathologic and both intrinsic and extrinsic, that modulate dynamic fetal biophysical activities. The observation of a normal given biophysical activity is strong presumptive evidence that the central nervous system (CNS) regulatory neurons are not hypoxic. In contrast, the failure to observe a variable necessitates a differential diagnosis. (Reproduced with permission from Manning FA, ed. Fetal Medicine: Principles and Practice. Norwalk, CT: Appleton & Lange, 1995.)
The mean pH + 2 SD observed in antenatal cord blood (cordocentesis) for each of the components of the biophysical profile score when normal (open circles) or abnormal (closed circles). A differential effect is observed with the nonstress test (NST), requiring the least perturbation in pH to become abnormal, and fetal movement requiring the greatest. (AFV, amniotic fluid volume; FBM, fetal breathing movement; FM, fetal movement; FT, fetal tone.) (Reproduced with permission from Manning FA, Snijders RL, Harman CR, et al: Fetal biophysical profile score. VI. Correlation with antepartum umbilical venous fetal pH. Am J Obstet Gynecol 1993;165:755 Oct 169(4):755-763.)
The fetus has a second adaptive response to hypoxemia, which is the aortic arch chemoreceptor reflex redistribution of cardiac output. This reflex, which probably requires either more severe hypoxemia or acidemia to be triggered, results in preferential shunting of blood flow away from all nonessential organs to essential organs (the heart, brain, placenta, and adrenals).15 The measurable clinical effect manifest over days is oliguric oligohydramnios and over weeks is intrauterine growth restriction (IUGR). This reflex accounts for an important principle of fetal assessment by the BPS, which is that in the presence of intact membranes and a functional genitourinary tract oligohydramnios is near certain presumptive evidence of fetal compromise. Although exceptions to this clinical dictum may occur, they must be exceedingly rare because our group has yet to identify one in more than 160,000 tests.
The time differential between the immediate adaptive response to hypoxemia, acidemia (loss of acute biophysical variables), or both, and the delayed reflex response (oliguric oligohydramnios) permits an assessment of the chronicity of the insult. The differential sensitivity of the regulatory centers provides some insight into the severity of the insult. These 2 components are critical to the testing frequency and interpretation in specific risk categories. Thus, for example, in clinical circumstances in which fetal compromise is apt to be sudden (eg, insulin-dependent diabetes), testing is frequent (twice weekly) with an emphasis on acute biophysical variables. In other conditions where fetal compromise is rapidly progressive, as, for example, with severe alloimmune anemia, testing may occur very frequently (daily or twice daily), with emphasis on the acute variables, and continue until treatment (intravascular transfusion) restores normal oxygen-carrying capacity. With indolent progressive placental failure, as may occur in the postdate pregnancy, the focus of biophysical scoring is to detect evidence of chronic adaptation (oligohydramnios), the superimposition of acute on chronic hypoxemia (loss of some or all acute variables), or both. Because the rate of deterioration in these circumstances may be rapid, the testing interval is shortened to at least twice weekly. It is likely that, as our understanding of the pathophysiology of other abnormal fetal conditions improves, the frequency and emphasis of fetal biophysical profile scoring will be altered.