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30 The physiology and hemodynamics of the normal venous circulation
https://t.me/med1917
e venous wall is considerably thinner than the arterial wall, but consists of the same elements—intima, media,
and adventitia. e walls of the subfascial deep veins have a
relatively uniform thickness. In comparison to supercial
tributary veins, the walls of the major supercial venous
trunks—the saphenous, basilic, and cephalic veins—are
relatively thick. Pliability is a key feature of venous or
capacitance vessels. However, when fully distended at high
pressures, a vein loses this pliability and becomes as sti as
an artery.10 Another key feature related to capacitance function is the ability to constrict or dilate over a wide range
of diameters. For example, venoconstriction oen follows
failed venipuncture or exposure for harvest in the operating room, and venodilation oen follows increased ambient
temperature, warmed acoustic gel, and general anesthesia.
3.3.3 Physiological control: Reflex,
hormonal and local mechanisms
Volume ow through splanchnic, muscle, and cutaneous
veins can change enormously in response to various stimuli. Reex impulses are transmitted through sympathetic
nerves, which predominantly exert their eects as arterial
constriction. Baroreceptor- and chemoreceptor-mediated
eects are the most eective acute adjustments to the distribution of blood ows.1 Fluid shis and hormonal mechanisms become more important with chronic adjustments
to volume status. Although ow is largely controlled by the
small resistance arterial beds, capacity is largely adjusted by
dilation or constriction of the venous network.
Adrenergic innervation is distributed to both arteries
and veins. Furness and Marshall,21 in an elegant physiologic/anatomic study, demonstrated that the relative densities of these adrenergic endings in the microcirculatory bed
are far greater in the arterial (resistance) circulation (Figure
3.3). e splanchnic and cutaneous distributions receive the
greatest venous concentration of adrenergic bers. ese
distributions also have the largest complement of smooth
muscle.1 Marked arteriolar smooth muscle hypertrophy
facilitating precapillary vasoconstriction is one of many
adjustment in the extremity skin of the girae, which helps
in the animal’s adaptation to extreme vertical physiologic
22
stress.
e splanchnic circulation normally contains approximately 18 mL/kg or about 25% of the total blood volume
and accounts for approximately 27% of the total blood ow.
Although normal splanchnic demand is determined from
local regulatory mechanisms, acute control of splanchnic
volume may be mediated by baroreceptors via adrenergic
2,4
bers.
In severe hypotension, circulating vasopressin and
catecholamines may exert a substantial additive eect on
the splanchnic adjustments. ese redistributions account
for approximately 50% of the acute volume compensation
following a hemorrhage. Although a small proportion of
this volume shi may result from active venoconstriction,
the majority results from passive elastic recoil and redistribution of arterial ow.
Figure 3.3 Diagrammatic representation of the relationship
between adrenergic nerves and the mesenteric blood vessels. The adrenergic nerves are represented by the heavy
lines. Arrows indicate the direction of blood flow. Note that
the precapillary arterioles and the collecting venules are
not innervated. pa: principal artery; pv: principal vein; sa:
small artery of the microvasculature; ta: terminal arteriole;
pca: precapillary arteriole; c: capillary; cv: collecting venule;
sv: small vein. (Reproduced with permission from Furness
JB, Marshall JM. J Physiol 1974;239:75–88.)
minute/100 g of tissue, but because of its large mass, this
accounts for approximately 15% of the total blood volume. Adrenergic stimulation has little inuence on skeletal
muscle ow, which is primarily controlled by locally mediated stimuli.
fold to 80 mL/minute/100 g tissue with sustained exercise.
Venoconstriction occurs in response to exercise, although
local heating abolishes this response in active muscle.3 e
increased volume of ow with exercise, along with the heat
generated, secondarily recruits dilation of the cutaneous
venous network.
whereas skin temperature varies markedly with the ambient temperature. Overall, temperature control is maintained by the hypothalamus, whereas cutaneous circulation
responds to both reex innervation and direct local stimuli.
Cutaneous blood ow is approximately 3 mL/minute/100 g
of tissue in cool weather, which accounts for approximately
6% of the total blood ow,
30-fold. Conservation of body heat is achieved by constriction of the cutaneous network, which lowers ow even further. e deep veins are unaected by cold.
cold also concentrates venous ow in the deep system, where
a countercurrent heat exchange eciently preserves thermal
pv
pa
sv
sa
ta
pca
c
c
cv
e blood ow to inactive skeletal muscle is only 3 mL/
1,2
Skeletal muscle ow may increase many-
Core temperature is maintained at a constant 36–37.5°C,
16
and may vary by as much as
17
us, extreme
3.4 The peripheral muscle pump mechanism 31
(a)(b) (c)
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energy. A reduction in body temperature markedly enhances
venoconstriction in response to local cooling through potentiation of the threshold of the adrenergic receptors of cutaneous veins.17 In a warm environment, heat loss is facilitated in
order to maintain homeostatic body temperature. Skin blood
ow increases with reduced adrenergic impulses, leading to
both arterial and venous dilation.16 In severe heat stress, the
skin blood ow may reach 2–3 L/minute.
Local injury leads to the release of histamine and bradykinin, which produce localized vasodilation. ere is
mounting evidence to suggest that the vasodilatory actions
of progesterone seem to increase venodilation and even the
incidence of varicose veins.4 Despite having been evaluated
by a number of investigators, only a limited role has been
identied for nitric oxide in venous regulation.
23,24
3.4 THE PERIPHERAL MUSCLE PUMP
MECHANISM
Flow against gravity is maintained by a system of muscle
pumps to eject the blood combined with internal valves to
prevent retrograde ow (Figure 3.4). In normal individuals, this mechanism is remarkably ecient. e complex
relationship between pressure and volume is integral to the
comprehension of venous function.
3.4.1 Valvular function
Duplex surveys have dened normal valvular function as a
duration of retrograde ow that is <0.5 seconds for all deep
and supercial veins of the lower extremities, except for
the femoral and popliteal veins (<1.0 seconds).
15,25,26
Soleal
sinuses have no valves and a relatively xed volume.27 e
paired gastrocnemius muscles also have sinuses, but apparently of reduced volume and number. Although the role of
valves in the prevention of reux ow is obvious, the importance of dysfunction (incompetence) of a single or even
several valves is not clear. Incompetence of a single valve
produces no known physiological consequences.
25
e importance of various anatomic sites of valvular
dysfunction is incompletely resolved. Some have ascribed
great pathophysiological signicance to the femoral and
popliteal valves, while others have emphasized abnormalities of the distal valves.
25,28–30
In an analysis of 155 patients
from a series of randomized trials, incompetence of the
popliteal vein valve was the only signicant risk factor for
delayed healing.28 Rosfors et al.30 determined that distal
valvular dysfunction was of greater signicance than popliteal valvular dysfunction, but combined disease categories
were most likely to be associated with severe chronic venous
insuciency (CVI).13 e increased number of valves in
the infrapopliteal segments suggests that their functional
importance is greater in that location.
Perforating vein valves prevent outward ow when func-
tioning properly.
27, 31
is concept is consistent with the
pressure/ow relationships of the calf pump. Cockett27 colorfully captured the image of perforating vein malfunction
with his description of the “ankle-blow-out” syndrome.
3.4.2 The calf pump
Figure 3.4 Drawing illustrating “operation of the muscle
pump”: (a) resting, (b) muscle contraction, and (c) muscle
relaxation. Venous pressure in the distal leg is indicated
by the length of the hydrostatic column. (From Sumner
DS, Zierler E. Vascular physiology: Essential hemodynamic
principles. In: Rutherford RB, ed. Vascular Surgery, 6th Ed.
Philadelphia, PA: Saunders-Elsevier, 2005.)
Contraction of the gastrocnemius and soleus muscles expels
blood into the large-capacity popliteal vein. e normal limb
has a calf volume ranging from 1500 to 3000 mL, a venous
volume of 100–150 mL, and ejects over 60% of the venous
volume with a single contraction.
12,32,33
Christopoulos etal.32
normalized the reporting of air plethysmographic volumes
in order to facilitate comparison of clinical groups and eliminate such eects as edema and variance in calf size. An ejection volume of 2.5–3.7 mL/100 mL of calf tissue volume was
described for normal limbs. Expressing the ejection fraction
as a ratio serves the same comparative function.
From a high resting hydrostatic pressure, venous pressure is substantially reduced within several contractions
(Figure 3.5).
5
e end-exercise pressure, referred to as the
AVP, is maintained at a relatively low value with continued
calf contractions. When active contraction ceases, 31 seconds are required to restore hydrostatic pressure in the normal limb. Measurements of changes in venous pressure and
volume during repetitive contractions of the normal calf
transcribe similar curves (Figure 3.6a–c).
5,6,32,33
Separation
of venous pressure relationships from musculofascial pressures is accomplished by simultaneous measurement of
33,34
compartmental and venous pressures.
>90% of volume requires over 70 seconds to rell the calf.
Restoration of
32
In the normal resting state, the veins of the calf are
lled at a rate of 1–2 mL/second by both active and passive
32 The physiology and hemodynamics of the normal venous circulation
150
70
Venous pressure in mmHg
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120
1st step
90
2nd step
Figure 3.5 Mean pressure changes in the dorsal foot vein during standing, calf exercise, and the subsequent resting state.
(From Pollack AA, Wood EH. J Appl Physiol 1949;1:649–62.)
mechanisms. e calf pump is actively primed by compression of the plantar venous plexus. Passive lling occurs during muscle relaxation when blood ows into the recently
emptied deep veins from the muscle itself, the distal deep
veins, and the supercial veins. Venous blood ows through
perforating veins following the pressure gradient from elevated hydrostatic pressures in the supercial veins to the
rhythmically decreased mean pressure in the deep veins
of the calf. Not all perforating veins have valves, but those
that do are oriented to prevent ow from the deep to the
supercial system.27 Abnormal function of either the deep
or supercial venous system will commonly result in an
increased venous pressure, an increased venous volume,
and a shortened rell time.
sion would benet this ow pattern by actively encouraging
ow into the deep system and reducing calf volume, thus
eectively priming the peripheral pump.
Radiographic visualization of contrast movement during active calf contraction was described by Almén and
Nylander.31 e intramuscular soleal and gastrocnemial
sinuses ll from the deep muscle compartment and empty
completely with a single calf contraction. e intermuscular, paired, deep tibial veins, which lie between the muscle
bundles, are substantially compressed, but are never completely empty. e proximal valves open during active calf
contraction. e distal deep vein valves close during active
calf contraction, along with those in the perforating veins,
thus preventing retrograde or outward ow during the contraction cycle.
gests a major role for the plantar venous plexus in lling the
deep tibial veins.
e use of direct pressure measurements in the tibial,
popliteal, and saphenous veins has provided invaluable
evaluations of hydrostatic pressure, pressure reduction with
single and multiple calf contractions, and time for recovery
60
30
0
5,14 ,32
Notably, external compres-
31
In addition, phlebography of the foot sug-
35
3rd step
5th step
Maximum
7th step
pressure
Minimum pressure
l
04812 16 20 24 28 32 36 40 50 60
eadmill
step
Last
Stop tr
Time (seconds)
of resting pressure. However, despite innovative and extensive experimental observations, the invasive aspects of
these investigations have precluded repetitive examination.
Plethysmography, whether by foot volume, air, or strain
gauge, is well accepted, such that longitudinal data with
these non-invasive methods are now appearing. Various
authors have described the volume changes associated with
elastic compression, surgical intervention, CEAP clinical
class, late-day deterioration of venous function, and diminished joint function.
11,12,15,32,36,37
3.4.3 Thigh and foot contributions to the
peripheral venous pump
Although the thigh veins are surrounded by muscle, the
contribution of the active contraction of thigh muscle to
venous return is thought to be minimal. Ludbrook33 was
surprised by his data demonstrating that it required fewer
than 10 seconds for normal venous lling in the thigh
compared with over a minute for the calf. e virtually
instantaneous rell of this segment is consistent with endexercise pressure measurements in the popliteal vein.
thigh segment ejection fraction of 20% was measured with
a 15-cm air plethysmographic cu.33 Considerably less ecient venous return from the thigh segment was attributed
to the observed rapid rell and less compressible intermuscular location of the deep veins in the thigh.
Compression of the plantar venous plexus actively pumps
blood proximally.
veins are also intermuscular in location, intrinsic muscle
contraction coincides with the timing of maximal weight
bearing on the foot; compression then forces blood out of
the foot. Blood ow from the plantar venous plexus is primarily directed into the paired, deep tibial veins; however,
there is disagreement about whether it is all retained in the
35
Although the medial and lateral plantar
18,38
A
(a)
(c)
mmHg
Seconds
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deep system. Several investigators describe ndings which
suggest that ow passes from these and other deep foot veins
into both the deep and the supercial venous networks.
39,40
Kuster etal.40 studied the veins communicating between the
deep and suprafascial systems of the foot in 10 unembalmed
limbs and identied 6–12 communicating veins per foot.
Approximately 50% of these veins had valves that, unlike
the perforating veins of the calf and thigh, only allowed ow
from the deep veins toward the supercial veins. Even with
intraosseus tarsal phlebography, an ankle tourniquet was
still needed to direct ow into the deep veins.
39
Although the interactions between the various leg pumps
are not fully understood, they all work together with competent valve function to return the venous blood from one
segment of the extremity to another.
3.4.4 Stroke volume and calf pump output
Like many biological systems, the provision for normal
venous return from the peripheral muscle pump greatly
exceeds the minimum required for normal function.
If we postulate a conservative normal walking cadence
of 100 steps/minute and a median ejection volume of
3.0 mL/100 mL in a 2.0-L calf, the calf pump output (CPO)
would be 6.0 L/minute. e CPO per limb would be half of
this, or 3.0 L/minute. Even by employing these conservative
assumptions, the estimated CPO exceeds the resting cardiac
output. Logically, if the proportion ejected was reduced, the
result would be a less ecient pump and a decreased CPO.
For example, in deep venous insuciency, if the median
ejection volume was decreased to 1.7 mL/100 mL, the CPO
would still be 3.4 L/minute.
3.4.5 Pressure relationships in the lower
extremity
3.4 The peripheral muscle pump mechanism 33
Pressure (mmHg)
(b)
Volume
120
↓ Standing o-wt
100
80
60
Volume %
40
20
0
–10 01020
10 Heel raises or
↑
walking in place
Volume
Pressure
Standing–limb relaxed
30
40 50 60 70
–100
–0
100
80
60
40
20
0
In the normal limb, the pressure is reduced from the resting
hydrostatic pressure (~90 mmHg) to a mean of 22 mmHg
with ambulatory calf contractions, a value that is reached
within 7–12 steps.5 Similar pressure changes were observed
with standing ankle plantar exion or heel raising, which
transfers weight to the forefoot (the tip-toe maneuver).
5,6 ,14
When resuming a static standing position, the hydrostatic
pressure is restored in a mean of 31 seconds (Figure 3.6a–c).
As a practical matter, venous pressure studies have generally
been obtained from the dorsal foot veins, assuming that the
pressure accurately reects pressure determined from direct
cannulation of the deep veins of the calf (posterior tibial).
Several authors have compared simultaneous pressures
from deep and supercial vein catheters placed at the same
anatomic height.
8,18,38,40
ese investigations demonstrated
that pressures measured in the supercial veins at the ankle
closely reected those in the deep system. However, pressures measured in the skin and subcutaneous (supercial)
venous network are most likely to be associated with dermal
pathophysiologic changes. e incidence of cutaneous ulceration has a linear relationship with increases in AVPs above
Figures 3.6 The pressure and volume changes with
activation of the calf muscle pump are demonstrated.
Beginning in the standing posture, the hydrostatic
pressure baseline is demonstrated in a dependent, but
non-weight-bearing limb. The subject then performs 10
tip-toe (heel raising) maneuvers and resumes the nonweight-bearing posture. (a) Pressure changes during
these maneuvers are illustrated in this recording from
cannulation of a dorsal foot vein, reported in mmHg. (b)
Volume changes during these maneuvers are illustrated
in this air plethysmographic examination. The volume
remaining in the limb after exercise divided by the venous
volume standing still is reported as the residual volume
fraction (RVF, %). (c) This schematic compares the pres-
sure and volume changes along a concomitant timeline.
Note the efficiency of the calf pump in terms of rapidly
reducing either volume or pressure upon the commencement of muscle activity. Although volume filling begins
within 5–7 seconds, pressure does not rise substantially
for 30–40 seconds. Alterations in these relationships can
generate chronic, sustained venous pressure elevations,
the end products of which are the symptoms and findings
of chronic venous insufficiency.
34 The physiology and hemodynamics of the normal venous circulation
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30 mmHg. Ulceration and an increased AVP was also associated with a 90% rell time of <20 seconds.14 In addition,
rapid reux (i.e., venous lling of greater than 7 mL/second)
is also associated with a high incidence of ulceration.
32
Contracting muscle and an intact limb fascia are integral components of the peripheral musculovenous pump.
During maximal contraction, intramuscular pressures
of 250 mmHg are generated in the soleus muscle, and
215 mmHg in the gastrocnemius.33 More recent studies
have suggested that pressures measured within the fascial
envelope of the leg ranged from 80 to 90 mmHg in various
postural positions.34 Intravenous pressures taken from the
proximal posterior tibial vein rose to >200 mmHg during
initial calf contraction, with subsequent peak pressures of
>150 mmHg on repetitive contractions. ese deep calf
pressures fell to 30 mmHg on relaxation.18 Saphenous vein
measurements at the same anatomic height had a lesser initial peak pressure and also demonstrated declining peak
pressures with each contraction. e pressure gradient thus
favors supercial to deep ow only during the post-contraction relaxation phase of the calf muscle cycle. Pressures
in the popliteal vein demonstrate a short rise during the
initial calf contraction, which corresponds to expulsion of
blood from the calf, but popliteal pressures do not decrease
following relaxation; thus, the baseline, resting popliteal
vein pressure remains close to the hydrostatic pressure for
the greater proportion of the walking cycle.
18,38
e xed,
non-elastic investing fascia of the lower leg provides an
unyielding envelope that permits the generation of these
high pressures, but also prevents dilation of the capacitance
chamber, eliminating an increase in stroke volume as a
potential compensatory mechanism for calf pump failure.
Unlike the fascia, normal skin is elastic and can stretch in
response to a susta ined increase in subc utaneous pressure. e
combination of stretched skin, edema, venous hypertension,
and minor injury may predispose to ulceration. In contrast
to humans, the girae exhibits several physical adaptations
to its exaggerated physiological demands; these include an
elevated interstitial uid pressure (mean 40–50 mmHg) and
a skin structure that is characteristic of a tight and unyielding fascia.
22
Clinically, these considerations are incorporated
into therapeutic devices, such as the adjustable Velcro wrap
and Unna’s boot, which also provide an unyielding external
envelope. e gradient compression stocking utilizes elastic
in order to provide convenient, exible, external support.
3.5 PHYSIOLOGIC COMPENSATIONS
3.5.1 Compensation for upright posture
In humans, the primary peripheral circulatory adaptation
to the assumption of an upright posture is made by changes
in arterial resistance and not by adjustments in venous tone
or capacitance.
in position is largely achieved by immediate changes in
heart rate and then adjustment in arterial resistance.
When the dependent capacitance vessels (veins) are allowed
3,41
Circulatory homeostasis with this switch
2,5,41
to continue to ll passively without emptying, the redistribution of blood volume may result in syncope. is is a
common problem in fresh military recruits who are learning to stand in formation. Normal individuals who are
standing in a static position dget and shi weight from one
leg to another at least once per minute; this frequency is not
diminished by extreme heat or cold.
38,42
3.5.2 Volume depletion: Hemorrhage
(acute) and dehydration (chronic)
Compensation for an acute reduction in blood volume
and the resulting decrease in venous return is mediated by
baroreceptor stimulation and increased sympathetic output. Loss of approximately 10% of the circulating volume
may be accommodated without changes in cardiac output
or systemic pressure by sympathetic-mediated arteriolar
constriction, venoconstriction, and increases in heart rate.
Acute loss of approximately 30%–40% of the volume can be
tolerated without death, but requires maximal utilization of
compensatory mechanisms. Reex vasoconstriction, which
is most prominent in the splanchnic and cutaneous distributions, is accompanied by increased circulating catecholamines in severe acute blood loss. Canine studies suggest
that acute volume depletion of approximately 29% (20 mL/
kg) can be compensated for by the combination of vasoconstriction and transcapillary uid reabsorption (6 mL/kg).
us, 10–15 mL/kg is compensable by active venoconstriction and passive elastic recoil resulting from both reduced
arterial pressure and vasoconstriction.
1,2
Over a prolonged time interval, an individual can compensate for loss of almost 50% of the blood volume (35 mL/
kg). e transfer of extracellular uid volume to the circulating volume and the hormonal eects of aldosterone
and the renin–angiotensin system are both involved in the
accommodation of chronic volume loss of this degree.
Both acute and chronic adjustments to volume depletion
are primarily achieved through the control of arterial resistance, with veins playing a passive, but essential role.
3.5.3 Musculoskeletal activity
To supply the enormous blood ow required by exercising muscle, three major circulatory accommodations take
place.1 First, cardiac output may increase by ve to seven
times relative to the normal resting values. Second, the mean
arterial pressure rises by 20–80 mmHg. ird, the mass
sympathetic discharge produces diuse arteriolar constriction and venoconstriction. Local eects produce vasodilation of the muscle arterioles because local metabolic eects
override the sympathetic signals to vasoconstriction.
Deterioration of calf pump function at the end of the day
was observed using both photo and air plethysmography.
Although the variance was relatively limited, these ndings
suggest that venous return from the limb deteriorates with
prolonged upright activity. e explanation for these ndings
may be related to stress relaxation of venous smooth muscle.
36,37
1,2
3.6 Summary 35
(c)
(a)
Seconds
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It is probable that the calf pump mechanism normally
compensates for venous insuciency, whether reuxive or
obstructive in nature. However, calf pump function and
ankle range of motion are progressively diminished with
increasing severity of CVI.
6,7,11,12
e potential role of the
calf pump in venous insuciency has been known for some
time, but little has been done in a direct attempt to eect a
therapeutic intervention. e hypothesis that physical conditioning that is directed to improve calf pump function
could be of therapeutic value was addressed in a small, randomized controlled trial; both improved calf pump function and muscle strengthening were observed.
43
3.5.4 Temperature adjustment
Regulation of heat loss from the body is a major determinant of skin blood ow. A decrease in temperature produces
cutaneous arterial vasoconstriction as well as subcutaneous venoconstriction. e combination of local and central
eects can reduce skin blood ow to less than 3 mL/minute/100 g.16 Additional physiologic compensations for cold
include shivering, hunger, and catecholamine secretion.
Compensatory mechanisms to achieve heat loss include
increased cutaneous arterial ow and increased subcutaneous venous capacitance. Maximal skin blood ow may
increase by over 10-fold to 30 mL/minute/100 g with ows
of 2–3 L/minute.16 Additional physiologic compensations for
heat include sweating, increased respiration, and decreased
activity. At the extremes of ambient temperature (0–55°C),
venous pressure measurements in normal individuals
exhibit pathological ndings.42 By gradually adjusting ambient temperatures between 0°C and 55°C, toe temperatures
of 23°C and 39°C, respectively, were recorded when subjects were stressed to the clinical end-points of shivering or
sweating (Figure 3.7).42 A cold extremity never achieved a
full hydrostatic pressure head and required prolonged lling to reach even a reduced hydrostatic pressure. A warm
extremity achieved a full hydrostatic pressure almost immediately, making assessment of post-exercise pressures dicult.42 Although specically determined in relatively extreme
temperatures, these ndings for AVP determinations have
implications for other methods of venous testing as well.
erefore, the rooms used for these examinations should be
maintained within a reasonable range of comfortable ambient temperatures.
mmHg
93
39°C
0
(b)
93
33°C
0
93
25°C
Figure 3.7 Changes in an ambulatory venous pressure
tracing at extremes of ambient temperature (the temperature markings indicate toe temperatures). At a toe temperature of 33°C (b), ambulatory venous pressure returns
to the baseline hydrostatic pressure at 40 seconds, which
is considered normal. Note the absence of a return to the
baseline hydrostatic pressure (93 mmHg) in
tions, and the immediate return to baseline hydrostatic
pressure in
J Clin Invest 1950;29:855–61.)
(c) hot conditions. (From Henry JP, Gauer OH.
12080400
(a) cold condi-
its vasodilator eect in the venous circulation is minimal
compared with its eects in the arterial circulation. A clinical correlate was described by Lüscher etal.,24 who studied
internal mammary arteries, internal mammary veins, and
saphenous veins harvested for coronary arterial bypass
gras. e relaxation response of the veins was markedly
reduced compared with the artery (Figure 3.8). e authors
postulated that these physiological characteristics inuenced the patency of arterial and venous bypass conduits.
3.6 SUMMARY
3.5.5 Other
Active venoconstriction occurs with hyperventilation,
cold showers, strong emotion, and muscular exercise; it is
mediated by the adrenergic (sympathetic) nervous system.3
Ongoing research continues to seek eective pharmacological solutions for venotonic therapy.
Although a specic neural pathway for venodilation has
not been identied in humans, the paracrine mechanism of
the endothelial-derived relaxing factor has been an important focus of recent research. Now recognized as nitric oxide,
Understanding the normal venous circulation requires
mastery of complex hemodynamic and physiologic concepts. Gravity-induced hydrostatic pressure encourages
ow into the dependent capacitance network. e distensibility of the venous wall permits the system to accept (or
contribute) large-volume adjustments with a minimal rise
4
(or fall) in pressure.
Venous return ows along a pressure gradient, just as
the arterial and microcirculation ows do. e return of
venous blood against gravity is accomplished by breaking
the system into multiple pumped segments with internal
36 The physiology and hemodynamics of the normal venous circulation
Without endothelium (n = 9)
Without endothelium (n = 9)
Relaxation % of contraction to norepinep
hrine
Acetylcholine (–logM)
(a) (b)
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0
20
With endothelium (n = 22)
40
50
80
100
Figure 3.8 Endothelium-dependent relaxation responses to acetylcholine (ACH) in (a) human saphenous vein and
(b)human internal mammary artery. (From Lüscher TF etal. N Engl J Med 1988;319:462–7.)
valves preventing the return of ejected blood. e calf
muscle pumping mechanism is very ecient and empties
into a capacious, valved, popliteal vein. Acute circulatory
adaptation associated with standing, volume deciencies,
or changes in temperature are largely compensated for by
Guidelines 1.2.0 of the American Venous Forum on the physiology and hemodynamics of the normal venous circulation
No. Guideline
1.2.1 Venous return follows a continued dynamic pressure gradient.
The majority of the energy imparted by the pumping action of
the heart is dissipated in distribution to the arterial circulation.
1.2.2 The hydrostatic pressure in the venous system is directly related
to the height of the column of blood in relation to the zero
point of the right atrium.
1.2.3 Venous return against gravity is accomplished by the combined
action of an active extremity muscle pump and one-way
venous valves.
1.2.4 The plantar venous pump acts to prime the calf muscle pump. C
1.2.5 The thigh muscle pump contributes little to venous return. B
1.2.6 The anatomic structure of a vein allows for great variation in its
diameter. This facilitates the capacitance function of the
venous system for adjustment to volume and temperature
changes.
1.2.7 External pressure on collapsible proximal veins increases distal
venous pressure.
789
5
6
With endothelium (n = 27)
4
789
5
6
4
reex alterations in resistance vessels, in conjunction with
adjustments of venous tone. e complex physiologic interactions of the return circulation provide a homeostatic
milieu that supports varied human demands for function in
a wide variety of circumstances.
Grade of evidence (A: high quality; B:
moderate quality; C: low or very low quality)
A
A
A
A
B
References 37
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Classification and etiology of chronic
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venousdisease
ROBERT L. KISTNER AND BO EKLÖF
4
4.1 Development of the CEAP classification 39
4.2 “Revised” CEAP document 40
4.3 Terminology and new definitions 41
4.4 Writing of the CEAP 43
4.5 Clinical application of CEAP 44
e need for an accurate classication system in venous disease is fundamental to understanding the clinical disease
processes and to inter-institutional communication about
the separate entities. e imprecise diagnoses that were
the norm in venous disease throughout the ages have been
replaced by accurate imaging studies since the introduction
of noninvasive ultrasound scans in the 1980s. Once presented with the ability to make accurate diagnoses of the
cause and mechanism of chronic disease in the individual
segments of the lower extremity veins, it was necessary to
devise a classication system that was capable of organizing
the data in a meaningful way.
In 1994, the American Venous Forum convened a subcommittee of world experts in chronic venous disease
(CVD) to address this challenge. Recognizing that a modern classication of CVD must now embrace more than
just the clinical state of the patient, this committee created
the “CEAP” classication, which provides a system where
the multiple variations of CVD can be communicated in a
clinically and scientically meaningful manner, enabling
analysis and comparison of treatment modalities for similar conditions.
Because identical clinical presentations of CVD arise
from dierent etiologies and the distribution of specic
pathologic processes have dierent implications for treatment and long-term prognosis, the CEAP classication
organizes these elements into its methodology. In the CEAP
system, the clinical state (C) is amended by the etiologic
basis (E) for the disease in each case, and this is described in
terms of the anatomic distribution (A) of the pathophysiologic process (P) throughout the axial venous drainage from
1
4.6 Importance of defining etiology 45
4.7 Comparison of primary and secondary CVD 45
4.8 Conclusions 47
References 48
the calf to the diaphragm. is organization of information has been successfully promulgated around the world
by the international representation that devised it. Its wide
acceptance has become fundamental to inter-institutional
communication and to the description of chronic venous
disorders.
4.1 DEVELOPMENT OF THE CEAP
CLASSIFICATION
e CEAP classication that was introduced in 19941 provides a framework around which the clinical manifestations
found in CVD are paired with key pathologic elements of
causation and physiologic mechanisms in specic anatomic
locations of the lower extremity. Specically, for each clinical condition, it distinguishes:
●
Primary from secondary and from congenital causes of
the problem
●
Reux from obstructive pathophysiology
●
e precise anatomic segments aected by reux or
obstruction through 18 named segments of the lower
extremity venous tree
In this way, clinical manifestations are coupled with the
precise pathological entity from which the natural history
of the pathologic processes and the eects of management
alternatives for similar clinical states can be identied and
studied. e classication describes the status of the disease
process at a point in time; these details can change over time
with the introduction of interval treatments and with the
39
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