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42 Chapter 4/Venous Anatomy, Physiology, and Pathophysiology
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stress. Valve closure develops when the vortical fl ow pressure exceeds the proximally directed jet fl ow.
The role of venous valves in an individual quietly standing is not well understood. Pressures in the superfi cial and
deep veins are essentially the same during quiet standing,
but as Arnoldi has found, the pressure in the deep veins is
1 mm higher, which would tend to keep the valves in the
perforating veins closed.8 Normally functioning perforating
vein valves protect the skin and subcutaneous tissues from
the effects of muscular contraction pressure. This muscular
contraction pressure may exceed 100 to 130 mmHg.
Intuitively, the role of venous valves during muscular
exercise is obvious, since their major purpose is to promote
antegrade fl ow from superfi cial to deep. Volume and pressure changes in veins within the calf occur with muscular
activity. In the resting position, with the foot fl at on the fl oor,
there is no fl ow. However, in the heel strike position, the
venous plexus under the heel and plantar surface of the foot
(Bejar’s plexus) is emptied proximally. Blood fl ows from
the foot and ankle into the deep veins of the calf. Then, calf
contraction transports this blood into the deep veins of the
thigh, and henceforth, blood fl ow proceeds to the pelvic
veins, vena cava, and ultimately to the heart all due to the
infl uence of lower extremity muscular contraction.
9
PATHOPHYSIOLOGY
Abnormal functioning of the veins of the lower extremities is recognized clinically as venous dysfunction or, more
commonly, venous insuffi ciency. Cutaneous telangiectases
and subcutaneous varicose veins usually are grouped together
under the title Primary Venous Insuffi ciency, and limbs
with skin changes of hyperpigmentation, edema, and healed
or open venous ulceration are termed Chronic Venous
Insuffi ciency (CVI).
Primary Venous Insuffi ciency
Explanations of venous pathophysiology as published in
reviews, texts, and monographs are now for the most part
out of date. The new science as we now know it is incorporated in the following summary.
A dysfunctional venous system follows injury to vein
walls and venous valves. This injury is largely due to infl ammation, an acquired phenomenon.10 Factors, which are not
acquired, also enter into such injury. These include heredity,
obesity, female gender, pregnancy, and a standing occupation in women. Vein wall injury allows the vein to elongate
and dilate thus producing the visual manifestations of varicose veins. An increase in vein diameter is one cause of
valve dysfunction that results in refl ux. The effect of persistent refl ux through axial veins is a chronic increase in distal
venous pressure. This venous pressure increases as one pro-
ceeds from the inguinal ligament past the knee to the ankle.
Prolonged venous hypertension initiates a cascade of pathologic events. These manifest themselves clinically as lower
extremity edema, pain, itching, skin discoloration, and
ulceration.
11
The earliest signs of venous insuffi ciency often are elongated and dilated veins in the epidermis and dermis, called
telangiectasias. Slightly deeper and under the skin are fl at,
blue-green veins of the reticular (network) system. These
may become dilated and elongated as well (see Figure 4.4).
And fi nally, still deeper but still superfi cial to the superfi cial
fascia are the varicose veins themselves. All of these abnormal veins and venules have one thing in common: they are
elongated, tortuous, and have dysfunctional venous valves.
This implies a common cause, which is infl ammation.
Chronic Venous Insuffi ciency
Skin changes of hyperpigmentation, scarring from previous ulceration, and active ulcerations are grouped together
under the term chronic venous insuffi ciency (CVI). Numerous theories have been postulated regarding the cause of
chronic venous insuffi ciency and the cause of venous ulcer-
12,13
ation.
been disproved. An example is the theory of venous stasis,
fi rst proposed in a manuscript by John Homans of Harvard
in 1916.14 It was a treatise on diagnosis and management of
patients with chronic venous insuffi ciency, and in it, Dr.
Homans coined the term “post-phlebitic syndrome” to
describe the skin changes of CVI. He stated that, “Overstretching of the vein walls and destruction of the
valves . . . interferes with the nutrition of the skin . . . therefore, skin which is bathed under pressure with stagnant
venous blood will form permanent open sores or ulcers.”
That statement, like many others that describe venous conditions and their treatments, is steeped in dogma and is short
of observational fact. The erroneous term stasis ulcer honors
that misconception, as do the terms venous stasis disease
and stasis dermatitis.
proved the stasis theory by studying oxygen content from
varicose veins and normal veins.
oxygen content of the femoral vein in patients with severe
chronic venous insuffi ciency was greater than the oxygen
content of the contralateral nonaffected limb. Because
oxygen content was higher, some investigators felt that
arteriovenous fi stulas caused venous stasis and varicose
veins.
basis in fact since the entire thermal regulatory apparatus in
limbs depends on the opening and closing of arteriovenous
shunts. These shunts are important as they explain some
terrible accidents that happen during sclerotherapy when
sclerosant entering a vein is shunted into the arterial system
and distributed in its normal territory.
All the theories proposed in the past century have
Alfred Blalock, who later initiated cardiac surgery, dis-
15
He pointed out that the
16,17
That explanation, though disproved, has some
18
Microsphere inves-
Pathophysiology 43
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FIGURE 4.4 This cross-sectional view of the subcutaneous venous circulation shows how venous hypertension is
transmitted to the unsupported veins of the dermis and subcutaneous tissues from axial veins (GSV) and the deep veins
of the muscular compartments. (Redrawn from Reference 6.)
tigations have failed to show any shunting and the theory of
arteriovenous communications has died despite the fact that
these shunts actually exist and do open under the infl uence
of venous hypertension.
Hypoxia and its part in causation of chronic venous insuffi ciency was investigated throughout the last 25 years of the
twentieth century. English investigators thought that a fi brin
cuff, observed histologically, blocked transport of oxygen
and was responsible for skin changes of CVI at the ankles
and distally.19 That theory has been abandoned even though
a true periarteriolar cuff is easily identifi ed histologically.
The two elements that make up all the manifestations of
lower extremity venous insuffi ciency are failure of the vein
valves and vein walls and skin changes at the ankles, both
of which are related to venous hypertension.
20
Failure of Vein Walls and Valves
Our work suggests that venous hypertension causes a
shear stress dependent leukocyte-endothelial interaction,
which has all the manifestations of chronic infl ammation.21
These are leukocyte rolling, fi rm adhesion to endothelium,
and subsequent migration of the cells through the endothelial barrier into parenchyma of valves and vein walls.
22
There, macrophages elaborate matrix metalloproteases,
which destroy elastin and possibly collagen as well. Vein
walls become stretched and elongated. Vein valves become
perforated, torn, and even scarred to the point of near total
absence. These changes are seen both macroscopically and
angioscopically.
23
Similar changes have been produced in
the experimental animal by constructing an arteriovenous
fi stula to mimic the venous hypertension of venous dysfunction in humans.
24
Skin Changes
The second manifestation of chronic venous insuffi ciency
is expressed in the skin where leukocytes also are implicated
in the observed changes. There is evidence that leukocyte
activation in the skin, perhaps related to venous hypertension, plays a major role in the pathophysiology of CVI.
Thomas, working with Dormandy, reported that 25% fewer
white cells and platelets left the dependent foot of the
patients with venous hypertension. When the foot was elevated there was a signifi cant washout of white cells but not
platelets, suggesting platelet consumption within the microcirculation of the dependent foot.25 They concluded that the
decrease in white cell exodus was due to leukocyte trapping
in the venous microcirculation secondary to venous hypertension. They further speculated that trapped leukocytes
may become activated, resulting in release of toxic metabolites causing damage to the microcirculation and overlying
skin. Apparently, the primary injury in the skin is extravasation of macromolecules and red blood cells into the dermal
44 Chapter 4/Venous Anatomy, Physiology, and Pathophysiology
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interstitium. Red blood cell degradation products and interstitial protein extravasations are potent chemoattractants and
represent the initial chronic infl ammatory signal responsible
for leukocyte recruitment.
The important observations of Dormandy’s group were
historically the fi rst to implicate abnormal leukocyte activity
in the pathophysiology of CVI.
The importance of leukocytes in the development of
dermal skin alterations was further emphasized by Coleridge
Smith and his team.26 They obtained punch biopsies from
patients with primary varicose veins, lipodermatosclerosis,
and patients with lipodermatosclerosis and healed ulcers.
They counted the median number of white blood cells per
high power fi eld in each group but there was no attempt to
identify the types of leukocytes. In patients with primary
varicose veins, lipodermatosclerosis, and healed ulceration
there was a median of 6, 45, and 217 WBCs per mm2,
respectively. This demonstrated a correlation between clinical disease severity and the number of leukocytes in the
dermis of patients with CVI.
The types of leukocytes involved in dermal venous stasis
skin changes remain controversial. T-lymphocytes, macrophages, and mast cells have been observed on immunohistochemical and electron microscopic examinations.
27,28
The
variation in types of leukocytes observed may refl ect the
types of patients investigated. The London group biopsied
patients with erythematous and eczematous skin changes,
whereas Pappas has evaluated predominantly older patients
with dermal fi brosis. Patients with eczematous skin changes
may have an autoimmune component to their CVI whereas
patients with dermal fi brosis may have experienced pathologic alterations consistent with chronic infl ammation and
altered tissue remodeling Skin biopsies have shown that in
liposclerotic, eczematous skin macrophages and lymphocytes were predominant in such diseased skin. Infi ltration of
leukocytes into the extracellular space has been documented
by observing the localization of these leukocytes around
capillaries and post-capillary venules. Accompanying the
leukocytes is a disorganized collagen deposition. Clearly,
chronic venous insuffi ciency of the skin and its subcutaneous tissues is a disease of chronic infl ammation, again
dependent upon venous hypertension.
SUMMARY AND CONCLUSIONS
Knowing the normal anatomy of the venous system of
the lower extremities and the normal functioning of its elements is essential to understanding the pathologic processes
of venous dysfunction. Both processes, valve and vein wall
damage, and the advanced skin changes of CVI are the result
of sterile infl ammatory reactions. Both appear to be triggered by venous hypertension and, therefore, therapy must
be directed at correcting such venous hypertension.
References
1. Federative International Committee for Anatomical Terminology,
Terminologia Anatomica. George Thieme Verlag, Stuttgart. 1998.
2. Bundens WP, Bergan JJ, Halasz NA, Murray J, Drehobl M. The superfi cial femoral vein: A potentially lethal misnomer, JAMA 1995. 274:
1296–1298.
3. Caggiati A, Bergan JJ, Gloviczki P, Jantet G, Wendell-Smith CP,
Partsch H. International Interdisciplinary Consensus Committee on
Venous Anatomical Terminology. Nomenclature of the veins of the
lower limbs: An international interdisciplinary consensus statement, J
Vasc Surg. 2002. 36: 416–422.
4. Weiss RA, Weiss MA. Controlled radiofrequency endovenous occlusion using a unique radiofrequency catheter under duplex guidance to
eliminate saphenous varicose vein refl ux: A 2-year follow-up, Dermatol Surg. 2002. 28: 38–42.
5. Bush RG, Hammond KA. Tumescent anesthetic technique for long
saphenous stripping, J Am Coll Surg. 1999. 189: 626–628.
6. Somjen GM. Anatomy of the superfi cial venous system, Dermatol
Surg. 1995. 21: 35–45.
7. Lurie F, Kistner RL, Eklof B, Kessler D. Mechanism of venous valve
closure and role of the valve in circulation: A new concept, J Vasc
Surg. 2003. 38: 955–961.
8. Arnoldi CC. Venous pressures in the leg of healthy human subjects at
rest and during muscular exercise in the nearly erect position, Acta
Chir Scand. 1965. 130: 520–534.
9. Gardner AMN, Fox RH. The Return of Blood to the Heart, 2e. John
Libbey Publisher, London. 1993. p.81.
10. Schmid-Schönbein GW, Takase S, Bergan JJ. New advances in the
understanding of the pathophysiology of chronic venous insuffi ciency,
Angiology. 2001. 52: Suppl 1: S27–34.
11. Chronic Venous Insuffi ciency: Diagnosis and Treatment. Ballard JL,
Bergan JJ, eds. Springer-Verlag, London Berlin Heidelberg. 2000.
12. Homans J. The etiology and treatment of varicose ulcer of the leg, Surg
Gynecol Obstet. 1917. 24: 300–311.
13. Browse NL, Burnand KG. The cause of venous ulceration, Lancet.
1982. 1998-ii: 243–245.
14. Homans J. The operative treatment of varicose veins and ulcers based
on a classifi cation of these lesions, Surg Gynec Obst. 1916. 22: 143–
158.
15. Blalock A. Oxygen content of blood in patients with varicose veins,
Arch Surg. 1929. 19: 898–904.
16. Piulachs P, Vidal Baraquer F. Pathogenic study of varicose veins,
Angiology. 1953. 4: 59–100.
17. Brewer AC. Arteriovenous shunts, Br Med J. 1950. 2: 270.
18. Bergan JJ, Weiss RA, Goldman MP. Extensive tissue necrosis following high-concentration sclerotherapy for varicose veins, Derm Surg.
2000. 26: 535–542.
19. Coleridge Smith PD. Microcirculation disorders in venous leg ulcer.
Microcirculation in CVI, Microcirculation. 2001. pp. 1–10.
20. Takase S, Lerond L, Bergan JJ, Schmid-Schönbein GW. The infl ammatory reaction during venous hypertension in the rat, Microcirculation. 2000. 7: 41–52.
21. Takase S, Schmid-Schönbein G, Bergan JJ. Leukocyte activation in
patients with venous insuffi ciency, J Vasc Surg. 1999. 30: 148–156.
22. Takase S, Pascarella L, Lerond L, Bergan JJ, Schmid-Schönbein GW.
Venous hypertension, infl ammation and valve remodeling, Eur J Vasc
and Endovasc Surg. 2004. 28: 484–493.
23. Hoshino S, Satokawa H, Ono T, Igari T. Surgical treatment for varicose
veins of the legs using intraoperative angioscopy. In: RaymondMartimbeau P, Prescott R, Zummo M, eds. Phlebologie 92. Paris: John
Libbey Eurotext. 1992. pp. 1083–1085.
24. Takase S, Pascarella L, Lerond L, Bergan JJ, Schmid-Schönbein GW.
Venous hypertension, infl ammation and valve remodeling, Eur J Vasc
Endovasc Surg. 2004. 28: 484–493.
References 45
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25. Thomas PR, Nash GB, Dormandy JA. White cell accumulation in
dependent legs of patients with venous hypertension: A possible mechanism for trophic changes in the skin, Br Med J (Clin Res Ed). 1988.
18; 296(6638): 1693–520.
26. Scott HJ, Smith PDC, Scurr JH. Histological study of white blood cells
and their association with lipodermatosclerosis and venous ulceration,
Br J Surg. 1991. 78: 210–211.
27. Wilkerson LS, Bunker C, Edward JCW, Scurr JH, Coleridge Smith
PD. Leukocytes, their role in the etiopathogenesis of skin damage in
venous disease, J Vasc Surg. 1993. 27: 669–675.
28. Pappas PJ, DeFouw DO, Venezio LM, Gorti R, Padberg FT, Jr., Silva
MB, Jr., et al. Morphometric assessment of the dermal microcirculation
in patients with chronic venous insuffi ciency, J Vasc Surg. 1997. 26:
784–795.
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CHAPTER
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5
Role of Physiologic Testing in Venous Disorders
JEFFREY K. RAINES and JOSE I. ALMEIDA
Of the 25 million Americans with venous insuffi ciency,
approximately 7 million exhibit serious symptoms such as
edema, skin changes, and venous ulcers.1 About 1 million
seek formal medical advice annually and do so for symptoms of venous insuffi ciency. Approximately 80% of venous
patients are managed conservatively with observation, leg
elevation, and support stockings; the remainder are treated
surgically with vein stripping or endovenous ablation. Most
investigators acknowledge with the development of safe,
less traumatic, and effective endovenous techniques for
venous insuffi ciency, more individuals in the population will
seek treatment, and physicians will be more inclined to
move from conservative therapy to surgical therapy.
Physiologic testing is used to defi ne deep venous thrombosis and identify, grade, and follow venous insuffi ciency.
Since more patients will be presenting for therapy because
of improved outcomes with endovenous techniques over
traditional surgery, physiologic testing will take on increasing importance. For purposes of this chapter, physiologic
testing includes the various devices based on plethysmographic concepts, and color fl ow duplex imaging. The goal
of these studies is to provide accurate information describing
the hemodynamic or anatomic characteristics of the patient
with chronic venous insuffi ciency, precluding the need for
invasive studies.
2
BACKGROUND
Venous insuffi ciency of the lower extremity is far more
frequent than venous insuffi ciency in any other part of the
human circulation. This chapter will therefore be limited to
the lower extremity. The venous system in the lower extremities is composed of three interconnected parts: the deep
system, perforating (i.e., communicating) system, and superfi cial system. By virtue of the venous muscular pump and
bicuspid/unidirectional valves, in healthy veins, blood fl ows
toward the right side of the heart (i.e., upward) and from the
superfi cial system to the deep system (i.e., inward).
Lower extremity muscle compartments contract during
ambulation. This contraction compresses the deep veins,
producing a pumping action, which propels blood upward
toward the right side of the heart. This pumping action is
signifi cant; transient pressures in the deep system have been
recorded as high as fi ve atmospheres during strenuous lower
extremity exertion. This pumping action secondary to ambulation has the effect of reducing pressure within the superfi cial system. With this in mind, it is instructive to comment
on the hydrostatic pressure under which all three venous
systems of the lower extremity are subjected. A fl uid column
has weight and can produce a pressure gradient. In an individual six feet in height, the distance from the level of the
right atrium to the ankle is 120 cm and produces a hydrostatic pressure of approximately 90 mmHg.
Deep veins can withstand elevated pressure because the
fascia in which they exist limits dilation. In contrast, the
superfi cial system, surrounded by elastic skin, is constructed
for low pressure; therefore, elevated pressure in the superfi cial system can produce dilation, elongation, and valve
failure. Dilation increases the diameter of the veins and
elongation causes them to be more tortuous.
Consider the following cascade of events. Because of
valve failure, above-physiologic pressure develops in the
superfi cial system. With time, nearby superfi cial valves
begin to fail (i.e., lose their ability to direct fl ow in one
direction). With dilation and multiple valve failure, venous
blood will fl ow in the direction of the pressure gradient,
which is downward and outward. This fl ow direction is
The Vein Book
47
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Copyright © 2006, Elsevier Inc.
48 Chapter 5/Role of Physiologic Testing in Venous Disorders
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pump. In subjects with venous insuffi ciency, the fl uid column
will not drop to normal levels. If a subject’s fl uid column
falls to normal levels while occluding the superfi cial system,
the observer knows the deep system is intact and the superfi cial system is incompetent. If the fl uid column remains
elevated with exclusion of the superfi cial system, the
observer knows the deep system is incompetent. As will be
illustrated, physiologic venous testing is based on the principles outlined in this experiment.
Although the morbidity secondary to venous insuffi ciency and varicose veins is signifi cant,3 the most devastating consequence is due to life-threatening venous
thromboembolism to the lungs. In a study from the Mayo
Clinic, during 14,629 person-years of follow-up, 1333
patients died. Seven-day, 30-day, and 1-year venous throm-
FIGURE 5.1 The stick fi gure on the left illustrates a normal subject erect
and motionless with a venous cannulation in the left foot. Venous pressure
rises to the level of the right atrium. The stick fi gure on the right illustrates
the effect of the normal lower extremity venous pump and the unidirectional valves activated by walking or ankle fl exion. The fl uid column is
reduced to between 50–60% of its resting value. Failure to reduce the height
of the fl uid column results in ambulatory venous hypertension (i.e., venous
insuffi ciency).
boembolism survival rates were 75%, 72%, and 64%,
respectively.
Two statements may summarize this section. First, the
culprit in venous insuffi ciency syndrome is elevated pressure when limbs are dependent or ambulating. Measuring
and understanding venous hemodynamics is the cornerstone
of this diagnosis. Second, deep venous thromboembolism
may result in venous insuffi ciency and may develop independently. This diagnosis is less hemodynamically oriented
and more focused on sonographic visualization of thrombi.
4
directly opposite physiologic fl ow (i.e., upward and inward).
The early result is varicose veins and telangiectasia, which
are visible on the skin surface.
Early or mild venous insuffi ciency produces low-level
pain, edema, burning, throbbing, and leg cramping. As the
disease progresses patients can develop venous stasis
changes that can lead to debilitating severe soft tissue ulceration. We know from hemodynamics and clinical experience, on eliminating high pressure or fl ow in diseased
superfi cial venous channels, symptoms can improve
dramatically.
In understanding lower extremity venous hemodynamics,
the following experiment is instructive (see Figure 5.1).
First, a superfi cial vein in the foot of a normal subject is
cannulated and connected to a fl uid column (sterile saline
with vitamin A to add color to the column). With the subject
standing erect, the fl uid column will rise to the level of the
right atrium. This is due to the fact that the pressure at the
right atrium is near zero and therefore, the venous pressure
at the cannulation site is almost entirely based on the subject’s hydrostatic blood column (the subject’s blood and the
fl uid in the column have nearly the same Specifi c Weight).
When the subject is asked to perform sustained ankle fl exion,
the fl uid column drops to between 50 to 60% of its resting
height. This simulates walking and the reduction in superfi cial venous pressure secondary to the ambulatory venous
PLETHYSMOGRAPHY
Plethysmographs are devices that measure volume
change. Over the last 50 years plethysmographs have been
developed and used clinically that employ completely different principles. Descriptions of four plethysmographs are
given next.
Impedance Plethysmograph (IPG)
This device is based on a fundamental principle of electronics, which states that voltage (V) across a localized
segment is equal to the impedance (Z) (i.e., resistance, inertance, and capacitance) of the segment times the current (I)
fl owing through the segment of interest (V = Z × I). It is
possible to isolate a portion of a limb (thigh, calf, lower leg,
etc.) and subject the limb segment to a standard and known
current while measuring the voltage across the segment. In
this setting the measured voltage is proportional to the
impedance of the segment. Most materials demonstrate
impedance. Therefore, blood, subcutaneous tissue, and even
bone have impedance. If we make the assumptions that
impedance of a limb segment can be measured accurately,
blood volume is the only signifi cant variable with time, and
that arterial blood volume change is electrically fi ltered or
small compared to venous blood volume measured, then
voltage is proportional to venous volume in the segment.
Plethysmography 49
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In practice the operator places circular electrodes around
the segment of interest, generally the proximal calf, and
connects the electrodes to the electrical console. The subject
is asked to perform a series of maneuvers, and outputs from
the device are recorded. The maneuvers and outputs are
similar for all plethysmographs described in this chapter and
are given later. This method has been used with success by
some investigators in the assessment of DVT and venous
insuffi ciency.
5,6
However, there are a number of factors that
limit its accuracy. First, the set-up is tedious and must be
done with care. Second, the coupling of the device to the
skin surface is important and unfortunately variable between
measurements and during examinations. Third, the signalto-noise-ratio between the real physiologic change and the
baseline error is low. For these reasons and the fact that more
clinically oriented plethysmographic methods have been
developed, the technique is not used routinely.
Strain-Gauge Plethysmograph (SGP)
This device measures circumference of a selected limb
segment. Circumference is related to segment crosssectional area, and cross-sectional area multiplied by length
is volume. In using SGP the following assumptions are
made. First, blood volume is the only signifi cant variable
with time, and second, arterial blood volume change is small
compared to venous blood volume changes.
The device is constructed using a small hollow elastic
tube, mercury, and an electrical circuit capable of measuring
voltage across the tubing length. The hollow fl exible tube is
fi lled with mercury, which conducts electricity well.
The tube containing the mercury is carefully placed
around the limb segment of interest and connected to the
electric circuit. The subject is asked to perform a series of
maneuvers, and outputs from the device are recorded. The
maneuvers and outputs are similar for all plethysmographs
described in this chapter and are given later. As the limb
segment circumference is changed secondary to venous
blood volume, the length of elastic tube changes. The voltage
is measured and displayed by the circuit. By measuring
circumference as a function of time, venous blood volume
as a function of time may be measured.
7,8
This technique has a number of drawbacks. First, the
instrumentation is diffi cult to construct. Second, the assumption that circumference measured over a very small slice of
the limb segment represents volume change in the segment
is often not true. Third, as in the case of IPG, the signal-tonoise-ratio is low. Along with IPG, this method is rarely
used in contemporary clinical settings.
Photoplethysmograph (PPG)
Photoplethysmographs are not true plethysmographs
because the measure they provide is qualitative and cannot
be used to determine volume. Despite this limitation, PPG
9,10
is used in many clinics to assess venous insuffi ciency.
The
device measures phenomenon limited to the microvasculature of the cutaneous skin. PPG instrumentation includes a
surface transducer, which is taped to the lower leg just above
the medial malleolus and connected to an electrical circuit.
The electrical circuit excites the transducer and records and
interprets the returning signal.
The PPG transducer is designed with an infrared light
emitting diode and a photosensor. The transducer transmits
light to the skin, which is both scattered and absorbed by
the tissue in the illuminated fi eld. Blood is more opaque than
surrounding tissue and therefore attenuates the refl ected
signal more than other tissue in the fi eld. The intensity of
refl ected light is reduced with more blood in the fi eld. If the
electrical circuit fi lters the higher frequency arterial pulsations it is possible to register a signal, which qualitatively
corresponds to venous volume in the segment of interest.
PPG therefore is able to detect changes in venous fi lling
secondary to various patient maneuvers, which will be
described later. PPG has found a role in the clinical assessment of venous insuffi ciency.
Air Plethysmograph (APG)
Properly designed air plethysmographs more accurately
measure true volume than IPG, SGP, or PPG and are easier
to use in the clinical setting.
characterized by three major components. The fi rst component is the transducer, which is a form of closed air
bladder used to surround the limb segment of interest. The
second component is a pressure sensor, which can accurately measure the pressure in the air bladder as a function
of time. The third component is the electrical circuit necessary to control the pressure sensor and display the measured
results.
As mentioned earlier, use of the APG is relatively simple.
The air bladders are generally self-contained units similar to
standard blood pressure cuffs and are designed for specifi c
limb segments. The connection to the console generally is
limited to a single rubber tube with connector. With the air
bladder surrounding the limb segment of interest, any change
in volume in the limb segment will cause the pressure within
the bladder to change. For example if limb volume increases
the bladder volume will decrease. Since the bladder is a
closed system, this will cause the bladder pressure to
increase. Accurate APG carefully correlates bladder state
(i.e., mean bladder pressure and volume), instantaneous
change in bladder pressure, and limb volume change. APG
is able to detect changes in venous limb volume secondary
to various patient maneuvers. The maneuvers and outputs
are similar for all plethysmographs described in this chapter
and are given later. APG is used in the clinical assessment
of venous insuffi ciency and DVT.
11–14
The instrumentation is
50 Chapter 5/Role of Physiologic Testing in Venous Disorders
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Defi nition of Parameters and Maneuvers
Used in Generic Plethysmography for
Venous Insuffi ciency
Venous insuffi ciency causes the three venous systems in
the lower extremity to misdirect venous blood volume.
Therefore, the goal of this testing is to characterize misdirection of venous blood volume, if present.
Our test subject is placed in the supine position. This will
lower venous pressure in the lower extremities to a value
only slightly above right atrial pressure (∼0 mmHg). Using
a plethysmograph an operator can obtain a baseline volume
in the segment of interest. When the subject is placed in the
erect position, lower extremity venous pressure increases
due to the hydrostatic column of blood extending from the
right atrium to the segment of interest. Since veins are compliant (i.e., increase volume with increased internal pressure), vein blood volume in the segment of interest increases.
This volume increase is displayed on a graph from which
measurements may be taken. The Y-axis is volume, and the
X-axis is time. Since all measurements are either times or
ratios, the Y-axis is not required to be strictly calibrated as
volume. However, its display on the graph must correlate
with volume change (see Figure 5.2).
The measurement between the supine baseline volume
and the erect volume plateau is known as the Venous Volume
(VV). From this same curve the operator can determine the
Venous Refi lling Time (VRT). This is the time measured
from when the baseline volume begins to increase to its
plateau. With the subject in the erect position, the operator
instructs the subject to perform a single brisk ankle fl exion.
This will produce a momentary reduction in Y-axis volume.
This change in volume is called the Ejection Volume (EV).
To calculate the Ejection Fraction (EF), the operator divides
EV by VV. The subject is then instructed to perform 10 brisk
ankle fl exions. This will produce a reduction in Y-axis
volume, which will be larger than the volume reduction
experienced with one fl exion. This allows the operator to
measure Residual Volume (RV). This is defi ned as the dif-
ference between the volume after 10 fl exions and the baseline volume. Finally, the operator can calculate the Residual
Volume Fraction (RVF) by dividing RV by VV.
15–17
Simplifi ed Diagnostic Criteria for
Venous Insuffi ciency
These criteria may be applied to any plethysmograph.
The only restriction is that the volume measurements be
taken accurately. In order to simplify the diagnostic criteria
for venous phlethysmographic studies we have focused on
three parameters. The fi rst is Venous Refi lling Time (VRT).
In patients with signifi cant venous insuffi ciency, venous
refi lling develops secondary to venous refl ux and clearly
reduces the time necessary to complete the process. If VRT
is >20 seconds, the limb is not demonstrating signifi cant
refl ux. If VRT is <20 seconds, the diagnosis of venous refl ux
should be considered.17 This should be taken in light of the
fi nding that subjects with VRT <10 seconds very often
present with venous ulceration.18 The second parameter is
Ejection Fraction (EF). In patients with deep or superfi cial
venous insuffi ciency or deep venous thrombosis, EF is
reduced. If EF is >60% the limb is presenting with normal
venous hemodynamics. For superfi cial venous insuffi ciency
the average EF is 50%. Average EF is reduced to 40% in
subjects with deep venous insuffi ciency and 35% in deep
venous obstruction. The third measurement is Residual
Volume Fraction (RVF). If RVF is elevated, the limb is
demonstrating venous ambulatory hypertension. A normal
value for RVF is <35%. Subjects with RVF >35% should
be evaluated further for venous disease.
17
FIGURE 5.2 This fi gure illustrates parameter defi nitions and maneuvers
used generically in plethysmographic studies for venous insuffi ciency.
Deep Venous Thrombosis—Examination
by Plethysmography
The four plethysmographs just described have been used
for the identifi cation and monitoring of DVT. For purposes
of this text a generic procedure for DVT will be described.
Deep venous thrombosis is a life-threatening disease; for
that reason alone accurate diagnosis and therapy are essential. The deep venous system is not only a conduit for returning blood to the right side of the heart; it is also a storage
or capacitant system. This means its volume changes rapidly
as pressure within the deep system changes. If one examines
a vein at low pressure the walls are nearly fully collapsed
and only a small fl ow channel is present. It takes very little
increase in internal fl uid pressure to expand the fl ow channel
of a vein. Finally, if there is obstruction in a segment of
deep vein, despite rich venous collateral channels, venous
Continuous-Wave Venous Doppler (CW Doppler) 51
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pressure distal to the obstruction will increase. Examination
by plethysmograph makes use of these two principles (i.e.,
volume change with increased pressure and resistance).
Typically a plethysmograph transducer is placed at the
calf or distal thigh with the patient lying supine on a table.
In the case of APG the transducer is an air bladder infl ated
to 5 mmHg; in the case of PPG the transducer is a light emitting diode. Proximal to the transducer a method of rapidly
occluding the deep system must be used. For all transducers
this can be a thigh cuff infl ated rapidly by hand bulb or
automatic infl ator.
With the transducer recording a stable venous signal at
5 mm/second chart speed, the pressure in the proximal
occluding cuff is rapidly elevated to 50 mmHg. The transducer is measuring absolute levels of volume.
With the increased pressure in the proximal cuff, venous
blood in the deep system cannot pass under the cuff until
the venous pressure reaches approximately occluding cuff
pressure. This increase in venous pressure (i.e., pooling)
develops because the proximal cuff does not obstruct the
arterial infl ow. After about 20 to 40 seconds, pressure in the
distal venous system reaches the pressure in the occluding
cuff and venous volume reaches a plateau. Once the plateau
has been reached, the operator rapidly releases the pressure
in the occluding cuff. The pooled venous blood can then
return to the right side of the heart via the larger veins
upstream. Two measures of venous hemodynamics are taken
during this test. First, there is the volume increase from the
baseline to the plateau. This is known as Segmental Venous
Capacitance (SVC) and represents the blood storage capacity of the segment vein. This generally is quoted in mm of
defl ection or ml if the system is calibrated to volume.
The second measurement is the slope of the volume-time
curve immediately after the pressure in the occluding cuff
is released. This is known as Maximum Venous Outfl ow
(MVO) and represents resistance to blood fl ow in the deep
system. This may be quoted in mm of defl ection/second
or ml/second if the system is calibrated to volume. The
next two sections defi ne the diagnostic use of these
parameters.
Maximum Venous Outfl ow (MVO)
As in the case of SVC, vascular technologists and physicians are able to identify a normal range of MVO with their
specifi c plethysmographic equipment. Normal veins exhibit
a very rapid decrease in volume on defl ation of the occluding cuff. When deep system resistance is increased due to
deep venous obstruction, the reduction in MVO is dramatic.
Again, in the case of unilateral disease, the normal limb can
serve as a control. A difference in MVO between limbs of
25% is abnormal.
11
When Continuous-wave Venous Doppler measurements,
SVC, and MVO are performed as a diagnostic package,
sensitivity and specifi city of the combined testing reach
85%, respectively.11 It should be acknowledged Duplex
Venous Doppler Ultrasonic Imaging, which requires more
expensive equipment, clearly demonstrates a higher sensitivity and specifi city. Further, ultrasound is able to more
accurately localize obstruction and age thrombus. For this
reason, plethysmographic methods have limited diagnostic
use. There is one area in venous disease where SVC and
MVO provide unique and important information. This is in
the determination of venous collaterization following a
DVT. Patients that normalize SVC and MVO rapidly have
an improved prognosis when compared to subjects in which
normalization is prolonged.
CONTINUOUS-WAVE VENOUS
DOPPLER (CW DOPPLER)
CW Doppler instruments are widely available, relatively
inexpensive, and used extensively to rapidly investigate the
peripheral vascular system. CW Doppler measurements can
be used independently, or as mentioned earlier, combined
with measurements from a plethysmograph. The purpose of
this section is to outline how CW Doppler is used to facilitate the diagnosis of venous insuffi ciency of the deep system,
specifi cally deep vein refl ux and deep venous thrombosis.
Segmental Venous Capacitance (SVC)
With experience, vascular technologists and physicians
are able to identify a normal range of SVC with their specifi c
plethysmographic equipment. With the subject supine,
normal veins have signifi cant capacitance. If proximal deep
venous obstruction is present, pressure distal to the obstruction increases and SVC is markedly reduced. Therefore, if
SVC reduces more than 25% when compared to normal
levels, venous abnormality is suggested.
that SVC always be measured bilaterally. In the case of
unilateral disease, the normal limb can serve as a control,
which increases both sensitivity and specifi city.
11
It is recommended
Deep Venous Thrombosis
Strandness and Baker introduced CW Doppler in the
1960s.19 Its initial application was peripheral arterial assessment. With the development of additional maneuvers the
instrumentation was applied fi rst to the diagnosis of DVT
and later to deep vein insuffi ciency.
We recommend that the subject be studied on a fl at examining table in which the lower extremities may be placed in
the dependent position at approximately 15 degrees. This
slight angle dilates the deep system, which makes the identifi cation of veins easier and improves the velocity signals.
We recommend that target veins include the common
femoral vein at the inguinal ligament, popliteal vein at the
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