Acta Neurochir (Wien) (1996) 138:68-76
Acta Neurochirurgica
9Springer-Verlag 1996
Printed in Austria
Cerebral Haemodynamic Considerations in Obstructive Carotid Artery
Disease
A. Sorteberg, W. Sorteberg, K.-F. Lindegaard, and H. Nornes
Department of Neurosurgery, Rikshospitalet, The National Hospital, University of Oslo, Oslo, Norway
Summary
46 subjects with obstructive carotid artery disease were investigated with transcranial Doppler ultrasonography. Their baseline
blood velocities (V) in the middle, anterior and posterior cerebral
artery (MCA, ACA and PCA) and in the extracranial internal carotid
artery (ICA) were measured and the pulsatility index (PI) calculated
for each vessel. Thereafter the vasomotor reserve in both MCAs
was tested.
Typical patterns of V, PI and vasomotor reactivity are presented. Arterial collaterals were recognized by their relatively
increased velocities. We demonstrated a close association of the
baseline variables V and PI and the total vasomotor reactivity
(hypocapnic plus no, hypercapnic response) by calculating an
index of ghemrelated to the cerebrovascular tone. The Uhem index is
expressed by:
ghe m index = VMcA'PIMcA/VpcA'PIpcA
The relationship between Uh~mindex and the total vasomotor
reactivity seemed to correspond to a hyperbolic curve. The hyperbolic tangent of Uhem index and total vasomotor reactivity correlated highly significantly, r = 0.8203, p <0.0001, n = 49, the best fit
for the regression line was Y = -0.005+Uh~m index 51.3. On the
99% significance level an Uhem index >0.94 indicated normal total
cerebral vasomotor reactivity in contrast to an impaired reactivity
when ~<0.81. Findings in 20 patients investigated post hoc supported the validity of our concept.
Keywords: Transcranial
Doppler sonography; vasomotor
reserve; arterial collaterals; cerebrovascular impedance.
Introduction
In obstructive carotid artery disease the cerebral
circulatory status can be evaluated by assessing the
cerebral v a s o m o t o r reserve [2, 3, 8, 10, 14, 16, 21,
30]. Using non-invasive transcranial Doppler ultrason o g r a p h y (TCD), this is c o m m o n l y done by measuring changes in blood velocity (V) in response to step
changes in the carbon dioxide partial pressure (pCO2)
[14]. Individuals with reduced cerebral v a s o m o t o r
reserve m a y be especially prone to l o w - f l o w cerebral
infarction [6, 16] and could benefit from surgery [6, 8,
22, 29].
The functional state o f the cerebral microvascular
bed exerts considerable influence both on the magnitude o f the cerebral v a s o m o t o r reserve [7] and on the
T C D variables blood velocity and the pulsatility
index (PI). Functional changes in the cerebral microcirculation should therefore alter the cerebral vasom o t o r reserve as well as V and PI. Attempts to define
this relationship have so far been unsatisfactory [9],
although a trend has been shown [13].
The aim of this study was to investigate the association o f cerebral v a s o m o t o r reserve and the T C D variables V and PI in patients with inflow disturbance,
n a m e l y obstructive carotid artery disease. Based on
these clinical findings we introduce a concept to estimate the total cerebral v a s o m o t o r reserve in individual subjects from their T C D baseline variables.
Theoretical Considerations
The oscillating velocity of the b l o o d flow in arteries can be regarded as the rheological analogue to an
electrical alternating current [15]. The blood velocity
V (in cm.s -i) then represents the current (I) and the
vascular
impedance
(Z, in dyn.s.(cm3) -I or
0.1-kg.(m.s) -1) the total opposition to flow. The electromotive force (U) is represented by the contractile
state, or tone (in dyn.(cm2)-l), of the heart and vasculature. The relationship between these units is derived
f r o m O h m ' s law (I.Z = U), and we then obtain:
V(cm.s-1).Z(dyn.s.(cm3) -1) = tone (dyn.(cm2) -1) (1)
With the heart generating a continuous train o f
pressure waves, the vascular impedance determines
the shape o f the pulsatile blood velocity w a v e f o r m in
A. Sorteberg et
al.:
Cerebral Haemodynamic Considerations
69
one cardiac cycle. Exact description o f this w a v e f o r m
envelope requires c o m p l e x analysis, in clinical routine we might therefore use a m o r e simplified procedure. The pulsatility index, PI (Systolic minus diastolic blood velocity divided by the time mean, [5]),
serves to describe the blood velocity w a v e f o r m and
will be an approximation of the vascular impedance.
Replacing Z with the PI in (1), incorporates this
approximation into the equation, thus the product
V.P1 will, instead of representing the vascular tone,
express a unit closely related to it (Uhem):
V - PI = Uhem
(2)
Absolute values of V and PI in h u m a n cerebral
arteries m a y show large inter-individual differences.
However, in the normal situation there is a relatively
constant relationship between blood velocities and
the PI values observed in one brain hemisphere [27].
Thus, normalized values, the so-called hemispheric
indices, allow for the detection of h a e m o d y n a m i c
alterations that might be obscured when considering
absolute values only [12, 27].
In the present study on patients with obstructive
carotid artery disease we chose to emphasize the hemispheric middle cerebral artery/posterior cerebral
artery ( M C A / P C A ) indices because: the M C A is the
end artery to the obstructed carotid artery and the
P C A is the only collateral channel which usually has
its source in a separate arterial system (the vertebrobasilar) and can develop Willisian collaterals
(through the posterior c o m m u n i c a t i n g artery) as well
as supra-Willisian collaterals (through small pial
arteries and arterioles). In accordance with (2) we
obtain:
VMcA'PIMcA/VpcA'PIpcA = Uhem index
(3)
C o m p l e x m e c h a n i s m s regulate the tone o f the vascular bed. The regulatory upper and lower v a s o m o t o r
endpoints are m a x i m a l constriction and complete
dilation, respectively. In a given situation the vascular
tone should therefore determine the amount o f vasom o t i o n (further constriction and/or dilation) to a
vasoactive stimulus.
Materials and Methods
Patients
The study comprised 46 individuals, 8 females and 38 males
with a median age of 61 years (range 41-76 years). The diagnosis
of obstructive carotid artery disease was established by angiography and confirmed by means of Doppler ultrasonography.
All subjects first underwent an examination at rest (baseline
examination) followed by investigation of their cerebral vasomotor
reserve. Lying supine in a comfortable position they initially adapted to the situation.
Blood Velocity Measurements
The blood velocity measurements were performed on 2 MHz
range-gated Doppler instruments, either an EMETrans-scan
(Ueberlingen, Germany)(first 38 patients) or a Multi Dop X
(DWL, Sipplingen, Germany) (last 8 patients).
Baseline examination: Using a hand-held probe, the MCA,
anterior cerebral artery (ACA), PCA and proximal and distal portion of the extracranial internal carotid artery (ICA) were identified
in sequence and their highest blood velocity reading scored by the
procedure previously described [1, 12]. The PI was calculated for
each artery; the percentage area stenosis estimated from the carotid
artery blood velocity readings [11].
Vasomotor reserve testing: The subjects now breathed through
a mouthpiece with a one-way valve. After achieving a stable normocapnic state, changes in pCOz were obtained by breathing 5%
CO2 in air directly followed by voluntary hyperventilation. The
end-expiratory pCO2 was recorded continuously on an infrared
CO2 analyser (CD-102, Normocap, Datex, Finland). Using the
fixed probe technique, the blood velocity was monitored at the
same time in both MCAs [19]. Under off-line data processing, samples from stable normo-, hyper- and hypocapnic conditions were
extracted. The vasomotor reserve is expressed as percentage
change in V per unit change in pCO2 in kPa (1 kPa equalling 1
Vol%) referred to each individual's normocapnic state. Hyperplus
hypocapnic response is denoted as total vasomotor reactivity
(VMRtotal).
Arterial Blood Pressure (ABP)
During the vasomotor reactivity testing, the ABP was repeatedly measured using a conventional manual blood pressure cuff.
Mean ABP was calculated as the diastolic pressure plus one third
of the systolic-diastolic difference. The values obtained were averaged separately for the three pCO2 levels for each indiviual.
Patients Examined Post Hoc
After completion of the study, the next 20 subjects with
obstructive carotid artery disease, 3 females and 17 males with a
median age of 61 years (range 38-74 years), were examined in
order to validate our concept for estimating the VMRtotat from V
and PI. Using the Multi Dop X, they were investigated according to
the protocol described above.
Results
In the following, the hemisphere above by the
(more) obstructed I C A is termed side A and the contralateral hemisphere side B.
We identified 92/92 M C A s , 72/92 A C A s , 49/92
P C A s , and 83/92 I C A s in the 46 subjects (9 I C A s
were occluded). T h e y were divided into five groups
according to our findings: Patients with unilateral stenoses and antegrade A C A flow (group 1, n = 15) or
retrograde A C A flow (group 2, n = 8), those with
bilateral stenoses and antegrade (group 3, n = 10) or
retrograde (group 4, n = 4 )
A C A flow and those
A. Sorteberg et al.: Cerebral Haemodynamic Considerations
70
Table 1. Percentage Area Stenosis of the Carotid Artery (Median
Values with Ranges)Estimated fi'om the Carotid Artery Blood
Velocity Readings
Group
No.
Hemisphere A
Hemisphere B
1
2
3
4
5
15
8
l0
4
9
76(42-92)
80(72-90)
81(53-89)
93(75-94)
100
59 (25-73)
47 (30-62)
70(10-87)
For all 46 subjects combined, the VMCA was lower
on side A than on side B (61 vs 75 cm.s -1, p <0.001);
especially when ACA flow was reversed (groups 2, 4,
and 5, Fig. 1). The PINTA o n side A was also
dampened (0.71 vs 0.85, p <0.01, Fig. 2). Similarly,
in the distal extracranial ICA the V was lower and the
PI was dampened on side A compared with side B
(VIcA: 31 vs 44 cm.s -1, p <0.001 and PIIcA: 0.83 vs
0.94, p <0.001). With antegrade ACA flow (groups 1
and 3), the VACA o n side A was normal to low
(53 c m . s -1, h e m i s p h e r i c
VAcA/VMcA = 0.76).
When
ACA flow was reversed (groups 2, 4, and 5), the
with unilateral stenoses and contralateral occlusion
(group 5, n = 9).
Table 1 gives the percentage carotid artery area
stenosis in the five groups.
TCD Baseline Variables
In this section we used the Wilcoxon test for paired
observations for statistical purpose; the results are
presented as mean values.
....
HUA
[CA
....
HL:-A
1
3
2
4
VACA e x c e e d e d the i p s i l a t e r a l VMCA (VAcA 60 c m . s -1,
hemispheric VAcAfVMca = 1.35).On side B, the VACA
was highly increased (92 cm.s -1, hemispheric
VAcA/VMcA = 1.30).'No clear tendency was found for
the PIAcA (0.76 VS 0.77, n.s.). The VpcA on side A was
higher than on side B (70 vs 59 cm-s -1, p <0.05). No
definite relation between the PIpcA and ICA obstruction was detected.
ICA
GROUP
I
IV
'-'*-'
PC_A
ICA
....
~
ICA
.....
t-t.~
ICA
VELOCITIES ( c m . s - 1 )
Fig. 1. Blood velocities in the middle, anterior and posterior cerebral arteries (MCA, ACA, PCA) and the extracranial internal carotid arteries (ICA) in obstructive carotid artery disease and in the normal situation. Groups 1 and 2: unilateral stenosis with antegrade and retrograde
ACA flow; groups 3 and 4: bilateral stenosis with antegrade and retrograde ACA flow; group 5: unilateral stenosis with contralateral occlusion. A hemisphere above the (more) obstructed ICA. B contralateral hemisphere. + from Sorteberg et al. [27]
A. Sorteberg et aL: CerebraI Haemodynamic Considerations
71
0Z
,
JB
3
A
IVCA f ~ A K ' ~
ICA
"-"
I
Group
t-~A ICA
3
NORMAL
-t"
PULSATILITY INDICES
!
.2
:.:.:.:.:.
:.:.:.:.:.
:.:.:.:.:.
:.:.:.:.:.
:.:.:.:.:.
:.:.:.:.:.
:.:.:.:.:.
:.:.:.:,:.
:.:.:.:.:.
:.:.:.:,:.
:.:.:.:.:.
:.:.:,:.:.
:.:.:.:.:,
:.:.:.:.:.
:,:.:.:.:.
:.:.=.:.
:.:.:.:.:.
:.:.:.:.:.
:.:.:.:.:.
:.:.:.:.:.
:.:.:q.:.
:.:.:.:.:.
I~
IW-A/~C-A FCA EA
" - " H.YA ICA
2
A
[vr~ 'z~'A
~ I:C_.A
4
ICA
5
Fig. 2.The Pulsatility Index, PI (systolic minus diastolic blood velocity divided by the time mean) in the MCA, ACA, PCA, and tCA in
groups 1-5 of obstructive carotid artery disease and in the normal situation. A hemisphere above the (more) obstructed ICA. B contralateral
hemisphere. + from Sorteberg et al. [27]
VASOMOTOR
REACTIVITY
{V%.kPa-1)
29
30
23
/
6O
50,
" --.
20 ~ - ' - ~.~.. ~.
49
,
18
-,
18
.
51
44
43
".
43
40
10
i
I
-
I
43
I 5% CO2
0
4O
1
30
30
2
3
22
20
4
5
31
30
2O
22
26,
20
10
!21
TOTAL
t6
10
0
1
2
3
4
5
ItV
0
3
4
5
Fig. 3. Total, hypercapnic (5%
CO2) and hypocapnic (HI/) vasomotor reactivity in the cerebral
hemisphere above the (more)
obstructed ICA (straight line, A)
and the contralateral hemisphere
(dotted line, B) in groups 1-5 of
obstructive carotid artery disease
A. Sorteberg et al.: Cerebral Haemodynamic Considerations
72
(ANOVA, F = 1.06, n.s.). There were considerable
individual variations within each group.
V%kPa-1
60
O
n
50
9
" Z'"Y
O 9D
DO
30
20
~o
TCD Baseline Variables and Vasomotor Reactivity
*
o
"
40
9
":~
o
~176
4, 9
go ~ 9
Y
10
0
I
I
I
I
I
I
0.5
1
1.5
2
2.5
3
Uhem index
a
V%kPa-1
60
50
40
De
ip
,1~
30
Oo
D
~3
20
D
10
0
I
1
I
1
I
0.2
0.4
0,6
0.8
1
tanh (ghe m index)
b
Fig. 4. (a) The relationship between the index of Uhem,expressed as
VMcA'PIMcA/VpcA'PIpcA and the total cerebral vasomotor reactivity
(VMRtotal) in 46 patients with obstructive carotid artery disease in
this study (black squares) and 20 patients examined post hoc (white
squares). The graph suggests a hyperbolic curve. (b) Correlation of
the hyperbolic tangent (tanh = e2•215
of Uhem index and
VMRtotal, r = 0.8203 (p <0.0001, n = 49). The best fit for the regression line w a s Y = - 0 . 0 0 5 + U h e m index.51.3 (black line). Study
series (black squares) and patients examined post hoc (white
squares)
For all 46 patients combined, there was no significant correlation of VMCA and PIMcA (r = 0.0237, n.s.)
or of VMCA and VMRtotai (r = 0.2689, n.s.). The
PIMCA and VMRtotai correlated with r = 0.459
(p <0.0001, n = 92).
The relationship between Uhem index and the
VMRtotat are illustrated in Fig. 4 a (black squares).
The graph suggests a hyperbolic curve. The hyperbolic tangent (tanh = eZ•
2x+1) of Uhem index and
VMRtotal correlated highly significantly (Fig. 4 b,
black squares) with r = 0.8203 (p <0.0001, n = 49)
and the best fit for the regression line was
Y = --0.005+Uhem index.51.3.
The VMRtotal was also estimated according to the
best fit for the regression line. The relationship
between measured and estimated VMRtotai is shown in
Fig. 5 (black squares). When calculating on the precision of the estimated VMRtota], we defined a "critical"
Uh~m index for the 99% confidence interval. An Uhem
index />0.94 then indicates a normal VMRmtai ( > / 3 6
V%.kPa -~) in contrast to a n Uhem index ~<0.81 when
the VMRtotal is impaired.
Substituting contralateral ACA values for the ipsilateral P C A p a r a m e t e r s in (3), Uh~m index and
VMRtotal led to r = 0.2524, p <0.05.
V%kPa-1
60 measured
n 9~
50
9
30
[]
9
*
Vasomotor Reactivity
For all 46 patients combined, the VMRtotal was
lower on s i d e A than on s i d e B (38+12 vs 46+8
V%-kPa <, p <0.00t, t = 5.587, t-test for paired samples). Figure 3 (left) gives the VMR~ot~Iin groups 1-5,
showing no significant difference between groups and
hemispheres (ANOVA, F = 2.85, n.s.). While the
hypercapnic response (Fig. 3, upper right) was significantly
lower
on
side A ( A N O V A ,
F = 5.42,
p <0.001), the hypocapnic response (Fig. 3, lower
right) was similar between groups and hemispheres
20
oD, , ~
0
0
=
10
=
20
I
30
=
I
40
50
estimated
I V%kPa-1
60
Fig. 5. The relationship between measured and estimated VMetotal
in patients with obstructive carotid artery disease in the study
(black squares) and those examined post hoc (white squares)
A. Sorteberg et
al.:
Cerebral Haemodynamic Considerations
Arterial Blood Pressure
The mean ABP increased 9% (range 1-29%)in
hypercapnia and decreased 2% (range -22-14%) in
hypocapnia. In 25 normotensive patients the cerebral
vasomotor reactivity was independent of the ABP
(side A: r = - 0 . 1 6 3 5 , n.s. and side B: r = - 0 . 0 5 6 8 ,
n.s.).
In 21 subjects where the systolic ABP exceeded
170 mmHg during the vasoreactivity testing (all 21
had chronic hypertension) the vasomotor reactivity
was also independent of the ABP in hemispheres
above obstructed carotid arteries (side A: r = 0.0506,
n.s. and side B: r = -0.1327, n = 9, n.s.). There was,
however, an inverse relation between mean ABP and
the hypercapnic response for the 12 hemispheres
above nonobstructed arteries in the hypertensive
patients (Side B in groups 1 and 2, r---0.6444,
p <0.01).
Patients Examined post hoc
The 20 patients examined post hoc belonged to the
different groups as follows: group 1, n = 6; group 2,
n = 6; group 3, n = 1; group 4, n = 3; group 5, n = 4.
Uhom index and its hyperbolic tangent were calculated from the V and PI in 35/40 hemispheres (five
PCAs were not identified). These values and the
measured VMRtotal are presented in Fig. 4 a and b,
respectively (white squares). Using the best fit for the
regression line, we also estimated the VMRtotal in the
35 hemispheres. The relationship between measured
and estimated VMRtotal is shown in Fig. 5 (white
squares). We obtained a mean of 38.8 V%.kPa -1 for
the measured - versus 39.6 V%-kPa -~ for the estimated VMRtotal; the mean difference was 0.8 V%.kPa -1
and the standard error of the mean was 0.8 V%.kPa -1.
The nine hemispheres where the measured VMRtotal
was ~<36V%, were also estimated to be impaired.
Correspondingly, the 26 hemispheres with measured
VMRtot~l >~36V% were also recognized as being normal by estimation.
Discussion
TCD Baseline Variables
The TCD baseline variables, blood velocity and
pulsatility are resultants of complex factors interacting, including the size and quality of the input signal,
rheological/chemical properties of the blood and
organ related factors [ 13]. These factors have equivalent influence on the different brain regions [23].
73
Superimposed on this, local factors such as intracranial space occupying lesions or disease altering the
cerebral haemodynamics exert regional influences on
the V and PI [17].
In obstructive carotid artery disease, the cerebral
circulation depends on the degree of carotid artery
lumen narrowing as well as on the extent of the collateral blood supply [29]. Using TCD, functioning collaterals can be recognized by analysing the
individual's cerebral haemodynamic pattern: In the
normal situation, the blood velocities in the two hemispheres show no significant side differences (Fig. 1,
upper right). Moreover, within each hemisphere they
are subject to characteristic proportions forming a
"stairway pattern" (Fig. 1, upper right). Alterations in
this pattern suggest a haemodynamic situation related
to pathology. Figure 1 thus illustrates how increasing
ICA pathology distorts this stairway pattern more and
more. Communication through the circle of Willis
also makes it necessary to consider the blood velocities in a bilateral context, even when the obstruction
is unilateral.
Typically, collateral flow patterns are recognized
from the relatively increased blood velocity in the
collateral arteries, an increase reflecting enlargement
of the respective arteries' perfusion territories [26]. In
obstructive carotid artery disease, the main collaterals
are the contralateral ACA and the ipsilateral PCA.
Potential collaterals may be revealed by compressing
the common carotid artery [24]; however, we do not
use this as a routine procedure. The stenosis itself is
recognized by the increased blood velocity at the
point of obstruction and the decreased velocity and
pulsatility distally. The present findings of decreased
ipsilateral VMCA and PIMcA concur with previous
studies [13, 21, 25].
Not only velocity, but also the pulsatility contains
information about the capacity of collateral channels.
Collaterals showing more distinct pulsatile patterns
have thus been found to have the highest index of collateral capacity, while those with a low collateral
capacity have a throttled pulsatile flow [18]. The
observation of an undampened pulsatility was considered indicative of low impedance in the collateral vessel [18]. In our subjects investigated there was a!so a
tendency towards higher PIs in the collaterals with the
relatively most increased velocities (ipsilateral PCA
in groups 3, 4, and 5 and reversed ipsilateral ACA in
groups 2 and 5, Figs. 1 and 2).
The PI is often associated with the cerebrovascular
74
resistance, which is mainly confined to the cerebral
microvasculature. However, the bloodstream in the
cerebral arteries is oscillating and subjected to the
more complicated cerebrovascular impedance,
including the vascular closing pressure and the total
system compliance distal to the point of observation.
The term resistance is used in steady flow dynamics
[15]. Nornes [19] described how mean ICA flow and
flow pulsatility decreased similarly during graded
ICA clamping for saccular aneurysm, while a corresponding reduction of ICA flow caused by hyperventilation increased the ICA flow pulsatility. He
explained this with a nearly similar "resistance" to
flow in the two situations, but with different impedances.
Ffirst et al. [4] used the Purcelot Index to express
vascular impedance. However, this index' only takes
into consideration the systolic and diastolic extremes.
The PI seems physiologically more relevant for such
evaluations because it takes account of the waveform
envelope [13].
T C D Baseline Variables and Vasomotor Reactivity
The correlation of single TCD baseline variables
and the VMRtotal was lower than when using calculations of the Uhem index in (3). The PIMcA and the
VMRtotal correlated with r = 0.459, which is close to
the results of Ley-Pozo et al. [9] and Lindegaard [13].
We observed that the more the ipsilateral VPCA
increased, the more the VMRtotal was impaired. This
might seem paradoxical since a good collateral function should in fact prevent the vasomotor reserve
from becoming exhausted. However, one must bear in
mind that our series probably were selected in the
sense that they were healthy enough to be considered
for surgery. To this end, only those with the "fittest"
collateralization system survive [21]. The maximum
exploitation of dilatatory ability goes hand in hand
with the maximum use of collateral capacity; a highly
increased VecA therefore reflects a marginal ipsilateral hemispheric perfusion.
The collateral function on the contralateral ACA
acts via the anterior communicating artery (ACoA).
Being shorter (average length: 2.6 vs 14 mm) and
most often wider (average diameter: 2.3 vs 1.2 mm)
than the posterior communicating artery [28], the
resistance to flow through the ACoA will usually only
be a fraction of that in the posterior communicating
artery. Dependence of a hemisphere on ipsilateral
PCA collateral flow therefore may reflect a situation
A. Sorteberget al.: CerebralHaemodynamicConsiderations
where the capacity of the anterior circle of Willis is
inadequate. This also explains why our contralateral
ACA values showed a poor correlation in the estimation of the VMRtotal.
Widder et al. [30] found the normal vasomotor
reactivity to be 23_+5 V%.kPa q, and considered it
p/~thological when <18 V%.kPaq. Based on their
findings, we presently set the lower limit for the normal VMRtotal at 36 V%.kPa-1. The vasomotor tone
defines the microvascular capacity to further dilatation and/or constriction. It is therefore appropriate to
link the g h e m index in the VMRtot~. This relationship
suggests a hyperbolic curve with a breakpoint close to
0.94; which is the lower limit for the compatibility
with a normal VMRtot~. Above this threshold, the vasomotor reactivity has a physiologically broader variation than the Uhe m index.
Given adequate MCA and PCA blood velocity signals, we could presently estimate the VMRtotal from
the baseline variables V and PI. Moreover, findings in
the 20 patients examined post hoc (Figs. 4 a, b and 5,
white squares) support the validity of this concept.
Such an estimation offers an alternative to reactivity
testing and is of special interest in subjects in whom
such a test is not feasible. Our concept also broadens
the view on cerebral haemodynamics in obstructive
carotid artery disease because it includes both the
vasomotor and collateral capacity.
Arterial B l o o d Pressure
Hypercapnia presently elevated the mean ABP by
about 10%, which is of the same magnitude as reported previously [3, 14, 30]. We also confirm the findings of Widder et al. [30] that the cerebral vasomotor
reactivity is independent of ABP at systolic pressures
<170 mm Hg. For values >170 mm Hg, however, we
obtained an inverse relation between hypercapnic
reactivity and the ABP in hemispheres above nonobstructed ICAs. This can be explained by constriction of the cerebral microvasculature to the increased
ABP counteracting the vasodilatatory response to
hypercapnia.
In hemispheres severely affected by obstructed
ICAs, an elevated ABP may protect the brain by helping to maintain an adequate cerebral perfusion pressure. An increase in ABP might then not be counteracted by microvascular contraction to the same extent
as in the normal situation. Correspondingly, a reduction of the ABP in patients with haemodynamically
significant ICA obstruction could in fact provoke
low-flow cerebral infarction.
A. Sorteberg et al.: Cerebral Haemodynamic Considerations
Acknowledgement
The authors wish to thank Robert Innes, MD, for reviewing the
English manuscript.
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Correspondence: Angetika Sorteberg, M.D., Department of
Neurosurgery, Rikshospitalet, The National Hospital, University of
Oslo, N-0027 Oslo 1, Norway.
Comments
In this paper the group of the Rikshospitalet in Oslo presents a
very original and well clone study on cerebral haemodynamics in
obstructive carotid artery disease. 46 patients were investigated
76
using transcranial Doppler ultrasonography and the velocities and
pulsatility-index of the basal cerebral arteries and of the extracranial internal carotid artery were measured and correlated with the
vasomotor reserve in both MCAs. The authors demonstrate a close
association of the velocity, the pulsatility-index and the vasomotor
reactivity. By the non-invasive Doppler technique, relevant hae-
A. Sorteberg et al.: Cerebral Haemodynamic Considerations
modynamic information can be gained as demonstrated in this
paper. The method used is correct and the results are significant.
The manuscript deserves the attention of the readers of Acta Neurochirurgica.
R. Seiler