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Cardio defect embryo

Membranous VSD Faulty formation of membranous VSD. L-->R shunt, with pulmonary HTN and excessive fatigue, exertion
Eisenmenger Occurs because of faulty VSD which leads to increased in pulmonary HTN. This leads to narrowing of pulmonary arteries. R--> L shunt develops with cyanosis
Muscular VSD Single/multiple perforations in the musclar IV septum
Common ventircle (cor triocularare biatrium) failure of the membranous/muscular IV to form
X-ray of VSD increased size of pulmonary artery and cardiomegaly
ASD findings S1 with fixed split S2, L--> R shunt
Foramen primum defect failure of the AV septum to fuse with the septum primum (abnormal mitral valve)
Tricuspid atresia AV defect (hypoplastic right heart). Insufficient amount of tissue to form tricuspid valve causing complete agenesis of the tricuspid valve . Cyanosis, patent foramen ovale, IV septal defect occurs
Ebstein's anomaly failure in the development of the tricuspid valve
Persistant truncus arteriosus AP septum doesn't completely form. Both ventricles pump into the aortic arch
D-Transposition of vessels Co-truncal septum fails to follow its normal spiral course and runs straigt down. Aorta orignates from R. Ventricle, pulmonary artery originates form L. ventricle. Ductus arteriosus remains open.
L-transposition of vessels Left and right ventricle are mixed up. Normal blood flow occurs
Tetrology of fallot Unequal divison of conus. Reuslts in 4 CV alterations: 1) narrow r. ventricle outflow tract (pulmonary infundibular stenosis), 2) hypertrophy of the R. ventricle wall because of higher pressure on R. Side, 3) IV defect, 4) overriding aorta (more to r)
Created by: ddecampo



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