Talk:Cardiovascular System - Developmental Shunts

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Cite this page: Hill, M.A. (2021, November 30) Embryology Cardiovascular System - Developmental Shunts. Retrieved from


Prenatal cardiovascular shunts in amniotic vertebrates

Respir Physiol Neurobiol. 2011 Apr 13. [Epub ahead of print]

Dzialowski EM, Sirsat T, van der Sterren S, Villamor E. Source Department of Biological Sciences, University of North Texas, Denton, TX 76203, USA.


During amniotic vertebrate development, the embryo and fetus employ a number of cardiovascular shunts. These shunts provide a right-to-left shunt of blood and are essential components of embryonic life ensuring proper blood circulation to developing organs and fetal gas exchanger, as well as bypassing the pulmonary circuit and the unventilated, fluid filled lungs. In this review we examine and compare the embryonic shunts available for fetal mammals and embryonic reptiles, including lizards, crocodilians, and birds. These groups have either a single ductus arteriosus (mammals) or paired ductus arteriosi that provide a right-to-left shunt of right ventricular output away from the unventilated lungs. The mammalian foramen ovale and the avian atrial foramina function as a right-to-left shunt of blood between the atria. The presence of atrial shunts in non-avian reptiles is unknown. Mammals have a venous shunt, the ductus venosus that diverts umbilical venous return away from the liver and towards the inferior vena cava and foramen ovale. Reptiles do not have a ductus venosus during the latter two thirds of development. While the fetal shunts are well characterized in numerous mammalian species, much less is known about the developmental physiology of the reptilian embryonic shunts. In the last years, the reactivity and the process of closure of the ductus arteriosus have been characterized in the chicken and the emu. In contrast, much less is known about embryonic shunts in the non-avian reptiles. It is possible that the single ventricle found in lizards, snakes, and turtles and the origin of the left aorta in the crocodilians play a significant role in the right-to-left embryonic shunt in these species.

Copyright © 2011. Published by Elsevier B.V.

PMID: 21513818

Transient hepatic nodular lesions associated with patent ductus venosus in preterm infants

Am J Perinatol. 2011 Mar;28(3):177-80. Epub 2010 Sep 16.

Schierz IA, La Placa S, Giuffrè M, Montalbano G, Lenzo M, Corsello G. Source Unità Complessa di Pediatria e Terapia Intensiva Neonatale, Dipartimento Universitario Materno Infantile, Università degli Studi di Palermo, Via Alfonso Giordano 3, Palermo, Italy.


We report on two cases of low-birth-weight preterm infants with patent ductus venosus associated with hepatic hypoechoic lesions of the fourth segment in an otherwise normal liver. Although tumorlike hepatic lesions have been previously reported in association with portosystemic shunts in children and adults, they were never described in preterm infants during physiological patency of ductus venosus. In our patients, hepatic lesions disappeared shortly after the spontaneous ductus closure. Physiopathologic interactions are discussed regarding altered portal blood supply caused by ductus venosus shunt.

© Thieme Medical Publishers.

PMID: 20848372


Preferential streaming of the ductus venosus and inferior caval vein towards the right heart is associated with left heart underdevelopment in human fetuses with left-sided diaphragmatic hernia

Heart. 2010 Oct;96(19):1564-8. Epub 2010 Aug 11.

Stressig R, Fimmers R, Eising K, Gembruch U, Kohl T. Source Department of Obstetrics and Prenatal Medicine, University Hospital of Bonn, Bonn 53105, Germany.


OBJECTIVE: Left heart underdevelopment is commonly observed in fetuses with left diaphragmatic hernia. This finding has been attributed to compression of the left atrium by herniated abdominal organs, redistribution of fetal cardiac output and/or low pulmonary venous return. As preferential right or left heart underdevelopment is usually not a feature of right diaphragmatic hernia, we searched for an alternative mechanism. Since in normal fetuses the major fraction of left heart filling is provided by the ductus venosus via the inferior caval vein and oval foramen, our study focused in particular on the streaming direction of these structures.

PATIENTS AND METHODS: We prospectively studied 32 fetuses with left diaphragmatic hernia between 19 + 6 weeks and 38 + 6 weeks of gestation by echocardiography. The fetuses were divided into two groups: Group I fetuses exhibited abnormal streaming of ductus venosus and inferior caval vein blood flow towards the right side of the heart; group II fetuses did not exhibit this abnormal flow direction. Cardiac inflow and outflow dimensions were compared in the two groups.

RESULTS: 18 of 19 group I fetuses with left diaphragmatic hernia exhibited disproportionately smaller left than right heart dimensions; 12 of 13 group II fetuses exhibited similar sized left and right cardiac inflow and outflow dimensions (p<0.05).

CONCLUSIONS: Preferential ductus venosus and inferior caval vein streaming towards the fetal right heart offers another haemodynamic mechanism for left heart underdevelopment in fetuses with left diaphragmatic hernia. The pathoanatomical basis of this abnormal flow pattern results from intrathoracic abdominal organ herniation and rightward displacement of the heart.

PMID: 20702536


Ductus venosus shunting in the fetal venous circulation: regulatory mechanisms, diagnostic methods and medical importance

Ultrasound Obstet Gynecol. 2006 Apr;27(4):452-61.

Tchirikov M, Schröder HJ, Hecher K. Source Department of Obstetrics, University Medical Center Hamburg-Eppendorf, Germany.


The fetal liver is located at the crossroads of the umbilical venous circulation. Anatomically, the ductus venosus (DV) and the intrahepatic branches of the portal vein are arranged in parallel. The actual DV shunting rate, i.e. the percentage of umbilical blood flow entering the DV measured by Doppler velocimetry, seems to be lower than that estimated using radioactively-labeled microspheres. In human fetuses the DV shunting rate is about 20-30%. Increases in the DV shunting rate are a general adaptational mechanism to fetal distress. Hypoxia results in a significant increase in the DV shunting rate, most probably in order to ensure an adequate supply of oxygen and glucose to vitally important organs such as the brain and heart. The mechanism of blood flow redistribution between the fetal liver and the DV is still a matter of debate. The isthmic portion of the DV contains less smooth muscle tissue than the intrahepatic branches of the portal vein, which in vitro react more forcefully in response to catecholamines than the DV. In growth-restricted human fetuses DV shunting is increased and the umbilical blood supply to the fetal liver is reduced. The long-term reduction of the hepatic blood supply may be involved in fetal growth restriction. The occlusion of the DV leads to a significant increase in cell proliferation in fetal skeletal muscle, heart, kidneys and liver, and possibly to an increase in insulin-like growth factor (IGF)-I and -II mRNA expression in the fetal liver. These findings hint at the possible role of the perfusion of the fetal liver in the control of the growth process. The quantification of DV shunting by Doppler velocimetry may improve the early recognition of fetal compromise in prenatal medicine. In this Review we summarize the published data on the anatomical structure and histology of the DV, the mechanisms of regulation of DV shunting, its role in fetal survival and growth and the possible use of the measurement of DV shunting in clinical practice.

Copyright 2006 ISUOG.

PMID: 16565980


The ductus venosus

Semin Perinatol. 2001 Feb;25(1):11-20.

Kiserud T.

Department of Obstetrics and Gynecology, Bergen University Hospital, Norway.


Until recently, our information on the ductus venosus was based on postmortem and experimental studies. The present review relates to the modern concept of this vein predominantly founded on clinical studies. Recent publications show that the blood distribution through the ductus venosus is particularly sensitive to changes in umbilical venous pressure, blood viscosity, and an active regulation of diameter of the entire ductus venosus. The mean fraction of umbilical blood shunted through the ductus is reduced from 30% to 20% during the second half of the human pregnancy, indicating that, during this period, the fetal liver has a higher priority than the shunting through the ductus venosus, apart from the compensatory redistribution needed during extreme challenges of placental compromize and hypoxemia. Additionally, the ductus venosus acts as a transmission line to the umbilical vein for pulse waves generated in the heart. These waves, reflecting cardiac function, are substantially influenced by the local variation of impedance and compliance.

PMID: 11254155


Prenatal diagnosis of abnormalities of the fetal venous system

Ultrasound Obstet Gynecol. 2000 Mar;15(3):231-41.

Hofstaetter C, Plath H, Hansmann M. Source Department of Obstetrics and Gynecology, University of Bonn, Germany. Abstract OBJECTIVE: To present our experience in the prenatal diagnosis of anomalies of fetal veins using high-resolution color Doppler ultrasound.

DESIGN: An observational study of 16 fetuses with abnormalities of the umbilical, portal, hepatic and caval venous system being diagnosed at the Division of Prenatal Diagnosis and Therapy (Bonn, Germany) over the past 5 years. The abnormality of the venous system, the underlying embryologic disorder and the outcome of the pregnancy are presented and compared with the literature.

RESULTS: In group A, eight fetuses had an abnormal course of the umbilical vein with a patent (n = 3) or absent (n = 5) ductus venosus. No portal veins and absent or abnormal hepatic veins were visualized by color Doppler sonography. Six fetuses (75%) did not have an associated malformation and have survived. Two pregnancies with fetal hydrops due to a small heart and to Turner's syndrome were terminated or ended in fetal demise. In group B, seven of eight fetuses with an abnormal caval system had a situs ambiguus or an atrial isomerism. A cardiac defect was detected in six cases (86%). These six pregnancies ended in four terminations of pregnancy and two infant deaths due to the severity of the congenital cardiac defect. One child with a normal heart and a child with an isolated abnormal course of the lower inferior vena cava are developing well.

CONCLUSIONS: In a targeted fetal scan the course of the umbilical vein, ductus venosus, the portal and hepatic veins and inferior vena cava should be carefully examined using color Doppler. Any suspicious finding should be followed by a detailed assessment of the specificity of this abnormality taking into consideration the embryologic development of the fetal venous system together with the associated malformations.

PMID: 10846780


Hepatic manifestations of familial patent ductus venosus in adults

Gut. 1999 Sep;45(3):442-5.

Jacob S, Farr G, De Vun D, Takiff H, Mason A. Source Section of Gastroenterology and Hepatology, Ochsner Medical Institutions, 1520 Jefferson Highway, New Orleans, LA 70121, USA.


BACKGROUND: The ductus venosus connects the umbilical vein to the inferior vena cava during fetal life and subsequently closes rapidly after birth. It is known as patent ductus venosus when it remains patent in adulthood.

PATIENTS: A 43 year old man with a history of panhypopituitarism presented with recurrent bouts of pedal oedema associated with fatigue, hypoalbuminaemia, and elevated prothrombin time. An ultrasound examination of his abdomen with Doppler revealed notable attenuation of the main portal vein with diminished intrahepatic branches; a computed tomography scan with angiography revealed a large collateral vein within the liver consistent with a patent ductus venosus. Sequential liver biopsies showed a considerable reduction in the calibre and number of the portal veins. His younger brother, who was diagnosed with alcohol related cirrhosis, suffered from intermittent bouts of encephalopathy and was found to have the same vascular lesion. A third brother was found to have a patent ductus venosus as well as two large hepatic masses consistent with focal nodular hyperplasia.

CONCLUSION: The syndrome of familial patent ductus venosus has only previously been described in three infant brothers who presented with hepatic encephalopathy and fatty degeneration of the liver. This report documents three brothers with a patent ductus venosus presenting in adulthood with different manifestations of liver disease. The presence of the same vascular anomaly in three brothers is highly suggestive of a recessive genetic trait with an anatomical manifestation of patent ductus venosus.

Comment in Gut. 1999 Sep;45(3):329-30.

PMID: 10446116


Hepatic and ductus venosus blood flows during fetal life

Hepatology. 1983 Mar-Apr;3(2):254-8.

Rudolph AM.


The course of the venous circulation in the fetal liver has been studied in fetal lambs by means of the radionuclide-labeled microsphere technique. About 50% of umbilical venous blood passes through the ductus venosus, while the remainder is distributed to both lobes of the liver. Portal venous blood is largely distributed to the right lobe of the liver, with a small proportion passing through the ductus venosus and none to the left lobe. Because of these flow patterns, oxygen saturation is lower in the right than in the left hepatic vein. Left hepatic venous blood joins the ductus venosus stream and these preferentially pass through the foramen ovale, whereas right hepatic venous blood joins the distal inferior vena caval stream and preferentially passes through the tricuspid valve. These patterns favor distribution of well-oxygenated blood to the fetal heart and brain. Hypoxia and reduced umbilical venous return are associated with reduced flow through the hepatic microcirculation with proportionately greater ductus venosus flow. In the fetus, the liver has a major role in influencing venous return to the heart and in regulating distribution of oxygen and energy substrate supply to different fetal organs.

PMID: 6832717