23 Superior Vena Cava Syndrome

3. Pathophysiology 

The pathogenetic basis of SVCS is obstruction to the blood flow. It can result from 

intrinsic or extrinsic obstacles. The former are uncommon and are represented by 

thrombosis or invading tissue. Extrinsic factors develop from compression or stricture of 

the vein.  

In physiologic conditions, blood return to the right atrium is facilitated by the pressure 

gradient between the right atrium and venae cavae. When obstruction of the SVC occurs, the 

vascular resistances rise and the venous return decreases. SVC pressure may increase 

consistently [4]. 

When SVC shows a significant stenosis (3/5 of the lumen or more), blood flow is redirected 

through the collateral circulation in order to bypass the obstruction and restore the venous 

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return [5]. The timing of the obstruction development is important for its clinical 

implications. In acute impairments, the blood flow is not rapidly distributed through the 

collateral network so symptoms arise markedly. In the case of slow-growing diseases, the 

collateral venous network has enough time to expand in order to receive the circulating 

volume. For this reason, long-lasting, severe SVC obstruction can sometimes be found 

without significant related signs and symptoms [3,6].