Peripheral Venous Disease Part 1

Chronic venous insufficiency and hypertension
Any condition obstructing normal venous drainage will lead to a backlog of blood
which will increase the pressure within the veins. This increased pressure will damage
the venous valves which do not have good powers of recovery. As a result an episode
of acute venous hypertension may result in a permanent reduction in the efficiency
of the venous return mechanisms. Reduced efficiency of venous return will lead to
a chronic increase in the pressure within the effected peripheral veins. These factors
explain why DVT is the most important pathogenic mechanism in the causation of
chronic venous insufficiency. This insufficiency can contribute to the development
of varicose veins and venous leg ulcers.
As a result of the venous insufficiency there is a chronic backlog of blood in
the peripheral veins. As the volume of blood in these veins increases so does
the pressure. Increased hydrostatic pressure in the veins in turn increases
hydrostatic pressure in the capillaries. Backlog of blood in the capillaries reduces
the rate of circulation as arterial blood is not able to enter efficiently. As a
result there is reduced delivery of nutrients and oxygen to the tissues as well as
inhibited removal of waste products such as carbon dioxide and nitrates.
Increased pressure in the venous ends of capillaries also reduces the rate of
reabsorption of tissue fluid; this increases the volume of tissue fluid resulting in
oedema. Oedema in tissues increases the volume of fluid through which nutrients
must diffuse in order to pass from capillary blood into the tissue cells. Also
oedematous swelling increases the diffusional distance from blood to tissue cells.
This reduces the efficiency of transporting oxygen and nutrients to cells and removing
carbon dioxide and other metabolic waste products. Both of these effects will reduce
the viability of tissue cells in the presence of oedema.
Increased pressure in a capillary will also lead to dilation of the vessel. This
will stretch the capillary walls and so widen the gaps (or pores) between individual
cells which compose the endothelial wall. Increased capillary pore size allows
larger molecules such as proteins to migrate from blood into the tissue spaces.
One of the plasma proteins is fibrinogen which can pass through the enlarged
pores. Once in the tissues fibrinogen is converted into the clotting protein
fibrin. Fibrin is composed of long sticky strands which may form a cuff around
a dilated capillary. It may be that the presence of such a ‘fibrin cuff’ further
reduces the interchange of oxygen, nutrients and waste products between capillary
blood and tissue fluids and so further reduces tissue viability.