Cyanotic versus Acyanotic Congenital Heart Disease - Emergency Medicine
This section summarises the pathophysiology, typical lesions, emergency department (ED) recognition, immediate stabilisation and escalation priorities for cyanotic and acyanotic congenital heart disease (CHD). It emphasises newborn screening context, practical bedside checks and the temporising measures an ED clinician must be prepared to start before specialist arrival.
Definitions and key mechanisms
- Cyanotic CHD: lesions that allow deoxygenated venous blood to enter the systemic circulation (right→left shunt), causing low arterial oxygen saturation and central cyanosis. Many present in the neonatal period; some are duct‑dependent.
- Acyanotic CHD: lesions characterised by left→right shunts or obstructive lesions that preserve systemic oxygenation but cause pulmonary overcirculation, heart failure and later complications. Cyanosis may occur only after pulmonary vascular disease with shunt reversal (Eisenmenger).
Representative lesions (common, ED‑relevant)
- Cyanotic: Tetralogy of Fallot (TOF), transposition of the great arteries (TGA), tricuspid atresia, Ebstein’s anomaly, hypoplastic left heart syndrome (HLHS).
- Acyanotic: Ventricular septal defect (VSD), atrial septal defect (ASD), patent ductus arteriosus (PDA), atrioventricular septal defect (AVSD), pulmonary/aortic stenosis, coarctation of the aorta.
How they present in the ED
- Neonates: central cyanosis, tachypnoea, poor feeding, lethargy, poor perfusion. Duct‑dependent lesions frequently deteriorate as the ductus arteriosus closes (typically within the first days of life).