Register for email alerts and news feeds:
This journal | BMJ Group
rss
Heart 2005;91:871-873; doi:10.1136/hrt.2004.047399
Copyright © 2005 BMJ Publishing Group Ltd & British Cardiovascular Society
Heart 2005;91:871-873
© 2005 by BMJ Publishing Group & British Cardiac Society

MINI-SYMPOSIUM

Response of the fetal heart to changes in load: from hyperplasia to heart failure

H M Gardiner

Correspondence to:
Correspondence to:
Dr Helena M Gardiner
Institute of Reproductive and Developmental Biology, Faculty of Medicine, Imperial College, Queen Charlotte’s and Chelsea Hospital, Du Cane Road, London, W12 ONN, UK; helena.gardiner@imperial.ac.uk

Keywords: fetal heart; hyperplasia; heart failure

The first 150 words of the full text of this article appear below.

The fetal circulation works in parallel with the dominant right ventricle, ejecting approximately 60% of the combined ventricular output. Three important communications exist between the two circulations (oval foramen and the arterial and venous ducts) that influence loading conditions. In particular, the determinants of fetal left ventricular filling differ considerably from those seen in the adult heart. Pulmonary venous return contributes only a small proportion to left ventricular preload because of the relatively low pulmonary blood flow in fetal life (rising from an estimated 11% to 25% of right ventricular output by the third trimester).1 Left ventricular filling depends predominantly on patency of the oval foramen to allow the relatively oxygen-rich blood returning from the placental circulation, via the umbilical vein and venous duct, to stream through the right atrium and enter the left side of the heart.2 The right ventricle fills from mostly upper body systemic venous return and . . . [Full text of this article]


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

This article has been cited by other articles:

  • Gardiner, H M (2009). The case for fetal cardiac intervention. Heart 95: 1648-1652 [Abstract] [Full Text]  
  • Gardiner, H. M., Belmar, C., Tulzer, G., Barlow, A., Pasquini, L., Carvalho, J. S., Daubeney, P. E.F., Rigby, M. L., Gordon, F., Kulinskaya, E., Franklin, R. C. (2008). Morphologic and Functional Predictors of Eventual Circulation in the Fetus With Pulmonary Atresia or Critical Pulmonary Stenosis With Intact Septum. J Am Coll Cardiol 51: 1299-1308 [Abstract] [Full Text]  
  • van den Wijngaard, J. P. H. M., Westerhof, B. E., Faber, D. J., Ramsay, M. M., Westerhof, N., van Gemert, M. J. C. (2006). Abnormal arterial flows by a distributed model of the fetal circulation. Am. J. Physiol. Regul. Integr. Comp. Physiol. 291: R1222-R1233 [Abstract] [Full Text]  

eLetters:

Read all eLetters

Physiological fetal to neonatal transition is safer.
David J R Hutchon, et al.
Online, 4 Sep 2008 [Full text]

This Article

Services
Citing Articles
Google Scholar
PubMed
Topic Collections
Bookmark with

Register for free content

The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.