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Feature
Acyanotic Congenital Heart Disease
Cyanotic Congenital Heart Disease
Primary
Mechanism
Typically involves Left-to-Right shunts (oxygenated blood flows back to the lungs) or Obstructive lesions without shunts.
Typically involves Right-to-Left shunts (deoxygenated blood bypasses the lungs and enters the systemic circulation).
Cyanosis
(Clinical)
Absent initially.
Present (usually evident when arterial saturation is ≤85%).
Type of
Cyanosis
If cyanosis develops late (e.g., Eisenmenger's syndrome), it is Central Cyanosis.
Primarily Central Cyanosis.
Physiological
Effect
Increased pulmonary blood flow and volume overload of certain chambers (e.g., RV enlargement in ASD).
Systemic hypoxemia due to desaturated venous blood entering the arterial circulation.
Onset of
Symptoms
Often asymptomatic until adulthood (e.g., ASD) or symptoms related to heart failure (VSD, PDA).
Symptoms, such as anoxic spells and severe dyspnea, may present anytime after birth or later in infancy.
Late Progression
Risk
Left-to-right shunts (ASD, VSD, PDA) can lead to severe Pulmonary Hypertension (PHT) and subsequent shunt reversal (Right-to-Left flow), resulting in late cyanosis (known as Eisenmenger’s syndrome or cyanosis tardive).
Shunting usually dictates cyanosis early, and the degree of cyanosis in conditions like Tetralogy of Fallot depends on the severity of the obstruction to right ventricular outflow.
Examples of
Conditions
With Shunts: Ventricular septal defect (VSD), Atrial septal defect (ASD), Patent ductus arteriosus (PDA).
Without Shunts: Aortic stenosis, Coarctation of aorta.
With Shunts: Tetralogy of Fallot, Transposition of great vessels, Tricuspid atresia, Epstein’s anomaly, Truncus arteriosus, Total anomalous pulmonary venous communication.
Without Shunts: Pulmonary stenosis.

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