Ventricular Septal Defect

  • Ventricular Septal Defects (VSDs) involve defects of the interventricular septum and allow for inappropriate communication between the right and left ventricles.
Clinical Consequences
  • Overview
    • The quantity of shunted blood between the ventricles depends on the size of the defect and the relative resistances to blood flow into the pulmonary and systemic circulation. In general, VSDs result in holosystolic heart murmurs whose intensity in inversely proportional to the size of the defect as smaller defects result in more turbulent blood flow.
  • Small Defects
    • Small defects generally provide much higher resistances to blood flow through the defect as compared to flow through the pulmonary artery or aorta. Consequently, little blood volume is thus clinical consequences typical of shunts do not arise. However, although little blood volume is shunted through small defects, the speed of blood flow may be very high and result in a focused jet of blood emerging from the left ventricle and impacting on the right ventricular endocardium. This can lead to significant hemodynamic endocardial damage and increase the propensity for development of infective endocarditis.
  • Large Defects
    • Large defects result in a relatively low-resistance channel between the two ventricles and consequently the directionality of shunting is largely dependent on the relative resistances offered by the pulmonary and systemic circulations. During fetal life pulmonary vascular resistance is similar or higher than the systemic vascular resistance and so blood is appropriately shunted from the right to left heart as is physiological for the fetal circulation.
    • After birth the pulmonary vascular resistance drops significantly compared to the systemic vascular resistance, resulting in the development of a significant left-right shunt. Because shunted blood must ultimately return to the left heart, over time the left heart undergoes volume overload and enters a spiral of left heart failure. Additionally, through poorly-understood processes, chronically increased blood flow through the pulmonary circulation due to left-right shunting results in pulmonary hypertension which can increase the pulmonary vascular resistance beyond that of systemic vascular resistance]], ultimately yielding reversal of the shunt. This physiological scenario, termed Eisenmenger's Syndrome, yields a right-left shunt can result in hypoxemia and symptomology of cyanosis at this late stage.