16 Venous Doppler Sonography

F. Bahlmann

Historical Development

Since its initial description by Fitzgerald in 197713, the Doppler ultrasound assessment of the fetomaternal vascular system has become widely utilized in the surveillance of high-risk pregnancies. In the past, scientific and clinical attention was focused primarily on examination of the uteroplacental vascular system and on the arterial system of the fetus. In recent years, there have been increasing numbers of Doppler ultrasound studies of the physiological and pathophysiological changes in the fetal heart and circulatory system, with special emphasis on the cardiac and venous vascular systems. Although Doppler studies of volume flow in the intrahepatic umbilical vein were already being done in the early 1980 s, this method has not become widely established because of its poor reproducibility^{11,12,18,19,20,35,36,41}. With technical advances in ultrasound instrumentation and especially the advent of color Doppler sonography, it became possible to make a detailed evaluation of the fetal venous system. Besides the umbilical vein, inferior vena cava, and hepatic veins, Doppler examination of the ductus venosus has become a particular object of current scientific interest.

Physiology

Streaming effect. The ductus venosus represents the first of three specific shunts in the fetal circulation and appears to be an important regulator in the distribution of oxygen-enriched blood. Studies in experimental animals have demonstrated the existence of two different directions of blood flow (streaming effect) in the thoracic portion of the inferior vena cava9. Studies in fetal lambs showed that approximately 50% of oxygenated umbilical venous blood flows through the ductus venosus. The narrow ductal lumen causes marked acceleration of the blood flow, creating a stream in the left dorsal portion of the inferior vena cava with the preferential direction of flow through the foramen ovale into the left atrium and left ventricle. This streaming mechanism ensures an optimum oxygen supply to the brain and myocardium. The considerably slower blood flow in the distal inferior vena cava forms a stream in the right ventral portion of the inferior vena cava that is directed into the right atrium and then into the right ventricle (Fig. 16.1).

This streaming effect appears to be supported by the crestlike caudal border of the foramen ovale⁹. Similar findings were made in color Doppler studies of human fetuses⁴². An approximately 70% increase of blood flow through the ductus venosus was documented in response to hypoxemia in fetal lambs¹⁰. The exact pathophysiological mechanism of this effect is still uncertain.

Umbilical Vein

Quantitative determination of blood flow. Eik-Nes and Gill11,18 used Doppler ultrasound to evaluate fetal blood volume in the early 1980 s. They found a relatively constant mean volume flow of 110–125 ml/(kg min) in the third trimester, which decreased to 90 ml/(kg min) toward the end of pregnancy^11,12,18 (Fig. 16.2). The following formula (equation 1) is used for the quantitative determination of blood flow in the umbilical vein⁴⁷:

Fig. 16.1 “Streaming effect” demonstrated by experimental studies in fetal sheep9.

Q_VU = V × (D/2)² × π × 0.6 ml/min

Venous umbilical blood flow in this equation (Q_VU) is dependent on the blood flow velocity (V) and the vascular crosssectional area (D/2)² × π. The quantitative analysis of umbilical blood flow is problematic, however, in that even slight deviations in the vessel diameter lead to a large scatter of flow values⁴⁷. Because of its poor reproducibility, this quantitative method of blood volume determination is not widely utilized¹².

Fig. 16.2 Mean volume flow in the umbilical vein during pregnancy19.

Locating the umbilical vein. Doppler spectra are recorded from either the intra-amniotic or intrahepatic segment of the umbilical vein. The intrahepatic segment is preferred for its better reproducibility11,12,18. It is sampled by imaging the fetal abdomen in a transverse plane and placing the sample volume at an acute angle (<30°) in the central part of the intrahepatic umbilical vein¹¹.

Findings. The umbilical venous waveform generally shows a monophasic pattern with a mean flow velocity of 10–15 cm/s. Under physiological conditions, umbilical vein pulsations occur until the end of the first trimester or in response to fetal breathing movements^33,58 and normally are no longer seen after 13 weeks’ gestation. Umbilical vein pulsations in the second or third trimester may signify a cardiac anomaly or congestive heart disease, or they are commonly associated with absent end-diastolic flow in the umbilical artery as a result of chronic placental insufficiency^22,49 (Fig. 16.3). Umbilical vein pulsations in these cases show a temporal correlation with atrial systole and are an expression of myocardial insufficiency. Pulsations in the umbilical vein may take the form of single pulsations, double pulsations, or a triphasic Doppler spectrum^1,3,22,49. A markedly increased mortality rate of 50–60% is reported when these flow patterns are detected^22,33,49.

Ductus venosus

Locating the ductus venosus. The ductus venosus and its flow pattern can be demonstrated with two-dimensional real-time ultrasound and also with color Doppler (Fig. 16.4). Of all the precardial veins, the ductus venosus yields the best and most reliable information on the myocardial hemodynamics and function of the fetal heart, with good reproducibility of the Doppler spectra⁶¹. Doppler signals are recorded most easily and quickly when the fetus is in a dorsoposterior lie. For rapid venous orientation, the intrahepatic portion of the umbilical vein should be imaged first. The best view is obtained in either a midsagittal plane or oblique transverse plane of the fetal abdomen^24,30,42,43. The entry of the intrahepatic umbilical vein into the ductus venosus is located in continuity with the vein. The diameter of the ductus venosus rarely exceeds 2 mm and shows a slight funnel-shaped expansion up to 20 mm long⁴⁴.

A marked difference in blood flow velocities between the umbilical vein and ductus venosus can be recognized with color Doppler. The 3–4 times higher flow velocity in the ductus venosus causes aliasing, which appears as an area of color reversal (Figs. 16.5, 16.6). Flow signals are acquired by positioning the Doppler sample volume directly at the entrance to the ductus venosus, at the site of the color reversal^24,42 (Fig. 16.7). The width of the sample volume should just cover the vessel lumen to avoid detecting signals from the adjacent hepatic veins and umbilical vein. The use of color Doppler makes it much easier to locate the ductus venosus and accurately position the sample volume. Owing to the funnel shape of the ductus venosus, the flow velocities directly at the entrance are higher than at the outlet⁵³. An insonation angle less than 30° (or 50°) is recommended to obtain an optimum waveform⁴⁴. The wall filter should be set as low as possible—between 125 Hz and 100 Hz, depending on the type of equipment used.

Waveforms and indices. A sonographer experienced in Doppler ultrasound can obtain clear Doppler signals from the ductus venosus in 94% of cases²⁴. The normal velocity waveform of the ductus venosus exhibits continuous, triphasic forward flow throughout the cardiac cycle. Absent or low pulsatility is noted in 3% of cases and is considered a normal variant⁴⁴; a brief waiting period is recommended in these cases. The maximum flow velocities in the ductus venosus are the highest in the venous system and appear to be responsible for the “streaming effect.” As in the arterial system, the flow velocities in the ductus venosus are dependent upon gestational age, fetal breathing and body movements, and the fetal heart rate⁴⁴. The maximum blood flow velocity rises on average from 65 cm/s to 75 cm/s between 18 and 40 weeks’ gestation⁴⁴. The blood flow velocity in the ductus venosus can rise to double or triple the normal value during inspiration, depending on the intensity of the breathing movements.

The quantities that are determined for ductus venosus waveform analysis are the maximum flow velocities during ventricular systole (S), ventricular early diastole (D), and ventricular late diastole (atrial contraction [a]) (Fig. 16.8). Hemodynamically, these phases reflect the rapidly time-varying pressure gradient between the umbilical vein and right atrium. The highest pressure gradient between the ductus venosus and right atrium occurs during ventricular systole. This gradient is produced by the descent of the atrioventricular (AV) valve plane, resulting in antegrade flow that fills the atria. Subsequent early diastole is marked by opening of the AV valves and passive filling of the ventricles. This phase corresponds to the E component of the biphasic atrioventricular waveform. During atrial contraction, which coincides with the A component of the atrioventricular waveform, the foramen ovale closes and the rest of the atrial blood volume is actively pumped into the right ventricle. By analyzing these patterns, the sonographer can obtain information on the end-diastolic right ventricular pressure and the central venous pressure. The angle-independent parameters listed in Table 16.1 are used for the qualitative assessment of pulsatility. These parameters can be used to evaluate the cardiac preload⁸.

Normal and abnormal changes during the course of pregnancy. The end-diastolic ventricular pressure declines with advancing gestational age as a result of placental maturation processes that lower the placental resistance. This decrease is manifested by a decline of venous pulsatility and falling preload indices and is due mainly to the rising flow velocity during atrial contraction (Figs. 16.9, 16.10). A rise in the preload indices reflects an increased end-diastolic ventricular pressure in the heart. In a healthy fetus, the umbilical venous pressure during atrial contraction is higher than the central venous pressure. When there is severe centralization of the fetal circulation due, for example, to chronic placental insufficiency or hypovolemia, a hypoxia-induced myocardial insufficiency develops, leading to a rise of central venous pressure in the fetal right heart. The result is a fall of maximum flow velocities in the ductus venosus or even reverse flow during atrial contraction (Fig. 16.11)^{23,25,27,46,62}. Complete cardiac exhaustion and decompensation are manifested by sinus bradycardia, which is marked by a decrease in systolic and early diastolic antegrade flow velocities and an increase in retrograde late diastolic flow velocities.

S = systole, D= diastole, a = atrial contraction, Tamx = time-averaged maximum velocity.

Inferior Vena Cava

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