Abnormal arterial flows by a distributed model of the fetal circulation

Wijngaard, Jeroen P. H. M. van den; Westerhof, Berend E.; Faber, Dirk J.; Ramsay, Margaret M.; Westerhof, Nico; Gemert, Martin J. C. van

doi:10.1152/ajpregu.00212.2006

Cited by 38 publications

(44 citation statements)

References 62 publications

(89 reference statements)

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“…First, our pulse arterial propagation model (48), and second, our TTTS model with nonpulsating circulations (46). The resulting new model incorporates 13 differential equations for each twin, coupled by the net fetofetal transfusion of blood volume and blood constituents, i.e., colloids, osmoles, and vasoconstrictive peptides.…”

Section: Methodsmentioning

confidence: 99%

“…As described previously (48,54,55), the fetal arterial tree was constructed using 13 viscoelastic tubes representing the arteries and 9 three-element windkessels representing the peripheral organ beds. Details on anatomical parameters, i.e., arterial lengths and radii, wall thicknesses and viscoelastic wall properties, and blood viscosity, all as a function of gestational age, were adapted from the literature (20,32,48). The model uses a normal cardiac flow waveform entering the ascending aorta.…”

Section: Methodsmentioning

confidence: 99%

“…One computer run took ϳ2.5 min on a Pentium 4.8 GHz personal computer. Details of the model can be found elsewhere (48).…”

Section: Methodsmentioning

confidence: 99%

“…We recently modeled (48) pulsating arterial flow of the fetoplacental circulation, using viscoelastic tube segments and three-element windkessels to simulate the arteries and fetal organs, respectively. In the present study, we sought to extend the TTTS model, including our model of pulsating arterial circulations and multiple cardiovascular parameters, to simulate the onset and development of abnormal umbilical arterial pulsations (stage III) and to examine the progression of TTTS from stage 1 to stage IV in relation to the placental angioarchitecture.…”

mentioning

confidence: 99%

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A mathematical model of twin-twin transfusion syndrome with pulsatile arterial circulations

Wijngaard¹,

Westerhof²,

Ross³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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December 7, 2006; doi:10.1152/ajpregu.00534.2006.-The twin-twin transfusion syndrome (TTTS) is a severe complication of monochorionic twin pregnancies caused by a net transfusion of blood from one twin (the donor) to the other (the recipient) through placental anastomoses. To examine the pathophysiology of TTTS evolving through clinical stages I to IV, we extended our mathematical model to include pulsating circulations propagating along the arterial tree as well as placental and cerebral vascular resistances, and arterial wall thickness and stiffness. The model demonstrates that abnormal umbilical arterial flow (TTTS stage III) in the donor twin results from increased placental resistance as well as reduced resistance in the cerebral arteries. In contrast, recipient twin abnormal umbilical arterial flow requires a significantly greater increase in placental resistance, resulting from the compressive effects of high amniotic fluid pressure. Thus simulated abnormalities of donor umbilical arterial pulsations occur in the donor more commonly and earlier than in the recipient. The "normal" staging sequence (I, II, III, IV) correlates with the presence of compensating placental anastomoses, constituting the majority of monochorionic twin placentas. However, TTTS stage III may occur before manifestations of stage II (lack of donor bladder filling), in our model correlating with severe TTTS from a single arteriovenous anastomosis, an infrequent occurring placental angioarchitecture. In conclusion, this mathematical model describes the onset and development of the four stages of TTTS, reproduces a variety of clinical manifestations, and may contribute to identifying the underlying pathophysiology of the staging sequence in TTTS. stage III; quintero staging sequence IN THE UNITED STATES, about 10% of all monochorionic twin pregnancies, resulting in ϳ3,000 fetal twin pairs each year, develop twin-twin transfusion syndrome (TTTS). Caused by uncompensated fetofetal transfusion through a placental arteriovenous (AV) connection from one twin (the donor) to the other (the recipient), TTTS often leads to intrauterine fetal death or premature delivery (24, 49). TTTS severity can be mitigated by other, compensating anastomoses, which return part of the AV transfusion back to the donor twin [i.e., opposite arteriovenous (VA), arterioarterial (AA) (45), and venovenous (VV) anastomoses].TTTS is believed to progress through four worsening stages of severity with both twins alive (36). Stage I TTTS is diagnosed by the oligo-polyhydramnios sequence, where the donor has almost no amniotic fluid and the recipient simultaneously has excess amniotic fluid. More severe stages of TTTS often develop subsequently: stage II includes lack of donor bladder filling; stage III, abnormal umbilical flows in either twin (i.e., reduced or reversed end-diastolic flow) (21); and stage IV, congestive cardiac failure and hydrops in the recipient.The syndrome has a largely inaccessible pathophysiology, because invasive fetal study is unethical and an ani...

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…One computer run took ϳ2.5 min on a Pentium 4.8 GHz personal computer. Details of the model can be found elsewhere (48).…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

A mathematical model of twin-twin transfusion syndrome with pulsatile arterial circulations

Wijngaard¹,

Westerhof²,

Ross³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

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“…Hence, the use of a mathematical model is very helpful in the assessment of fetal well-being. Computational studies based on mathematical models of fetal cardiovascular blood flow redistribution [28,29] are already present. Some are based on fetal lamb circulation [30].…”

Section: Introductionmentioning

confidence: 99%

Simulation and Analysis of Umbilical Blood Flow using Markov-based Mathematical Model

Queyam¹,

Pahuja²,

Singh³

2017

IJISA

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Abstract-The intra-uterine development of the fetus depends on various factors, one such critical factor is umbilical blood flow because the quantity of oxygen delivered to the placenta and to the fetus is directly limited by umbilical blood flow rate. Since the measurement of the hemodynamic quantities such as blood pressure and blood flow rate is not possible in utero hence the use of patient-specific mathematical modeling is beneficial for the assessment of feto-maternal wellbeing. A Markov model based mathematical model of fetal circulation is developed by taking three node concept. The fetus, the umbilical cord, and the placenta represent the 3 nodes of Markov model. A LabVIEWbased virtual instrument is designed to simulate the mathematical model which results in waveform similar to Doppler blood flow velocimetry of umbilical artery. The model is simulated at various degree of conductivity of the umbilical cord to the oxygenated blood. Simulation results show that the umbilical artery blood flow velocity waveform depends on gestation age, fetal heart rate, uterine contraction and placental insufficiency. The Doppler indices calculated from simulation helps in predicting both fetal and maternal abnormalities at various degrees of the conductivity to the blood flow passage. Therefore, integrating patient-specific models along with established medical equipments will be helpful in identifying true intra-uterine growth restricted fetuses from normal fetuses and helps clinicians to take timely interventions.

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Hypothesized pathogenesis of acardius acephalus, acormus, amorphus, anceps, acardiac edema, single umbilical artery, and pump twin risk prediction

Gemert

Ross

Wijngaard

et al. 2021

Birth Defects Research

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Background: Acardiac twinning complicates monochorionic twin pregnancies in ≈2.6%, in which arterioarterial (AA) and venovenous placental anastomoses cause a reverse circulation between prepump and preacardiac embryos and cessation of cardiac function in the preacardiac. Literature suggested four acardiac body morphologies in which select (groups of) organs fail to develop, deteriorate, or become abnormal: acephalus (≈64%, [almost] no head, part of body, legs), amorphus (≈22%, amorphous tissue lump), anceps (≈10%, cranial bones, well-developed), and acormus (≈4%, head only). We sought to develop hypotheses that could explain acardiac pathogenesis, its progression, and develop methods for clinical testing.Methods: We used qualitatively described pathophysiology during development, including twin-specific AA and Hyrtl's anastomoses, the short umbilical cord syndrome, high capillary permeability, properties of spontaneous aborted embryos, and Pump/Acardiac umbilical venous diameter (UVD) ratios. Results:We propose that each body morphology has a specific pathophysiologic pathway. An acephalus acardius may be larger than an anceps, verifiable from UVD ratio measurements. A single umbilical artery develops when one artery, unconnected to the AA, vanishes due to flow reduction by Hyrtl's anastomotic resistance. Acardiac edema may result from acardiac body hypoxemia combined with physiological high fetal capillary permeability, high interstitial compliance and low albumin synthesis. Morphological changes may occur after acardiac onset. Pump twin risk follows from UVD ratios. Conclusion:Our suggested outcomes agree reasonably well with reported onset, incidence, and progression of acardiac morphologies. Guidance for clinical prediction and testing requires ultrasound anatomy/circulation study, from the first trimester onward.

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Abnormal arterial flows by a distributed model of the fetal circulation

Cited by 38 publications

References 62 publications

A mathematical model of twin-twin transfusion syndrome with pulsatile arterial circulations

A mathematical model of twin-twin transfusion syndrome with pulsatile arterial circulations

Simulation and Analysis of Umbilical Blood Flow using Markov-based Mathematical Model

Hypothesized pathogenesis of acardius acephalus, acormus, amorphus, anceps, acardiac edema, single umbilical artery, and pump twin risk prediction

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