Tricuspid atresia pathophysiology: Difference between revisions
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{{CMG}}; '''Associate Editor-In-Chief:''' {{Sara.Zand}} [[User:KeriShafer|Keri Shafer, M.D.]] [mailto:kshafer@bidmc.harvard.edu] [[Priyamvada Singh|Priyamvada Singh, MBBS]] [mailto:psingh13579@gmail.com]; '''Assistant Editor-In-Chief:''' [[Kristin Feeney|Kristin Feeney, B.S.]] [mailto:kfeeney@elon.edu] | {{CMG}}; '''Associate Editor-In-Chief:''' {{Sara.Zand}} [[User:KeriShafer|Keri Shafer, M.D.]] [mailto:kshafer@bidmc.harvard.edu] [[Priyamvada Singh|Priyamvada Singh, MBBS]] [mailto:psingh13579@gmail.com]; '''Assistant Editor-In-Chief:''' [[Kristin Feeney|Kristin Feeney, B.S.]] [mailto:kfeeney@elon.edu] | ||
==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 == | == 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. | *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.<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== | ||
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* [[Inferior vena cava]] and [[superior vena cava]] collect venous [[nonoxygenated blood]] into the [[right atrium]]. | * [[Inferior vena cava]] and [[superior vena cava]] collect venous [[nonoxygenated blood]] into the [[right atrium]]. | ||
* Through [[atrial septal defect]] (ASD)[[ blood ]] | * 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. | * This [[blood]] is a mixture of saturated and unsaturated O2. | ||
| Line 33: | Line 41: | ||
* 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 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]]. | * 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. | * [[Transpositioning great arteries]] (TGA) and [[subaortic stenosis]] are other associated anomalies. | ||
| Line 44: | Line 52: | ||
== Classification == | == Classification == | ||
Tricuspid atresia is classified according to connection between ventricles with great arteries(aorta, pulmonary) into two subgroups: | [[Tricuspid atresia]] is classified according to the connection between [[ventricles]] with great[[ arteries]] ([[aorta]], [[pulmonary]]) into two subgroups:<ref name="pmid13059216">{{cite journal |vauthors=ASTLEY R, OLDHAM JS, PARSONS C |title=Congenital tricuspid atresia |journal=Br Heart J |volume=15 |issue=3 |pages=287–97 |date=July 1953 |pmid=13059216 |pmc=479498 |doi=10.1136/hrt.15.3.287 |url=}}</ref> | ||
* Normal connection between [[ventricles]] with the [[aorta ]]and [[pulmonary artery]] which is the common type and is consistent with 70%-80% of cases. Most patients are [[ cyanotic]].<ref name="pmid19391004">{{cite journal |vauthors=Rao PS |title=Diagnosis and management of cyanotic congenital heart disease: part I |journal=Indian J Pediatr |volume=76 |issue=1 |pages=57–70 |date=January 2009 |pmid=19391004 |doi=10.1007/s12098-009-0030-4 |url=}}</ref> | |||
* | * [[Aorta]] originated from small [[right ventricle]] and the [[ pulmonary artery ]]comes from the [[ left ventricle]]. [[Heart failure]] and [[pulmonary hypertension ]] are common and patients are not [[cyanotic]]. Flow in the [[aorta]] is dependent on [[ventricular setrum defect]]([[VSD]]) size. [[Subaortic stenosis]] and [[aortic arch]] anomalies are common. | ||
* Aorta originated from small | |||
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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.
- The classic term of tricuspid atresia was used firstly by schuberg in 1861.
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
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Tricuspid Atresia
{{#ev:youtube|BsvdUEbHyDE}}
- 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.
Classification
Tricuspid atresia is classified according to the connection between ventricles with greatarteries (aorta, pulmonary) into two subgroups:[1]
- Normal connection between ventricles with the aorta and pulmonary artery which is the common type and is consistent with 70%-80% of cases. Most patients are cyanotic.[2]
- Aorta originated from small right ventricle and the pulmonary artery comes from the left ventricle. Heart failure and pulmonary hypertension are common and patients are not cyanotic. Flow in the aorta is dependent on ventricular setrum defect(VSD) size. Subaortic stenosis and aortic arch anomalies are common.
References
- ↑ 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.
- ↑ 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.