Cyanotic congenital heart disease is defined by structural lesions that deliver deoxygenated systemic venous blood to the systemic arterial circulation, producing hypoxemia that supplemental oxygen cannot correct (a failed hyperoxia test) because the defect is anatomic shunting or circulatory separation rather than impaired alveolar gas exchange. Truncus arteriosus exemplifies the mixing-lesion mechanism: failure of conotruncal septation leaves a single arterial trunk with a single semilunar valve overriding a ventricular septal defect, so one common vessel supplies both pulmonary and systemic circulations from blood of intermediate saturation. Transposition of the great arteries exemplifies the parallel-circulation mechanism: ventriculoarterial discordance places the aorta off the right ventricle and the pulmonary artery off the left ventricle, so the pulmonary and systemic circuits run in parallel rather than in series and survival depends entirely on an intercirculatory communication (patent ductus arteriosus, VSD, or ASD). Both belong to pediatric cardiology's classification of the five cyanotic lesions, where anatomy predicts saturation physiology, radiographic silhouette, and definitive surgical repair.
Cyanotic congenital heart disease is defined by structural lesions that deliver deoxygenated systemic venous blood to the systemic arterial circulation, producing hypoxemia that supplemental oxygen c…