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20 Development and anatomy of thevenoussystem
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Intersaphenous v.
Cranial extension
of the small saphenous v.
Great
saphenous v.
Saphenous n.
Medial
gastrocnemius
perforators
Small
saphenous v.
Figure 2.8 Posterior superficial and perforating veins of
the leg.
Popliteal v.
Lateral sural
cutaneous n.
Lateral
gastrocnemius
perforators
Sural n.
Lateral leg perforators
Dorsal venous arch
Lateral ankle
perforator
lateralvenous system. e lateral venous system is drained
through multiple small tributaries into the GSV and SSV or
through PVs into the deep system.
In the supercial veins, bicuspid valves secure unidirectional venous blood ow towards the heart. ere are more
constant valves, which are usually located at the termination
of the major venous trunks. ese valves have strong, white
cusps and marked sinusoid dilatation of the venous wall at
the origin of the valves. Other valves are delicate, almost
transparent structures. In the GSV, there are usually at least
six valves (maximum: 14–25). A constant valve is present
in the GSV within 2–3 cm of the saphenofemoral junction
in about 85% of veins.30 e frequency of valves is greater
below than above the knee. In the SSV, valves are numerous
(median: 7–10, range: 4–13) and more closely spaced. e
highest valve is usually situated close to the termination of
the SSV. Valves in communicating tributaries between the
two saphenous veins are always oriented in order to direct
blood from the SSV to the GSV.
Small supercial veins and venules, even those with a
diameter of <2 mm, may contain valves.
31,3 2
ese valves
likely play an important role in the development of the skin
changes in chronic venous insuciency.
9
2.2.4 Deep veins of the leg
Femoral v.
Perforators of the
femoral canal
Popliteal v.
Soleal v.
Paratibial
perforators
Soleal v.
Posterior tibial vv.
Posterior
tibial
perforators
Medial ankle
perforator
Medial plantar v.
Figure 2.9 Deep veins of the lower extremities.
Upper
Middle
Lower
Anastomosis to
deep femoral v.
Small saphenous v.
Medial and lateral
gastrocnemius vv.
Anterior tibial vv.
Soleal vv.
Peroneal vv.
Lateral leg
perforators
Lateral plantar v.
Deep veins accompany their corresponding arteries,
frequently in a paired fashion. On the sole, the richly anastomosing deep plantar venous arch collects blood from
the toes and the metatarsals. e deep plantar venous arch
continues into the medial and lateral plantar veins, which
become the posterior tibial veins behind the medial ankle
(Figure 2.9). On the dorsum of the foot, the major deep
veins—the dorsalis pedis veins—continue into the anterior
tibial veins.
In the calf, the paired posterior tibial veins run between
the edges of the exor digitorum longus and tibialis posterior muscles and under the fascia of the deep posterior
compartment (Figure 2.10). ey drain the muscles of the
deep and supercial posterior compartments and are connected to the GSV and posterior accessory saphenous vein
by perforators. e posterior tibial veins pierce the soleus
muscle close to its bony adherence (soleal arcade) and continue into the popliteal vein. e anterior tibial veins ascend
in the anterior compartment. Distally, there is a constant
connection between the anterior tibial and the peroneal
veins. e peroneal veins originate in the distal third of the
calf and ascend deep to the exor hallucis longus muscle.
ey receive the peroneal perforators and several large veins
from the soleus muscle. e anterior tibial and peroneal
veins form the short tibio-peroneal trunk, which joins the
posterior tibial veins to form the popliteal vein.
e popliteal and femoral veins are usually duplicated
in segments of various lengths and form a plexus around
the corresponding arteries similarly to the deep veins of the
calf (Figure 2.9). e gastrocnemius vein and the SSV are
2.2 Anatomy 21
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Lower posterior
tibial perforator
Great saphenous vein
Paratibial
perforator
PTVs
Posterior accessory
great saphenous vein
Middle posterior
tibial perforator
Figure 2.10 Relationship of the medial direct perforating veins to the deep and superficial posterior fascial compartments.
PTV: posterior tibial veins; SPC: superficial posterior fascial compartment.
SPC
Upper posterior
tibial perforator
PTVs
PTVs
SPC
SPC
the main tributaries of the popliteal vein. In the adductor
canal, the popliteal vein becomes the femoral vein and runs
initially lateral and then medial to the femoral artery. e
femoral vein unites with the profunda femoris (deep femoral) vein at about 9 cm below the inguinal ligament. In the
adductor canal or sometimes more distally, there is a consistent (~84%) anastomosis between the profunda femoris
and the femoral or popliteal veins that provides an important collateral channel in case of deep venous thrombosis.
e common femoral vein is the continuation of the femoral vein aer it joins the deep femoral vein. e GSV empties into the common femoral vein at the saphenofemoral
junction. Further tributaries of the common femoral vein
are the lateral and medial circumex femoral veins, which
can anastomose with the internal iliac vein. e common
femoral vein is medial to the corresponding artery and ends
at the inguinal ligament, where it continues as the external
iliac vein.
e frequency of valves in deep veins increases in the
proximal to distal direction. Deep veins of the foot, the posterior and anterior tibial, and the peroneal veins are profusely valved, containing valves at about 2-cm intervals.
e popliteal vein and the most distal part of the femoral
vein usually have one or two valves. ere are three or more
additional valves in the femoral vein, up to the junction
with the profunda femoris vein. One of these valves is consistently (~90%) found just distal to this junction.33 In the
common femoral vein, there is usually only one valve. It is
important to emphasize that in the external iliac and common femoral veins proximal to the saphenofemoral junction, there is only one valve or, in 37% of cases, there is no
valve at all. ecommon iliac and cava veins are valveless.
2.2.5 Perforating veins
ere are more than 150 PVs in the lower extremities;
however, the medial PVs are most signicant and have
been the center of debate for decades.
34–42
eir role in the
development of chronic venous insuciency and venous
ulcers is still not well dened. Signicant variation exists
in the location of leg perforators; however, the distribution
of clusters of PVs follows a predictable pattern (Table 2.2).
Dorsal, plantar, medial, and lateral foot perforators are the
main groups of PVs in the foot. A large PV runs between
the rst and second metatarsal bones and connects the
supercial dorsal venous arch to the pedal vein. e clusters of PVs at the ankle are the anterior, medial, and lateral
ankle perforators. e medial calf perforators exist in two
groups: posterior tibial and paratibial PVs. ree groups
(lower, middle, and upper) posterior tibial PVs (Cockett
I–III perforators) connect the posterior accessory GSV to
the posterior tibial veins (Figure 2.10). e paratibial perfo-
rators drain the GSV into the posterior tibial veins. Other
perforators of the leg below the knee are the anterior, lateral, medial, and lateral gastrocnemius, intergemellar, and
Achillean PVs. Infra- and supra-patellar and popliteal fossa
PVs are located around the knee. Perforators of the femoral
canal connect tributaries of the GSV to the femoral vein
(Figure 2.8). Inguinal perforators drain into the femoral
vein in the proximal thigh.
2.2.6 Venous sinuses of calf muscles
Venous sinuses are thin-walled, large veins in the calf
muscles, which have a capacity to hold great volumes of
22 Development and anatomy of thevenoussystem
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Table 2.2 Studies on the location of direct medial perforating veins in the leg
Number of legs Location of medial perforating veins
First author
(year)
Linton (1938) 10 50 Distal third of the leg Middle third of
Sherman (1948) 92 901 13.5 cm 18.5 cm 24 cm, 30 cm, 35 cm,
Cockett (1953) 21 201 13–14 cm 16–17 cm At the knee
O’Donnell (1977) – 39 Half of the incompetent PVs are between 10
Fischer (1992) – 194 Random distribution of incompetent PVs
Mózes (1996) 40 – 7–9 cm
Note: PV: perforating vein.
a
Distances measured from the sole.
b
Distances measured from the lower tip of the medial malleolus.
Anatomic
dissections
Surgical
findings Cockett II Cockett III Proximal paratibial PVs
the leg
and 15 cm
b
(15–20 cma)
b
(12–14 cma) 10–12 cmb
(15–17 cm
a
)
a
Proximal third of the leg
40 cm
Few incompetent PVs
b
18–22 cm
28–32 cm
(28–32 cm
, 23–27 cmb,
b
(23–27 cma),
a
), (33–37 cma)
venous blood. ey are embedded in skeletal muscles,
which contract rhythmically during ambulation; therefore, they serve as “chambers” of the “peripheral heart,”
the calf muscle pump. e soleus muscle is particularly
rich in venous sinuses; it may contain one to 18 of such
sinuses. ey are less developed in the gastrocnemius muscle. Venus sinuses are lled from the supercial veins and
from the reticular venous plexus through indirect, muscular perforators and from the muscles through postcapillary venules and small muscular veins. Venous sinuses of
the soleus muscle are drained into the posterior tibial and
peroneal veins by the soleus veins (Figure 2.9). e soleus
veins are large, short, and tortuous in order to accommodate the considerable range of muscular movements. In
the lower third of the leg, the soleus veins frequently join
directly into PVs before entering the deep veins. Bilateral
gastrocnemius veins draining the two heads of the gastrocnemius muscle usually empty into the popliteal vein,
distal to the conuence of the SSV with the popliteal trunk
(Figure 2.9). e venous sinuses themselves are valveless;
however, the small intramuscular veins linking them
and the muscular veins draining venous sinuses into the
deep veins contain numerous valves. Indirect PVs feeding venous sinuses are also valved. Valvular competence
plays a critical role in the ecient functioning of the calf
muscle pump.
2.2.7 Veins of the abdomen and pelvis
e external iliac vein begins at the inguinal ligament,
courses along the pelvic brim, and ends anterior to the
sacroiliac joint by joining the internal iliac to form the
common iliac vein.
epigastric, the deep circumex iliac, and the pubic veins,
which freely anastomose with the corresponding supercial
veins and with the obturator vein. e internal iliac vein is
43
Its tributaries are the (deep) inferior
a short trunk that is formed by the union of its extra- and
intra-pelvic tributaries. e extrapelvic tributaries are the
gluteal (superior and inferior), the internal pudendal, and
the obturator veins. e gluteal veins anastomose with
the medial circumex femoral vein and receive numerous
PVs from the corresponding supercial veins (Figure2.11).
e intrapelvic tributaries of the internal iliac vein, such
as the lateral sacral and several visceral (middle rectal,
vesical, uterine, and vaginal) veins, drain the presacral
venous plexus and the pelvic visceral plexuses (rectal, vesical, prostatic, uterine, and vaginal). ese plexuses and the
additional supercial (pudendal) plexus provide free communication for venous ow between the two sides of the
44
pelvis.
e common iliac veins begin at the sacroiliac joints
and form a conuence at the right side of the h lumbar
vertebra to form the inferior vena cava. e only tributary of the right common iliac vein is the right ascending lumbar vein, whereas the le drains the median sacral
vein as well. e ascending lumbar vein runs vertically
along the vertebral column, collects blood from lumbar veins, and proximally anastomoses with the azygos
system.
e inferior vena cava ascends on the right side of the
vertebral column and terminates in the right atrium very
shortly aer passing through the diaphragm (Figure 2.11).
Its tributaries are the lumbar veins, the right gonadal vein,
the renal veins, and the right suprarenal, the right inferior
phrenic, and the hepatic veins. e le gonadal and suprarenal veins join the le renal vein, and the le inferior phrenic
vein opens into the le suprarenal vein. In case of inferior
vena cava obstruction, anastomoses between the veins of
the chest and abdominal wall (thoraco-epigastric, internal
thoracic, and epigastric veins), the lumbar–azygos connections, and the vertebral plexuses can provide important
collateral avenues.
2.2 Anatomy 23
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Sup.
intercostal
v.
Arch of the
azygos v.
Azygos v.
Inf. vena cava
R. gonadal v.
Left innominate v.
Subclavian v.
Renal v.
Common
iliac v.
Int. iliac v.
Presacral
plexus
Gluteal v.
T12
Int. jugular v.
Cephalic v.
Sup.
vena
cava
Accessory
hemiazygos
Hemiazygos v.
L. gonadal v.
Ascending
lumber v.
Lumber vv.
Medial
sacral v.
Lat.
sacral v.
Obturator v.
Ext.
iliac v.
v.
Axillary v.
Cephalic v.
Cephalic v.
Basilic v.
Median cubital v.
Basiclic v.
Median v. of forearm
Visceral
plexus
Superficial plexus Profunda femoris v.
Great saphenous v.
Medical circumex v.
Femoral v.
Common
femoral
v.
Figure 2.11 Major veins of the pelvis, abdomen, and
thorax.
2.2.8 Veins of the upper extremity
andthethorax
2.2.8.1 UPPER EXTREMITY VEINS
Venous return from the arm is mostly maintained by the
functioning of the heart. Valves do not play an important
role in this venous circulation. e deep veins of the arm are
paired and follow their corresponding arteries. Perforators
between the deep and supercial veins are less numerous
inthe arm than in the leg.
e supercial veins of the upper limb are the cephalic
and basilic veins and their tributaries (Figure 2.12). e
dorsal venous plexus of the hand continues into the cephalic
Figure 2.12 Superficial veins of the upper extremity.
vein on the radial and into the basilica vein on the ulnar
side. e cephalic vein begins at the “anatomical snu box,”
courses over the distal radius to the ventral aspect of the
forearm, and ascends on the lateral side of the arm and
in the deltopectoral groove. It enters the infraclavicular
fossa, pierces the clavipectoral fascia, and empties into the
axillary vein. e basilic vein ascends on the ulnar side of
the forearm, perforates the deep fascia about midway in the
arm, and, aer receiving the deep brachial vein, it continues
into the axillary vein. e median cubital vein connects the
cephalic and basilic veins in front of the elbow. Variations
are common, including the presence of additional major
venous trunks, such as the accessory cephalic or antebrachial veins. e deep veins (radial, ulnar, brachial, and axillary
veins) are usually paired and follow the course of the main
arteries of the arm.
e axillary vein begins at the lower border of the teres
major, which corresponds with the lateral border of the
scapula on an anteroposterior chest roentgenogram. At
the outer border of the rst rib, it becomes the subclavian,
24 Development and anatomy of thevenoussystem
(b
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which ends at the medial border of the scalenus anterior
muscle, where it joins the internal jugular vein to form the
brachiocephalic vein. e brachiocephalic (innominate)
vein begins behind the sterno-clavicular joint. e le
brachiocephalic vein descends obliquely to join the right
one. Constant tributaries of the brachiocephalic vein are the
vertebral, internal thoracic, and inferior thyroid veins.e
superior intercostal vein drains the upper intercostal veins
and opens into the brachiocephalic vein on the le, whereas
on the opposite side it joins the azygos vein.
e superior vena cava is formed behind the rst right
costal cartilage by the union of the brachiocephalic veins.
It descends right of the ascending aorta and opens into the
right atrium at the level of the third right costal cartilage.
Halfway along its length, before it enters the pericardium,
itreceives the azygos vein from behind.
2.2.8.2 AZYGOS VEINS
e origin of the azygos vein is not constant. It may arise
from the back of the inferior vena cava at the level of the
renal veins or it may be the continuation of the right ascending lumbar vein (Figure 2.11). e azygos vein ascends on
the right side of the body until the fourth thoracic vertebra
and then passes anteriorly to join the superior vena cava.
Major tributaries of the azygos vein are the right superior
intercostal, the hemiazygos, and the accessory hemiazygos veins. e hemiazygos vein courses on the le side of
the vertebral column and its origin is similar to that of the
azygos vein. At the level of the eighth thoracic vertebra, it
crosses the column and joins the azygos vein. Oen, the
le renal vein communicates with the hemiazygos vein.
e accessory hemiazygos vein descends le to the vertebral column and parallel with the azygos vein. Proximally,
it anastomoses with the le brachiocephalic vein and ends
distally when it joins to the azygos or the hemiazygos veins
at the level of the seventh thoracic vertebra. e azygos veins
drain the intercostal veins on both sides, receive several visceral tributaries, and freely anastomose with the vertebral
venous plexuses. e azygos veins and their tributaries provide important collateral circulation in the face of superior
or inferior vena cava obstruction.
(a)
)
Figure 2.13 Proximal (a) and distal (b) aspects of a venous
valve (stereo microscopy, magnification: ×14).
2.3 HISTOLOGY
e venous wall is three layered: intima, media, and adven-
45,46
titia.
endothelial cells resting on scant connective tissue. e
e intima uniformly consists of a single layer of
internal elastic lamina, a layer of thick elastic bers at the
base of the intima, is frequently incomplete in mediumsized veins and absent in smaller ones. Venous valves are
bicuspid infoldings of the intima covered by endothelium on both sides, with an intervening connective tissue
skeleton(Figures 2.13a,b and 2.14). At the origin of valves,
the veins may be focally distended, forming small sinusoid
dilation, probably in response to the hemodynamic consequences of focally reversed ow.
Figure 2.14 Histology of a venous valve (orcein,
magnification: ×2.5).
e media is composed of layers of smooth muscle
cells and connective tissue. e relative thickness of the
media and the proportions of the two major components
vary considerably with dierent sizes and functions. e
major supercial veins, such as the greater and lesser
References 25
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saphenous, have thick muscular media, providing the
ability to contract and to resist the development of varicosities. Tributaries of the saphenous veins have thinner
media and can become more easily varicosed. e media
of the deep veins of the calf contain as much smooth muscle as saphenous veins; however, their collagen content
e adventitia is poorly demarcated and contains loose
connective tissue with lymphatics, vessels (vasa vasorum),
and adrenergic nerve bers. e GSV is ensheathed in
further layers of brous tissue associated with the deep
fascia, which makes this vein even more resistant to the
development of varicosities.
47
is higher, resulting in a more rigid wall. e larger deep
veins ( femoral, iliac, axillary, subclavian, and innominate) contain less smooth muscle cell mass, and the almost
complete lack of these cells in the media of the caval veins
is remarkable.
Guidelines 1.1.0 of the American Venous Forum on the development and anatomy of the venous system
No. Guideline
1.1.1 The main deep vein of the thigh between the popliteal and the common femoral
1.1.2 The main superficial veins of the lower limbs are the great saphenous vein and the
1.1.3 The old terms “Cockett” and “Giacomini” veins should be replaced by the new
20
vein is the femoral vein. The old term “superficial femoral vein” should be
abandoned.
small saphenous vein.
terms “posterior tibial perforating vein” and “intersaphenous vein,” respectively.
The use of eponyms is discouraged.
ACKNOWLEDGMENT
e author would like to acknowledge the major contribution of the late Dr. Geza Mozes to this chapter.
Grade of recommendation
(1:strong; 2: weak)
1
1
1
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38. O’Donnell TF, Burnand KG, Clemenson G, Thomas
ML, and Browse NL. Doppler examination vs.
clinical and phlebographic detection of the location of incompetent perforating veins. Arch Surg
1977;112:31–5.
39. May R. Nomenclature of the surgically most important connecting veins. In: May RPH, Staubesand
J, eds. Perforating Veins. Baltimore, MA: Urban &
Schwarzenberg, 1981, 13–8.
40. Fischer R, Fullemann HJ, and Alder W. About a phlebological dogma of the localization of the Cockett
perforators [in French]. Phlébologie 1992;45:207–12.
41. Mozes G, Gloviczki P, Menawat SS, Fisher DR,
Carmichael SW, and Kadar A. Surgical anatomy for
endoscopic subfascial division of perforating veins.
JVasc Surg 1996;24:800–8.
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42. Mozes G, Gloviczki P, Kadar A, and Carmichael SW.
Surgical anatomy of perforating veins. In: Gloviczki P,
Bergan JJ, eds. Atlas of Endoscopic Perforator Vein
Surgery. London: Springer-Verlag, 1998, 17–28.
43. Gabella G. Venous system. In: Gray’s Anatomy,
38th Ed. New York, NY: Churchill Livingstone, 1995,
1574–605.
44. Mavor GE and Galloway JM. Collaterals of the deep
venous circulation of the lower limb. Surg Gynecol
Obstet 1967;125:561–71.
45. Patrick JG. Blood vessels. In: Strenberg SS, ed.
Histology for Pathologists. New York, NY: Raven
Pres s, 1992, 195–213.
46. Parum DV. Histochemistry and immunochemistry
of vascular disease. In: Stehbens WE, Lie JT, eds.
Vascular Pathology. London: Chapman & Hall, 1995,
313 –27.
47. Thomson H. The surgical anatomy of varicose veins.
Phlebologie 1982;35:11–8.
The physiology and hemodynamics of the
https://t.me/med1917
normal venous circulation
FRANK T. PADBERG JR.
3
3.1 Introduction 27
3.2 Venous return 27
3.3 Physiologic components of the return circulation 28
3.4 The peripheral muscle pump mechanism 31
3.1 INTRODUCTION
Venous disorders have been recognized since antiquity, and
advances in physiology and diagnosis have led to improved
understanding and therapy over the past 150 years.
Anatomy and function are better appreciated now from
the perspective of twentieth-century testing modalities.
Studies from the middle of the twentieth century assessed
useful and unique physiological concepts. Although somewhat limited by the available diagnostic modalities of the
time, small sample sizes, and minimal descriptive statistics, these studies continue to oer valuable physiologic and
hemodynamic data on normal individuals. Ambulatory
pressure manometry, dynamic phlebography, plethysmographic evaluations, color ow duplex ultrasound, intravenous ultrasound, computed tomography, and magnetic
resonance venography have contributed substantially to the
advancement of current knowledge. Detailed discussions
of the major pathological conditions aecting the venous
circulation—obstruction and reux—will be found in later
chapters.
e primary purpose of the venous circulation is to
return blood to the heart for reoxygenation and recirculation. Understanding volume and pressure relationships is
essential for understanding normal and abnormal venous
function. e enormous capacity of the venous reservoir
plays a major role in the maintenance of cardiovascular
homeostasis by accommod ating volume shis. Regulation of
venous tone is an important aspect of volume accommodation and works in concert with arterial control mechanisms
that eect changes in the distribution of cardiac output.
Sympathetic-mediated adjustments of smooth muscle tone
3.5 Physiologic compensations 34
3.6 Summary 35
References 37
are most pronounced in the splanchnic and cutaneous distributions, which are also the most densely innervated. In
the upright posture, the physiological eects of gravity and
hydrostatic pressure would appear to oppose return ow,
but these eects are largely oset by competent valvular
function and an ecient peripheral pump mechanism.
3.2 VENOUS RETURN
Venous return is dened as the rate of blood ow toward
the heart, which in homeostatic circumstances must equal
cardiac output. It is expressed as volume per unit time and
varies with age, gender, and physical conditioning. Mean
human resting cardiac output (5040 mL/minute) is the
product of stroke volume (70 mL) and heart rate (72 bpm).1
Increasing ber length (volume) or heart rate will increase
cardiac output.
Active venoconstriction of capacitance vessels was once
thought to have been a major contributor to changes in
cardiac output. e accumulated evidence has now demonstrated that reex-mediated control of the resistance
(precapillary) vessels is the major determinant of the distribution of the circulation.
ity and posture, 60%–80% of human resting blood volume
(70 mL/kg in men and 65 mL/kg in women) resides in the
venous system. A total of 25%–50% of this volume resides
in the smaller post-capillary venules and their collecting systems. Approximately 25% (18 mL/kg) resides in the
splanchnic network.
e interaction of multiple components is required for
eective venous return, involving a central pump, a pressure gradient, a peripheral venous pump, and venous valves.
1–3
2–4
However, depending on activ-
27
28 The physiology and hemodynamics of the normal venous circulation
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3.2.1 Central
Blood moves through both arteries and veins because of the
pumping action of the heart. Venous ow follows a dynamic
pressure gradient toward the entry port of the central
pump—the right atrium. In the normal individual, atrial
pressures of 4–7 mmHg are relatively constant, regardless
of position. When supine, pressures at the venular end of
the capillary bed are estimated to be 12–18 mmHg, which
is consistent with the venous pressure measured in ankle
5–8
veins.
us, ow moves toward the lower pressures of
the right atrium. Pressures in the upper extremity in the
upright posture are increased by approximately 6 mmHg
at the level of the rst rib.
1,6
In an upright posture, with a
raised arm, gravitational or hydrostatic forces propel upper
extremity and cerebral blood toward the heart. e pliable
venous wall collapses above the height of the central venous
pressure, a fact that is utilized clinically during bedside
estimation of the height of distention in the external jugular vein. Whether standing or sitting, gravity is additive to
both arterial and venous pressures in the lower extremity.
However, since the force of gravity is equilibrated between
the arterial and venous circulation, it is not a signicant
factor when considering the pressure gradients inuencing
venous return in the normal lower extremity.
Venous return is enhanced by negative and neutral (usually 0 mmHg) intra-abdominal and intrathoracic pressures. Nevertheless, during inspiration, the increase in
intra-abdominal pressure causes a transient reduction in
ow from the lower extremities to the right atrium by acting as an external compressive force on ow through a collapsible tube such as the inferior vena cava (IVC).
9
Chronic,
sustained elevation of intra-abdominal pressure occurs
with clinical conditions such as ascites and morbid obesity;
venous pressure in the lower extremities must rise above
this chronically elevated pressure to eect ow through an
IVC that has collapsed because of external pressure.
In normal circumstances, a pressure gradient begins at
12–18 mmHg at the venous end of the capillary, and falls
steadily to 5.5 mmHg in the extrathoracic great veins.10
When blood reaches the right atrium, it is actively pulled
into the pump, oxygenated in the pulmonary circuit, and
recirculated. Since there are no valves in the large venous
conduits, the pathophysiologic consequences are generally
those of obstruction to venous ow. e consequences of
elevated central venous pressures are characterized by congestive heart failure, ascites, Budd–Chiari syndrome, morbid obesity, and superior vena cava syndrome.
3.2.2 Peripheral
Venous return from the dependent lower extremity is
achieved by active pumping of the calf muscle assisted by
competent venous valves. Normal valve closure eectively
prevents retrograde ow of blood. In the normal lower
extremity, venous return is primarily a function of the deep
veins. Valves are distributed throughout upper and lower
extremity veins, and are more numerous in the more distal
segments. e anatomic distribution and extent of valvular
incompetence that are necessary to produce clinical symptoms remain incompletely understood. As might be anticipated, the greater the valvular dysfunction or reux, the
greater the likelihood of symptoms from peripheral venous
insuciency arising.
11–15
e plantar venous plexus probably serves to ll or prime
the calf pump. Since most investigators have focused on the
calf pump, the role of the foot and thigh components are less
well dened. e calf pump is very ecient in the normal
limb; however, it is unknown whether or how it might compensate for deciencies such as outow obstruction, proximal
valvular failure, distal valvular failure, or muscle weakness.
3.3 PHYSIOLOGIC COMPONENTS OF THE
RETURN CIRCULATION
e prominent roles of hydrostatic pressure and capacitance
are unique to the venous circulation. Both interact with
other physiologic and hemodynamic factors to exert a variable inuence relative to circumstances such as posture, volume depletion, physical exercise, and ambient temperature.
Adrenergic-mediated reexes largely control the splanchnic circulation. Responding to local, hormonal, and reex
stimuli, blood ow to the skin and skeletal muscle uctuates
over a wide range.
2–4,16,17
3.3.1 Hydrostatic and dynamic pressure
relationships
Although local venous pressure varies with the recumbent, sitting, and standing positions, venous ow still follows a pressure gradient. e peripheral calf muscle pump
is eective at returning venous blood, but it only functions
when there are active muscle contractions. When active
movement is articially constrained, capacitance increases
and pressure slowly rises to that produced by gravity—the
hydrostatic pressure. Sustained exposure to elevated hydrostatic pressures is transmitted to the capillary bed, where the
balance of ltration favors transudation into the extracellular uid. Transient inactivity of the calf muscle pump may
lead to edema in otherwise normal individuals when the
extremity is immobilized for an extended period of time,
such as an “economy” intercontinental ight or immobilization in a long leg cast. Likewise, most individuals will
experience fatigue of the return system by an increasingly
snug t of their footwear near the end of the day.
e static or hydrostatic pressure represents the weight of
the column of blood from the point where active recirculation begins—usually the right atrium. Topographically, this
is assigned to the level of the fourth costosternal junction.
e hydrostatic pressure at a given anatomic point is determined by measuring the vertical distance below this land-
5,18
mark.
of height below the atria, with this constant being derived
from the product of the density of blood (1.056 g/cm
e eect of gravity increases by 0.77 mmHg/cm
3
) times
3.3 Physiologic components of the return circulation 29
A
HP
15
59
94
mmHg
Volume (mL)
Pressure (mmHg)
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the acceleration of gravity (980 cm/second2) divided by
13.33 mN/cm2.
1,10
As demonstrated in Figure 3.1, the hydrostatic pressure at the distal calf in the average 174-cm tall
American male is 94 mmHg when standing still.
6
Chronic, sustained venous pressure elevation, or venous
hypertension, is associated with pathologic consequences.
In the peripheral venous circulation, the major outcomes
are reected in the skin and subcutaneous tissues, and
include the typical changes described in CEAP clinical classications 3–6: edema, pigmentation, brosis, and ulceration. e frequency of cutaneous ulceration increases with
increasing end-exercise venous pressures above 30 mmHg14;
this condition, termed venous hypertension, is not the only
abnormality producing these symptoms, but remains a
major focus for surgical correction.
6,11,15
Reux, the most
common pathophysiological eect associated with venous
hypertension, may result from valvular insuciency of
either the deep or the supercial system.
3.3.2 Capacitance and pressure
relationships
e total body venous reservoir has an enormous capacity
for uid volume. e healthy individual can accommodate
as much as 20%–30% additional volume.
DP
15
0
0
1,2
e normal blood
cm
Ht
+/–R
174
+42
151
+19
volume is approximately 65 mL/kg in women and 70 mL/kg
in men, of which 60%–80% resides in the venous circulation. Assumption of an upright posture alone is responsible
for a 10% volume shi (7 mL/kg or 250–500 mL) into the
lower extremity.
2,3
e shape of the venous wall varies greatly depending
upon pressure, volume, and ow as demonstrated in Figure
3.2.9 When empty or accid, the walls are coapted and the
pressure low. As the cross-sectional prole changes to that
of a dumbbell or ellipse, large shis in ow (or volume) are
accommodated, with minimal changes in pressure. Until
the vein becomes circular in shape, the pressures remain
low. e enormous ow carried by an incompletely distended vein can be deceiving; just ask any surgeon who has
nicked a accid iliac vein or the vena cava!
Once a vein achieves a circular geometry, further distention is accompanied by a sharp increase in pressure per
unit volume (Figure 3.2). Over the normal pressure range
of 5–25 mmHg, capacitance volume may change by large
amounts without aecting ow or pressure.
2,9
As a result,
within the range of normal pressures, the venous hydrostatic pressure becomes an inactive factor in the mechanics of venous return. e higher pressure needed to produce
circular distention of the vein approximates that dened as
“abnormal” by ambulatory venous pressure (AVP) studies
(30 mmHg).14 is biological pressure threshold is similar to that associated with pulmonary dysfunction from
chronic obstructive or regurgitant valvular disease, as well
as to the threshold for tissue dysfunction resulting from
acute, sustained abdominal and extremity compartmental
pressure syndromes.
19,20
132
0
0
31 (leg)
(44 arm)
15
Figure 3.1 The relative pressures generated by dynamic
(cardiac pump) and hydrostatic (positional) influences are
illustrated in this schematic. The figure has been standing motionless with the dependent veins filling by gravity.
Upper extremity pressures vary with position of the arm.
DP: dynamic pressure; Ht: height; HP: hydrostatic pressure; RA: right atrium. (From Meissner MH etal. J Vasc
Surg 2007;46(Suppl.):4S–24S.)
0
112 –20
92 –40
56 –76
10 –122
14
12
10
8
6
4
2
–30–20 –100
Figure 3.2 Pressure/volume relationships in the dis-
tensible venous lumen are reflected in this diagram.
Considerable volume is introduced before pressure
rises; pressures begin to rise as the vein becomes elliptical and increase further as a circular configuration is
reached. (From Katz AI, Chen Y, Moreno AH. Biophys J
1969;9:1261–79.)
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