HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Corrected Table A corrigendum has been published All Versions of this Article: 291/5/R1222    most recent 00212.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by van den Wijngaard, J. P. H. M. Articles by van Gemert, M. J. C. Search for Related Content PubMed PubMed Citation Articles by van den Wijngaard, J. P. H. M. Articles by van Gemert, M. J. C.

TRANSLATIONAL PHYSIOLOGY

Abnormal arterial flows by a distributed model of the fetal circulation

¹Laser Center and Department of Obstetrics and Gynecology, ²BMEYE Cardiovascular Monitoring Company, and ³Laser Center, Academic Medical Center, University of Amsterdam, Amsterdam; ⁴Department of Obstetrics and Gynecology, Queen's Medical Centre, Nottingham, United Kingdom; and ⁵Laboratory for Physiology, Institute for Cardiovascular Research, Vrije Universiteit, University Medical Center, Amsterdam, The Netherlands

Submitted 24 March 2006 ; accepted in final form 8 June 2006

ABSTRACT

Modeling the propagation of blood pressure and flow along the fetoplacental arterial tree may improve interpretation of abnormal flow velocity waveforms in fetuses. The current models, however, either do not include a wide range of gestational ages or do not account for variation in anatomical, vascular, or rheological parameters. We developed a mathematical model of the pulsating fetoumbilical arterial circulation using Womersley's oscillatory flow theory and viscoelastic arterial wall properties. Arterial flow waves are calculated at different arterial locations from which the pulsatility index (PI) can be determined. We varied blood viscosity, placental and brain resistances, placental compliance, heart rate, stiffness of the arterial wall, and length of the umbilical arteries. The PI increases in the umbilical artery and decreases in the cerebral arteries, as a result of increasing placental resistance or decreasing brain resistance. Both changes in resistance decrease the flow through the placenta. An increased arterial stiffness increases the PIs in the entire fetoplacental circulation. Blood viscosity and peripheral bed compliance have limited influence on the flow profiles. Bradycardia and tachycardia increase and decrease the PI in all arteries, respectively. Umbilical arterial length has limited influence on the PI but affects the mean arterial pressure at the placental cord insertion. The model may improve the interpretation of arterial flow pulsations and thus may advance both the understanding of pathophysiological processes and clinical management.

pulsatility index; fetal pulsating arterial blood flow; mathematical model

This article has been cited by other articles:

				J. P. H. M. van den Wijngaard, B. E. Westerhof, M. G. Ross, and M. J. C. van Gemert A mathematical model of twin-twin transfusion syndrome with pulsatile arterial circulations Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2007; 292(4): R1519 - R1531. [Abstract] [Full Text] [PDF]