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42
()
2
PV
22
rr
VV
1
2
()
Chapter 1 · Fundamental Principles
1.2.2.3 Perfusion Regulation
1
Blood ow throughout the body is regulated to ensure
X
adequate perfusion of organs and tissues and to adjust
the blood supply to a body region in response to varying
X
demand (which is activity-dependent in the extremity arteries or increases aer a meal in the mesenteric arteries). Local
blood ow is regulated by arterioles and capillaries, which
can dilate or constrict selectively and are therefore referred
to as resistance vessels. Two types of regulation can be distinguished:
5 autoregulation to maintain constant perfusion (cerebral
perfusion, renal arteries) and
5 adaptive regulation to adjust blood supply to varying
demand (. Fig.1.45c).
V
1
V
e result is an idealized estimate because the equation does
not take into account other systemic factors (blood pressure,
wall elasticity, peripheral resistance) that may aect blood
ow velocity in the stenotic segment. A sudden decrease in
the cross-sectional area is associated with strong acceleration forces, which turn laminar ow into plug ow along the
æ
ö
V
=×-
100 1
1
ç
÷
V
è
ø
2
percentage stenosis degree
cross-sectionaal area reduction
prestenotic velocity
intrastenotic
vvelocity
constricted segment. e increase in kinetic energy resulting
Normal resting perfusion is maintained by constricted arterioles, resulting in high peripheral resistance and pulsatile
ow. Widening of the arterioles in response to an increase
in demand during exercise leads to augmented blood ow.
from the increase in average ow velocity in the stenosis leads
to a decrease in static (lateral) pressure. is conservation of
energy (7 Sect. 1.2.1) is expressed in the Bernoulli equation
as the sum of lateral pressure energy and kinetic energy:
e decreased peripheral resistance results in less pulsatile ow and a larger diastolic component (. Fig. 2.15 and
. Fig.1.45).
In autoregulation, the ability of the arterioles to adjust
their diameter serves to maintain constant blood ow and
compensates for changes in arterial blood pressure or other
systemic factors. A drop in perfusion pressure leads to compensatory vasodilation of resistance vessels, while an increase
in pressure leads to compensatory vasoconstriction.
1
+××=+××
PV
11
P
prestenotic lateral pressure
1
P
intrrastenotic lateral pressure
2
prestenotic flow velocity
1
iVV
nntrastenotic flow velocity
2
2
2
density of bloodr
1
2
2
Using the Bernoulli equation, the conversion of static pres-
1.2.3 Stenosis Grading andBlood Flow
Measurement
Volumetric blood ow measurement plays no role in daily
sure energy into kinetic energy resulting from a reduction in
the vessel cross-sectional area is expressed as follows:
PP
12 221
clinical practice, except for assessing ow in hemodialysis
access stulas. is topic is treated in a separate chapter
and details of ow volume measurement are provided in
7 Sect. 4.4.
Blood ow volume can be calculated from the vascular
cross-sectional area and mean ow velocity; however, this
method is prone to errors unless great care is taken in determining these two parameters (see
7 Sect. 1.1.2.4). erefore,
it is not recommended to calculate ow volume using inbuilt
soware tools.
The continuity equation states that the volume flow
rate (cross-sectional area multiplied by average flow
velocity) remains constant throughout a vessel. Therefore,
an abrupt decrease in arterial diameter in a stenotic vessel segment is associated with an increase in blood flow
velocity (a 50% decrease in diameter, corresponding to a
75% decrease in cross-sectional area, will result in a four
times higher flow velocity). The flow profile flattens out
(plug flow) when the blood enters a narrower segment.
If the increase in flow velocity is known, it is possible to
estimate the degree of stenosis using the continuity equation (. Fig.1.44a):
e poststenotic increase in the cross-sectional ow area
leads to turbulent ow, ow separation, and vortexing. e
pronounced turbulence occurring in the presence of highgrade stenosis is associated with eddy currents and backward
ow, resulting in the irreversible loss of most of the kinetic
energy, while the loss due to inertial and frictional forces is
negligible (Weber etal. 1992). e pressure drop across a stenosis (substantial portion of the Doppler-derived blood pressure) thus predominantly
the stenosis. erefore, the kinetic energy expressed as peak
systolic velocity (PSV) in the stenosis can serve as a measure
of the pressure drop across the stenosis (according to the
simplied Bernoulli equation: P
prestenotic velocity V1 in favor of intrastenotic velocity V2)
and the degree of stenosis (see 7 Sect. 2.1.6.1.1).
Blood ow resumes its laminar prole only farther downstream of the stenosis as a result of decreasing turbulence
and the inuence of mural friction. e conversion of much
of the remaining kinetic energy into static pressure energy
promotes dilatation of the atherosclerotic wall in the poststenotic arterial segment.
-=×× -
r
2
reects the lost kinetic energy in
– P2=4×V
1
2
; neglecting
2
()
1.2 · Hemodynamic Principles
43
1
An examiner using the Doppler-derived PSV to grade
stenosis should be aware, though, that, due to friction losses
inside the stenosis, this method is subject to some inaccuracy. In high-grade stenosis with a reduced volume ow rate,
ow velocity is already decreased in the prestenotic segment,
resulting in an intrastenotic increase in velocity that is lower
than expected from the diameter reduction. e maximum
intrastenotic velocity may thus be lower in high-grade stenosis with a reduced volume ow rate than in moderate stenosis
causing less pronounced ow reduction.
Stenosis grading based on absolute intrastenotic PSV
thresholds is also unreliable in patients with multilevel
steno- occlusive disease because the poststenotic pressure
drop downstream of a more proximal stenosis results in a
lower PSV upstream of the next (second or third) stenosis. To overcome this limitation, most examiners prefer to
identify and grade stenosis by determining the increase in
PSV in the stenosis in relation to the PSV in the prestenotic
segment (known as the PSV ratio). In general, a PSV ratio
greater than 2, indicating doubling of PSV inside the stenosis, is taken as the cuto for hemodynamically signicant
stenosis (>50%). Calculation of PSV ratios is less straightforward for stenoses occurring immediately downstream of
a vessel division, which is a common site of stenosis (origins
of profunda femoris or renal arteries, carotid bifurcation).
For these vessel segments, empirical threshold velocities
(reference value, angiography) must be determined to identify hemodynamically signicant stenosis. Such thresholds
are aected by systemic factors (hypercirculation, hypertension).
Careful adjustment of the Doppler angle of insonation
is crucial in measuring blood ow velocity for stenosis
grading. Ideally, the Doppler angle should be 60° or less to
minimize the eect of Doppler angle misreading on ow calculation; this eect becomes much larger when the Doppler
angle is 70° or greater. Alignment of the angle correction cursor may be technically challenging in curved or branching
vessels.
e maximum velocity, or PSV, is measured in the stenosis or the jet seen in the color duplex image. e intrastenotic increase in ow velocity in high-grade stenosis
results in a higher Reynolds number and is associated with
turbulent ow. Turbulence is characterized on color duplex
images by a typical mosaic pattern around the central stenosis jet with backward ow near the wall. Depending on
the increase in ow velocity, eddy currents may be seen over
a length of several centimeters downstream of the stenosis
. Fig.1.46).
(
e jet tapers o distal to the stenosis, while the zone
of turbulent ow widens until it occupies the entire lumen.
Further downstream, ow becomes laminar again. e pressure drop across a stenosis is determined by its length and
degree. ese two parameters, along with poststenotic turbulence, govern the loss of kinetic energy. e magnitude of the
intrastenotic pressure drop correlates with the kinetic pressure energy present in the stenosis jet. Based on measurement of the stenosis jet, the pressure drop across the stenosis
can be estimated using the simplied Bernoulli equation
(neglecting prestenotic ow velocity) as
PP jet velocity
12 2
e jet axis is typically not parallel to the vessel wall, especially when the stenosis is eccentric. Depiction of the stenosis
jet in the B-mode image can help the examiner in aligning the
angle correction cursor with the direction of ow for reliable
measurement of blood ow velocity in the jet (. Figs. 1.47
and 5.21).
A study comparing the invasively measured mean catheter pressure gradient across stenotic vessel segments with
the pressure gradient determined from the stenosis jet using
duplex ultrasound (Strauss etal. 1993) found a correlation of
R=0.77 for iliac artery stenoses. is investigation was based
on preceding model calculations and neglected viscous friction losses and energy losses due to poststenotic turbulence.
In vitro measurements in a model of pulsatile ow in
peripheral arteries demonstrated good agreement for the pressure decrease across a stenosis measured invasively and that
determined by Doppler ultrasound. e correlation found for
dierent degrees of stenosis was R=0.98 (Strauss etal. 1990;
Weber et al. 1992). Still, quantitative evaluation of stenosis
using only the absolute values of maximum intrastenotic frequency shis or peak velocities is discouraged, as the magnitude of intrastenotic ow velocity is also aected by various
other factors including central regulatory mechanisms (blood
pressure), collateral pathways, and peripheral resistance.
Empirical data show that a stenosis becomes hemodynamically relevant and causes clinical symptoms when the vessel
diameter is reduced by at least 30–50% (corresponding to a crosssectional area reduction of 50–75%). e pressure drop across a
stenosis increases with its degree and length and is reected in a
decrease in the Doppler-derived peripheral blood pressure.
Because PSV measured in a stenosis is inuenced by systemic factors (blood pressure during the examination, vessel
wall elasticity), stenosis grading based on absolute PSV cutos for dierent degrees of stenosis identied by ROC analysis is limited. To overcome these limitations, the use of a ratio
relating intrastenotic to prestenotic PSV (known as systolic
velocity ratio (SVR) or PSV ratio) was proposed as an alternative velocity parameter for stenosis grading and explored
in dierent vascular territories. Overall, the results come
close to the theoretical predictions of the continuity equation (see . Fig. 2.17), conrming that a ratio> 2 indicates
hemodynamically signicant stenosis (>50%) and a ratio>4
high- grade stenosis (>75%).
While stenosis grading based on PSV ratios yields the
most reliable results, there are some potential sources of
error the examiner should be aware of (. Table1.10):
5 Measurements using invitro ow models yielded
slightly lower PSV ratios than theoretically predicted
(loss due to intrastenotic friction)
5 Cutos for diameter reduction only apply to concentric
stenoses: an eccentric stenosis with the same diameter
reduction as a concentric stenosis produces a smaller
4-=×
2
V
44
bc
Chapter 1 · Fundamental Principles
1
a
def
. Fig. 1.46 a Blood ow patterns and eects on Doppler waveforms from dierent sites within and around a stenosis of the internal carotid artery
(ICA): 1=prestenotic ow (laminar, pulsatile); 2=intrastenotic ow (plug prole, maximum increase in peak systolic velocity (PSV), increase varies
with diameter reduction); 3=immediately poststenotic ow (marked turbulence, increased PSV); 4=poststenotic ow (return to lower ow velocity, residual turbulence); 5=poststenotic ow further downstream (return to laminar ow but decreased pulsatility, attened waveform with larger
diastolic component). b-f The waveform shapes in a illustrate stenosis-related ow changes in the carotid artery, but basically the same patterns
occur in a stenotic peripheral artery (see direct and indirect stenosis criteria in 7 Sect. 2.1.6.1.4), except that ow is more pulsatile (triphasic waveform). In this territory, loss of pulsatility in the poststenotic segment (with transition to a monophasic waveform) can serve as an indirect stenosis
criterion. b Popliteal artery stenosis: Proximal to the origin of hemodynamically signicant collaterals, the normal triphasic prestenotic waveform
may show reduced pulsatility. The extent to which pulsatility is decreased depends on the amount of collateral ow and compensatory ischemic
widening of arteries and arterioles in the periphery. When the sample volume is placed upstream of the origin of a collateral (KOL), there is only
a subtle incisure in the Doppler waveform in early diastole and continuous blood ow throughout diastole. Farther away from the transducer, a
collateral arising from the popliteal artery is seen, which provides signicant compensatory circulation. The hemodynamic eects of collateralization are rarely depicted in such an impressive manner. In this situation, two dierent prestenotic PSV values are obtained (due to ow division):
75cm/s proximal to the origin of the collateral versus 50cm/s distal to it (see c). Hence, the continuity equation will yield two dierent results for
the intrastenotic-to-prestenotic PSV ratio, depending on which of the two prestenotic PSVs is used (see . Fig. 2.16). The PSV ratio calculated with
the higher prestenotic PSV, measured proximal to the collateral origin, underestimates the degree of stenosis. c Distal to the collateral, the increased
pulsatility reects the ow resistance in the popliteal artery immediately before the stenosis. The abnormal diastolic ow is not only a function of
the stenosis- related peripheral resistance but also of vessel elasticity. Proximal to the sample volume, the hemodynamically signicant collateral
(KOL) arising from the popliteal artery is displayed in blue. The stenotic popliteal artery segment is not depicted but is likely to be located to the
right of the view presented. d The high-grade stenosis caused by a hypoechoic plaque produces aliasing in the color duplex image. The Doppler
spectrum shows the ow velocity to be increased to over 600cm/s (see waveform 2in a). In the segment depicted in the B-mode scan, the popliteal
artery stenosis appears to be less severe because the plaque predominantly involves the lateral vessel wall as compared with the spectral display,
which reects the hemodynamic signicance of the stenosis (see . Fig. 5.14). Like angiography, the B-mode scan reduces the three- dimensional
lumen to a two-dimensional, longitudinal plane. Depending on the plane of the gray-scale image, the severity of the stenosis caused by plaque may
be underestimated and may dier from the hemodynamic degree of stenosis based on PSV (see . Fig. 5.27). e In the immediate poststenotic segment, turbulent ow is predominant both in the color duplex image and in the Doppler waveform. PSV is still increased (300cm/s) (see waveform
3in a). f Three centimeters downstream of the stenosis, ow is monophasic with a delayed systolic rise and reduced PSV (see waveform 5in a)
reduction of the vascular cross-sectional area. Hence, the
eccentric stenosis has a less marked hemodynamic eect
and the resulting increase in PSV is smaller (see . Fig.
2.17
). is is important to keep in mind and explains
some of the discrepancies between a morphologic stenosis grading technique such as angiography and a hemodynamic technique such as duplex ultrasound.
5 When selecting the site of prestenotic PSV measurement
it is important to be aware of the eect of collaterals:
pre- and intrastenotic PSVs are higher in the absence of
collateralization, and prestenotic PSV is higher upstream
of the origin of a collateral than downstream of it (see
. Table 2.9 and . Figs. 2.16b and 1.46).
5 Ratios of intrastenotic to prestenotic PSV cannot be used
to grade stenosis at sites of vessel branching (femoral and
carotid bifurcation; see 7 Sects. 2.1.6.1.9 and 5.6.1.2) due
to dierences in diameter and hemodynamics between
stenotic and prestenotic segments and other inuencing
factors, e.g., steno-occlusive lesions in the other branch,
that are dicult to control. Empirical cutos dened for
the carotid bifurcation (see . Table 5.9) can be used as
secondary criteria but are only approximations.
Because stenosis most commonly develops at vessel origins
(renal arteries) and in bifurcations (carotid, femoral, and
iliac arteries), where the ratio of intrastenotic to prestenotic
for ICA stenosis)
150
100
50
100
150
200
250
300
400
500
1.2 · Hemodynamic Principles
PSV is of limited value, empirical data and graphic interpolations were used to establish nomograms and derive
thresholds for stenosis grading on the basis of intrastenotic
PSV in relation to PSV proximal or distal to the stenotic segment (Ranke etal. 1995). However, measuring the reference
velocity distal to the stenosis may introduce new sources of
error (hemodynamic eects of collaterals). Nomograms were
originally developed for the peripheral arteries but have since
been used to grade stenoses of the cerebral arteries as well.
e use of nomograms for stenosis grading is based on the
assumption that the nonstenotic vascular diameter in the
stenotic segment is identical to the diameter of the prestenotic or poststenotic segment in which the reference velocity
is measured (. Fig.1.48). It follows that the intrastenotic to
90
80
70
60
50
Percent stenosis
(distal degree
for ICA stenosis)
<60
60–70
70–80
45
1
60
70
80
90
. Fig. 1.47 In the eccentric high-grade stenosis of the internal
carotid artery (ICA) shown, the Doppler angle adjusted relative to the
vessel wall diers by approx. 10° from the angle relative to the stenosis
jet. Flow in the ICA is shown in blue (away from transducer) with aliasing indicating the stenosis jet. Distal to the hypoechoic plaque, blood
ow is red, indicating ow reversal resulting from ow separations and
eddy currents. The color change in the common carotid artery and the
bulb (red to blue) is due to a change in ow direction relative to the
ultrasound beam (ow toward and away from transducer) and ow
separation in the bulb (blue). Proper alignment of the Doppler angle
with the stenosis jet would have yielded a higher ow acceleration. The
turbulent ow components are reected more adequately in the Doppler waveform (see
. Fig. 5.21)
40
30
20
Prestenotic
PSV in cm/s
(poststenotic PSV
. Fig. 1.48 Nomogram for grading stenosis (Modied from Ranke
etal. 1995). Based on graphic interpolation, the degree of stenosis is
determined from the ratio of intrastenotic peak systolic velocity (PSV)
to the proximal or distal PSV.Example 1: 60–70% stenosis of the supercial femoral artery (red line) with a PSV of 320cm/s in the stenosis and
a prestenotic PSV of 95cm/s. Example 2: Internal carotid artery (ICA)
stenosis (blue line) with a PSV of 260cm/s in the stenosis and a poststenotic PSV of 80cm/s, yielding a distal stenosis degree of 60–70%. This
can be converted to a local stenosis degree of 70–80% (
80–90
>90
Intrastenotic
PSV in
cm/s
7 Sect. 5.5.1.1)
. Table 1.10 Duplex ultrasound stenosis grading based on the continuity equation. Dierences between theoretically predicted PSV
ratios (intrastenotic PSV divided by prestenotic PSV) and PSV ratios measured invitro are due to frictional losses within the stenosis. The
thresholds apply to stenosis caused by concentric plaque occurring in straight vessel segments
Degree of stenosis PSV ratio
Vascular cross-sectional area
reduction (%)
> 50 > 30 > 2 > approx. 1.8
> 75 > 50 > 4 > approx. 3.6
> 85 > approx. 60 > 6.66 > approx. 6.2
> 95 > approx. 80 > 20 > approx. 15
Diameter reduction(%) Theoretically predicted PSV ratio PSV ratio measured invitro
46
Chapter 1 · Fundamental Principles
poststenotic PSV ratio is used to grade a bifurcation steno-
1
sis, at the origin of the ICA, for instance (see . Fig. 5.9b).
Here, no collaterals enter the poststenotic segment, and in
accordance with the continuity principle, identical ow
velocities can be assumed proximal and distal to the stenosis
(except for losses due to the stenosis itself). is is why the
North American Symptomatic Carotid Endarterectomy Trial
(NASCET) used the so-called distal grading method for stenosis at the ICA origin, which is based on the measurement
of intra- and poststenotic PSV and graphic interpolation
but does not take plaque thickness in the carotid bulb into
account. Conversion tables (7 Sect. 5.2.1) are used to derive
the local degree of stenosis.
e main factors that may inuence the PSV and must
be considered in order not to over- or underestimate stenosis
severity are discussed in 7 Sect. 5.6.1.2.1 (“Critical Appraisal
of PSV: e Main Criterion of Carotid Stenosis”).
One important factor is that a decrease in peripheral
resistance, for example, during muscle activity, is associated with a relative increase in the degree of stenosis. e
increased blood volume required in the periphery per unit
time leads to a relatively greater reduction of the blood ow
through the narrowed segment above a certain degree of
stenosis, resulting in a greater discrepancy between the ow
volume required in the periphery and the volume that can
pass the stenotic segment. As a result, the peripheral dilatation associated with muscle activity can reduce the stenosisrelated perfusion pressure to such an extent that relative or
absolute ischemia may occur. e hemodynamic eects of
an
exercise- induced, hemodynamically significant per-
fusion reductio
n in the presence of a stenosis that is not
hemodynamically signicant at rest are also reected in the
Doppler waveform: there is a more pronounced increase
in the diastolic component during exercise but, above all,
a longer rest aer exercise is required before the postocclusive Doppler waveform returns to its normal triphasic
pattern (as compared with the contralateral side). In addition to the local degree of stenosis, the severity of peripheral perfusion reduction is also aected by other occlusive
processes and above all by cardiac function (in particular
systolic pressure) and the extent of collateralization.
e decrease in pulsatility is primarily due to the high
pressure gradient associated with luminal narrowing. e
changes in the spectral waveform proximal to a vessel
obstruction vary with collateral perfusion and the distance
between the site of sampling and the vessel lesion. Close to
the lesion, pulsatility increases as a result of the high resistance. When the Doppler information is sampled proximal to
the origin of relevant collateral vessels, peripheral resistance
causes a less pulsatile ow prole (
. Fig. 1.46). e hemo-
dynamic changes resulting from widening of the arterioles,
which decrease their tone as the blood supply drops, aect
the ow pattern in the prestenotic vessel segment through
the collateral pathways.
Grading of stenosis at arterial origins (ICA, profunda
femoris, and renal arteries) relies on empirical data as the
continuity equation does not apply to vessel divisions. In the
clinical setting, it is not generally necessary to determine an
exact percentage as the therapeutic management of a hemodynamically signicant stenosis is guided by the patient’s
clinical symptoms and the vessel segment aected.
On color duplex images acquired with adequate settings, aliasing will already suggest a stenosis. Nevertheless,
quantitative evaluation must be performed by analysis of the
Doppler waveform with angle-corrected velocity measurement using the criteria outlined above.
Again and again it has been proposed to measure
the degree of a stenosis
planimetrically by determining
the residual patent lumen, visualized in the color ow
mode, in relation to the vessel lumen (wall). However,
this approach is oen impaired or yields unsatisfactory
results due to inaccuracies resulting from color overow
(few color scan lines with interpolation) and scattering or
acoustic shadowing due to intrastenotic structures such as
calcied plaques. Under ideal conditions with complete
direct visualization of the stenotic segment, absence of
aliasing, and localization of the stenosis outside a bifurcation, determination of the residual lumen by color duplex
ultrasound was found to have a satisfactory diagnostic
accuracy of 85% compared with angiography (Steinke etal.
1990). Planimetric measurement appears to be most suitable for estimating the degree of mild to moderate stenosis
(see
. Figs. 5.53 (Atlas), 5.69 (Atlas), and 5.14) but should
not be used unless plaque echogenicity enables reliable definition of the patent lumen on B-mode images. Planimetric
stenosis grading on the basis of the cross- sectional area
reduction is justied only because these stenoses have no
hemodynamically relevant eect and therefore will not be
detected by spectral Doppler. e more complex plaque
congurations typically encountered when higher- grade
stenosis is present may not allow adequate identication
of the residual lumen, precluding grading on the basis of
B-mode imaging.
e use of color duplex images for dening the patent
lumen for stenosis grading has inherent methodological
limitations and is discouraged.
With the angle of incidence perpendicular to the vessel
(i.e., α = 90°) in the transverse plane, the Doppler equation
predicts Doppler-shied frequencies approximating zero,
resulting in poor or very inadequate visualization of blood
ow. ese limitations can be overcome to some extent, but
the remedies are likewise subject to error:
5 Slightly tilting the transducer to obtain a Doppler angle
<90° will improve the Doppler signal, but this comes at
the expense of introducing errors into the measurement
of the vascular diameter and cross-sectional area, which
becomes an oblique plane not showing the exact cross-
section but rather an ellipsoid vessel section.
5 e second remedy is to increase the color gain to make
up for the inadequate color display of the patent lumen,
but, as described above, this may result in color spillover
obscuring the vessel wall and plaque edge.
1.3 · Machine Settings
47
1
1.2.3.1 Poststenotic Parameters
1.2.3.1.1 Acceleration Time– Resistive Index
Another important Doppler parameter is the systolic acceleration time (also known as the systolic rise time) or acceleration index. Normal arterial blood ow is characterized
by a rapid systolic upstroke with a short rise time of a few
hundredth of a second before peak systolic velocity (PSV)
is reached. Distal to a high-grade stenosis or occlusion, the
upstroke is delayed, resulting in a longer acceleration time
and a reduced acceleration index (δV/δT)– mainly because
ow through collaterals is slower.
Acceleration time measurement is mainly used in the
sonographic evaluation of the renal arteries, where a prolonged acceleration time measured at the hilum is considered
a sign of a severe proximal stenosis (. Figs.1.49 and 6.8).
e delayed systolic upstroke in the poststenotic Doppler
waveform is also due to the slower systolic pressure buildup in the poststenotic segment. A longer acceleration time
in the poststenotic waveform is an indirect sign of a hemodynamically signicant stenosis. Behind high-grade stenosis,
the delayed equalization of central and peripheral (prestenotic and poststenotic) pressure during the cardiac cycle also
contributes to the persistent diastolic ow. is postocclusive increase in diastolic pressure is due to the decreased
peripheral resistance resulting from arteriolar widening in
response to reduced perfusion (. Fig.1.45). A stenosis may
be identied faster by obtaining Doppler spectra at selected
sites and evaluating them for prestenotic and poststenotic
criteria. If a stenosis is suspected in a vessel segment that is
dicult to interrogate directly, the so-called damping factor
can be calculated from the resistive indices (pulsatility indices) proximal and distal to the suspected stenosis in order to
estimate the signicance of the ow obstruction.
Pr
oximal pulsatility index
Dampingfactor
=
Distal pulsatilit
yyindex
Stenosis of less than 60% has little eect on the poststenotic
Doppler waveform. Only higher-grade stenoses are associated with an increasing reduction in poststenotic PSV, a less
steep systolic upslope, and delayed diastolic decrease with
persistent ow to the periphery. e decreased PSV and
delayed systolic rise are primarily due to the proximal ow
obstruction, while the monophasic ow prole results from
peripheral vasodilatation secondary to a mismatch of blood
supply and demand. e latter can thus also inuence the
prestenotic waveform via the collateral vessels.
1.3 Machine Settings
Proper selection of scanning parameters is of utmost importance for vascular examinations using color-coded duplex
ultrasound (. Tables 1.11 and 1.12). Adjustment is done
v
+
0
–
a
v
+
0
–
b
. Fig. 1.49a, b A longer systolic acceleration time and a reduced
acceleration index in a postobstructive vessel segment indicate
higher-grade stenosis and can be used as indirect stenosis criteria. The
increase in acceleration time is proportional to the degree of stenosis
(see . Fig. 6.8)
Systolic acceleration time
V
T
Systolic acceleration index
V
=
T
t
t
. Table 1.11 Optimal machine settings for specic diagnostic
tasks: Color-coded duplex ultrasound
Parameter Evaluation of ow
pattern
Evaluation for
stenosis
PRF As high as possible Low
Color box Small Fairly large
Doppler angle Intermediate (50°–60°) As small as possible
Wall lter Intermediate Low
Color gain Intermediate High
. Table 1.12 Optimal machine settings for specic diagnostic
tasks: Pulsed Doppler ultrasound
Parameter Evaluation of fast
ow
PRF As high as possible As low as possible
Wall lter Intermediate Low
Doppler angle 70°–90° As small as possible
Transducer Low frequency Higher frequency
Evaluation of small
vessels
Measurement of
slow ow
Evaluation of slow
ow
48
ab
Chapter 1 · Fundamental Principles
1
. Fig. 1.50a, b An acute angle of insonation is a prerequisite for reliable Doppler-based stenosis grading including hemodynamic parameters.
When the target vessel is insonated at a larger angle of say 70°, a small angle error of 5°, which is unavoidable, results in a disproportionate error
in the measured fow velocity. Selection of a proper transducer can make it easier for the examiner to obtain an adequate Doppler angle. a A
linear transducer, with a beam steering range of 20°, does not allow interrogation of an artery or vein coursing parallel to the skin surface with
an angle of less than 70°. b A curved array transducer with a small footprint can be titlted and, with the sample volume placed at the edge of the
scan sector, a Doppler waveform can be obtained with a small angle of insonation. In this way, vessels running parallel to the skin surface can be
interrogated with a Doppler angle of 50–60° (57° in the example shown). For the higher-grade stenosis in a and b, a peak systolic velocity (PSV) of
380cm/s was measured
individually for the respective vessel to be interrogated, in
particular when spectral Doppler information is collected.
e most important aspects are summarized below.
5 Transducer
5 Selection of a suitable frequency
5 Adequate presetting (magnication, gain, focusing,
PRF, wall lter, etc.)
5 Adjustment of B-mode scanning parameters
5 Identication of the target vessel in the transverse
plane
5 90° clockwise rotation of the transducer to depict the
vessel in the longitudinal plane
5 Focusing of the target vessel
5 Optimization of the image size
5 Optimization of gain and TGC: black vessel lumen,
walls sharply delineated
Color Doppler
5
5 Angling of the transducer to interrogate the vessel in
the longitudinal plane (to improve angle of incidence)
5 Positioning of the color box, possibly tilting it
(parallel transducer), to ensure the smallest angle
possible in relation to the vessel axis
5 Selecting the size of the color box in such a way as to
ensure a high enough frame rate
5 Optimizing gain
5 Adjusting PRF (. Fig.1.50):
Ȥ Higher PRF when aliasing occurs
Ȥ Lower PRF when no ow is detected but slow ow
is expected
5 Adjusting high-pass lter (HPF) (rarely necessary as
mostly coupled to PRF)
Ȥ Lower cuto to detect very slow ow
Ȥ Higher cuto when motion artifacts occur
5 If color lling of the vessel is insucient, a lower-
frequency transducer should be selected to improve
penetration depth. e poorer spatial resolution is
negligible in the color mode as it is compensated for
by the superior color signal.
5
Pulsed Doppler
5 Placing the Doppler gate in the center of the lumen in
the color-mode viewnder at an angle <70° relative to
the longitudinal vessel axis
5 Angle correction
5 Adjusting the Doppler gate width to cover the entire
lumen
5 If the Doppler signal is poor, the color mode should
be frozen in triplex scanning to improve Doppler
resolution
Optimizing the spectral waveform (. Figs.1.35, 1.36,
5
1.37, 1.38, 1.39, and 1.40)
5 Gain:
Ȥ Absent or sketchy curve: gain ↑
Ȥ Overmodulation (complete lling-in of systolic
window, mirror image): gain ↓
5 PRF:
Ȥ Peak frequency/velocity cut o (aliasing): PRF ↑
Ȥ Spectrum too “small”: PRF ↓
5 Filter:
Ȥ Depiction of slow ow: HPF ↓
Ȥ Elimination of interfering low frequencies: HPF ↑
An optimal waveform can be sampled from the site interrogated by minimally changing the transducer position using
for orientation the Doppler tracing but above all the acoustic
1.3 · Machine Settings
49
1
Doppler signal. An abnormal signal is oen heard before the
transducer provides the corresponding graphic information
(in particular when there is scattering due to plaque).
It is important to note that, in vessel segments with highgrade stenosis and very turbulent ow, high-energy frequencies from slow ow are predominant. For stenosis grading,
however, it is important to register the fast ow that oen has
a low energy and is concentrated in a thin jet. e following
measures are recommended to determine peak ow veloc-
ity in high-grade stenosis
5 Selection of a high PRF
5 Overmodulation of the spectrum by a higher gain to
also depict the low-energy, high Doppler frequencies
5 Localization of the jet by minimally and carefully chang-
ing the transducer position under acoustic and visual
guidance.
:
51
Extremity Arteries
2.1 Pelvic andLeg Arteries – 53
2.1.1 Vascular Anatomy – 53
2.1.1.1 Pelvic Arteries – 53
2.1.1.2 Leg Arteries – 53
2.1.2 Examination Protocol andTechnique – 55
2.1.2.1 Pelvic Arteries – 55
2.1.2.2 Leg Arteries – 56
2.1.3 Specic Aspects oftheExamination fromthePerspective
oftheAngiologist andVascular Surgeon – 61
2.1.4 Interpretation andDocumentation – 64
2.1.5 Normal Duplex Ultrasound ofPelvic andLeg Arteries – 64
2.1.6 Abnormal Findings – 65
2.1.6.1 Atherosclerotic Occlusive Disease – 65
2.1.6.1.1 Pelvic Arteries – 67
2.1.6.1.2 Time-Ecient Examination Based onWaveform Analysis – 68
2.1.6.1.3 Stenosis Grading – 70
2.1.6.1.4 Leg Arteries – 71
2.1.6.1.5 Stenosis Grading: Ultrasound Versus Angiography – 75
2.1.6.1.6 Role ofCollateralization inStenosis Grading – 77
2.1.6.1.7 Eects ofCollateralization onPre- andPostocclusive
Spectral Doppler Waveforms – 78
2.1.6.1.8 Plaque Conguration andStenosis Degree – 79
2.1.6.1.9 Profunda Femoris Artery – 81
2.1.6.1.10 Spectral Doppler Imaging below theKnee – 83
2.1.6.1.11 Role ofContrast-Enhanced Ultrasound – 84
2.1.6.1.12 Identication ofPedal Target Artery forBypass Grafting – 85
2.1.6.1.13 Multilevel Obstruction – 85
2.1.6.1.14 Arterial Occlusion – 85
2.1.6.2 Arterial Embolism – 88
2.1.6.3 Aneurysm – 89
2.1.6.3.1 True Aneurysm – 89
2.1.6.3.2 Pseudoaneurysm – 89
2.1.6.4 Rare Stenosing Arterial Diseases ofNonatherosclerotic Origin – 92
2.1.6.4.1 Adventitial Cystic Disease – 93
2.1.6.4.2 Popliteal Artery Entrapment Syndrome – 95
2.1.6.4.3 Raynaud’s Disease – 98
2.1.6.4.4 Paraneoplastic Disturbance ofAcral Perfusion – 98
2.1.6.4.5 Buerger’s Disease – 98
2.1.6.4.6 Vascular Inammatory Disease – 99
2
© Springer International Publishing AG, part of Springer Nature 2018
W. Schäberle, Ultrasonography in Vascular Diagnosis, https://doi.org/10.1007/978-3-319-64997-9_2
2.1.6.4.7 Dissection – 100
2.1.6.4.8 Arteriovenous Fistulas – 100
2.1.6.4.9 Chronic Recurrent Compartment Syndrome oftheCalf – 100
2.1.7 Follow-Up After Surgical andInterventional Treatment – 102
2.1.7.1 Thromboendarterectomy – 102
2.1.7.2 Percutaneous Transluminal Angioplasty andStenting – 102
2.1.7.3 Bypass Graft Surveillance – 104
2.1.7.3.1 Methodological Considerations andStenosis Criteria – 105
2.1.7.3.2 Controversy About theBenet ofDuplex Bypass
Graft Surveillance Programs – 107
2.1.7.4 Ultrasound Vein Mapping Prior toPeripheral Bypass Surgery – 110
2.1.8 Role of(Color) Duplex Ultrasound Compared withOther
Modalities: Problems andPitfalls – 112
2.1.8.1 Comparison ofHemodynamic andMorphologic Imaging
Modalities – 114
2.2 Arm Arteries – 116
2.2.1 Vascular Anatomy – 116
2.2.2 Examination Protocol andTechnique – 117
2.2.3 Clinical Role ofDuplex Ultrasound – 118
2.2.3.1 Atherosclerosis – 118
2.2.3.2 Vascular Compression Syndromes – 118
2.2.4 Documentation – 119
2.2.5 Normal Findings – 119
2.2.6 Abnormal Findings, Duplex Ultrasound Measurements,
andClinical Role – 119
2.2.6.1 Atherosclerosis – 119
2.2.6.2 Vascular Compression Syndromes – 120
2.2.6.3 Vascular Inammatory Disease – 122
2.2.6.4 Buerger’s Disease – 122
2.2.6.5 Raynaud’s Disease – 122
2.3 Atlas: Extremity Arteries – 124