Ventricular septal defects
Clinical presentation depends largely on VSD size and pulmonary physiology. An unrestrictive VSD is one that allows the free flow of blood from LV into PA (via the RV) without pressure restriction.
- RV systolic pressure in unrestrictive VSDs is by definition systemic.
- Flow-through large VSDs may be restricted by TV tissue or trabeculations.
- The pathophysiology of a VSD is related to (1) elevated pulmonary artery pressure (since aorta=LV=RV=PA pressure during systole if VSD is unrestrictive), (2) elevated pulmonary artery flow, and (3) left ventricular volume loading (since the LV performs the stroke work of all blood pumped across the VSD as well as normal cardiac output; the RV serves as an LV-PA connection). When severe, these lead to pulmonary edema and clinical heart failure, cardiomegaly, LA enlargement, left bronchial compression. The pulmonary lymphatics become congested with lung water, which may increase the risk of infection.
- Symptoms include tachypnea, growth failure, feeding intolerance.
- Medical treatment often includes diuretics.
- The timing of surgery is determined by symptoms (and therefore the size of the defect). Typically large defects present in the first 6 weeks to 2 months of life. Preterm infants often become symptomatic earlier.
Repair of VSDs
Technical. Closure of VSD is typically performed through TV, including the takedown of the septal leaflet for inlet defects. Small patch margin leaks are common in defects around conduction tissue due to interrupted sutures used to avoid heart block. Bypass in uncomplicated VSDs is typically brief and bleeding is typically minimal in the virgin chest.
Physiology. Closure of a VSD results in several immediate improvements in physiology. The left (LV) to right (PA) shunt is significantly decreased (or removed completely). This lowers PA pressure, as well as LA pressure and LVEDP due to the significant reduction in LV volume load. The presence of LV dysfunction on postoperative echo is common due to this acute reduction in LV preload and resolves over time. Because the circulation is significantly more efficient following VSD closure, postoperative hypertension is common.
•Assessment for residual VSD includes: echocardiogram sweeps of the ventricular septum, direct stick for RV pressure (presuming that RVP decreases when VSD is closed and that there is not pulmonary vascular HTN), LA pressure (to the extent that a VSD is an LV volume load), and increase in oxygen saturations between RA and PA (i.e. step-up on ‘sat run’); a PA saturation >10% points higher than RA sat may be clinically significant.
Postoperative course. Heart block may occur following repair of membranous defects, though this is typically transient. Junctional rhythm may also occur due to the proximity of conduction tissue to surgical stretching of the TV annulus during closure.
•Residual elevation in PA pressure following VSD closure (i.e. pulmonary HTN) may occur in older patients or in those with prematurity or chromosome disorders. These patients should be weaned more slowly, care taken during suctioning, and consideration is given to iNO use.
•The presence of pre/postoperative pulmonary edema is very common. However, most patients who were not intubated preoperatively are able to be extubated soon after VSD closure. Pulmonary edema resolves over time. Patients with intercurrent illness (e.g. viral infection) may take longer to extubate, and may have symptoms of pulmonary hypertension. Patients with other associated defects (e.g. CoA) may have restrictive LV physiology, LA hypertension, and a protracted postoperative course.