VENOUS PATHOPHYSIOLOGY

VENOUS PATHOPHYSIOLOGY

The purpose of the venous system is primarily to return blood back to the heart so that it can be delivered into the pulmonary circulation. The venous system contains approximately 60% of the total blood volume, with an average pressure of around 5–10 /uni00A0 mmHg. Mechanical factors, alongside the autonomic nervous and endocrine systems, control the rate at which - blood is delivered to the right atrium. Through its e ff ects upon myocardial contractility via the Starling mechanism, venous return is one of the factors responsible for determining cardiac output. teral Blood enters the lower limb through the femoral arteries before passing through arterioles into the capillaries, which have a pressure of about 32 /uni00A0 mmHg at their arterial ends. This pressure is reduced along the course of the capillaries and is approximately 12 /uni00A0 mmHg at the venular end of the capillary . The pressure continues to fall in the main veins, and is as low as 5 /uni00A0 mmHg at the upper end of the vena cava where it enters the right atrium. The venous pressure in a foot vein on standing is equiv alent to the height of a column of blood extending from the heart to the foot, e.g. approximately 100 /uni00A0 mmHg. To enable blood to be returned against gravity in the standing position a pressur e gradient must exist between the veins in the leg and those in the chest. This gradient is created in two ways. First, the increase in thoracic volume during inspiration decreases intrathoracic pressure. Second, the pressure in the veins of the leg is increased by compression by the surrounding mus cles (the ‘calf muscle pump’) and to a lesser extent the tone of the venous wall. The deep veins of the calf are capacious and are joined by blind-ending sacks called the soleal sinusoids, which force b lood into the popliteal and crural veins during calf muscle pump contraction, e.g. walking. The foot pump also ejects blood from the plantar veins during walking. As the calf muscles contract, the veins are compressed and the valves only allow blood to pass in the direction of the heart. The pressure within the calf compartment rises to 200–300 /uni00A0 mmHg during muscle contraction. Rapid blood flow in the deep veins at junctions and perforators draws blood from the superficial veins, driving this up the deep veins also. During muscle relax ation, the pressure falls and further blood from the superficial veins enters the deep vein. Each time this occurs the pressure falls in the superficial venous compartment until a thr is reached, when the venous inflow keeps pace with ejection from the deep veins. This is normally around 30 /uni00A0 mmHg, a fall of approximately two-thirds of the resting venous pressure. The net reduction in the pressure of the superficial system is Rudolf Virchow , 1821–1902, pathologist, Charité Hospital, Berlin, Germany , was the first to be credited with describing iliac vein compression. It was not until 1957 that May and Thurner (Innsbruck, Austria) clearly described compression of the left common iliac vein by the right common iliac artery . leg and the thorax and a patent and compliant venous system containing competent valves ( Figure 62.2 ). An absence of one or more of these results in venous hypertension, which leads to further vein wall damage, including loss of compliance, thickening, dilatation and valvular dysfunction. This venous damage goes on to reduce the function of the a ff ected veins, worsening the venous hypertension in a vicious cycle. When exposed to high venous and capillary pressures chronically , the soft tissues of the leg will be damaged, causing a spectrum of damage that becomes irreversible. The causes of venous hypertension are listed in Table 62.1 . /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF The majority of patients with venous disease have a problem primarily with the vein wall structure and in most this is confined to the superficial veins. Little is known about the mechanism of initiation of the changes in the vein wall. These changes are complex, but are typified by valvular failure allowing retrograde flow within the vein with gravity - (venous incompetence). It is no longer thought that venous incompetence is caused by a primary mechanical valvular failure. eshold The vein wall changes include inflammatory cell infiltration and activation, dysfunctional smooth muscle cell proliferation, collagen deposition, decreased elastin content and increased matrix metalloproteinases. These e ff ects typically lead to loss

limb Standing 80 70 60 50 40 30 Normal limb 20 Foot vein pressure (mmHg) 10 Walking Standing 0 0 10 20 30 40 Time (seconds) Figure 62.2 Effect of exercise on the super /f_i cial venous pressure in health and disease. The light blue line demonstrates the reduction in pressure primarily related to the action of the calf muscle pump. The dark blue line demonstrates how venous dysfunction is associated with reduced net antegrade /f_l ow during exercise, resulting in a relative increase in venous pressure when compared with normal (venous hypertension). TABLE 62.1 Factors causing venous hypertension. Pressure gradient dysfunction Increased abdominal or thoracic pressure COPD Pregnancy Obesity Large tumour Constipation Decreased calf muscle pump function Immobility Ankle joint fusion Paralysis Dysfunction of the venous system Venous structural de /f_i cit Valvular agenesis Valvular incompetence Venous dilatation Venous tortuosity Loss of vein wall compliance Loss of venous tone Arteriovenous /f_i stula Venous occlusion Agenesis Thrombosis Iatrogenic/trauma Venous compression May–Thurner syndrome Pelvic/abdominal tumour Pelvic/abdominal radiotherapy COPD, chronic obstructive pulmonary disease.

of compliance, dilatation, elongation (causing tortuosity) and secondary valvular dysfunction. This process can be initiated anywhere in the venous tree. Secondary varicose veins may develop in patients with post-thrombotic limbs and in patients with congenital abnormalities such as the Klippel–Trénaunay syndrome or multiple arteriovenous fistulae. The extent and number of incompetent veins governs the extent of the venous hypertension and correlates with the severity of the soft-tissue complications seen. Importantly however, neither the reflux burden nor the presence of skin changes, short of ulceration, correlate with the presence or degree of symptoms.

Figure 62.3 Varicose veins: (a) left leg varicose veins in the distribution of an incompetent great saphenous vein (marked for intervention); /uni00A0 (b) right leg varicose veins in the distribution of the small saphenous system with a recent episode of phlebitis; distribution of an isolated incompetent anterior accessory of the great saphenous vein with associated gaiter area skin changes.