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Ductus venosus blood‐flow patterns: more than meets the eye?

2012; Wiley; Volume: 39; Issue: 5 Linguagem: Inglês

10.1002/uog.10151

1469-0705

Ahmet Baschat, Özhan Turan, S. Turan,

Cardiovascular Function and Risk Factors

The Doppler evaluation of fetal venous flow-velocity waveforms is of clinical relevance in conditions that are associated with cardiovascular manifestations. In contrast to arterial flow, velocity waveform characteristics of the venous-flow profile relate to atrial pressure and volume changes throughout the entire cardiac cycle, producing a multiphasic flow pattern1. Among the fetal venous vessels, the ductus venosus has a special role because its flow is under active regulation and its anatomy results in a flow-velocity profile that is typically antegrade throughout the entire cardiac cycle and, therefore, lends itself to qualitative assessment1, 2. Designation of the individual phases of the venous flow-velocity waveform is based on the timing of the cardiac cycle. With the initiation of ventricular systole the descent of the atrioventricular (AV) valve ring decreases atrial pressure and increases the amount of venous return that can be accommodated by the atria. This produces the first increase in venous forward velocities, which peak at the S-wave. As the ventricle relaxes in the second half of systole the AV valve ring ascends towards its resting position, atrial pressures rise and venous forward velocities fall to the first trough, designated as the v-descent. Once ventricular relaxation is complete, the higher pressures in the atria lead to an opening of the AV valves, allowing for an increase in venous forward velocities towards the second peak during passive diastolic ventricular filling (D-wave). With the discharge of the sinoatrial node, atrial contraction initiates active ventricular diastolic filling and produces a sharp increase in atrial pressures. The fall in venous forward velocities produces the second trough, designated the a-wave (Figure 1). Representation of the major cardiac events that coincide with the four phases of the ductus venosus flow-velocity waveform. The S-wave (S) and v-descent (v) occur during ventricular systole and the D-wave (D) and a-wave (a) during ventricular diastole. During descent of the atrioventricular valve ring with ventricular contraction, atrial pressures fall and capacity is increased, resulting in increased forward velocities. During ventricular relaxation this process reverses, producing the v-descent. During early passive ventricular filling, atrial pressure falls and capacity rises. With atrial systole there is a sharp rise in atrial pressure and a decrease in capacity, producing a corresponding decrease in forward velocity. There are several variables including afterload, cardiac contractility, compliance and vascular volume that can affect cardiac function and therefore intra-atrial pressure–volume relationships. Because of the timing of events during the cardiac cycle, individual aspects of myocardial dysfunction may be more apparent during specific phases of the venous flow-velocity waveform (Figure 1). Accordingly, increased afterload or decreased cardiac contractility may affect S-wave velocities, as well as D and a-wave velocities, because of the increase in end-systolic ventricular volumes that may impair diastolic ventricular filling. In contrast, abnormalities in ventricular relaxation, an oxygen-dependent process in the fetus, may predominantly affect the v-descent. Restriction to ventricular filling, either by extracardiac compression or decreased cardiac compliance, is more likely to affect the D- and a-waves. Finally, restriction to atrial systolic emptying, for example due to valvular disease, may have its predominant effect during atrial systole. The association of specific cardiac functional abnormalities with characteristic patterns of the jugular venous pulse has been long recognized in adult medicine3. But while more sophisticated direct measurements of cardiac functional variables have replaced clinical evaluation in adult medicine not all of these techniques are available for examination of the human fetus. Our primary assessment of the ductus venosus flow velocity waveform is by Doppler indices that predominantly reflect S/a and to a lesser degree D/a and S/D velocity relationships, or by qualitative analysis focusing on the a-wave4-6. There is increasing evidence that such assessment has limitations in assessing the primary underlying cardiac functional component when the Doppler index is elevated. During the construction of reference ranges it has been recognized that diastolic AV waveforms do not relate to ductus venosus or inferior vena cava peak velocity or pulsatility index (PIV)7. During simultaneous evaluation of placental and venous Doppler measurements we realized that afterload has the greatest impact on the ductus venosus PIV and the least impact on the inferior vena cava S/a ratio6. In fetal growth restriction (FGR) it is known that high placental afterload, myocardial dysfunction and ductus venosus dilatation can all be associated with abnormal index elevation8. Accordingly, global myocardial dysfunction is not universally present in all cases of FGR with elevated ductus venosus Doppler index9. These observations raise the possibility that ductus venosus waveform analysis as it is currently practiced potentially provides insufficient or misleading information on the nature of cardiovascular compromise in various fetal conditions. During the management of various fetal conditions we have noticed several types of ductus venosus waveform abnormalities10. A familiar type of waveform abnormality is decreased forward velocity during atrial systole and during the D-wave (Figure 2a). In some fetuses we notice an abnormally low v-descent, sometimes as low as the a-wave. This is often associated with loss of the typically smooth contour of the venous flow profile, resulting in an 'M' shaped waveform (Figure 2b). In patients with obstructive AV valve disease we have observed marked reversal of the a-wave of a magnitude comparable with that of the D-wave (Figure 2c). Finally, in a small number of fetuses with visually asynchronous left and right ventricular relaxation we have observed a tetraphasic waveform pattern (Figure 2d). These differences in waveform abnormalities suggest the possibility of different underlying mechanisms. Evaluation of this possibility requires a departure from the current semiquantitative waveform analysis to a more systematic evaluation of the relationships between the individual phases of the ductus venosus waveform and direct measurements of related cardiovascular variables. The aim of this Letter is to suggest that such detailed venous waveform analysis is likely to provide greater insight into the pathophysiology of many fetal conditions, with a potential for greater discrimination in assessment and improvements in management. Abnormal ductus venosus waveforms in fetuses with different underlying causes. (a) Recipient twin in twin–twin transfusion syndrome at 22 weeks' gestation, showing a predominant decrease in a-wave velocities and, to a lesser degree, of D-wave velocities. (b) A growth-restricted fetus at 28 weeks' gestation, showing reduced v-descent and loss of the smooth waveform contour, giving it an 'M' shape. (c) A 29-week fetus with Ebstein anomaly, showing marked reversal of the a-wave, which is comparable with the 'cannon a-wave' described in adult medicine. (d) A fetus with cardiomyopathy secondary to maternal Sjögren syndrome, showing visual asynchrony between left and right ventricular relaxation potentially contributing to the tetraphasic pattern with two troughs during v-descent. A. A. Baschat*, O. M. Turan*, S. Turan*, * Department of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland, 22 South Greene Street, 6th floor, 6NE12 Baltimore, MD 21201, USA