A 3-month-old infant born to non-consanguineous parents presents with a harsh holosystolic murmur best heard at the position marked **A** in the diagram. The murmur is accompanied by a palpable thrill. Chest X-ray shows cardiomegaly with pulmonary plethora. The infant is feeding poorly and has failed to gain weight appropriately. Which of the following clinical findings would you expect given the location and character of this murmur?

Explanation

## Why Left ventricular hypertrophy on ECG with evidence of volume overload is right The harsh holosystolic murmur best heard at the **lower left sternal border (LLSB)** is the classic presentation of a ventricular septal defect (VSD). The clinical picture—cardiomegaly, pulmonary plethora, poor feeding, and failure to thrive—indicates a moderate to large VSD with significant left-to-right shunt causing pulmonary overcirculation. This hemodynamic burden causes LEFT VENTRICULAR VOLUME OVERLOAD (the LV must pump both systemic and shunted pulmonary blood), resulting in LV hypertrophy on ECG. This is the expected electrocardiographic finding in moderate-to-large VSDs per Nelson 21e and Harrison 21e Ch 264. ## Why each distractor is wrong - **Right ventricular outflow tract obstruction with right axis deviation**: This describes Tetralogy of Fallot (VSD + RVOT obstruction + overriding aorta + RVH), which is a different congenital lesion. A pure VSD does not have RVOT obstruction; right axis deviation would only appear if pulmonary hypertension develops (late finding in Eisenmenger syndrome), not in the acute presentation of a moderate VSD. - **Diastolic murmur at the apex with opening snap**: This describes mitral stenosis (position **B** in the diagram—apex). A VSD produces a holosystolic murmur at the LLSB, not a diastolic murmur at the apex. - **Ejection systolic murmur at the right upper sternal border with wide fixed splitting of S2**: This describes an atrial septal defect (ASD), which produces an ejection systolic murmur at the pulmonary area (position **C**) with fixed wide splitting of S2. A VSD produces a holosystolic (pansystolic) murmur at the LLSB, not an ejection murmur. **High-Yield:** VSD at LLSB = holosystolic murmur; intensity INVERSELY correlates with defect size (small hole = loud turbulent murmur; large hole = softer murmur but more hemodynamic impact). Moderate-large VSD → LV volume overload → LVH on ECG. [cite: Nelson 21e; Harrison 21e Ch 264]