Relationship of fetal Doppler indices to hypoxemia and acidemia

Data from direct animal experiments and indirect animal and human studies using Doppler techniques have demonstrated circulatory adaptations to impaired placental function and progressive hypoxemia (Hornbuckle and Thornton, 1998). Most of the human studies have been conducted on fetuses with fetal growth restriction (FGR) but are of direct relevance to pre-eclampsia, where FGR frequently coexists. An overview of Doppler changes is shown in Figure 32.2.

Under hypoxic conditions there is centralization of the fetal circulation with redistribution to preferentially supply the fetal brain, heart, spleen and adrenal glands. An increased amount of umbilical venous blood flow is also directed through the DV to maintain the oxygen tension in the left atrium (Edelstone, 1980). Doppler indices in fetal peripheral arteries are increased consistent with peripheral vasoconstriction. The ability to undergo these physiological adaptations to hypoxemia is likely to be gestation-dependent.

Umbilical artery Doppler indices provide an indirect measure of downstream placental resistance; reduction of end-diastolic velocities (EDV) is associated with impaired placental villous development and a reduction in the number of small villous arteries and arterioles (Giles et al., 1985). Umbilical artery indices correlate with fetal pO2 and pH at cordocentesis; 40—45% of fetuses with abnormal UA FVW but end-diastolic frequencies present are hypoxemic (pO2 > 2 SD below mean for gestation) and 20—30% are acidemic (pH > 2 SD below mean for gestation) (Nicolaides et al., 1988; Nicolini et al., 1990; Yoon et al., 1994). In contrast, 80—90% of fetuses with absent

Mca Doppler Fetal For Antikell
Figure 32.2 Summary of circulatory changes in fetal growth retardation. Abbreviations: PI, pulsatility index; AREDF, absent/ reversed end-diastolic frequencies; UA, umbilical artery; MCA, middle cerebral artery; LV, left ventricle; RV, right ventricle; DV, ductus venosus; UV, umbilical vein.

end-diastolic velocities are hypoxemic and 45—80% are acidemic (Nicolaides et al., 1988; Nicolini et al., 1990; Yoon et al., 1994).

Hypoxemia leads to redistribution of left cardiac output with cerebral vasodilatation. This is reflected by a decrease in MCA PI values, maximal when fetal pO2 is 2—4 SD below the mean for gestation (Vyas et al., 1990). An increase in MCA PI (or an increase in UA/MCA PI ratio) is the earliest and most sensitive indicator of fetal hypoxemia (Rizzo et al., 1995a). The reported rates of circulatory redistribution (MCA PI < 2 SD below mean for gestation) among growth restricted fetuses range from 20—76% and even with AREDV only 60—70% of fetuses show a reduction in MCA PI (Hornbuckle and Thornton, 1998). Importantly in some fetuses MCA PI subsequently normalizes (Konje et al., 2001; Rowlands and Vyas, 1995). This ''loss of brain sparing'' is thought to represent a change in the vascular sensitivity to hypoxia and a decrease in left cardiac output.

With progressive hypoxemia/acidemia, systemic vascular resistance and afterload on the right heart increases, resulting in an increase, in the depth of the venous ''a'' wave. Changes in the DV PIV correlate closely with the presence or absence of acidemia (Rizzo et al., 1995a). Reversal or absence of the ''a'' wave represents a near-terminal event (Baschat et al., 2000; Muller et al., 2002); in a study of 37 fetuses with UA AREDV increased PIV or reversed ''a'' wave in the DV was documented in 14/15 (93%) perinatal deaths (Hofstaetter et al., 2002). With increasing cardiac dysfunction the abnormal venous pulsations are transmitted distally ultimately resulting in pulsations in the umbilical vein (UV). Pulsations may become evident prior to reversal of the DV ''a'' wave and are reported in 25-75% of fetuses with UA AREDV (Baschat et al., 2003; Hofstaetter et al., 2002). Rizzo et al. (1995b) reported that all fetuses with UV pulsations were hypoxemic and 91% acidemic, while their occurrence has a 71% sensitivity (and

95% specificity) for predicting perinatal death (Hofstaetter et al., 2002). In a study of UA, DV and UV Doppler waveforms in 224 fetuses with FGR, Baschat et al. (2003) concluded that DV "a" wave reversal and UV pulsations offered the best prediction of acidemia and perinatal death, irrespective of the UA waveform.

With deterioration of the fetal arterial Doppler waveforms there is progressive change in fetal cardiac function. Longitudinal studies show that right heart diastolic function, as measured by DV and right E/A (ratio of early and active filling of the ventricle), is affected earlier and to a greater degree than systolic function and changes in the right heart precede those on the left (Figueras et al., 2003).

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