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Importance of venous flow assessment for clinical decision-making

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Importance of venous flow assessment for clinical decision-making
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  European Journal of Obstetrics & Gynecology andReproductive Biology 84 (1999) 173–178 Importance of venous flow assessment for clinical decision-making *Saemundur Gudmundsson ¨ University of Lund  ,  Department of Obstetrics and Gynecology ,  University Hospital MAS  ,  S  - 205 02   Malmo ,  Sweden Abstract In recent years Doppler ultrasound examinations of fetal venous circulation has given new insight into fetal hemodynamics. Blood flowin the systemic circulation has a pulsating pattern which reflects fetal central venous pressure. Characteristic changes in the blood velocitywaveform have been described in different clinical conditions like congestive heart failure, imminent fetal asphyxia and arrhythmias.Recording fetal venous blood flow by Doppler ultrasound can thus give important clinical information and has with time gained a place asone of the most valuable tools for fetal surveillance in high-risk pregancies.  ©  1999 Elsevier Science Ireland Ltd. All rights reserved. Keywords :   Doppler ultrasound; Venous blood flow; Fetus; Pregnancy; Review 1. Introduction  (A), which frequently has reversed blood velocities awayfrom the heart. The degree of reversion in blood velocitiesDuring the 1990s, Doppler ultrasound examinations of depends on the site of measurement, being most prominentfetal venous blood flow have given additional knowledge near the heart and is hardly ever reversed in the moreon fetal physiology that has given valuable clinical in- peripheral veins.formation on fetal condition in high-risk pregnancies. The At the isthmus of the ductus venosus (DV), pulsatingfollowing is a summary of the present knowledge on high blood velocities can be recorded as an expression of ´venous blood velocities and its implication in clinical the difference in umbilical venous and central venousmanagement. pressure. Blood velocities in the umbilical vein (UV) andportal circulation are, in contrast to the systemic venouscirculation, even and without fluctuation. Heart synchro- 2. Normal fetal venous circulation  nous pulsating patterns in the UV can normally be seen inearly pregnancy, but disappear between 9 and 13 weeks of Blood velocities in the fetal systemic venous circulation gestation. Single rhythmic systolic pulsating pattern in thehas a typical pulsating pattern as a reflection of central UV has also been reported in otherwise normal pregnan-venous pressure [1] (Fig. 1). There are normally two peaksof blood velocity towards the heart. The first (S) corre-sponds to the filling of the atria during ventricular systole,which might be explained by reduced pressure in the atriacaused by atrial wall relaxation and because of downwardmovement of the atrio-ventricular valves (AV-valves) an-nulus during ventricular contraction. The second peak of blood velocity (D) occurs at the onset of diastole corre-sponding to the opening of the AV-valves and early fillingof the ventricles. Finally, at the end of diastole, a reductionin blood velocity occurs corresponding to atrial contraction *Tel.:  1 46-40-333412; fax:  1 46-40-962600. Fig. 1. Spectrum of normal fetal inferior vena cava blood velocity. S,  E  - mail address :   saemundur.gudmundsson@obst.mas.lu.se (S. Gud- peak systolic blood velocity; D, peak diastolic blood velocity; and A,mundsson) reversed blood flow during atrial contraction.0301-2115/99/$ – see front matter  ©  1999 Elsevier Science Ireland Ltd. All rights reserved.PII: S0301-2115(98)00326-1  174  S  .  Gudmundsson  /   European Journal of Obstetrics  &   Gynecology and Reproductive Biology  84 (1999) 173  – 178  Fig. 2. Spectrum of umbilical artery and vein blood velocity. Pulsatingumbilical venous blood velocity during systole due to umbilical cordocclusion. cies with partial umbilical cord occlusion or a knot on thecord. The rhythmic decrease in UV blood velocity iscaused by the umbilical arterial wall pulsating against thevein (Fig. 2). Similar pattern can be seen during fetalbradycardia. 3. Diagnosis of fetal arrhythmia Blood velocity in the inferior vena cava (IVC) andhepatic veins (HV) is pulsating as a reflection of centralvenous pressure and therefore shows characteristic bloodvelocity changes during different types of fetal arrhythmia.Premature heart beats of supra-ventricular or ventricular  Fig. 3. Schematic illustration of inferior vena cava blood velocity origin can be differentiated due to characteristic differ-  waveforms. Highest panel: normal blood velocity pattern; middle panel:blood velocity pattern during premature ventricular extra-systole (VES); ences in reversal of blood velocity during atrial contrac- lowest panel: blood velocity pattern during premature supraventricular tion. During premature beats of atrial srcin an exaggerated extra-systole (SVES). reversed blood velocity caused by atrial contraction isrecorded earlier than expected during the heart cycle (Fig.3). However, during premature beats of ventricular srcinthe reversed velocity comes at the right moment in end-diastole, but with increased intensity due to the atriacontracting against closed AV-valves (Fig. 3). A typicaltime-lag pattern in blood velocity is seen after the ventricu-lar premature beat.IVC blood velocity recordings can also diagnose atrialflutter with a typical multispiked waveform pattern asillustrated in Fig. 4. A typical pattern can also be seenduring supraventricular tachycardia (SVT) as illustrated inFig. 5 and discussed under the next section on congestivefetal heart failure. 4. Diagnosis of fetal congestive heart failure Non-immune hydrops fetalis (NIHF) is a severe clinicalfetal condition of varying etiology with overall poorprognosis. In some of the fetuses, hydrops resolves within  Fig. 4. Inferior vena cava blood velocity pattern in a fetus with atrial days or weeks without treatment [2]. Differentiating be-  flutter.  S  .  Gudmundsson  /   European Journal of Obstetrics  &   Gynecology and Reproductive Biology  84 (1999) 173  – 178   175 whom SVT was treated successfully in-utero; one withcytomegolovirus cardiomyopathy; and one pregnancy witha suspected viral infection that developed placental abrup-tion 1 day after the examination. All except one of theeight cases with normal UV blood flow pattern survived;one case with polyhydramnios was delivered prematurelyat 29 weeks of gestation and died due to lung hypoplasia.Hydrops in the fetus with normal UV blood velocitiesusually disappeared within 4 weeks if not delivered shortlyafter the examination and laboratory analysis confirmed orgave suspicion of a viral cause of hydrops.Fetuses showing heart failure with pulsations in the UVhad a characteristic blood velocity pattern in the IVC (Fig.7). The early diastolic blood velocity (D), as a sign of passive filling of the ventricles, had disappeared during Fig. 5. Renal vein blood velocity. Upper panel: in normal pregnancy; SVT as illustrated in Fig. 5 or nearly disappeared in the lower panel: in a fetus with supraventricular tachycardia. fetus with normal heart rhythm (Fig. 7). Pulsating bloodvelocity patterns in the UV in cases of NIHF might between NIHF caused by congestive heart failure and other caused by absent or reversed diastolic (ARED) flow in thenon-cardiac causes was difficult before the introduction of umbilical artery, but ARED flow in the umbilical arteryDoppler ultrasound in perinatal medicine. The diagnosis of was only seen in four of the fetuses. Umbilical venouscongestive heart failure was mostly based on increased pulsations are therefore probably caused by transmission of fetal heart size, decreased heart ventricle shortening frac- pressure waves across the DV into the umbilical cord. Intion on ultrasound imaging and/or M-mode echocardiog- the terminal case of fetal heart failure, the umbilicalraphy. venous blood velocity had similar blood velocity pattern asGudmundsson et al. [2] studied 24 cases with NIHF. Of the IVC (Fig. 8), which might suggest a widely open DVall cardiovascular parameters analyzed, only the presence probably due to increased central venous pressure duringof abnormal pulsating pattern of blood velocities in the UV congestive fetal heart failure.was found in relationship with poor perinatal outcome. Fetal echocardiographic examination of the fetus withAbnormal UV blood velocity pulsations are illustrated in abnormal umbilical venous pulsations showed many fac-Fig. 6. The results were first presented after the examina- tors suggesting a state of congestive heart failure whention of 18 cases [2] and the results were then confirmed by compared to the fetus with normal venous blood velocitiesan expanded study of 24 cases [3]. Of the 16 fetuses with [3]; the IVC diameter was larger, there was a decreasedabnormal UV pulsations four survived (25%); two in right and left heart ventricular fractional shortening, de-creased peak velocity at the aortic and pulmonary valvesand in the ductus arteriosus. Decreased d v  /d t   of the Fig. 6. Spectrum of umbilical venous blood velocity. Upper panel:normal blood velocity recording; middle panel: fluctuating blood velocity Fig. 7. Spectrum of inferior vena cava blood velocity. Upper panel:during fetal breathing movements; lower panel: umbilical venous pulsa- normal blood velocity tracing; below: blood velocity in a fetus withtions. From Gudmundsson et al. [2] Am J Obstet Gynecol 1991;164:33, non-immune hydrops due to congestive heart failure. From Gudmundssonwith permission. et al. [2] Am J Obstet Gynecol 1991;164:33, with permission.  176  S  .  Gudmundsson  /   European Journal of Obstetrics  &   Gynecology and Reproductive Biology  84 (1999) 173  – 178  IVC due to differences in atrial pressure caused by thepartial obstruction to flow by the foramen ovale (Fig. 9).The echocardiographic information on entrance of thepulmonary veins into the left atrium can be of majorimportance for the newborn baby and minimize the risk of unexpected life threatening crises due to pulmonary venousdrainage into the right atrium. 6. Diagnosis of imminent fetal asphyxia During the early 1980s, examination of umbilical ven-ous volume blood flow was the main focus of interest[4,5]. The results in high-risk pregnancies were, however,disappointing for the prediction of fetal compromise. The Fig. 8. Spectrum of umbilical artery and vein blood velocity just before terminal fetus usually seemed to be able to maintain blood intra-uterine fetal death. Umbilical venous blood velocity pulsating as in flow through the placenta [5]. This might be due to an the inferior vena cava. increase in fetal blood pressure. Technical errors, especial-ly difficulties in measuring vessel diameter might also be aaccelerating slope at the pulmonary valve and during cause of the poor correlation to fetal condition.tricuspid regurgitation (TR) was also recorded in fetus with Rhythmic decrease in end-diastolic UV blood velocityabnormal venous pulsations. TR might be suggested as has been demonstrated during hypoxia in a lamb prepara-being the cause of abnormal venous pulsations by in- tion [6,7] and in human high-risk pregnancies suspected of creased atrial blood volume, but no relationship to TR was chronic fetal hypoxemia. Perinatal mortality is frequentlyfound in these cases of NIHF. TR was found in five of the associated with UV pulsations, suggesting that it is a late11 survivors and in seven of the 13 non-survivors. sign of fetal compromise in high-risk pregnancies [8–10].Abnormal umbilical venous pulsation and increased rever- The exact physiological cause of UV pulsations issal of blood flow in end-diastole in the IVC in pregnancies unclear, but changes in blood flow might be caused bywith NIHF might therefore differentiate between hydrops factors influencing forward blood flow through thecaused by virus or congestive heart failure and predict placenta and/or in the cord, or retrograde transmission of outcome of pregnancy. pressure waves across the DVcausing rhythmic decrease inUV flow. Decreased forward flow across the placenta indiastole due to absent or reversed flow in the umbilical 5. Pulmonary venous drainage into the atrium  artery (ARED-flow) might be a cause of reduction in bloodflow in end-diastole (single pulsation, Fig. 10). DuringPulmonary venous blood velocity has a characteristic umbilical cord occlusion or bradycardia the umbilicalpulsating pattern as a reflection of pressure in the left artery might squeeze the vein and cause a single pulsationatrium. The blood velocity pattern is different to that in the in systole (Fig. 2). Double UV pulsation, however, isdiphasic with a similar pattern as the normal fluctuation of blood flow in the IVC. This might suggest that it representscentral venous pressure waves transmitted retrograde overthe DV into the cord. Primary opening of the DV duringfetal hypoxia might also be a cause of diphasic UV Fig. 9. Spectrum of venous blood velocity. Upper panel: blood velocitytracing in a hepatic vein; lower panel: blood velocity tracing in a Fig. 10. Spectrum of umbilical artery and vein blood velocity. Pulsatingpulmonary vein. umbilical venous blood velocity in end-diastole.  S  .  Gudmundsson  /   European Journal of Obstetrics  &   Gynecology and Reproductive Biology  84 (1999) 173  – 178   177Table 1Causes of umbilical venous pulsations Single pulsation: changes in forward flow from placenta  During diastole :ARED-flow in umbilical artery  During systole :BradycardiaUmbilical cord occlusionTrue knot on the cord Diphasic pulsation: increased central venous pressureand/or opening of the ductus venosus Fetal congestive heart failureImminent fetal asphyxia pulsation. Different types of umbilical venous pulsationsand the pathophysiological processes causing it are sum-marized in Table 1.During chronic hypoxia, the fetus reacts by redistribut- Fig. 11. Spectrum of ductus venous blood velocity. Upper panel: normal ´ing its cardiac output to organs of greater need like the blood velocity tracing; lower panel: blood velocity tracing in a compro- brain, heart and adrenals [11]. Consequently the fetus can mised fetus. maintain blood acid-base levels within normal limits[12,13]. However, the redistribution can cause ischemicdamage in deprived organs that can be a clinical problem during atrial systole despite minimal changes in umbilicalafter birth such as necrotizing enterocolitis. artery pulsatility index. Decreased blood flow towards thePresently, the umbilical artery blood velocity waveform heart during diastole might suggest an early sign of fetalcan give information on increased feto-placental vascular congestive heart failure. Subsequent studies have, how-resistance, i.e. ARED-flow. Fetuses with ARED-flow ever, not been able to repeat these findings and reportedusually have poor growth potential and usually can not minimal changes in central venous blood flow in thecope with the stress of vaginal delivery. Delivering these high-risk fetuses [8,19]. The authors have suggested thatfetuses after lung maturation is therefore a routine in most the fetal heart like the brain is spared during chronic fetalhands, but management before 31 weeks of gestation is hypoxemia. Changes in central venous blood velocitycontroversial. The clinical dilemma is between being might therefore be a late sign of fetal compromise.active with early delivery and the risk of damage due to DV blood velocity has been studied intensively in recentimmaturity, or wait and react on worsening fetal condition, years in order to find a more intermediate signal of fetalwhich might cause cerebral damage in the newborn [14]. compromise [20–24]. The results have been promisingFetal redistribution has been studied intensively in especially in early third trimester of pregnancy showingrecent years, hoping it might assist in optimal timing of characteristic decrease in end-diastolic blood velocity indelivery with minimal damage to the premature fetus. the compromised fetus (Fig. 11). The first prospectiveMiddle cerebral artery blood velocity has been studied study on DV blood velocity in high-risk pregnanciesintensively as a sign of brain sparing, but it seems to be a showed, however, no relationship between abnormal DVvery early sign of fetal hypoxia in a fetus that still has blood velocity waveform and adverse perinatal outcomereserves to cope with the stress of vaginal delivery [15,16]. [25]. In animal studies, DV blood velocity seems to beUV pulsations are a late sign of hypoxia with high greatly influenced by central venous pressure and heart rateperinatal mortality, a more intermediate sign of fetal [26]. Recording at the proximal or distal part of the DVcompromise is therefore badly needed. might also give different results. More studies on DVExaminations of central fetal veins have been also been blood velocity are therefore needed before it can beundertaken in order to earlier predict worsening fetal introduced in the clinical setting.condition and deliver the fetus with less risk of cerebraldamage. Reed et al. [17] studied IVC blood velocity in 15IUGR fetuses with absent end-diastolic blood velocities in  References the umbilical artery and found an increased S/D-ratio inthese fetuses, with lower blood velocities during early  [1] Reuss ML, Rudolph AM, Dae MW. Phasic blood flow patterns inthe superior and inferior venae cavae and umbilical vein of fetal diastole and increased reversed blood velocity during atrial sheep. Am J Obstet Gynecol 1983;145:70–8. systole (A). Rizzo et al. [18] examined fetuses with [2] Gudmundsson S, Huhta JC,Wood DC, Tulzer G, Cohen AW,Weiner absence of end-diastolic blood velocity in the umbilical S. Venous Doppler in the fetus with non-immune hydrops. Am J artery longitudinally and reported a significant progressive  Obstet Gynecol 1991;164:33–7. increase in IVC S/D-ratio and percentage of reverse flow  [3] Tulzer G, Gudmundsson S, Wood DC, Cohen AW, Weiner S, Huhta
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