U.S. patent application number 12/740623 was filed with the patent office on 2010-12-16 for venous modulation of collateral perfusion of cerebral ischemia.
This patent application is currently assigned to The Regents of the University of California. Invention is credited to David S. Liebeskind, Mindaugas Pranevicius, Osvaldas Pranevicius.
Application Number | 20100318114 12/740623 |
Document ID | / |
Family ID | 40591507 |
Filed Date | 2010-12-16 |
United States Patent
Application |
20100318114 |
Kind Code |
A1 |
Pranevicius; Osvaldas ; et
al. |
December 16, 2010 |
Venous Modulation of Collateral Perfusion of Cerebral Ischemia
Abstract
A patient in whom blood diversion due to cerebral venous steal
is present, and abolishment of the cerebral venous steal is
indicated, is treated by increasing the cerebral venous pressure in
the patient. This increase in cerebral venous pressure restores the
collapsed cerebral vasculature, thereby increasing cerebral blood
flow. The increase in cerebral venous pressure may be achieved
using an occluding catheter in the superior vena cava or the
internal jugular veins, using external compression of the cervical
veins, or any other suitable mechanism. The occlusion may be
controlled precisely during treatment, possibly as a function of
cerebral blood flow, and after treatment the patient may experience
a persistent effect because the cerebral vasculature is no longer
collapsed.
Inventors: |
Pranevicius; Osvaldas; (New
York, NY) ; Pranevicius; Mindaugas; (Forest Hills,
NY) ; Liebeskind; David S.; (Los Angeles,
CA) |
Correspondence
Address: |
FENWICK & WEST LLP
SILICON VALLEY CENTER, 801 CALIFORNIA STREET
MOUNTAIN VIEW
CA
94041
US
|
Assignee: |
The Regents of the University of
California
Oakland
CA
|
Family ID: |
40591507 |
Appl. No.: |
12/740623 |
Filed: |
October 31, 2008 |
PCT Filed: |
October 31, 2008 |
PCT NO: |
PCT/US08/82161 |
371 Date: |
April 29, 2010 |
Related U.S. Patent Documents
|
|
|
|
|
|
Application
Number |
Filing Date |
Patent Number |
|
|
60984372 |
Oct 31, 2007 |
|
|
|
Current U.S.
Class: |
606/194 |
Current CPC
Class: |
A61M 2025/1052 20130101;
A61M 25/10 20130101; A61M 25/10181 20131105; A61M 25/1018 20130101;
A61M 25/10184 20131105; A61B 17/1322 20130101; A61B 17/1204
20130101 |
Class at
Publication: |
606/194 |
International
Class: |
A61M 29/02 20060101
A61M029/02 |
Goverment Interests
STATEMENT REGARDING FEDERALLY SPONSORED RESEARCH OR DEVELOPMENT
[0002] The U.S. Government has certain rights in this invention
pursuant to Grant No(s). 5K23NS054084-03 awarded by the National
Institutes of Health.
Claims
1. A method for treating cerebral ischemia, comprising: selecting a
patient in whom blood diversion due to cerebral venous steal is
present and abolishment of the cerebral venous steal is indicated,
the cerebral venous steal caused by focally collapsed cerebral
vasculature; increasing a cerebral venous pressure in the patient
using an occlusion of one or more veins coupled to the collapsed
cerebral vasculature; maintaining the increased cerebral venous
pressure for a period of time sufficient to restore at least a
portion of the patient's collapsed cerebral vasculature; and
removing the occlusion of the one or more veins coupled to the
collapsed cerebral vasculature.
2. The method of claim 1, wherein the patient is suffering from a
stroke.
3. The method of claim 1, wherein the occlusion is of a portion of
the patient's superior vena cava.
4. The method of claim 1, wherein the occlusion is of a portion of
the patient's superior vena cava between the patient's right aorta
and azygos vein.
5. The method of claim 1, wherein the occlusion is of one or both
of a patient's interior jugular veins.
6. The method of claim 1, wherein the occlusion is achieved by an
expandable balloon placed in the one or more veins.
7. The method of claim 1, wherein the occlusion is achieved by
expanding a cervical cuff placed around the patient's neck to press
against the patient's cervical veins.
8. The method of claim 1, further comprising: mapping the cerebral
blood flow and the venous pressure while the increased cerebral
venous pressure is being maintained; and adjusting the increased
venous pressure as a function of at least the cerebral blood
flow.
9. The method of claim 8, wherein the cerebral blood flow is mapped
using TCD waveforms.
10. The method of claim 1, wherein cerebral blood flow
heterogeneity and blood flow in ischemic areas of the patient's
brain are maintained above the critical ischemic threshold.
11. An apparatus for treating cerebral ischemia, comprising: an
elongated tubular member for insertion into a patient's superior
vena cava, the tubular member having proximal and distal ends; an
expandable occluder located at the distal end of the tubular
member, the occluder having an expanded state and a collapsed
state; a pressure measurement device coupled to the tubular member
and configured to measure a pressure at the distal end of the
tubular member; a hemodynamic effect measurement device configured
to obtain a measure of cerebral blood flow in a patient; and a
controller coupled to the occluder for actuating the occluder
between the expanded and collapsed states, and in communication
with the pressure measurement device to obtain a measured venous
pressure and to the hemodynamic effect measurement device to obtain
the measure of cerebral blood flow, wherein the controller is
programmed to actuate the expandable occluder as a function of the
measured venous pressure and the measure of cerebral blood
flow.
12. The apparatus of claim 11, wherein the expandable occluder
comprises an elastomeric balloon.
13. The apparatus of claim 11, wherein the expandable occluder is
configured to fit within a portion of a patient's superior vena
cava.
14. The apparatus of claim 11, wherein the expandable occluder is
configured to fit within one or both of a patient's interior
jugular veins.
15. The apparatus of claim 11, wherein the expandable occluder
comprises an expandable cervical cuff configured to be placed
around a patient's neck to press against the patient's cervical
veins.
16. The apparatus of claim 11, wherein the hemodynamic effect
measurement device obtains a measure of cerebral blood flow using
TCD waveforms.
Description
CROSS REFERENCE TO RELATED APPLICATIONS
[0001] This application claims the benefit of U.S. Provisional
Application No. 60/984,372, filed Oct. 31, 2007, which is
incorporated by reference in its entirety.
BACKGROUND
[0003] This invention relates generally to medical devices and
methods, and more particularly, to catheters, systems, kits, and
methods for treating cerebral ischemia, such as acute or chronic
ischemia associated with stroke.
[0004] Stroke remains a devastating and common clinical disorder,
yet treatment options are limited. In recent years, the field of
cardiology has witnessed remarkable advances in the prevention and
treatment of ischemic heart disease. However, cerebral ischemia has
eluded the stroke research community's fervent efforts to reverse
or even limit the degree of neurologic injury that develops within
only minutes or hours of stroke onset yet may result in lifelong
disability.
[0005] Much attention has been devoted to the ischemic cascade, or
sequence of cellular and molecular events that occur in the brain
when arterial blood flow is diminished. Traditional descriptions of
the ischemic cascade in stroke focus on organ-specific aspects of
pathophysiology such as deleterious events in brain tissue,
neglecting critical vascular elements such as hemodynamic
compensation, endothelial ischemia, or blood-brain barrier
permeability that accompany early phases of acute ischemic stroke.
Recognition of the neurovascular unit has recently shifted focus to
the complex interaction between vascular elements and specific
pathophysiologic events in the ischemic brain. Increasing use of
advanced noninvasive imaging modalities and endovascular procedures
for acute ischemic stroke has also provided a wealth of information
regarding the critical role of collateral perfusion.
[0006] The emphasis on vascular aspects of acute ischemic stroke
prevails in the clinical realm. Almost a dozen years after the
introduction of thrombolysis for acute ischemic stroke, the only
advance in treatment has been the US Food and Drug Administration
(FDA) clearance of the Merci device (Concentric Medical, Mountain
View, Calif.) for mechanical thrombectomy. As a result, the only
approved means to treat stroke is to remove the clot obstructing an
artery feeding the brain with essential oxygen and nutrients.
Unfortunately, this approach can only be used in a subset of
cases.
[0007] Recent investigational strategies have attempted to improve
upon this approach with newer and potentially safer clot-busting
approaches. Novel thrombolytic and antithrombotic drugs,
alternative endovascular thrombectomy devices, and even noninvasive
use of ultrasound have been proposed to enhance recanalization.
Although recanalization is an important facet of acute stroke
therapy, numerous limitations abound. Persistent arterial occlusion
occurs in a substantial subset of cases, and recanalization is not
tantamount to reperfusion, as distal emboli may ensue. Rethrombosis
may occur in one of every three thrombolysis cases. Reperfusion of
the proximal artery may also not herald improved neurologic
outcome, as some regions of downstream ischemia may not be
vulnerable due to established compensation via collateral
perfusion. Proximal recanalization may also hasten hemorrhagic
transformation or bleeding into areas of severe ischemic injury.
Neuroprotective strategies have attempted to circumvent this aspect
by conducting clinical trials that consider ischemia and
hemorrhage. However, effective delivery of neuroprotective agents
is also dependent on collateral perfusion, underscoring the
emphasis on vascular pathophysiology.
[0008] The introduction of devices to treat acute ischemic stroke
has also transformed the field. Endovascular devices for
neurointerventional procedures have been proliferating for many
years. Debate concerning these techniques has focused on the
distinction between clinical outcomes and vascular end points, such
as the technical efficacy of arterial recanalization. The
dissimilar regulatory processes for approval of drugs and devices
have also received much attention. More subtle issues relate to the
nature of these different therapeutic approaches. Devices may
selectively target specific biophysical mechanisms and thereby
enhance an endogenous pathophysiologic process, whereas drugs may
exhibit more complex interactions.
[0009] Unlike drugs administered in a standard fashion, the
efficacy of devices may depend on operator experience, as
procedural variables may be difficult to ascertain. Devices have
flourished in the growing competition to develop effective
therapies for acute ischemic stroke. Current investigational device
strategies include infrared laser therapy transmitted through the
skull, stimulation of the sphenopalatine ganglion, and endovascular
catheters for novel recanalization approaches, induction of
hypothermia, and perfusion augmentation.
[0010] The concept of blood diversion due to vascular collapse as a
mechanism of perifocal cerebral ischemia, and the possibility to
abolish this diversion with increased venous pressure, has been
previously described. However, this has never been applied to treat
patients in whom venous steal is present, where blood, flowing in
the path of least resistance, is diverted from areas where it is
needed (e.g., in the immediate peristroke vicinity). Moreover, none
of the existing methods for treatment of stroke or cerebral
ischemia directly address enhancement of penumbral blood flow.
SUMMARY
[0011] Although previous approaches have emphasized pressure
augmentation in arterial inflow routes providing collateral blood
flow, the critical pathophysiology may actually involve downstream
resistance of venous outflow pathways. Cerebral venous steal, or
diversion of blood volume to the periphery of the ischemic
territory, may thus occur caused by the collapsible nature of
venous circuits in the brain. Such displacement of blood volume may
lead to increasing downstream resistance due to focally collapsed
veins once critical closing pressures are compromised. Conversely,
increased blood volume and distension of cerebral veins may enhance
tissue perfusion.
[0012] Accordingly, embodiments of the invention target ischemia
rather than clot disruption or consideration of venous hemodynamics
and flow redistribution. For acute and chronic treatment of stroke
and other cerebral ischemia, embodiments of the invention use
cerebral venous outflow modulation to abolish cerebral vessel
collapse and venous steal, thereby increasing cerebral collateral
and penumbral flow. The venous outflow modification method
described herein may be used in combination with antegrade
perfusion enhancement methods.
[0013] Accordingly, embodiments of the invention provide devices
and methods for improving cerebral collateral perfusion in patients
suffering from either local or global ischemia, in either the acute
or chronic timeframes. In one embodiment, the apparatus comprises a
catheter which includes an elongated tubular member having a
proximal end, a distal end, and first and second lumens. The first
lumen communicates with the proximal end and a port at the distal
end of the catheter. The second lumen communicates with the
proximal end of the catheter and a port proximal to the expandable
occluder. An expandable occluder, which may be an elastomeric
balloon in certain embodiments, is mounted on a distal region of
the catheter between the proximal port and the distal port. A
manometer, or other pressure measurement device, is mounted to the
proximal end of the second lumen, which is located proximal to the
occluder for measuring venous pressure proximal to the
occluder.
[0014] Embodiments of the invention are capable of rapidly
reestablishing collateral cerebral blood flow (cCBF) at a rate
sufficient to relieve penumbral ischemia distal to the occlusion.
The techniques described herein could be adaptable for use both in
an emergency situation (e.g., outside the hospital), within a
hospital environment, or even in an outpatient or chronic setting.
To avoid reperfusion injury, embodiments of the invention may
enable control over the rate of cCBF and/or cessation of cCBF to
the ischemic region. In addition to treating ischemia, the
embodiments of the invention may provide access and support for
performing other therapeutic interventions to treat the ischemia,
including drug interventions to treat stroke and to provide
supportive therapy. Additionally, embodiments of the invention may
use access routes that are familiar to most health care
professionals, so as to permit rapid and wide spread adoption.
BRIEF DESCRIPTION OF THE DRAWINGS
[0015] FIG. 1 is a diagram of a patient, and a portion of the
patient's vascular system, being treated in accordance with an
embodiment of the invention.
[0016] FIG. 2 is a diagram of a device for treating cerebral
ischemia in accordance with an embodiment of the invention.
[0017] FIG. 3 is a diagram of a patient, and a portion of the
patient's vascular system, being treated in accordance with another
embodiment of the invention.
[0018] FIG. 4 is a diagram of a patient, and a portion of the
patient's vascular system, being treated in accordance with another
embodiment of the invention.
[0019] The figures depict various embodiments of the present
invention for purposes of illustration only. One skilled in the art
will readily recognize from the following discussion that
alternative embodiments of the structures and methods illustrated
herein may be employed without departing from the principles of the
invention described herein.
DETAILED DESCRIPTION
Overview of Pathophysiology
[0020] In accordance with embodiments of the invention, treatment
of ischemia in the brain is achieved by the control of the
collapsibility factor in the cerebral vasculature. It may therefore
be deemed pertinent to review basic physiological effects, related
to collapsibility of intracranial vessels, before discussing
specific embodiments of the invention.
[0021] Cerebral vessels like other collapsible tubes tend to
collapse when external pressure exceeds intravascular (negative
transmural pressure). When intravascular pressure is increased
(i.e., positive transmural pressure), vessels reopen and their
diameter increases. It has been demonstrated that resistance in the
collapsible vascular beds decreases when transmural pressure
increases. Active wall tension also contributes to vessel collapse
and results in critical closing pressure. Critical closure pressure
is the inflow pressure at which flow through the vascular bed
stops. Due to pressure drop through the feeding arteries and active
autoregulation, intravascular pressure at the microcirculation is
not directly related to systemic arterial pressure. However, it is
directly proportional to the venous pressure. The dependence of
intravascular pressure, resistance, and collapsibility on the
venous pressure allows venous pressure to be used to modify
perifocal blood vessel collapse and flow distribution. Increasing
venous pressure may seem counterintuitive; however, this approach
or mechanistic modification of the circulatory bed may actually
augment cerebral blood flow and open collaterals circuits in
penumbral regions that are at-risk for evolving infarction.
[0022] Experimental physiological data indicate that intracerebral
vein pressure is slightly above intracranial pressure (ICP).
However, dural sinus pressure is lower than that in the smaller
veins and not related to ICP. Spontaneous increase in ICP does not
affect jugular vein bulb pressure (JVBP). Similarly, a small JVBP
increase does not affect ICP, although a more extensive increase of
JVBP raises both cerebral venous pressure and ICP to an equal
extent. If JVBP is low, its drop does not affect ICP or cerebral
venous pressure. If JVBP is high, its drop affects ICP and cerebral
venous pressure to an equal extent. This is caused by an
interesting physiological phenomenon referred to as a "vascular
waterfall." When this happens, flow rate through a collapsible tube
will depend only on an upstream pressure at the feeding segment and
will be independent of downstream pressure at the exit end. This
behavior is similar to that of a mountain waterfall, where the flow
rate depends on the quantity of flow at the source and not on the
height of the vertical drop or fall. This is in a sharp contrast to
ordinary laminar or turbulent flow in rigid pipes, where flow is
simply proportional to the pressure gradient between the ends.
[0023] Analysis of vessel collapse shows that under some
circumstances provision of resistance to the outflow end might
actually enhance flow through a collapsed tube segment. This is
because distal resistance increases distending pressure on the
collapsed segment, which may eliminate the most effective hindrance
to flow, progressive and recurrent narrowing of the collapsed
segment. This is because collapsible tubes have an unequivocal and
nonlinear flow (Q) pressure (P) interrelationship. When transmural
pressure (Ptm) is positive, the cerebral veins assume a circular
cross shape. If external pressures exceed venous pressure, the vein
wall is subjected to circumferential compression with subsequential
diminution of their cross-sectional area and full collapse. Between
a fully-distended and fully-collapsed state, the cerebral veins
exhibit a highly nonlinear and unequivocal P-Q interrelationship,
part of which is inverted when veins are partially collapsed. In
this part, flow through the vein increases as pressure gradient
along it falls. In other words, it is possible to augment cerebral
blood flow (CBF) by decreasing an extra-intracranial pressure
gradient. This is a physiological basis for reestablishing CBF via
the collateral circulation in the brain, in accordance with
embodiments of the invention.
Device and Method
[0024] Accordingly, embodiments of the invention are used to treat
a patient who is suffering from venous steal due to cerebral vessel
collapse, which may otherwise lead to cerebral ischemia, by
increasing the cerebral venous pressure in the patient. FIG. 1 is
diagram of a patient illustrating a portion of the patient's
vascular system, including interior the jugular veins (IJ), the
superior venous cava (SVC), the right atrium (RA), and the azygos
vein. FIG. 1 illustrates a oxygen demand directed technique for
treating the patient.
[0025] As illustrated, distal end of an occluding catheter 12 is
inserted through a percutaneously accessible vein, such as the
jugular or subclavian vein, into the SVC. The distal region of the
occluding catheter 12 contains an expandable balloon 32, or other
expanding mechanism, which is positioned in the SVC at a location
above the RA and below where the azygos vein connects to the SVC.
The position of the occluding catheter 12 and balloon 32 may be
confirmed, for example, via x-ray.
[0026] Once the occluding catheter 12 is in place, the balloon 32
is expanded to occlude blood flow in the SVC at least partially.
The degree of occlusion in the SVC may be varied according to the
venous pressure, which may be recorded by a pressure sensor that
records pressure proximal to the balloon 32 or other portion of the
occluding catheter 12. In addition, the occluding catheter 12 may
include mechanisms to measure other physiological parameters. For
example, flow may be measured by Doppler ultrasonography,
electromagnetic flow meters, or heat dilution; and blood
oxygenation may be measured by fiberoptic oximetry or concentration
of metabolites or markers.
[0027] In addition, the patient may be connected to a hemodynamic
effect monitor 40, which measures the cerebral blood flow in the
patient's head. In this way, the hemodynamic effect monitor 40
provides feedback for whether and to what extent the treatment
results in the desired increased cerebral blood flow. In one
embodiment, the hemodynamic effect monitor 40 uses TCD waveforms to
obtain a mapping of the patient's cerebral blood flow. In other
embodiments, the hemodynamic effect may be monitored using
spectrometry or CT angiography.
[0028] FIG. 2 is a diagram of the venous occlusion catheter 12,
which may be used in connection with the embodiment illustrated in
FIG. 1. The catheter 12 is of a length sufficient to extend from an
insertion point to the SVC. The outer diameter of the catheter is
less than the inner diameter of the SVC at a location whether the
SVC is to be occluded. The catheter 12 is preferably opaque to
X-rays and may be marked at the tip for easy visualization using
conventional X-ray equipment.
[0029] In one embodiment, the catheter 12 comprises a main lumen 26
opening at the tip 28 of the catheter. The catheter further
comprises a balloon lumen 30 that forms a low resistance connection
between an inflatable balloon 32 and a pump, e.g., via a reservoir.
The inflatable balloon 32 is preferably made from a highly
compliant or easily folding material so that the balloon 32, the
low resistance balloon channel 30, and the reservoir together form
a high compliance system. This system may be filled with a low
viscosity gas, such as helium.
[0030] The catheter 12 may incorporate a conventional optic fiber
34 to allow for oxygen saturation measurement in the SVC. The
catheter 12 may further incorporate a thermistor 36, positioned
close to the catheter tip 28 and proximally to the balloon 32 for
cerebral blood flow (CBF) measurement. The main lumen 26 of the
catheter 12 is coupled to the controller 22 for pressure sensing of
the SVC. Alternatively the SVC pressure can be sensed through a
conventional fiberoptic pressure sensor in the catheter 12. The
main catheter lumen 26 is also connected to a pump for fluid
injection/withdrawal to actuate the balloon 32.
[0031] In another embodiment for treating venous steal due to
cerebral vessel collapse, illustrated in FIG. 3, the occluding
catheter 12 may comprise a plurality of expandable balloons 32,
each coupled to controller 22 and individually expandable. In
operation, a lower balloon 32 may be positioned between the RA and
the inferior venal cava (IVC), and the upper balloon 32 positioned
between the RA and the SVC. This embodiment allows control of flow
from the IVC while the outflow in the SVC is being occluded. Using
this dual balloon embodiment, an operator may alternatively or
simultaneously occlude only the jugular vein or the jugular with
the azygos veins (which collects blood from the vertebral plexus).
This allows for improved control; otherwise, the azygos vein
outflow can be controlled only with hydrostatic pressure (e.g., by
placing the patient's head down).
[0032] In another embodiment for treating venous steal due to
cerebral vessel collapse, cerebral venous pressure increase is
achieved by occluding one or both of the internal jugular veins.
This may be achieved, for example, by inserting the distal end of
an occluding catheter 12 in the right or the left internal jugular
vein. In such an embodiment, the occluding catheter 12 is modified
to fit within the structure of the interior jugular vein. A balloon
32 of the occluding catheter 12 is expanded within the jugular vein
to occlude the return flow from the brain to the heart. As with
occluding flow in the SVC, this may also increase the cerebral
venous pressure and thereby restore collapsed cerebral veins to
increase the cerebral blood flow therethrough. Advancing jugular
catheter into the intracranial portion of venous circulation (e.g.,
the sigmoid sinus or straight sinus) allows venous pressure control
in the selective part of cerebral venous circulation. In another
embodiment, cerebral venous pressure increase can be achieved by
inserting the distal ends of an occluding catheter 12 in each of
the right and the left internal jugular veins.
[0033] FIG. 4 illustrates another embodiment in which cervical vein
occlusion is achieved with external cervical compression device. In
this embodiment, a cervical cuff 54 is placed around a patient's
neck, where the cervical cuff 54 is coupled to the controller 22
via a hose 56. The controller 22 may include a pump to actuate the
cervical cuff 54 via the hose 56, causing the cervical cuff 54 to
tighter around the patient's neck and partially occlude the
cervical veins. In this way, increased cerebral venous pressure can
be achieved quickly and without any invasive procedure.
[0034] There are several advantages in using the various
embodiments of the devices and methods disclosed herein for
protecting the brain and cerebral vasculature of patients suffering
from global or local ischemia due to venous steal. For example,
compared with known techniques for retrograde cerebral venous
perfusion, the retrograde venous perfusion of the invention (1)
does not produce backflow of blood to the brain, thereby
eliminating retroperfusion injury; (2) eliminates the need for IVC
clamping, thereby avoiding damage to the IVC; (3) provides an
accurate measurement of the jugular venous pressure; (4) is very
easy to administer (akin to placement of central venous catheters
that most physicians learn during early training stages) so does
not require specialized medical personnel; (5) is expected to have
very low complication rates due to its simplicity; and (6) can be
combined with IVC catheterization procedures for administration of
fluids, drugs, and the like.
[0035] In one embodiment, the degree of vessel occlusion may be
controlled by a balloon inflator (e.g., a pump) in the controller
22, which can be manually or automatically controlled. Balloon
inflation is preferably limited to a value of pressure and/or
volume selected as maximal safe level (P_balloon_max and/or
V_balloon_max). Once the balloon is maximally inflated, a before
and after balloon pressure gradient (dPmax) is measured. The
balloon is then gradually deflated until dP diminishes. The level
of balloon inflation that maintains dP near dPmax is
P_balloon_submax. In one embodiment, this pressure is selected as
the optimal inflation pressure at which to maintain the occluding
catheter 12 during treatment of the patient.
[0036] In one embodiment, the expandable balloon may have a
large-volume, high-compliance design with or without a fixed
pressure external inflation reservoir. This embodiment allows a
fixed-pressure, variable-volume balloon inflation. Fixed balloon
pressure limits dP increase to P_balloon.
[0037] In one embodiment of the treatment procedure, a patient is
initially selected who is experiencing an acute onset of
neurological deterioration due to stroke or cerebral ischemia,
cause by venous steal. The patient is screened for an ability to
modify cerebral blood flow or collateral flow augmentation by
trendelenburg/valsalva.
[0038] Once the patient is determined to be a candidate for the
procedure, the occluding catheter 12 is inserted into the patient's
venous system and positioned in the body as desired. In position,
the balloon 32 of the occluding catheter 12 is inflated, using for
example the controller 22. (Alternatively, occlusion may be
achieved externally using the cervical cuff 54, shown in FIG. 4.)
The venous pressure is measured using the catheter 12, and the
cerebral blood flow response is assessed using the hemodynamic
effect monitor 40, which data may be provided to the controller 22.
Responsive to the venous pressure and cerebral blood flow
measurements, the occlusion of the catheter 12 is modulated to
achieve an optimal response (e.g., maximal cerebral blood flow).
This therapy is continued until the patient's condition improves,
or for a predetermined time period. Beneficially, the improvement
in the patient's condition is expected to have a persistent effect
even after treatment is ceased, since the increased cerebral blood
flow will tend to keep the cerebral venous structure from
collapsing without need for continued increased venous
pressure.
[0039] In one embodiment, the following control algorithm is used
to determine the optimal occlusion by the occluding catheter 12.
This algorithm optimizes regional cerebral blood flow (CBF) by
increasing venous pressure via occlusion, responsive to the
measured venous pressure and CBF. The steps of the algorithm are:
[0040] 1. Obtain baseline CBF(t0), map rCBF(t0), collateral
flow(t0) [0041] 2. Obtain baseline MAP(t0), CVP(t0) [0042] 3.
Calculate CPP(t0)=MAP(t0)-CVP(t0) [0043] 4. Change CVP by
DPv(t0+dt) [0044] 5. Map rCBF response to DPv: [0045] a. ohms
response (rCBF reduction ptoportional to CPP reduction):
d(rCBF)=(CBF(t0)-0)/CPP(t0)-Dpv) [0046] b. Starling response
(rCBF=const or changes little)--characteristic for the large
regions with increased tissue pressure or when CBF autoregulation
is preserved (CBF independent of CPP):
d(rCBF)<(CBF(t0)-0)/CPP(t0)-Dpv); or d(rCBF)=0 [0047] c. steal
response--rCBF increases while CPP decreases--characteristic for
heterogenous perifocal regions with rCBF diversion [0048] 6.
Determine from rCBF mapping (step 1) regions with critically
reduced rCBF (at risk for permanent injury) [0049] 7. Determine
from the step 5 whether critical regions have steal response (5c)
[0050] 8. Elevate CVP to the level where rCBFSc (steal) is
maximized and exceeds critical flow threshold, while rCBFSa (ohm's
response) decreases, but stays above the ischaemic threshold [0051]
9. Reassess rCBF response to CVP periodically [0052] 10. Result:
optimized rCBF distribution with the decreased chance of permanent
ischaemic injury in perifocal regions
SUMMARY
[0053] The foregoing description of the embodiments of the
invention has been presented for the purpose of illustration; it is
not intended to be exhaustive or to limit the invention to the
precise forms disclosed. Persons skilled in the relevant art can
appreciate that many modifications and variations are possible in
light of the above disclosure.
[0054] Some portions of this description describe the embodiments
of the invention in terms of algorithms and symbolic
representations of operations on information. These algorithmic
descriptions and representations are commonly used by those skilled
in the data processing arts to convey the substance of their work
effectively to others skilled in the art. These operations, while
described functionally, computationally, or logically, are
understood to be implemented by computer programs or equivalent
electrical circuits, microcode, or the like.
[0055] As used herein, the term "proximal" refers to a position
closer to the catheter end outside the body and venous circulation
part away from the heart. If the catheter is inserted so that is
distal part is closer to the brain (e.g., inserted via inferior
vena cava), the terms "proximal" and "distal" still apply to the
catheter, but when referred to the venous system they refer to the
part closer to the brain (i.e., proximal) or closer to the heart
(i.e., distal). Usage of the lumens is reversed in the latter
case.
[0056] Finally, the language used in the specification has been
principally selected for readability and instructional purposes,
and it may not have been selected to delineate or circumscribe the
inventive subject matter. It is therefore intended that the scope
of the invention be limited not by this detailed description, but
rather by any claims that issue on an application based hereon.
Accordingly, the disclosure of the embodiments of the invention is
intended to be illustrative, but not limiting, of the scope of the
invention, which is set forth in the following claims.
* * * * *