Peripheral venous pressure is regulated by central and
peripheral mechanisms. Peripheral venous hypertension is an
important pathologic component of chronic venous disease and
is present in about two-third of patients with chronic venous
disease. It can result from reflux, obstructive lesions or high
arterial inflow. The dominant influence in patients with
peripheral venous hypertension appears to be obstruction
rather than reflux. Reflux can be superficial or deep or both. In
about 70% of patients with reflux, valvular incompetence is
present in the superficial, deep and perforator systems in some
combination. In an ex vivo experimental model, conduit pressure
increased with smaller native or functional caliber, focal
stenosis and increased post-capillary inflow. Venous pressure
in the lower limb can be measured in a variety of ways: supine
resting pressure, erect resting pressure and ambulatory venous
pressure. These measurements are affected by factors such as
intra-abdominal pressure, intra-thoracic pressure, gravity,
venoarteriolar reflux, valve reflux and venous obstruction.
Venous obstruction is associated with elevated supine
pressures while reflux is associated with elevated erect resting
and ambulatory venous pressures. Ambulatory venous pressure
reflects venous hypertension in patients with advanced venous
disease. However, our investigation has shown that ambulatory
venous pressure hypertension is rarely present if air
plethysmography testing is negative. Consideration maybe given
to the omission of the ambulatory venous pressure testing if air
plethysmography testing is normal.
The inability of venous occlusion air plethysmography to identify patients who will benefit from stenting of deep venous obstruction
