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346
ABP (mm Hg)
FV-MCA (cm/s)
0
FV-MCA (cm/s)
0
a
b
C. Puppo et al.
200
160
120
200
160
120
CrCp
80
40
0
0204060
CrCp
80
40
Vasospasm
basal
80
ABP (mm Hg)
ipsilateral
100120 14
contralateral
0
0204060
80
100120 14
Fig. 20.2 Critical closing pressure values in two different patients [modied from [7]] Critical
closing pressure (CrCP) in a patient who developed vasospasm in the middle cerebral artery
(FV
) is shown in panel “a”. CrCP value during vasospasm was lower than 10mmHg, while the
MCA
baseline value, prior to the onset of vasospasm, was 40mmHg. In panel “b” the difference in CrCP
between the vasospasm side and the contralateral (no vasospasm), is shown, with values close to
15 and 30mmHg respectively. In this way, a temporary and regional evaluation of the changes of
the CrCP was obtained. A CrCP decrease was demonstrated in cerebral vasospasm. The hypothesis
of the researchers was the opposite, since they had assumed that the increase in resistance caused
by middle cerebral artery vasospasm would increase CrCP.The importance of distal vasodilation
of small arteriolar vessels, as the origin of this decrease in CrCP is underlined. Since TCD insonates
the spastic segment, the increased FV at this level is the result of a decrease in the diameter of the
artery; on the other hand, the decrease in cerebrovascular resistance is due to arteriolar reactive
vasodilation. [ABP: arterial blood pressure]
20 Critical Closing Pressure in Acute Brain Injury: Usefulness of Transcranial…
347
20.5.2 Critical Closing Pressure
andIntracranial Hypertension
With controlled increase in ICP in patients with normotensive hydrocephalus, we
will refer to two research papers on ICP-controlled increase in patients with normotensive hydrocephalus.
(a) Monitoring data obtained in a clinical study in patients with suspected normo-
tensive hydrocephalus were retrospectively used to study CrCP and its changes
during a controlled rise in ICP [11]. The lumbar infusion test evaluates how
cerebral hemodynamics reacts to an increase in volume; in patients with normotensive hydrocephalus, it helps to predict the need for placement of a peritoneal
ventricular shunt or to change a dysfunctional shunt. Thirty-seven patients were
studied. ICP was recorded by means of a lumbar catheter, continuous noninvasive ABP with Finapres and CBFV with TCD, during a slow lumbar infusion of normal saline. CrCP was calculated using three methods: A method
described by Aaslid using the rst harmonics of ABP and CBFV pulsatile waveforms and two methods based on Varsos cerebrovascular impedance model,
using CPP or ABP [appendix]. They found good agreement among the three
CrCP calculation methods, with correlation coefcients greater than 0.8. During
the controlled increase in ICP, CrCP values increased signicantly with all
three methods. The strongest correlation between ICP and CrCP was found for
the impedance method that used CPP in its formula. This study evaluates and
compares the three methods. With the Aaslid method [appendix], negative
results of CrCP frequently appear; they were not observed with the impedance
multiparameter methods. These researchers conclude that invasive CrCP
(Varsos method including CPP instead of ABP) is more sensitive to variations
in ICP and can be used as an indicator of the reserve of the cerebrovascular
system during infusion tests. The authors do not discuss the origin of the
increase in the CrCP in this work. As CrCP is the sum of two components, ICP
and parietal tension, the interpretation of this CrCP increase has to be searched
in the behavior of these two parameters. ICP increased (it was the objective of
the test). Wall tension may have decreased or increased, since the change in the
vasoconstriction or vasodilation state of the resistance arterioles depends on the
CPP that reaches the arteriolar sector and the state of autoregulation. In the
event of an increase in ICP without compensation, CPP would go down, but a
reex increase in ABP may turn up to maintain (or even raise) CPP.In case of a
not compensated decrease in CPP, this should cause an autoregulatory response
with vasodilation of small resistance vessels, with a decrease in wall tension. If
CPP were maintained, there would be no changes in wall tension, and if it
increased, the normal autoregulatory response would generate an increase in
resistance. We can conclude that compensatory vasodilation, if it existed, was
of a lesser degree than the rise of ICP.
348
(b) Another work by Varsos etal. [12] studied the possible correlations between
cerebral hemodynamic indices based on CrCP and the compensatory dynamics
of cerebrospinal uid, also evaluated during lumbar infusion tests. They evaluated data from 34 patients with normotensive hydrocephalus undergoing infusion tests, with simultaneous monitoring of CBFV by TCD.CrCP was calculated
from the monitored signals: ICP, ABP, and CBFV, while the vascular wall tension was estimated as WT=CrCP- ICP.The closing margin was calculated as
the difference between ABP and CrCP.ICP increased during the infusion from
7±5 to 25 ± 11mmHg (mean±SD), which caused an increase of CrCP of
23%, with WT decreasing by 11% due to vasodilation. CM showed a tendency
to decrease, although not signicantly, due to a 9% increase in ABP.In general,
CrCP increases and WT decreases during infusion tests, while the initial CM
may act as an indicator that characterizes the compensatory reserve of the cerebrospinal sector.
C. Puppo et al.
20.5.3 Spontaneous Increase inICP inPatients
withNeurotrauma
This second study aimed to describe the behavior of CrCP and WT during spontaneous increases in ICP, with the characteristics of plateau waves. The objective of this
work was to quantify the ischemic risk during these waves. These researchers used
Varsos’s multiparametric method, which is based on the cerebrovascular impedance
module. Arteriolar WT was estimated as CrCP–ICP.Clinical data included records
of ABP, ICP, and CBFV of 38 plateau wave events, recorded in 20 patients with
TBI.CrCP increased signicantly from 52±9mmHg at the beginning of the study
to 63±11 mmHg at the top of the plateau waves (mean±SD; p<0.001). WT
decreased signicantly during plateau waves by 34.3% (p< 0.001), which is in
favor of their vasodilator origin. No non-physiological negative values of CrCP
were observed that have been described with the traditional methods for its calculation; therefore, the method used resulted in a more plausible estimate of the CrCP
than the “graphic” methods. The researchers conclude that increased CrCP during
plateau waves increases the likelihood of cerebral vascular collapse and zero ow
when the difference: ABP–CrCP (“the collapsing margin”) becomes zero or
negative.
20.5.4 Critical Closing Pressure inSeptic Patients
20.5.4.1 Experimental Endotoxemia
A prospective study in critical care studied CrCP in 40 volunteers and 10 septic
patients [13]. An experimental endotoxemia was generated in volunteers by the
administration of bacterial lipopolysaccharides (LPS). The registered changes were
20 Critical Closing Pressure in Acute Brain Injury: Usefulness of Transcranial…
349
compared with those of 10 septic patients with or without septic shock. CrCP was
estimated using the cerebrovascular impedance model, recording CBFV and invasive ABP (no ICP). Volunteers who received LPS were randomized to receive an
infusion of one of the following vasopressor drugs: norepinephrine (NE), phenylephrine (PhE), or vasopressin (VP). The corresponding vasopressor drug was started
1 hour before the administration of LPS, and the infusion was administered for
5hours. In the third group, placebo was administered. In septic patients, the decision to use vasopressors and uids, as well as which uid to use, was freely taken
by the treating medical team. The objective was to achieve normovolemia and an
average blood pressure>65mmHg, using NE.
The LPS bolus was followed by a decrease in CrCP, without differences
between groups.
In septic patients, CrCP was 35.7mmHg, lower than that presented by volunteers
after receiving LPS.After the administration of LPS, CBFV decreased, most likely
as a result of the decrease in Circle of Willis outow to the middle and anterior
cerebral arteries, not compensated for by distal vasodilation. This decrease in ow
shows that autoregulation is not functioning at the pressures studied. However, the
decrease in CrCP maintains for a longer time an adequate effective cerebral perfusion pressure constituting a protective mechanism against ischemia. The authors
conclude that human experimental endotoxemia results in a decrease in CrCP due
to the decrease in resistance of the cerebral arterial bed (arteriolar dilation), which
is not prevented by vasopressors. The alterations presented in septic patients are
similar to those of volunteers who are administered LPS.
20.5.5 Critical Closing Pressure inSurvivors ofCardiac Arrest
A study estimated CrCP during post-cardiac arrest syndrome (post-CA) and determined whether it differs between survivors and non-survivors [14]. It also compared
post-CA patients with normal controls. This prospective observational study was
conducted in the ICU of a tertiary university hospital in Nijmegen, the Netherlands.
Eleven patients in coma resuscitated from CA, treated with mild therapeutic hypothermia, and 10 normal controls were studied. CBFV was recorded in the middle
cerebral artery at several time points after admission to the ICU.CrCP was determined by Varsos model using ABP instead of CPP.CBFV at ICU admission was
similar in patients who survived and in those who died, but throughout the observation period it increased in patients who evolved to death compared to survivors.
Immediate post-CA CBFV was signicantly lower in survivors compared to normal
controls, with a gradual restoration to normal values. CrCP decreased signicantly
from 61mmHg to 42mmHg in the rst 48hours and remained stable. CrCP was
signicantly higher in survivors compared to non-survivors. CrCP immediately
post-CA was also signicantly higher compared to the control group. The researchers concluded that CrCP rises post-CA with high cerebrovascular resistance and low
CBFV.This means that the effective CPP or closing margin is lower, suggesting that
cerebral perfusion pressure should be maintained at a sufciently high level in
350
patients in post-CA, to avoid further ischemic brain damage. On the other hand, the
lack of normalization of the cerebrovascular prole can be a predictor of poor
results.
C. Puppo et al.
20.6 Conclusion
Intracranial hypertension, during controlled (infusion tests) or spontaneous (plateau
waves) ICP increases, causes an increase in CrCP, and simultaneously a lower closing margin with higher risk of ischemia if we are guided by CPP calculated as
ABP–ICP.CrCP decreases in sepsis, which helps to maintain longer adequate effective cerebral perfusion pressure constituting a protective mechanism against
ischemia.
Appendix
Methods
Methods used to measure CrCP can be divided into two groups. All are based on
data acquired with ABP and TCD, at a frequency that allows to reproduce arterial
pulse and CBFV waves, for example, at 50Hz (50 measurements in 1second).
Group 1: Graphic Methods
The rst group is based on “graphic” concepts. The data used are non-invasive. It
assumes that the relationship between ow and pressure is linear; therefore, when
pressure falls below the minimum value recorded in the patient, the ow pressure
relationship would be unchanged.
Changes in cerebral blood ow (through changes in CBFV) and arterial blood
pressure are graphically evaluated; the line of best t between recorded values is
found and its equation is calculated. This line is extrapolated to cross the pressure
axis at a point (CrCP) where ow would be theoretically zero. There are three different models using this approach.
Method Using theValues ofSeveral Pulse Waves (“Systo-Diastolic Method”)
Several simultaneous ABP and CBFV waves are selected, and only the maximum
(systolic) and minimum (diastolic) values of each one are plotted, ABP in the x-axis
and CBFV in the y-axis. Thus, a cloud of systolic points and another of diastolic
Systolic and diastolic acquired values CrCp estimated with systole-diastole method
time (seconds)
ABP (mmHg)
FV (cm/s)
20 Critical Closing Pressure in Acute Brain Injury: Usefulness of Transcranial…
45
130
120
110
100
40
35
30
25
20
15
90
80
70
650 660 670
680 690 700 20
60
50
40
30
20
FV (cm/s)
10
0
–10
–20
CrCp 27 mmHg
40 60 80 100 120
ABP (mmHg)
351
Fig. 20.3 Systole and diastole method. All waves of a certain time period are studied. In this case
about 100seconds. Two values are obtained from each BFV pulse wave: maximum systolic and
nal diastolic. The same process is repeated with the maximum and minimum values of each ABP
wave (left panel). These values are shown on a scatterplot (right panel) displaying BFV in the
abscissa (cm/s) and ABP in the ordinates (mmHg). Two point clouds are thus obtained: one with
the systolic values of the selected BFV and ABP pulsatile waves (red line around the blue wave)
and another with their diastolic values (blue wave). A line of best t is inserted between these
points. The ABP point corresponding to the BFV zero value is the CrCP.In this example, the value
of CrCP is 27mm Hg
points are obtained. These clouds are joined with the corresponding best t line, and
this line is extrapolated to zero ow. The cut-off point of this line on the ABP axis
(zero ow) corresponds to CrCP (Fig.20.3).
“Beat-by-Beat Method”
Instead of using several beats, one value per pulse is calculated. The descending
values of a CBFV wave (in most models all points—ascending and descending—
are used) are plotted against the simultaneous descending values of ABP (each point
in the ABP pulse curve has its corresponding point in the descending part of the
CBFV pulse curve). CBFV does not reach zero in diastole, but the line with the best
t is extrapolated to the zero-ow point. The point in the abscissa (ABP) where this
line reaches zero corresponds to the CrCP value (Figs.20.4 and 20.5).
Method Described by Aaslid
This method is similar to the previous ones, but instead of taking the recorded ABP
and CBFV values, the values of the rst harmonic of both variables are taken. It has
the advantage of eliminating the upper harmonics that distort the arterial wave. It
uses Fourier analysis to determine the amplitude of the rst harmonic in the ABP
and in the CBFV register. With this approach, it is possible to perform the regression
analysis with almost perfect linear data. Using the value of the rst harmonic
352
seconds
100
125
100
ABP
ABP
C. Puppo et al.
75
50
25
,50
,30
,10
90
80
70
60
50
40
1,08 1,10 1,12 1,14 1,16 1,18 1,20
,70
seconds
1,10
,90
1,30
1,50
1,70
1,90
FV
ABP
FV
ABP
ABP
FV
ABP
FV
125
100
FV
FV
75
50
25
,90
,94
,98
1,02
1,06
1,10
1,14
1,18
1,22
1,26
1,30
1,34
1,38
seconds
Fig. 20.4 “Beat to beat” measurement method of the critical closing pressure of the cerebral circulation. CrCP is studied for each pulse. The record of several simultaneous waves of arterial blood
pressure (ABP) and BFV is displayed on the left panel. A blue rectangle shows an ABP wave and
the simultaneous PV wave. The values of the descending zones of each beat are displayed in blue
in the central panel. The simultaneous studied data is shown in the right panel
eliminates, the distortions generated by the fact that the measurements are recorded
at different sites and with artifact values due to the Windkessel effect. The Windkessel
effect is the cushioning effect that ensures that the blood ow that is generated intermittently in the heart reaches the arteries, arterioles, and capillaries continuously.
The ideal way of measuring these parameters (but for now impossible in clinical
practice) would be to take both measures at the brain level. Actually, ABP is measured far away from cerebral arteries, such as the radial artery. In this location, the
wave is distorted with respect to what would be recorded directly in the cerebral
vessels. This is due to the transmission of the pulse and the existence of reections
or reverberations of the waves. The high-frequency components of the wave are
more distorted than the fundamental component (rst harmonic). Therefore, eliminating the error caused by higher frequency harmonics before processing the data
()
()
11
ABP (mmHg)
FV (cm/s)
20 Critical Closing Pressure in Acute Brain Injury: Usefulness of Transcranial…
353
Fig. 20.5 Linear
correlation between data
shown in (Fig.20.3), right
panel. Each point in this
graphic corresponds to a
ABP and CBFV (FV)
simultaneous value. The
best t line is calculated
and its linear extrapolation
to zero ow crosses ABP
axis at a value which is the
CrCP of this pulse wave. In
this case the value is higher
than 40mm Hg
80
70
60
50
40
40 50 60 70
y=5,4+0,78*x
80 90 100
results in a more accurate estimate of the CrCP.For this reason, the waves are analyzed with a Fourier transform, which nds the amplitude of the rst harmonic of
both the ABP and the BFV, and its relative intensity. With this model, the formula
that calculates the intersection of the descent of the ow with the axis of the abscissa,
corresponding to zero ow, is the following:
CrCP ABP CBFVABP CBFV
=-
f
00
´
/
where CrCPf is the critical “ltered” closing pressure (calculated with the variables
devoid of the mentioned distortion); ABP0 and CBFV0 refer to the average values of
ABP and CBFV of each beat; and ABP1 and CBFV1 refer to the amplitude of the
rst harmonic of ABP and CBFV (after the higher frequency components have been
removed).
The above-analyzed methods, or “graphic methods,” are based on the shape of
the recorded waves. They have the main drawback that negative, non-physiological
CrCP values may result. If we rethink the concept of critical closure pressure, such
as the blood pressure at which the circulation stops, we cannot nd a plausible
physiological or pathophysiological explanation. Anyhow, these approaches can be
used to see the trends of CrCP over time, evaluating the effects of drugs, pathological situations, etc., on the state of vasodilation or vasoconstriction of the arteriolar
bed, and not as an absolute value. These values away from the physiological values
are probably due to the fact that in the “graphic” models it is assumed that there is a
linear relationship between the variables, a circumstance that is probably more
complex.
354
()
21
C. Puppo et al.
Group 2: Multiparameter or Impedance Methods [14]
To overcome the negative value problem, researchers at the University of Cambridge
have generated a more complex model, multiparameter model, or “impedance”
model [14].
It is called multiparameter because, in addition to the values recorded directly
from the ABP and the CBFV, it uses other parameters derived from the cerebral
circulation for CrCP calculation. Several of them originate in turn from ABP and
CBFV, such as arterial complacency and cerebrovascular resistance. The formula
also uses heart rate, which can be inferred from any of the registers, from ABP or
CBFV.Impedance is a similar concept to cerebrovascular resistance, but variable
throughout the cycle (remember that the circulation is pulsatile). The formula used is
CrCP ABP
=-
CVRCaHR
CPP
´´ ´
2
+
p
As we can see, CPC value is included in this formula (CPP = ABP – ICP).
However, in patients in whom there is no suspicion of an increase in ICP, this same
formula has been used with ABP instead of ICP.
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