Key result
A prolonged hypoxia-induced fetal heart rate deceleration during labor resulted in an atypical ductus venosus waveform with marked prolongation of ventricular diastole and delayed A-wave onset.
Case Report (n=1)
Hypoxia-induced fetal bradycardia can cause atypical ductus venosus waveforms with prolonged ventricular diastole and delayed A-wave onset, which normalize upon heart rate recovery.
Hypoxia-induced fetal bradycardia may alter ductus venosus waveforms; leaves open its role in intrapartum monitoring.
The incidence of atypical ductus venosus (DV) waveforms is under-reported in the literature. We read with interest the article of Smrcek et al.1 on seven cases of atypical DV waveform patterns due to structural cardiac defects. In all seven cases severe tricuspid valve regurgitation was present. Such a phenomenon may be accompanied by systolic notching and may cause reduced peak systolic velocity (S-wave) compared to the peak diastolic velocity (D-wave) in the DV, especially after the conversion from tachycardia to sinus rhythm. Besides such cases with structural heart defects, atypical DV waveforms can be observed as a result of different fetal positions in healthy fetuses2, 3. We report on a case with an atypical DV waveform at the very last moments of a term labor, recorded during a prolonged deceleration. At the time of examination the fetal heart rate (FHR) was 80 beats per min (Figure 1). This coincided with a sudden decrease in arterial oxygen saturation, measured by pulse oxymetry, from 40% to values below 10% (Figure 2). Ductus venosus waveform during a prolonged fetal heart rate deceleration in labor. Cardiotocographic pattern with pulse oxymetry recording showing a prolonged deceleration and a concomitant drop in the fetal oxygen saturation. A similar characteristic DV pattern was observed by Gudmundsson et al.4 during hypoxemia-induced bradycardia in ovine fetuses. An explanation for this could be that fetal heart rate affects central venous pressure and DV blood flow velocities in a parabolic fashion4. Accordingly, an increase in venous pressure and a corresponding decrease or absence of end-diastolic blood velocities during atrial contraction occur regularly but are dependent on the severity of bradycardia. In our case, a hypoxia-induced deceleration of the FHR (bradycardia) occurred, which lasted several minutes. As a result, a characteristic DV tracing was recorded, demonstrating a marked prolongation of ventricular diastole with a delayed onset of the A-wave (Figure 1). Spontaneous normalization of the waveform was observed after 5 min once the FHR had returned to normal. Since similar phenomena are rarely discussed in the literature, the present report illustrates an interesting physiological variation of the DV waveform that is dependent on the FHR. N. Szunyogh*, S. Galo*, P. Zubor*, J. Visnovsky*, * Department of Obstetrics and Gynecology, Jessenius Faculty of Medicine, Martin Faculty Hospital, Kollarova 2, 036 59 Martin, Slovakia
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Szunyogh et al. (2006) conducted a case report in Fetal heart rate deceleration in labor (n=1). Prolonged fetal heart rate deceleration (hypoxia-induced bradycardia) was evaluated on Atypical ductus venosus waveform. A prolonged hypoxia-induced fetal heart rate deceleration during labor resulted in an atypical ductus venosus waveform with marked prolongation of ventricular diastole and delayed A-wave onset.
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