In tricuspid atresia (TA) there is no communication between right atrium (RA) and right ventricle (RV) due to absent tricuspid valve. The floor of RA may be muscular or membranous. Blood flows from RA through the interatrial communication to LA then to LV and aorta and from LV to pulmonary artery through VSD. Interatrial communication is obligatory. Anatomy beyond mitral valve determines type of TA and clinical features. In Type I there is normally related great arteries, in Type II there is d-transposition and in Type III there is l-transposition. When ventricular septum is intact, there is pulmonary atresia (low pulmonary flow with severe cyanosis and duct dependent pulmonary flow) and when VSD is large, there is no pulmonary stenosis (large pulmonary flow with heart failure). TA usually consists of a restrictive VSD, pulmonary stenosis and normally related great arteries (Type 1b). Cyanotic infants are symptomatic from infancy with or without CHF depending upon size of VSD and severity of pulmonary stenosis. LV apex, single S2, Ejection systolic murmur over left sternal border with ECG showing left axis and left ventricular hypertrophy are diagnostic features. Echocardiographic features are absence of communication and flow from RA to RV, interatrial communication with right to left shunt. VSD size, severity of PS and great arterial relations are also well demonstrated by Echo. Severely cyanotic newborns may require prostaglandin E1 infusion or ductal stenting before subjecting for surgery. Cavo-pulmonary shunt, Hemi-Fontan or modified Fontan operations are the surgical options for treatment.