holosystolic murmur in VSD

Septal defects at the ventricular level create a left-sided volume load because blood traversing the defect in systole is entrained into right ventricular outflow and returns to the left atrium, and thus the left ventricle is recirculating volume. Right ventricular afterload is increased by the augmented flow. This differs from atrial septal defects, in which left-to-right flow creates right-sided volume load.

Ventricular septal defects typically present with a harsh holosystolic murmur, and a parasternal thrill can be present as well. The intensity of the murmur depends on the size of the defect and the pressure gradient across it. Elevated right ventricular pressure decreases the gradient across the defect and thus diminishes the volume of the murmur; as such, a very loud murmur reflects normal right ventricular pressure (choice A is correct). Pulmonary hypertension decreases the gradient and the murmur (choice D is incorrect). In large (nonrestrictive) defects, pressures in the right and left ventricles equalize; flow is determined by the relative resistance in the pulmonary and systemic circuits, so flow across the defect is not turbulent and thus is not loud (choice B is incorrect). In fact, small shunts may have very turbulent flow and present with a loud murmur. The intensity of the murmur is not dependent on the location of the defect (choice C is incorrect).

Ventricular septal defects can be congenital, but in the ICU, most ventricular septal defects are acquired in the setting of acute myocardial infarction. Understanding their physiology and the importance of right ventricular function to prognosis can be important.123

Footnotes

  1. SEEK Questionnaires ↩

  2. Fuster V, Brandenburg RO, McGoon DC, et al. Clinical approach and management of congenital heart disease in the adolescent and adult. Cardiovasc Clin. 1980;10(3):161-197. PubMed ↩

  3. Perloff JK, Marelli AJ. Ventricular septal defect. In: Perloff JK, Marelli AJ, eds. Perloff’s Clinical Recognition of Congenital Heart Disease. 6th ed. Philadelphia, PA: WB Saunders;2012:283-315. ↩