Angioplasty of Branch Pulmonary Artery Stenosis

One of the most important areas of interventional catheterization has been the dilation and stenting of hypoplastic or stenotic branch pulmonary arteries. In patients with tetralogy of Fallot with hypoplastic pulmonary arteries, pulmonary atresia, or single ventricle with surgically induced peripheral stenoses, the use of balloon angioplasty and stenting procedures creates favorable pulmonary artery anatomy and reduces the risk of subsequent surgical repairs ( Fig. 51-18 ).

Balloon angioplasty is accomplished by tearing the vascular intima and media, allowing the vessel to remodel and heal with a larger diameter. The balloon is placed across the stenotic lesion so the middle of the balloon is at the stenosis. The balloon is inflated until the waist of the balloon is eliminated. Ideally, the most stenotic lesions are dilated first to minimize the impact on pulmonary blood flow and cardiac output. When the balloon is inflated, pulmonary blood flow is reduced, right ventricular afterload is increased, and cardiac output falls. In patients with an associated VSD or ASD, right-to-left shunting and desaturation occur with balloon inflation. Occasionally, balloon catheters must be placed across aortopulmonary shunts, significantly reducing pulmonary blood flow.

The procedure is successful in approximately 60% of patients. In an early series, complications included hypotension (40%), pulmonary artery rupture (3%), unilateral reperfusion pulmonary edema (4%), aneurysmal dilation of the dilated pulmonary vessel (8%), death (1.5%), and transient post-procedural right ventricular dysfunction.^[260] Improved techniques and patient selection have favorably influenced the results with superior balloon catheters and stents, while significantly reducing serious complications. Anesthetic support minimizes hemodynamic compromise by anticipating changes in blood flow patterns, treating transient hypotension, and providing airway support to minimize the risks associated with pulmonary artery disruption and acute unilateral pulmonary edema.^[260]