Tricuspid atresia pathophysiology: Difference between revisions

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*The classic term of [[tricuspid atresia]] was used firstly by schuberg in 1861.<br />
*The classic term of [[tricuspid atresia]] was used firstly by schuberg in 1861.<br />
==Overview==
[[Tricuspid atresia]] occurs during [[prenatal]] development. In [[tricuspid atresia]], there is no continuity between the [[right atrium]] and [[right ventricle]]. [[Inferior vena cava]] and [[superior vena cava]] collect venous [[nonoxygenated blood]] into the [[right atrium]]. Through [[atrial septal defect]] (ASD), [[ blood ]] come into the [[left atrium]], then [[left ventricle ]]and[[ aorta]].This [[blood]] is a mixture of saturated and unsaturated O2. If there is a [[ventricular septal defect ]](VSD), this mixed blood in the [[left ventricle]] flows into the [[right ventricle]], then via [[pulmonary artery]] reaches [[pulmonary bed]] and becomes [[oxygenated]], then returns back into the [[left atrium]] via[[ pulmonary veins]]. In diminished [[pulmonary blood flow]] whether the flow is dependent on [[patent ductus arteriosus]] (PDA), the mixed-blood in [[aorta]] flows from this passage into[[ pulmonary artery]] and [[pulmonary bed]]. In the presence of normal positioning of [[great arteries]], [[cyanosis]] is more prominent and is affected by the size of [[ VSD]]. [[Transpositioning great arteries]] (TGA) and [[subaortic stenosis]] are other associated anomalies.


==Pathophysiology==
==Pathophysiology==

Latest revision as of 15:16, 8 November 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Sara Zand, M.D.[2] Keri Shafer, M.D. [3] Priyamvada Singh, MBBS [4]; Assistant Editor-In-Chief: Kristin Feeney, B.S. [5]


Overview

Tricuspid atresia was first discovered by Friedrich Ludwig kreysig in 1817, a German physician who found the obstruction between the right atrium and right ventricle in the autopsy of cyanotic infants. The classic term of tricuspid atresia was used firstly by schuberg in 1861

Historical perspective

  • Tricuspid atresia was first discovered by Friedrich Ludwig kreysig in 1817, a German physician who found the obstruction between the right atrium and right ventricle in the autopsy of cyanotic infants.


Overview

Tricuspid atresia occurs during prenatal development. In tricuspid atresia, there is no continuity between the right atrium and right ventricle. Inferior vena cava and superior vena cava collect venous nonoxygenated blood into the right atrium. Through atrial septal defect (ASD), blood come into the left atrium, then left ventricle andaorta.This blood is a mixture of saturated and unsaturated O2. If there is a ventricular septal defect (VSD), this mixed blood in the left ventricle flows into the right ventricle, then via pulmonary artery reaches pulmonary bed and becomes oxygenated, then returns back into the left atrium viapulmonary veins. In diminished pulmonary blood flow whether the flow is dependent on patent ductus arteriosus (PDA), the mixed-blood in aorta flows from this passage intopulmonary artery and pulmonary bed. In the presence of normal positioning of great arteries, cyanosis is more prominent and is affected by the size of VSD. Transpositioning great arteries (TGA) and subaortic stenosis are other associated anomalies.

Pathophysiology

Normal Human Heart

Caption:Anterior (frontal) view of the opened heart. White arrows indicate normal blood flow. (Tricuspid valve labeled at bottom left.)
Caption:Anterior (frontal) view of the opened heart. White arrows indicate normal blood flow. (Tricuspid valve labeled at bottom left.)


Tricuspid Atresia


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Classification

Tricuspid atresia is classified according to the connection between ventricles with greatarteries (aorta, pulmonary) into two subgroups:[1]


References

  1. ASTLEY R, OLDHAM JS, PARSONS C (July 1953). "Congenital tricuspid atresia". Br Heart J. 15 (3): 287–97. doi:10.1136/hrt.15.3.287. PMC 479498. PMID 13059216.
  2. Rao PS (January 2009). "Diagnosis and management of cyanotic congenital heart disease: part I". Indian J Pediatr. 76 (1): 57–70. doi:10.1007/s12098-009-0030-4. PMID 19391004.

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