Tricuspid atresia pathophysiology: Difference between revisions
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'''Associate Editor-In-Chief:''' [[User:KeriShafer|Keri Shafer, M.D.]] [mailto:kshafer@bidmc.harvard.edu] [[Priyamvada Singh|Priyamvada Singh, MBBS]] [[mailto:psingh@perfuse.org]] | |||
'''Assistant Editor-In-Chief:''' [[Kristin Feeney|Kristin Feeney, B.S.]] [[mailto:kfeeney@perfuse.org]] | |||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 12:49, 22 July 2011
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor-In-Chief: Keri Shafer, M.D. [2] Priyamvada Singh, MBBS [[3]]
Assistant Editor-In-Chief: Kristin Feeney, B.S. [[4]]
Pathophysiology
This defect occurs during prenatal development. Because of the lack of an A-V connection, an atrial septal defect (ASD) must be present to maintain blood flow. Also, since there is a lack of a right ventricle there must be a way to pump blood into the pulmonary arteries, and this is accomplished by a ventricular septal defect (VSD).
Blood is mixed in the left atrium. Because the only way the pulmonary circulation receives blood is through the VSD, a patent ductus arteriosus is usually also formed to increase pulmonary flow.
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