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336
P. Castro and E. Azevedo
Fig. 19.2 Representative changes in cerebral blow ow velocity and cerebral vasculature calibre
during CO
patient is rst summited to hypercapnia, e.g. achieved by carbogen inhalation (CO
vasoreactivity testing. During CO2 vasoreactivity testing, after a resting period, the
2
at 5%) or
2
through manipulation of ventilator parameters and after recovery of physiological parameters, it
follows a hypocapnia challenge (hyperventilation less than 7–10mm Hg from baseline). In the
upper part of the gure, we see that cerebral resistance vessels (mainly small arterioles) vasodilate
in response to hypercapnia and vasoconstrict to hypocapnia. It should be noticed that despite transcranial Doppler insonates the M1 segment of middle cerebral artery, the changes in cerebral blood
ow velocity (CBFV) depicted in lower part of the gure, are caused by the calibre changes in the
small distal parenchymal microvessels and not M1, which remains with constant diameter throughout the challenge. The lower part of the gure represents an actual record from a patient. When
compared to normocapnia, hypercapnia induces CBFV increase and a subtle hypocapnia causes a
visible CBFV decrease. End-tidal CO
(EtCO2) concomitant changes were derived by a nasal cap-
2
nograhy. By plotting the averaged mean CBFV and EtCO2 at each of the three stages we can calculate the vasoreactivity by deriving the inclination of that line (bottom left)
Fig. 19.3 Apparatus for measuring CO2 reactivity in a non-intubated patient. Transcranial Doppler
probes and bilaterally hold in place by a proper steady probe-holder. Nasal cannula is also in place.
A T-tube with a safety expansion bag is adapted for a supply gas (carbogen) for inhalation during
hypercapnia
()
/%
19 Acute Neurologic Injury in ICU: Vasomotor Reactivity Testing by Transcranial…
or a non-return valve. Hypercapnia is achieved by inhaling a 2–8% CO2 (carbogen) mixture, causing an increase in EtCO2 of at least 7–10mm Hg. In addition,
we can test response to hypocapnia through hyperventilation to reduce EtCO2 by
about 7–10mm Hg. In order to obtain the overall VMR (% or cm.s−1 per mm Hg
of CO2), we calculated the slope of the linear regression line between the mean
values of EtCO2 in the abscissa axis and the respective mean values of mean ow
velocity (MFV) in the phases of hyperventilation, resting and carbogen. We can
also calculate VMR values separately for the phases of hypercapnia and hypocapnia [9]. Another parameter that can be calculated, although less frequently, is
the total vasodilator capacity given by the following formula (Eq. 19.2):
337
MFVMFV MFV
hypercapnia hypocapniaresting
−
×
100
(19.2)
In intubated patients, EtCO2 can be measured directly from the capnography
linked to ventilatory apparatus. To achieve higher and lower CO2 levels of around
10mm Hg from baseline, we can manipulate the ventilator parameters.
3. Pharmacological Challenge [13]: Vasodilator substances such as L-arginine
(500mg/kg for 30minutes) or acetazolamide (15mg/kg for 5minutes, maximum
effect in 10–12minutes) are perfused, which promote cerebral vasodilation by
increasing the production of NO [10] or of cerebral tissue pH [11], respectively.
Diamox® (acetazolamide), a potent, reversible inhibitor of carbonic anhydrase,
is widely more frequently used. It is most probable that these effects are stimulated by metabolic acidosis but this is debatable in literature [1].
19.5 Vasoreactivity (VMR): Interpretation oftheResults
• The following criteria can be used to evaluate the breath-holding index results
[3, 5, 12]:
– >0.6 is normal.
– 0.21 to 0.60 is impaired.
– ≤0.20 is signicantly impaired VMR.
• The following criteria are used to evaluate the CO2 challenge results as vasomo-
tor reserve [4, 13, 14]:
– Normal vasomotor reserve 86%±16%.
– Mild to moderately reduced 69% to 39%.
– Severely reduced 38% to 16%.
– Exhausted <=15%.
• The following criteria are used to evaluate the CO
challenge as expressed by %
2
MFV per mm Hg (linear regression method) [15]:
– VMR to CO2 5.26±1.61 [%/mmHg].
338
– Relative reduction of VMR: side difference more than 3%/mmHg or 2%/
mmHg < VMR<5%/mmHg.
– Restricted VMR: VMR<2%/mmHg.
– Exhausted VMR: VMR<1%/mmHg.
• The following criteria are used to evaluate acetazolamide test [13]:
– VMR to acetazolamide: normal is ~40±15% increase in MFV.
– Pathological <10% increase in MFV.
P. Castro and E. Azevedo
19.6 Technical Tips
• There are standard normality values derived from larger cohorts, and the values
reported in this chapter are only for reference purposes.
• Use a TCD probe holder to minimize the errors in CBFV measurement.
• Use MCA M1 (45–60mm in depth) segment bilaterally since these are the values most frequently encountered in the literature.
• The times for hypercapnia or hypocapnia, as well as resting phases between
them are only references. It is possible that they can be shortened or increased
depending on the individual differences in reaching steady-state values of EtCO2
or CBFV.For this purpose, it is important to visually control capnography, and
CBFV time trends monitor to ensure that these plateau levels are reached.
• Before proceeding with the VMR tests, a complete extracranial and intracranial
examination is advisable to exclude the presence of haemodynamic stenosis that
may inuence the test results.
19.7 Vasoreactivity: Clinical Importance
The grade of cerebral vasoreactivity has been linked to prognosis in critical care
patients.
In a small cohort of patients with subarachnoid haemorrhage, impaired VMR to
CO2 challenge was more frequent in patients with a poor clinical grade on admission and at the time of examination [16]. A persistently decreased VMR to CO2 also
predicted those that developed delayed cerebral ischemia. In patients with carotid
occlusion, patients with exhausted, reduced and normal VMR to CO2 showed 50%,
28% and 18% suffering from ischemic stroke [17]. In intensive care unit patients,
was found clinical correlation between VMR and ICP variations [18], where progressive decrease in VMR (worse cerebral hemodynamic state) was associated with
worse clinical outcomes in long term [18].
19 Acute Neurologic Injury in ICU: Vasomotor Reactivity Testing by Transcranial…
339
19.8 Conclusion
Cerebral vasoreactivity or vasomotor reactivity is an index of cerebral blood ow or
velocity in response after administration of a vasomodulatory stimulus. It is a simple and non-invasive test that can inform you about the vasodilatory vasomotor
reserve of the cerebral microvascular bed. A transcranial Doppler with probe holder
and a capnographic line is all the necessary equipment. A persistently decreased
vasoreactivity predicted those that developed delayed cerebral ischemia in subarachnoid haemorrhage patients and those with increased risk of stroke in carotid
occlusion.
References
1. Gur A, Csányi A, Bornstein N. Vasomotor reactivity. In: Csibá L, Baracchini C, editors.
Manual of neurosonology. Cambridge: Cambridge University Press; 2016.
2. Malojcic B, Giannakopoulus P, Sorond FA, Azevedo E, Diomedi M, Oblak JP, etal. Ultrasound
and dynamic functional imaging in vascular cognitive impairment and Alzheimer’s disease.
BMC Med. 2017;15:27.
3. Silvestrini M, Vernieri F, Troisi E, Passarelli F, Matteis M, Pasqualetti P, etal. Cerebrovascular
reactivity in carotid artery occlusion: possible implications for surgical management of
selected groups of patients. Acta Neurol Scand. 1999;99:187–91.
4. Ringelstein EB, Sievers C, Ecker S, Schneider PA, Otis SM.Noninvasive assessment of CO2-
induced cerebral vasomotor response in normal individuals and patients with internal carotid
artery occlusions. Stroke. 1988;19:963–9.
5. Markus HS, Harrison MJ.Estimation of cerebrovascular reactivity using transcranial Doppler,
including the use of breath-holding as the vasodilatory stimulus. Stroke. 1992;23:668–73.
6. Segal SS.Regulation of blood ow in the microcirculation. Microcirculation. 2005;12:33–45.
7. Panerai RB.Complexity of the human cerebral circulation. Philos Transact A Math Phys Eng
Sci. 2009;367:1319–36.
8. Segal SS.Special circulations. In: Boulpaep WFBEL, editor. Medical physiology. Philadelphia,
PA, USA: W.B. Saunders Company; 2008.
9. Madureira J, Castro P, Azevedo E. Demographic and systemic hemodynamic inuences
in mechanisms of cerebrovascular regulation in healthy adults. J Stroke Cerebrovasc Dis.
2017;26:500–8.
10. Zimmermann C, Wimmer M, Haberl RL.L-arginine-mediated Vasoreactivity in patients with
a risk of stroke. Cerebrovasc Dis. 2004;17:128–33.
11. Vorstrup S, Henriksen L, Paulson OB. Effect of acetazolamide on cerebral blood ow and
cerebral metabolic rate for oxygen. J Clin Invest. 1984;74:1634–9.
12. Muller M, Voges M, Piepgras U, Schimrigk K.Assessment of cerebral vasomotor reactivity
by transcranial Doppler ultrasound and breath-holding. A comparison with acetazolamide as
vasodilatory stimulus. Stroke. 2005;26:96–100.
13. Ringelstein EB, Van Eyck S, Mertens I.Evaluation of cerebral vasomotor reactivity by vari-
ous vasodilating stimuli: comparison of CO2 to acetazolamide. J Cereb Blood Flow Metab.
1992;12:162–8.
14. Park CW, Sturzenneger M, Douville CM, Aaslid R, Newell DW.Autoregulatory response and
CO2 reactivity of the basilar artery. Stroke. 2003;34:34–9.
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15. Diehl RR, Henkes H, Nahser HC, Kuhne D, Berlit P. Blood ow velocity and vasomotor
reactivity in patients with arteriovenous malformations. A transcranial Doppler study. Stroke.
1994;25:1574–80.
16. Carrera E, Kurtz P, Badjatia N, Fernandez L, Claassen J, Lee K, etal. Cerebrovascular carbon
dioxide reactivity and delayed cerebral ischemia after subarachnoid hemorrhage. Arch Neurol.
2010;67:434–9.
17. Widder B, Kleiser B, Krapf H.Course of cerebrovascular reactivity in patients with carotid
artery occlusions. Stroke. 1994;25:1963–7.
18. Klinglelhofer J, Sander D.Doppler CO2 test as an indicator of cerebral vasoreactivity and
prognosis in severe intracranial hemorrhages. Stroke. 1992;23:962–6.
P. Castro and E. Azevedo
Chapter 20
Critical Closing Pressure inAcute Brain
Injury: Usefulness ofTranscranial Doppler
asNeuromonitoring
CorinaPuppo, LeandroMoraes, andBernardoYelicich
Key Points
1. CrCP is a blood pressure value, expressed in mmHg, greater than or equal to
ICP.It is the ABP at which small vessels collapse and circulation stops.
2. Negative values do not have a physiological explanation, being probably a meth-
odologic limitation.
3. The difference between ICP and CrCP represents the tone of cerebral arteriolar
vessels and has been called wall tension.
4. The difference between ABP and CrCP represents the effective cerebral perfu-
sion pressure or closing margin.
5. Vasospasm in the patient with SAH temporarily and spatially decreases CrCP.
20.1 Introduction
Before dening the critical closing pressure of cerebral circulation (CrCP) and in
order to better understand its concept, we must refer to another concept closely
related to CrCP: cerebral perfusion pressure (CPP). The perfusion pressure of an
organ is the pressure that propels blood through its vascular circuit, calculated as the
C. Puppo (*)
Intensive Care Unit, Clinics Hospital, Universidad de la Republica School of Medicine,
Montevideo, Uruguay
e-mail: coripuppo@gmail.com
L. Moraes
Intensive Care Center, Hospital de Clinicas, School of Medicine, University of the Republic,
Montevideo, Uruguay
B. Yelicich
Engineering (Ing), Universidad de la República – Montevideo Uruguay, Neuromonitoring
Group of the Hospital de Clínicas, Montevideo, Uruguay
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_20
341© Springer Nature Switzerland AG 2022
342
CPPABP CVP= –
CPPABP ICP=-
difference between the pressure in the arterial vessel arriving at the specic organ
and the pressure in the veins which drain it. In the case of the brain it should be the
arterial blood pressure minus the cerebral venous pressure (CVP) (Eq.20.1):
C. Puppo et al.
The veins that leave the brain and lead the blood to the dura sinuses are called
bridge veins. The pressure in these veins is the outlet pressure of the cerebral vascular circuit. These veins have thin, predominantly adventitious walls; the pressure
around them is transferred to them. On certain occasions, when there is an increase
in intracranial pressure (ICP), these veins are compressed. Cerebral bridge veins’
pressure is not measurable in clinical practice. The formula used for cerebral perfusion pressure is the difference between the arterial blood pressure that reaches the
brain and intracranial pressure. If ICP is normal, both pressures are similar, so the
formula is useful in both situations, during normal and high ICP:
From this formula, broadly used, it can be erroneously inferred that, if CPP
approaches zero, either because ABP decreases or ICP increases, cerebral circulation traverses the brain with decreasing driving force, and when it reaches zero,
circulation stops.
That is, if ABP=PIC, CPP=0 (Eq.20.2).
However, circulation stops before these pressures are equal. This is because the
small resistance vessels have a tone which exerts an inward force, facilitating the
closure of the vessels, before ABP and ICP are equal. This force is not included in
CPP formula.
Burton coined the term “critical closing pressure” for systemic circulation in
1951. He described, through a theoretical model, that brain vessels can collapse
when their pressure drops to a critical value, for which he coined the name “critical
closing pressure” (CrCP) [1].
Based on Burton’s model, critical closing pressure of the cerebral circulation is
dened as the arterial blood pressure (ABP) at which small cerebral arteries close and
cerebral blood ow (CBF) ceases [2–4]. That is, the force generated by the heart is
insufcient to propel circulation through the cerebral vascular bed. It is greater than ICP.
(20.1)
(20.2)
20.2 CrCP Therefore Represents aCritical Lower Threshold
20.2.1 What Is theImportance ofCrCP Concept?
When measuring CPP with the conventional formula presented above, there may be
an acceptable CPP value of 70mmHg, with an ABP of 90mmHg and an ICP of
20mmHg, for example, pressures that do not worry the intensivist. But if the tone
ofCerebral Circulation
CM ABPCrCP=-
20 Critical Closing Pressure in Acute Brain Injury: Usefulness of Transcranial…
CPP
CM or
Effective
CPP
343
CPP
MAP MAP
ICP ICP
Fig. 20.1 Scheme of the different pressures to which the text refers. On the left it is shown how
the cerebral perfusion pressure is conventionally measured (CPP). CPP is the difference between
the inlet pressure to the circuit (ABP) and the output pressure (ICP). On the right, vascular wall
tension (WT) added to ICP constitutes the critical closing pressure. Observe how “classical” CPP
calculation (left panel) can overestimate the effective CPP value (CM in the right panel).
[Abbreviations: MAP: mean arterial pressure; ICP: intracranial pressure; CPP: cerebral perfusion
pressure; CM: closing margin; WT: wall tension; CrCP: critical closing pressure]
WT
CrCP
of the cerebral arterioles is high, it may happen that the cerebral circulation of this
patient is at risk of stopping, which is not evidenced by CPP with its classical measurement. Therefore, some researchers have proposed the terms “effective CPP” [5,
6] or “collapsing” or “closing margin” (CM) [7, 8], to get a closer idea of the real
hemodynamic situation and the risk of arteriolar collapse. This closing margin is
calculated as the difference between the patient’s ABP and CrCP (Eq.20.3):
(20.3)
The difference between ICP and CrCP corresponds to the tone of cerebral arte-
riolar vessels and has been called “wall tension“(WT) (Fig.20.1).
20.3 Methods toStudy Cerebral Critical Closing Pressure
The advent of TCD has been extremely useful to non-invasively measure different
parameters of cerebral hemodynamics, based on the possibility of visualizing cerebral blood ow velocity (CBFV) at patient’s bedside, in real time, with excellent
temporal resolution. One of the calculated parameters based on CBFV has
been CrCP.
When using TCD, CBFV is measured in conductance brain basal large vessels.
When continuous monitoring is performed, the middle cerebral artery is the vessel
studied in more than 90% of the cases. This artery delivers approximately one-third
of the total CBF. This allows CBFV and ABP changes to be simultaneously followed. Since in most clinical situations ABP does not decrease to extreme values
leading to circulatory arrest, CrCP cannot be measured directly in clinical grounds.
344
Aaslid studied CrCP during transient cardiac arrest—generated at the evaluation of
patients with implantable debrillators—thus being able to directly visualize the
pressure at which cerebral blood ow stopped.
Methods initially used assumed that the relationship between ABP and cerebral
blood ow was linear in the dynamic situation of each arterial pulse, that is, if ABP
continued to decline, CBFV would continue to decrease at the same rate, proportionally to ABP descent. The relationship between rapid changes in CBF (studied
through CBFV recorded continuously with TCD) and the rapid changes in ABP
began to be studied graphically. The decrease in cerebral blood ow was virtually
continued (linearly extrapolated), projecting it to its zero value, recording the ABP
corresponding to zero ow as the CrCP.These methods can be displayed graphically for better understanding.
C. Puppo et al.
20.4 Parameters toMonitor
The methods which estimate CrCP use two parameters to measure CrCP: ABP and
CBF.Continuous recordings of both variables have to be obtained in order to calculate the ABP value at which ow stops. Changes in CBF, as explained above, are
estimated by a surrogate method: CBFV measured with TCD.This allows continuous monitoring of CBF changes occurring over time in one or both middle cerebral
arteries. Although TCD does not measure CBF in absolute values, CBFV changes
are proportional to CBF changes.
There are two types of methods to estimate CrCP:
1. What we will call “graphic” methods, based on comparing how the simultaneous
waves of ABP and CBFV behave graphically and calculate CrCP based on this
comparison.
2. Multiparameter or impedance methods, which add other high-frequency param-
eters of cerebral circulation, can be derived from CBFV and ABP, such as arterial compliance and cerebrovascular resistance, heart rate, and angular frequency.
Impedance concept is similar to resistance, but it varies with the cyclic variation
of the waves. Therefore, the multiparametric models use the value π (“pi”) and the
heart rate. These impedance methods have been initially described using ICP in
their formula, but eventually they were also calculated without this parameter if ICP
value was considered to be normal.
Details for its measurement or estimation can be seen in the appendix.
20.5 Clinical Importance ofCritical Closing Pressure
We will review here the most important experimental and clinical publications on
this subject.
20 Critical Closing Pressure in Acute Brain Injury: Usefulness of Transcranial…
345
20.5.1 Critical Closure Pressure During Vasospasm inPatients
withSubarachnoid Hemorrhage
Two papers were published by Czosnyka and coworkers [9, 10] (2004 and 2014).
(a) The rst one prospectively evaluated 32 patients with SAH.Patients were fol-
lowed with daily TCD studies, diagnosing vasospasm when mean blood ow
velocity (MFV) was greater than 120cm/s, and Lindegaard ratio was greater
than 3. CrCP was studied with two graphic-based methods [appendix]. Vasospasm
was identied in 18 patients. Three patients were excluded because vasospasm
was bilateral. In the 15 patients that were eventually included in the study, two
comparisons were performed: (1) the level of baseline, pre- vasospasm CrCP was
compared with the intra-vasospasm level and (2) CrCP ipsilateral to vasospasm
was compared with contralateral (no vasospasm side) CrCP (Fig.20.2).
(b) In the second study, also carried out by members of the same group 10years
later, CBFV and ABP records of 52 patients with SAH in whom cerebral vasospasm of the cerebral arteries had been diagnosed with TCD were retrospectively studied. The diagnosis of vasospasm was made with the measurement of
CBFV and Lindegaard ratio with TCD, using the same criteria as in the previous (2004) study. They used the impedance model described by Varsos (using
CPP in the formula in patients who had ICP monitoring, and ABP in those
without ICP). Since CrCP expresses the sum of intracranial pressure (ICP) and
vascular wall tension, the researchers used the estimation of CrCP to indirectly
evaluate the changes in vascular tone that occur in small vessels distal to vasospasm. From the pathophysiological point of view, when vasospasm develops,
the caliber of the spastic cerebral conductance arteries decreases, thereby
increasing the resistance to ow in that proximal sector.
This leads to a perfusion pressure decrease at the zone distal to vasospasm.
If autoregulation is maintained, the small arteriolar vessels of the hypoperfused
area, responsible for the so-called cerebrovascular resistance, will dilate,
decreasing resistance so that perfusion is maintained. This response decreases
these vessels’ wall tension.
The development of cerebral arteries vasospasm caused signicant decreases
in CrCP, without any signicant change observed in ICP.Vasospasm, as in the
previous study, induced asymmetry; CrCP ipsilateral to vasospasm of cerebral
arteries was signicantly lower than contralateral. Patients with poor clinical
outcomes (at discharge and at 3months) had a signicantly lower CrCP after
the onset of cerebral vasospasm. In other words, they also veried that CrCP is
reduced in the presence of cerebral vasospasm in both temporal and spatial
evaluations. Since ICP remained unchanged during vasospasm of the cerebral
arteries, all the change in CrCP was attributed to a decrease in cerebrovascular
resistance (CrCP= ICP+WT). This agrees with the interpretation that CrCP
evaluates the change in wall tension of small resistance vessels distal to vasospasm. They dilate during vasospasm as an autoregulatory response to a
decrease in regional perfusion pressure of the area irrigated by spastic arteries.