ABSTRACT
We start our consideration of cardiovascular disorders with the problems of vascular occlusion.
Vascular occlusion may be arterial or venous and the effect of any occlusion will depend on the following:
Collateral vessels provide an alternative route for the blood and they are sometimes able to compensate completely, especially if the occlusion develops slowly. The venous system has more collaterals than the arterial system, e.g. there are anastomoses between the portal and systemic veins, around the lower end of the oesophagus, and also linking veins between the deep and superficial venous plexus in the leg. This means that occlusion of a deep vein in the calf does not produce haemorrhagic infarction of the foot, but just a mild oedema of the tissues and congestion of the superficial veins because of their increased flow. Unfortunately, not all veins have a collateral system. If the central vein of the retina is occluded, as may happen in thrombosis of the cavernous sinus due to local infection, the tissue of the orbit becomes oedematous and congested so that the eye is pushed forward (proptosis), and there may be local haemorrhage as the small vessels rupture because of the increased pressure. In the worst cases the venous pressure rises until it exceeds the arterial pressure and prevents arterial flow. This produces infarction, i.e. death of the tissue, and the infarcted tissue is red or purple and
swollen because of the haemorrhagic oedema. The word ‘infarction’ actually comes from the Latin ‘farcire’ meaning to stuff, and it is thought to have originally been used for the appearance of venous infarcts stuffed with blood.
