The American College of Phlebology - Venous Anatomy = and Physiology

From: Subject: The American College of Phlebology - Venous Anatomy and Physiology Date: Sun, 21 Sep 2003 16:14:26 +0300 MIME-Version: 1.0 Content-Type: multipart/related; boundary="----=_NextPart_000_0000_01C3805B.6DB0FA00"; type="text/html" X-MimeOLE: Produced By Microsoft MimeOLE V6.00.2800.1165 This is a multi-part message in MIME format. ------=_NextPart_000_0000_01C3805B.6DB0FA00 Content-Type: text/html; charset="Windows-1252" Content-Transfer-Encoding: quoted-printable Content-Location: http://www.phlebology.org/syllabus1.htm The American College of Phlebology - Venous Anatomy = and Physiology

=20

VENOUS ANATOMY AND = PHYSIOLOGY

Excerpted from Peripheral Venous Disease=20

Craig Feied, MD, FACEP=20

Back to=20 Primer Table of Contents

=20

The peripheral venous system functions both as a = reservoir to=20 hold extra blood and as a conduit to return blood from the = periphery=20 to the heart and lungs. Unlike arteries, which possess three = well-defined layers (a thin intima, a well-developed = muscular media,=20 and a fibrous adventitia), most veins are composed of a = single=20 tissue layer. Only the largest veins possess internal = elastic=20 membranes, and at best this layer is thin and unevenly = distributed,=20 providing little buttress against high internal pressures. = The=20 correct functioning of the venous system depends on a = complex series=20 of valves and pumps that are individually frail and prone to = malfunction, yet the system as a whole performs remarkably = well=20 under extremely adverse conditions.=20

The entire cardiac output volume of 5 to 10 L/min is = received=20 into end-capillary venules for eventual delivery back to the = heart=20 and lungs. A large part of this volume passes into the = peripheral=20 venous system of the extremities, where it is received = against a=20 reverse pressure gradient, then is passed (mostly) uphill = against=20 gravity, against fluctuating thoracoabdominal pressures, and = sometimes in the face of additional back pressures such as = the=20 elevated right atrial pressures of congestive heart failure. = All of=20 this return circulation occurs with no obvious motive force. = Considered in this light, the venous system seems almost = magical in=20 its function.=20

Primary collecting veins of the lower extremity are = passive,=20 thin-walled reservoirs that are tremendously distensible. = Most are=20 suprafascial, surrounded by loosely bound alveolar and fatty = tissue=20 that is easily displaced. These suprafascial collecting = veins can=20 dilate to accommodate large volumes of blood with little = increase in=20 back pressure, so that the volume of blood sequestered = within the=20 venous system at any moment can vary by a factor of two or = more=20 without interfering with the normal function of the veins.=20 Suprafascial collecting veins belong to the superficial = venous=20 system. Outflow from collecting veins is via secondary, or = conduit,=20 veins that have thicker walls and are less distensible. Most = of=20 these veins are subfascial and are surrounded by tissues = that are=20 dense and tightly bound. These subfascial veins belong to = the deep=20 venous system.=20

The Superficial Venous System=20

The superficial venous system is a tremendously = complicated and=20 extremely variable weblike network of interconnecting veins, = most of=20 which are unnamed. A few larger truncal superficial veins = are fairly=20 constant in location; like the deep veins, these truncal = superficial=20 veins serve as a conduit to pass blood centrally and = eventually into=20 the deep venous system.=20

The principal named superficial veins of the lower = extremity are=20 the short saphenous vein (SSV), which usually runs from = ankle to=20 knee, and the greater saphenous vein (GSV), which usually = runs from=20 ankle to groin.=20

Anatomy of the Short Saphenous Vein=20

The short saphenous vein originates in the lateral foot. = It=20 passes posteriorly lateral to the Achilles tendon in the = lower calf.=20 The SSV usually lies directly above the deep fascia in the = midline=20 as it reaches the upper calf, where it enters the popliteal = space=20 between the two heads of the gastrocnemius muscles. In two = thirds of=20 cases, it joins the deep popliteal vein above the knee = joint, and in=20 one third of cases, it joins with other veins (most often = the GSV or=20 the deep muscular veins of the thigh).=20

Anatomy of the Greater Saphenous Vein=20

The GSV originates in the medial foot and passes upward = anterior=20 to the medial malleolus, then crosses the medial tibia in a=20 posterior direction to ascend in the medial line across the = knee.=20 Above the knee it continues anteromedially above the deep = fascia to=20 the thigh, where it passes through the foramen ovale and = joins the=20 (deep) common femoral vein at the groin crease. Large = branches of=20 the GSV are easily mistaken for the main trunk. Most = patients have=20 at least two major branches below the knee (the anterior and = posterior branches) and at least two above the knee (the=20 anterolateral and posteromedial branches). Up to 20% of = patients=20 have a duplicated main GSV trunk in the thigh.=20

Perforating Veins=20

Many superficial collecting veins deliver their blood = into the=20 truncal greater and short saphenous veins, which deliver = most of=20 their blood into the deep system through the saphenofemoral = junction=20 (SFJ) and the saphenopopliteal junction (SPJ). However, the = SPJ and=20 SFJ are not the only pathways from the superficial system to = the=20 deep system. Both the superficial collecting web and the = superficial=20 truncal veins are also connected to a variable number of = perforating=20 veins that pass through anatomic defects in the deep fascia = to join=20 directly with the deep veins of the calf or thigh. = Perforating veins=20 usually contain venous valves that prevent reflux of blood = from the=20 deep veins into the superficial system. A few named = perforating=20 veins are fairly constant in location and are named only as = vague=20 groupings.=20

The Deep Venous System=20

All venous blood eventually is received by the deep = venous system=20 on its way back to the right atrium of the heart. In most = cases=20 there are five major named branches to the deep venous = system, three=20 below and two above the knee. To confuse the issue, the = principal=20 deep venous trunk of the leg is called the popliteal vein = (PV) from=20 below the knee until it passes upward and anteriorly through = the=20 adductor canal in the distal thigh, where it is called the = femoral=20 vein (FV) for the remainder of its course in the thigh.=20

Deep Veins of the Calf=20

In the lower leg, three groups of deep vein exist: the = anterior=20 tibial vein (ATV), draining the dorsum of the foot; the = posterior=20 tibial vein (PTV), draining the lateral aspect of the foot. = From the=20 ankle, the anterior tibial vein passes upward anterolateral = to the=20 interosseous membrane, the posterior tibial vein passes = upward=20 posteromedially beneath the medial edge of the tibia, and = the=20 peroneal vein passes upward posteriorly through the calf. = Venous=20 sinusoids within the calf muscle coalesce to form soleal and = gastrocnemius intramuscular venous plexi, which join the = peroneal=20 vein in midcalf. In most patients, each one of these is = actually a=20 pair of veins flanking an artery of the same name; thus = there are=20 actually six named deep veins below the knee in a typical = patient.=20 Just below the knee, the four anterior and posterior tibial = veins=20 join with the two peroneal veins to become the single large=20 popliteal vein.=20

Deep Veins of the Thigh=20

The popliteal vein courses proximally behind the knee and = then=20 passes anteromedially in the distal thigh through the = adductor=20 canal, at which point it is called the FV. The PV and the FV = are one=20 and the same, and this is the largest and longest deep vein = of the=20 lower extremity. The deep femoral vein (DFV), is a short, = stubby=20 vein that usually has its origin in terminal muscle = tributaries=20 within the deep muscles of the lateral thigh, but may = communicate=20 with the popliteal vein in up to 10% of patients. In the = proximal=20 thigh, the FV and the DFV join together to form the common = femoral=20 vein (CFV), which passes upward above the groin crease to = become the=20 iliac vein. The FV is sometimes incorrectly referred to as = the=20 "superficial femoral vein" despite the fact that it is not a = part of=20 the superficial venous system.=20

The Calf Muscle Pump=20

The passage of blood upward from the feet against gravity = depends=20 on a complex array of valves and pumps. Muscle pumps of the = calf and=20 thigh provide the motive force for venous return. The most = important=20 of these is called the calf muscle pump, often referred to = as the=20 peripheral heart. The calf muscle pump is easy to understand = by=20 simple analogy to the common hand-pump bulb of a = sphygmomanometer.=20 Before pumping starts, the pressure is neutral and equal = everywhere=20 throughout the system. When the hand bulb is squeezed, the = intake=20 valve is forced closed and the outflow valve is forced open. = Air is=20 pumped into the cuff at high pressure. When the hand bulb is = allowed=20 to relax, the bulb re-expands. The outflow valve opens to = allow=20 refilling of the bulb.=20

Each segment of the calf muscle pump works in the same = way as the=20 hand bulb of the sphygmomanometer. Inflow to a segment of = deep vein=20 is through intake valves from perforating veins as well as = from the=20 deep vein segment below. Outflow is through an outflow valve = to the=20 deep vein segment above. Squeezing of the vein segment = occurs when=20 muscle contraction increases the pressure within a fascial = muscle=20 compartment. Just like a sphygmomanometer, the calf muscle = pump can=20 achieve pumping pressures of several hundred mm Hg before = valve=20 failure occurs.=20

Venous Pathology=20

Venous pathology develops when venous return is impaired = for any=20 reason. Venous pathology can be deep, superficial, or mixed. = It can=20 result from primary muscle pump failure, from venous = obstruction=20 (thrombotic or nonthrombotic), or from venous valvular = incompetence,=20 which may be segmental or whole leg. Immediately after = ambulation,=20 the normal pressure within the veins of the lower extremity = is=20 extremely low because both the superficial and deep venous = systems=20 have been emptied by a normally functioning muscle pump. = Normal=20 inflow to the lower extremity veins is purely via arterial = inflow,=20 thus the normal venous system will be more or less refilled = after 3=20 to 5 minutes of standing. When the entire venous system is = filled,=20 the valves float open and venous pressure rises to a maximum = exactly=20 equal to the height of the standing column of venous blood = from head=20 to foot. This condition triggers an urge to move the legs,=20 activating the muscle pumps and re-emptying the legs.=20

Primary Muscle Pump Failure=20

If the calf muscle pump does not work (because of muscle = wasting,=20 neuromuscular disease, deep fasciotomies, or local vein = valve=20 failure within the muscle fascia sheath), venous blood is = never=20 effectively pumped out of the distal extremity. The = immediate=20 postambulatory venous pressure will be nearly as high as the = pressure after prolonged standing. The volume of venous = blood that=20 suffuses the extremity and dilutes arterial inflow will be=20 increased. A smaller fraction of the extremity's venous = blood will=20 return to the central circulation each minute, and because = arterial=20 blood must flow into congested tissues with elevated = hydrostatic=20 pressure, the volume of arterial inflow will actually be = reduced.=20

Deep Obstruction=20

Partial obstruction of the deep veins may have little = effect on=20 venous outflow, but severe obstruction of the deep veins = produces=20 secondary muscle pump failure. In this case the muscle pump = produces=20 an appropriately high outflow pressure with each = contraction, but=20 the volume of venous blood pumped out of the calf is reduced = because=20 of the reduced diameter of the outflow tract.=20

Deep Incompetence=20

If outflow tracts are open and the muscle pump is = functional but=20 the valves of the deep veins permit reflux (because of = primary=20 agenesis, prior thrombosis, direct trauma, or dilatation = with=20 secondary valvular failure), venous blood will be pumped out = of the=20 calf in normal volumes but extremity refill will include = both normal=20 arterial inflow and pathologic venous retrograde flow. The = venous=20 pressure immediately after ambulation may be slightly = elevated or it=20 may even be normal, but the veins will refill and dilate = very=20 quickly. After a person with deep incompetence stands for = only a few=20 seconds, the venous pressure will be nearly as high as the = maximum=20 reached after prolonged standing. Again, the volume of = venous blood=20 that suffuses the extremity and dilutes arterial inflow will = be=20 somewhat increased. A smaller fraction of the extremity's = venous=20 blood will return to the central circulation each minute, = and=20 because arterial blood must flow into congested tissues with = elevated hydrostatic pressure, the volume of arterial inflow = will=20 again be somewhat reduced.=20

Perforator Incompetence=20

Under ordinary circumstances the bulk of venous blood = moves=20 strictly from the superficial to the deep system. Failure of = the=20 valves of communicating perforator veins can permit a = significant=20 volume of blood to flow from deep veins backward into the=20 superficial system, producing local congestion and venous=20 hypertension. More important, perforator incompetence allows = the=20 extremely high pressures generated within deep veins by the = calf=20 muscle pump to be communicated to the superficial veins, = which are=20 not strong enough to tolerate the pressure. This high = pressure (even=20 if intermittent and highly localized) can produce excessive = venous=20 dilatation and secondary failure of superficial vein valves. = This is=20 one of the major mechanisms for the development of = superficial=20 venous incompetence and varicose veins.=20

Superficial Incompetence=20

Superficial venous incompetence is the most common form = of venous=20 disease. Retrograde flow through the superficial venous = system=20 occurs when venous valve no longer perform their usual = function.=20 This can happen for a variety of reasons. Direct injury or=20 superficial phlebitis may cause primary valve failure. = Congenitally=20 weak vein walls may dilate under normal pressures to cause = secondary=20 valve failure, or congenitally abnormal valves may be = incompetent at=20 normal superficial venous pressures. Normal veins and normal = valves=20 may become excessively distensible under the influence of = hormones=20 (as in pregnancy). In most cases, however, superficial = venous reflux=20 is simply the inevitable end result of the introduction of = high=20 pressures into otherwise normal superficial veins that were = intended=20 to function as a low- pressure system. High pressure causes = normal=20 superficial veins to dilate so widely that the thin flaps of = venous=20 valves simply no longer meet in the midline.=20

High pressure can enter the superficial veins by failure = of key=20 valves at any point of communication between the deep and=20 superficial systems. Two clinical syndromes of high pressure = superficial system disease are recognized: junctional and=20 perforator. Junctional high-pressure disease results from = failure of=20 the primary valve at the junction between the GSV and the = CFV (the=20 SFJ), or at the junction between the SSV and PV (the SPJ). = Vein=20 dilatation in these cases proceeds from proximal to distal, = and=20 patients perceive that a large vein is "growing down to the = leg."=20 Perforator high-pressure disease results from failure of the = valves=20 of any perforating vein. The most common sites of primary = perforator=20 valve failure are at the canal of Hunter in the midproximal = thigh=20 (Hunterian vein) and in the proximal calf. If the primary=20 high-pressure entry point is distal, patients experience the = initial=20 development of large clusters of veins in the lower leg, = with large=20 veins eventually "growing up the leg" toward the groin.=20

Clinical Pathophysiology=20

A familial tendency toward development of varicose veins = is=20 understood by physicians and patients. It is felt by some to = be=20 dominant, while others believe it is a recessive trait. In = clinical=20 practice, usually 70% of patients can identify superficial = venous=20 disease as a familial trait. In addition, the severity of = venous=20 disease may also be familial. Patients whose parents had = venous=20 ulceration are at increased risk of this complication as = well.=20

Female hormonal influences on the veins are profound. For = example, when varicose veins develop in pregnancy, in 70-80% = of=20 cases, they appear in the first trimester. This development = is not=20 dependent upon size of the gravid uterus, increased blood = flow, or=20 iliac venous occlusion, but is due to the immediate rise of=20 progesterone. It has been found that diameter of the femoral = vein=20 increases by 50% within six weeks of the start of pregnancy. =

Two forces act on the hereditary/hormonal substrate to = produce=20 dilation and elongation of veins. The first, the weight of = the blood=20 column from the right atrium to the affected veins is a = constant=20 gravitational force and may be referred to as hydrostatic = pressure.=20 This is measured in millimeters of water. The Basle study=20 demonstrated that among workers in a factory, those with = standing=20 jobs were significantly more likely to have venous disease, = followed=20 by those with sitting jobs. Patients frequently comment that = the=20 adoption of a regular exercise program is followed by a = reduction in=20 their symptoms of aching and pain.=20

The second is pressure exerted by contracting muscles on = adjacent=20 veins. This may be called a hydrodynamic force. This = pressure,=20 measured in millimeters of mercury (13 times heavier than = water)=20 propels blood through open deep valves toward the heart. = However,=20 when valves in perforating veins fail, this force is exerted = on=20 subcutaneous veins and venules in the epidermis in a = pulsatile=20 fashion coincident with muscular contraction. It is no = wonder that=20 they become elongated and tortuous and that venous dilation = causes=20 their valves to fail in turn.=20

In summary, it follows that telangiectasias, reticular=20 varicosities, and varicose veins are derived from a=20 hereditary/hormonal substrate which is acted upon by static=20 gravitational pressure and dynamic muscular forces = transmitted=20 through failed venous valves. While neither the hereditary = nor the=20 hormonal substrate can be altered by intervention, the = influence of=20 hemodynamic forces and hydrostatic pressure can be modified = by=20 intervention.=20

References=20

1. Widmer LK: Peripheral Venous Disorders: Prevalence and = Socio-Medical Importance, Bern 1978, Hans Huber.=20

Back to=20 Primer Table of Contents

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