U.S. patent application number 09/968745 was filed with the patent office on 2002-02-07 for non-invasive aortic impingement.
This patent application is currently assigned to The Ohio State University Research Foundation. Invention is credited to Ward, Kevin R..
Application Number | 20020016608 09/968745 |
Document ID | / |
Family ID | 21963543 |
Filed Date | 2002-02-07 |
United States Patent
Application |
20020016608 |
Kind Code |
A1 |
Ward, Kevin R. |
February 7, 2002 |
Non-invasive aortic impingement
Abstract
A method for subdiaphragm hemorrhage control in a patient or for
non-invasively enhancing cerebral and myocardial perfusion in a
patient includes positioning a moveable surface through the
esophagus adjacent the patient's esophageal-gastric junction and
displacing the moveable surface thereby applying a force
posteriorly in the direction of the patient's descending aorta
sufficient to partially or substantially completely occlude the
descending aorta. The moveable surface may be positionable in a
lower portion of the esophagus where the esophagus and the aorta
pass through the diaphragm or may be positioned in a portion of the
patient's stomach juxtaposed with the patient's descending
aorta.
Inventors: |
Ward, Kevin R.; (Glen Allen,
VA) |
Correspondence
Address: |
VAN DYKE, GARDNER, LINN AND BURKHART, LLP
2851 CHARLEVOIX DRIVE, S.E.
P.O. BOX 888695
GRAND RAPIDS
MI
49588-8695
US
|
Assignee: |
The Ohio State University Research
Foundation
1960 Kenny Road
Columbus
OH
43210-1063
|
Family ID: |
21963543 |
Appl. No.: |
09/968745 |
Filed: |
September 28, 2001 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
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09968745 |
Sep 28, 2001 |
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09446288 |
Apr 28, 2000 |
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6296654 |
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09446288 |
Apr 28, 2000 |
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PCT/US98/13109 |
Jun 24, 1998 |
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60050133 |
Jun 27, 1997 |
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Current U.S.
Class: |
606/192 |
Current CPC
Class: |
A61B 2017/00243
20130101; A61B 17/12136 20130101; A61B 17/12 20130101; A61B
17/12022 20130101; A61B 2017/00557 20130101; A61B 17/12099
20130101 |
Class at
Publication: |
606/192 |
International
Class: |
A61M 029/00 |
Claims
The embodiments of the invention in which an exclusive property or
privilege is claimed are defined as follows:
1. A non-invasive method of subdiaphragm hemorrhage control in a
patient, including: positioning a moveable surface through the
patient's esophagus adjacent the patient's esophageal-gastric
junction; and displacing the moveable surface thereby applying a
force posteriorly in the direction of the patient's descending
aorta sufficient to at least partially occlude the descending
aorta.
2. The method of claim 1 including positioning said moveable
surface with an elongated member and wherein said applying said
force includes moving said moveable surface with a displacement
mechanism joining said moveable surface to said elongated
member.
3. The method of claim 2 including anchoring said elongated member
with an anchoring member in the patient's esophagus.
4. The method of claim 2 including anchoring said elongated member
with an anchoring member in the patient's stomach.
5. The method of claim 2 wherein said displacement mechanism
includes parallel linkages supporting said moveable surface in a
parallel relationship with said elongated member.
6. The method of claim 2 wherein said moveable surface pivots with
respect to said elongated member.
7. The method of claim 1 wherein said moveable surface is defined
by a cuff and wherein said displacing the moveable surface includes
inflating said cuff sufficiently to at least partially occlude the
descending aorta.
8. The method of claim 7 wherein said cuff inflates
unidirectionally.
9. A non-invasive method of enhancing cerebral and myocardial
perfusion in a patient, including: positioning a moveable surface
through the patient's esophagus adjacent the patient's
esophageal-gastric junction; and displacing the moveable surface
thereby applying a force posteriorly in the direction of the
patient's descending aorta sufficient to at least partially occlude
the descending aorta and thereby increasing central and
intracranial arterial pressure.
10. A non-invasive method of enhancing cerebral and myocardial
perfusion in a patient, including: positioning an inflatable device
through the patient's esophagus in a portion of the patient's
stomach juxtaposed with the patient's descending aorta and
inflating the inflatable device; and applying a force with the
inflated device posteriorly in the direction of the patient's
descending aorta sufficient to at least partially occlude the
descending aorta and thereby increasing central and intracranial
arterial pressure.
11. The method of claim 10 including positioning said inflatable
device with an elongated member attached to said inflatable device
and wherein said applying said force includes moving said
inflatable device in the direction of the patient's diaphragm by
applying traction to said elongated member.
12. The method of claim 10 wherein said applying a force includes
applying a force on an exterior surface of the patient.
13. The method of claim 12 using a belt around the patient's
thoraco-abdominal region to apply said force.
14. The method of claim 10 including positioning said inflatable
device with an elongated member and wherein said applying said
force includes moving said inflatable device with a connecting
member joining said inflatable device to said elongated member.
15. The method of claim 10 wherein said connecting member is a
lever.
16. The method of claim 14 including anchoring said elongated
member with an anchoring member in the patient's esophagus.
17. The method of claim 14 including anchoring said elongated
member with an anchoring member in the patient's stomach.
18. The method of claim 17 wherein said anchoring member is another
inflatable device positioned to react with the patient's
diaphragm.
19. The method of claim 10 including positioning said inflatable
device with an elongated member and wherein said applying a force
includes providing a substantially rigid portion of said elongated
member and expanding said inflatable device posteriorly from said
rigid portion.
20. The method of claim 19 including anchoring said elongated
member with an anchoring member in the patient's esophagus.
21. The method of claim 19 including anchoring said elongated
member with an anchoring member in the patient's stomach.
22. The method of claim 21 wherein said anchoring member is another
inflatable device positioned to react with the patient's
diaphragm.
23. A non-invasive method of subdiaphragm hemorrhage control in a
patient, including: positioning an inflatable device through the
patient's esophagus in a portion of the patient's stomach
juxtaposed with the patient's descending aorta and inflating the
inflatable device; and applying a force with the inflated device
posteriorly in the direction of the patient's descending aorta
sufficient to at least partially occlude the descending aorta
24. A non-invasive apparatus for at least partially occluding the
descending aorta of a patient, comprising: a tubular member
configured at least in part to a patient's esophagus; a selectively
moveable portion of the tubular member positioned adjacent the
patient's esophageal-gastric junction when said tubular member is
positioned in a patient's esophagus, said portion moveable a
sufficient distance and having a surface of sufficient area to at
least partially occlude the patient's descending aorta; and a
displacement mechanism for displacing said moveable portion in the
direction of the patient's descending aorta when said tubular
member is positioned in the patient's esophagus with a force
sufficient to cause at least partial occlusion of the patient's
descending aorta.
25. The apparatus in claim 24 including an anchoring member which
is adapted to anchoring said tubular member in the patient's
esophagus.
26. The apparatus in claim 24 including an anchoring member which
is adapted to anchoring said tubular member in the patient's
stomach.
27. The apparatus in claim 24 wherein said displacement mechanism
includes a connecting member joining said moveable portion to said
tubular member which is operable to move said moveable portion
posteriorly in the direction of the patient's descending aorta.
28. The apparatus in claim 27 wherein said connecting member is a
lever.
29. The apparatus in claim 28 wherein said moveable portion is an
inflatable member pivotally joined with said elongated member by
said lever.
30. The apparatus in claim 24 wherein said moveable portion
includes a moveable surface and said displacement mechanism
includes parallel linkages supporting said moveable surface in a
parallel relationship with said elongated member.
31. The apparatus in claim 30 including a sheath covering said
moveable surface.
32. The apparatus in claim 24 wherein said moveable portion is
defined by a cuff and wherein said displacement mechanism includes
an inflation mechanism adapted to inflating said cuff.
33. The apparatus in claim 32 wherein said cuff inflates
unidirectionally.
34. A non-invasive apparatus for at least partially occluding the
descending aorta of a patient, comprising: an inflatable member; a
positioning device which positions said inflatable member through
the patient's esophagus in a portion of the patient's stomach
juxtaposed with the patient's descending aorta; an inflation
mechanism which selectively inflates said inflatable member; and a
force-producing mechanism producing a force with a surface of said
inflatable member posteriorly in the direction of the patient's
descending aorta sufficient to cause at least partial occlusion of
the patient's descending aorta.
35. The apparatus in claim 31 wherein said positioning device is an
elongated member which positions said inflatable member in the
patient's stomach and wherein said force-producing mechanism
includes a connecting member joining said inflatable device to said
elongated member which is operable to move said inflatable member
posteriorly in the direction of the patient's descending aorta.
36. The apparatus in claim 35 wherein said connecting member is a
lever.
37. The apparatus in claim 35 including an anchoring member which
anchors said elongated member in the patient's esophagus.
38. The apparatus in claim 35 including an anchoring member which
anchors said elongated member in the patient's stomach.
39. The apparatus in claim 34 wherein said force-producing
mechanism includes a strap applied externally around the patient's
thoraco-abdominal region wherein tightening of the strap applies a
force on the inflatable member posteriorly in the direction of the
patient's descending aorta.
40. The apparatus in claim 39 wherein said inflatable device
substantially fills the patient's stomach.
41. The apparatus in claim 34 wherein said positioning device is an
elongated member which positions said inflatable member in the
patient's stomach and including a substantially rigid portion of
said elongated member wherein said force is produced by expanding
said inflatable device posteriorly from said substantially rigid
portion.
42. The apparatus in claim 41 including an anchoring member which
anchors said elongated member in the patient's esophagus.
43. The apparatus in claim 41 including an anchoring member which
anchors said elongated member in the patient's stomach.
44. A non-invasive apparatus for at least partially occluding the
descending aorta of a patient, comprising: an inflatable member; an
elongated member which positions said inflatable member through the
patient's esophagus in one of a portion of the patient's stomach
juxtaposed with the patient's descending aorta and adjacent the
patient's esophageal-gastric junction; an inflation mechanism which
selectively inflates said inflatable member; and a displacement
mechanism which is operable to displace said inflatable member from
said elongated member posteriorly in the direction of the patient's
descending aorta thereby producing a force posteriorly in the
direction of the patient's descending aorta sufficient to at least
partially occlude the descending aorta.
45. The apparatus in claim 44 including an anchoring member which
anchors said elongated member in the patient's esophagus.
46. The apparatus in claim 44 including an anchoring member which
anchors said elongated member in the patient's stomach.
47. The apparatus in claim 44 wherein said displacement mechanism
is a lever.
48. The apparatus in claim 44 wherein said inflatable member has a
diameter of between approximately 1.5 inches and approximately 10
inches when inflated.
49. The apparatus in claim 48 wherein said inflatable member has a
diameter of between approximately 2 inches and approximately 4
inches when inflated.
Description
BACKGROUND OF THE INVENTION
[0001] This invention relates generally to medical intervention
and, more particularly, to the treating of cardiac arrest patients,
patients in various forms of shock and patients with head injury.
More particularly, this invention relates to a method and apparatus
for a non-invasive alteration of arterial blood pressures,
myocardial and cerebral perfusion pressures, blood flow and cardiac
output.
[0002] Approximately one million people per year have cardiac
arrests in the United States. Less than 10% of these people are
discharged from the hospital alive without neurological damage.
This percentage of people discharged would be increased if the
treatment available after the onset of cardiac arrest was improved.
Areas in which this treatment could be improved include: (1)
artificial circulation during cardiopulmonary resuscitation (CPR);
(2) induction and maintenance of brief periods of cerebral
hypertension after return of spontaneous circulation; and (3)
continued circulatory support for the brain and heart after return
of spontaneous circulation from cardiac arrest.
[0003] The blood of a cardiac arrest patient is artificially
circulated during CPR by cyclically compressing the chest. One
major theory describing how artificial circulation is generated
during CPR states that compression of the chest causes global
increases in intrathoracic pressure. This increase in intrathoracic
pressure in the thoracic compartment is evenly distributed
throughout the lungs and the four chambers of the heart, as well as
the great vessels in the chest. The increase in thoracic pressure
is greater than in the compartments above and below the chest.
These compartments mainly include the neck and head above the chest
and the abdominal compartment below the diaphragm and the chest.
When thoracic pressure is increased above the pressure in these
compartments, blood within the thoracic cavity moves to the head
and abdomen with greater blood flow going toward the head. When the
chest is released, the pressure within the thoracic cavity drops
and becomes less than the pressure within the head and abdomen,
therefore allowing blood to return to the thoracic cavity from the
head and abdominal compartments. This theory of CPR-produced blood
flow is termed the "thoracic pump mechanism," whereby the entire
thorax itself acts as a pump with the heart itself acting as a
passive conduit for blood flow. This theory is different from the
cardiac pump mechanism, which states that compression of the chest
produces blood flow by compressing the heart between the sternum
and anterior structures of the vertebral column. In most patients,
blood flow produced during chest compressions is likely a
combination of the two theories. In each individual patient, blood
flow during CPR depends on various factors, such as body habitus,
with thinner individuals relying more on the cardiac pump mechanism
of blood flow, and in larger individuals with increased
anterior-posterior chest dimension relying on the thoracic pump
mechanism. Both mechanisms of blood flow have been shown to be
present in animal and human studies. Regardless of which mechanism
is invoked, currently performed standard chest compressions as
recommended by the American Heart Association produces 30% or less
of the normal cardiac output. This results in extremely poor
regional cerebral and myocardial blood flow during CPR. The level
of blood flow generated during CPR is usually insufficient to
re-start the heart and prevent neurologic damage. The purpose of
CPR is to attempt to sustain the viability of the heart and brain
until more definitive measures, such as electrical countershock and
pharmacotherapy, are administered to the patient.
[0004] A main determinant for successful resuscitation from cardiac
arrest is the coronary perfusion pressure produced during CPR.
Coronary perfusion pressure (CPP) is defined as the aortic
diastolic pressure minus the right atrial diastolic pressure. CPP
represents the driving force across the myocardial tissue bed.
Animal studies are plentiful which demonstrate that CPP is directly
related to myocardial blood flow. It appears in humans that a CPP
of at least 15 mm Hg is required for successful resuscitation. CPP
of this magnitude is difficult to achieve with chest compressions
alone. Patients, who utilize the thoracic pump mechanism for CPR,
are even more unlikely to be able to produce this level of CPP
during CPR alone. The major means for producing coronary perfusion
pressures high enough for successful resuscitation have been to
perform more forceful chest compressions and by administering
various adrenergic agonists, such as epinephrine. Unfortunately, it
has been shown that CPPs are difficult to augment with chest
compressions alone and that in some situations very high doses of
adrenergic agonists are required to produce higher CPPs. The
difficulty in trying to produce higher CPPs with CPR alone lies in
the fact that right atrial diastolic pressures are sometimes
increased to the same or greater magnitude as aortic diastolic
pressures. Using various adrenergic agonists, aortic diastolic
pressure is usually augmented to a higher degree than right atrial
diastolic pressure. However, the use of adrenergic agonists to
achieve this have several drawbacks. These include increasing
myocardial oxygen demands to a greater degree than can be met with
blood flow produced during CPR. In addition, there are lingering
effects of adrenergic agonists which may be detrimental after
successful return of spontaneous circulation. These include periods
of prolonged hypertension and tachycardia, which may further damage
the heart and possibly cause re-arrest.
[0005] Cerebral perfusion pressure is a main determinant of
cerebral blood flow. During cardiac arrest and CPR, autoregulation
of blood flow in the brain may be lost. Cerebral perfusion pressure
is defined as the mean arterial pressure minus the intracranial
pressure. The main determinant of mean arterial pressure during CPR
is aortic diastolic pressure. One of the main determinants of
intracranial pressure during CPR is the mean venous pressure in the
central circulation and the neck. Forward flow to the head is
produced during CPR because of functional valves at the neck veins
entering the thorax. These valves close during chest compressions,
which prevent venous pressure transmission and flow of blood back
into the neck and cranium. When these valves are not functioning,
pressure is transmitted during the chest compression to the neck
veins and into the cranium. This in effect decreases forward
cerebral blood flow. Methods that increase cerebral blood flow
during conventional CPR are mainly the use of adrenergic agonists.
These agents selectively increase arterial pressure over venous
pressure. Thus, mean arterial pressure becomes greater than
intracranial and cerebral venous pressure thus producing net
forward flow. However, use of adrenergic agonists have several
drawbacks. In conventional doses, increases in cerebral blood flow
are extremely variable with many individuals having no response at
all. The use of higher doses of adrenergic agonists may be
problematic as previously discussed under myocardial blood
flow.
[0006] In summary, the major deficiencies in CPR-produced blood
flow to the critical organs of the heart and brain are primarily
due to the inability of conventionally performed CPR to cause
highly selective increases in aortic diastolic pressure without
causing increases of similar magnitude in central venous pressures.
The ability to maximize the former while minimizing the latter
would be extremely advantageous especially if the effects could be
immediately reversed.
[0007] Several techniques have been developed to take advantage of
the various CPR-produced mechanisms of blood flow. Two techniques
that take advantage of the thoracic pump mechanism include
simultaneous ventilation compression CPR (SVC-CPR) and vest-CPR.
SVC-CPR is a technique that involves inflating the lungs
simultaneously during the chest compression phase of CPR. This
causes larger increases in intrathoracic pressure than external
chest compression alone without ventilation or without external
chest compression. This has been shown in animal studies to result
in higher cerebral blood flows than in conventionally performed
CPR. However, one major drawback is that coronary perfusion
pressures are not uniformly increased and, in some instances, can
be detrimentally decreased. When SVC-CPR was tested in a clinical
trial, no increases in survival were noted over standard CPR.
[0008] Vest-CPR is a technique which utilizes a bladder containing
vest analogous to a large blood pressure cuff and is driven by a
pneumatic system. The vest is placed around the thorax of the
patient. The pneumatic system forces compressed air into and out of
the vest. When the vest is inflated, a relatively uniform decrease
in circumferential dimensions of the thorax is produced which
creates an increase in intrathoracic pressure. Clinically, the vest
apparatus is cyclically inflated 60 times per minute with 100 mm
Hg-250 mm Hg pressure which is maintained for 30%-50% of each cycle
with the other portion of the cycle deflating the vest to 10 mm Hg.
Positive pressure ventilation is performed independent of the
apparatus after every fifth cycle. When studied clinically in
humans, and compared with manually performed standard external CPR,
the vest apparatus produced significantly higher coronary perfusion
pressures and significantly higher mean aortic, peak aortic, and
mean diastolic pressures. However, these changes are not uniformly
seen in all patients. Of note, when the vest has been studied in
the laboratory and clinical settings, larger doses of epinephrine
have been used to achieve these higher coronary perfusion pressures
since the thoracic pump model would predict aortic diastolic and
right atrial diastolic pressures to be equivalent during the
relaxation phase (when coronary perfusion occurs).
[0009] Another new technique, which takes some advantage of both
the thoracic and cardiac pump mechanism of blood flow, is called
"active compression/decompression CPR (ACDC-CPR)." This technique
utilizes a plunger-type device, which is placed on the patient's
sternum during cardiac arrest. The person performing chest
compressions presses on the device which causes downward excursion
of the anterior chest wall. The person then pulls up on the device.
Since the device is attached to the sternum by suction, this causes
the anterior chest to be actively recoiled instead of undergoing
the usually passive recoil of standard external CPR. This active
recoil is capable, in many individuals, of causing a decrease in
intrathoracic pressure, which is transmitted to the right atrium
thus lowering right atrial pressure during artificial diastole and,
in turn, increasing coronary perfusion pressure. This negative
right atrial pressure also has the effect of increasing venous
return to the thoracic cavity, which may enhance cardiac output.
Factors, such as body habitus and chest wall compliance, which
impact on the efficacy of ACDC-CPR have not been studied, but are
likely to have an effect. Persons with larger body habitus probably
would receive less benefit from the technique.
[0010] Two other techniques, which are being investigated to
resuscitate victims of cardiac arrest, and which do not rely on a
mechanism of CPR-produced blood flow, include selective aortic arch
perfusion and cardiopulmonary bypass. Both of these techniques
require access to the central arterial vasculature. Selective
aortic perfusion is experimental and involves percutaneously
placing a balloon catheter in the aortic arch through a vessel,
such as the femoral artery. The balloon catheter is placed in the
aortic arch and the inflated balloon positioned just distal to the
take-off of the carotid arteries. Perfusion takes place under
pressure with oxygenated fluids or blood for various lengths of
time. In this manner, the brain and heart are selectively perfused
with little or no perfusion taking place distal to the occluded
portion of the aorta. Over time, the central venous pressures will
rise. This technique has not been tested clinically, but is
expected to take a high level of expertise and cannot be readily
performed in a setting outside of the hospital where many cardiac
arrests occur.
[0011] Cardiopulmonary bypass during CPR is performed by obtaining
central arterial and venous access usually percutaneously through
the femoral artery and vein. This technique is capable of totally
supporting the circulation by producing near normal cardiac outputs
and blood flows to the heart and brain. Although shown to be
effective, there are many technical difficulties which make its
widespread use unfeasible. Large cannulas must be placed in the
femoral artery and vein, which is difficult in the collapsed
circulation. The bypass circuit is complicated and, if not properly
primed, may produce air emboli. In addition, the patient requires
systemic anticoagulation in most instances. The use of such a
technique during CPR can be performed only at specially equipped
centers with specially trained personnel.
[0012] Open-chest CPR is an old technique that was commonly
performed before the advent of modern-day CPR. This technique
involves opening the patient's chest by performing a thoracotomy.
The descending aorta is usually cross-clamped. The heart itself is
then manually massaged (compressed) with the hands. Although this
technique is effective in producing heart and brain blood flows
superior to standard CPR, it does not lend itself to widespread
performance especially in the out-of-hospital setting. Reasons for
this include the level of expertise required and the hazard of
blood-borne pathogens. Other special equipment, such as the Anstadt
cup, can be directly placed on the heart to mechanically compress
the heart but, of course, have the same disadvantage of requiring a
thoracotomy.
[0013] Two post-resuscitative interventions found to improve
neurologic outcome in animal models of cardiac arrest is a brief
period of immediate post-resuscitation hypertension and rapid
induction and maintenance of cerebral hypothermia. The mechanisms
for improved neurologic outcome with post-resuscitation
hypertension is unclear. It is thought that this brief period of
hypertension clears cerebral vessels of microthrombi, which may
clog the cerebral circulation following cardiac arrest. It is also
thought that this brief period of hypertension may help to prevent
some of the post-resuscitation cerebral low flow and "no flow
phenomenon," which contributes to neurologic injury.
Post-resuscitation hypertension may decrease the overall amount of
cerebral damage caused by cardiac arrest. One difficulty in
providing for post-resuscitation hypertension is that the common
means of producing this, through the use of adrenergic agonists,
also produces considerable metabolic demands on the cardiovascular
system.
[0014] Cardiogenic shock has many causes, including myocardial
infarction, various forms of myocarditis, and other causes of
myocardial injury. When severe, this condition becomes
self-perpetuating secondary to the inability of the host to provide
for adequate myocardial blood flow. This may result in further
myocardial dysfunction leading to inadequate cerebral and
myocardial blood flow and eventually to cardiac arrest. Cardiogenic
shock may also be first noted after resuscitation from cardiac
arrest depending on the length of the cardiac arrest. Cardiogenic
shock may sometimes be difficult to distinguish from other forms of
shock. Survival might be enhanced if myocardial and cerebral
perfusion could be maintained until other definitive diagnostic and
therapeutic measures could take place.
[0015] Immediate survival from cardiogenic shock will depend on
maintenance of myocardial and cerebral blood flow. Various forms of
treatment are available for cardiogenic shock, including various
forms of pharmacotherapy and intra-aortic balloon pumping.
Pharmacotherapy, while effective, requires invasive hemodynamic
monitoring, such as pulmonary artery catheter placement for optimal
titration. This may be difficult to institute in a timely manner
when severe cardiogenic shock is first encountered especially in
the pre-hospital setting. Intra-aortic balloon pumping in which a
balloon catheter is placed into the thoracic aorta is effective but
somewhat complicated to perform. Special equipment is needed for
its placement and can only be performed at facilities which are
capable of placing and maintaining such equipment and patients.
Intra-aortic balloon pumping increases cardiac output by decreasing
cardiac afterload. A balloon inflates during the diastolic portion
of a cardiac cycle. This reduces cardiac afterload, thus lessening
the workload on the heart. This balloon inflation during diastole
also forces blood cephalad, thus perfusing the myocardial and
cerebral tissues more effectively.
[0016] Other forms of shock, such as septic and neurogenic shock,
cause hypoperfusion of critical organs due to a relative
hypovolemia. Vascular tone is lost and requires a combination of
volume replacement and vasopressors to maintain critical perfusion
to vital organs. Immediate effective therapy aimed at maintaining
cerebral and myocardial perfusion is difficult to institute because
the various forms of shock are at times difficult to differentiate
and therapy may differ between types of shock, although the
immediate goal is to preserve myocardial and cerebral
perfusion.
[0017] The major underlying immediate cause of death from any shock
state is inadequate myocardial and cerebral perfusion. Survival
with intact neurologic function is likely to be enhanced if
myocardial and cerebral blood flow can be maintained until the
underlying cause of the shock state can be optimally diagnosed and
treated.
[0018] Head injury can be devastating. Much of the neurologic
damage that takes place occurs after the initial insult. Blood flow
to injured brain tissue is many times reduced below critical levels
required to maintain survival when intracranial pressure is
increased. Cerebral blood flow may be extremely difficult to
maintain after the initial injury especially when multiple organ
systems are involved in the trauma. Mean arterial blood pressure
can also be difficult to maintain because of the ongoing blood loss
into the thoracic and abdominal cavities or from extremity
injuries. Intracranial pressure increases because of brain edema
from the cerebral injury, or from expanding pools of blood from
torn vessels in the brain or skull itself. Currently, the main
mechanisms for reducing intracranial pressure involve the
administration of diuretics, such as furosemide and mannitol,
administration of steroids which reduce cerebral edema over time,
removal of cerebral spinal fluid, elevation of the head which
promotes venous drainage, administration of barbiturates which
reduce the metabolic demand of brain tissue, hyperventilation
producing hypocapnia and reduced cerebral blood flow which
decreases intracranial pressure, and, as a last resort, removal of
less necessary parts of the brain itself. Many of these therapies
cannot be performed during the initial care of the multiple injured
trauma patient who has both neurologic injury and multiple organ
system injury, or have significant side effects. Administration of
diuretics produce further volume depletion and may further reduce
mean arterial pressure. Steroids require several hours to begin
taking effect. Removal of cerebral spinal fluid and damaged brain
tissue itself may take several hours to perform. Administration of
barbiturates may also reduce the mean arterial pressure.
Hyperventilation, although effective in reducing intracranial
pressure, does so by decreasing cerebral blood flow which may be
injurious to damaged tissue. All of these therapies become more
complicated in the presence of other extra-cerebral organ
injury.
[0019] Occasionally, pharmacotherapy to raise mean arterial blood
pressure is used to help maintain cerebral perfusion pressure in
the face of rising intracranial pressure. This is difficult and
sometimes dangerous to institute early because vasopressors many
times increase the metabolic demands of other injured tissues.
[0020] Hemorrhagic shock is a leading cause of death from trauma.
Many times there are delays in reaching hospitals which are
qualified to take care of the complex injuries of such individuals.
Many patients who die of trauma, die from multi-system involvement.
Multi-system involvement may include head injury along with
injuries to organs of the thoracic and abdominal cavity.
Uncontrolled hemorrhage leading to hypovolemic shock is a leading
cause of death from trauma especially from blunt and penetrating
trauma of the abdomen. When head trauma occurs concomitantly with
thoracic and abdominal hemorrhage, the brain becomes hypoperfused
and, thus, becomes at greater risk for secondary injury. Currently,
in the pre-hospital and emergency department setting, there are
limited means to control exsanguinating hemorrhage below the
diaphragm while maintaining myocardial and cerebral blood flow.
Definitive control of hemorrhage is performed at surgery but this
may be delayed and may not occur within the golden hour (time from
injury to definitive treatment/repair) where the best opportunity
lies in salvaging the patient. Survival with improved neurologic
outcome might be enhanced if means were available to slow or stop
ongoing hemorrhage (especially below the diaphragm) while
maintaining adequate perfusion to the heart and brain until
definitive treatment of the hemorrhage is available. This would be
especially true of trauma victims whose transport to appropriate
medical facilities would be prolonged.
[0021] The use of the pneumatic anti-shock garment (PASG) has met
with varying degrees of success depending on the location of
injury. This garment is placed on the legs and abdomen and is then
inflated. Hemorrhage in the abdominal cavity, as well as the lower
extremities, is controlled through tamponade while systemic blood
pressure is raised partially through autotransfusion and by raising
peripheral vascular resistance. Use of the PASG can sometimes be
cumbersome and does not uniformly control hemorrhage or raise blood
pressure. In addition, persons with concomitant penetrating
thoracic injuries may hemorrhage more when the device is applied.
The device may also raise intracranial pressure, which might
detrimentally alter cerebral blood flow resulting in neurologic
injury.
[0022] Other more drastic means to control abdominal bleeding prior
to surgery have been the use of thoracotomy to cross-clamp the
thoracic aorta and the use of balloon catheters placed into the
aorta from the femoral arteries to a point above the celiac-aortic
axis. These techniques have met with varying degrees of success and
require a high degree of skill and cannot be performed in hospitals
not equipped to care for trauma patients or by paramedical care
personnel.
[0023] Deliberately keeping hemorrhaging trauma victims in a
hypotensive state is currently being examined as a means to improve
survival. This is done based on the premise that overall hemorrhage
(especially abdominal hemorrhage) is reduced if mean arterial
pressure is kept low by not aggressively volume-repleting the
victim prior to surgery. Unfortunately, this may be dangerous for
trauma victims with concomitant head injury or myocardial
dysfunction.
[0024] An important cause of hemorrhagic shock not caused by trauma
includes rupture of abdominal aortic aneurysms. These can occur
suddenly and without warning. Control of bleeding even at surgery
can be difficult. Temporary measures discussed above for hemorrhage
secondary to trauma have been tried for hemorrhage secondary to
aneurysm rupture. The same difficulties apply. Survival might be
enhanced if hemorrhage could be controlled earlier while
maintaining perfusion to the heart and brain.
SUMMARY OF THE INVENTION
[0025] The present invention provides a non-invasive method and
apparatus for enhancing cerebral and myocardial perfusion in a
patient, particularly cardiac arrest patients, and for hemorrhage
control of a patient for management of trauma.
[0026] A non-invasive method of subdiaphragm hemorrhage control in
a patient or of enhancing cerebral and myocardial perfusion in a
patient particularly during cardiopulmonary resuscitation includes
positioning a moveable surface through the patient's esophagus
adjacent the patient's esophageal-gastric junction. The moveable
surface is displaced thereby applying a force posteriorly in the
direction of the patient's descending aorta sufficiently to at
least partially occlude the descending aorta. This decreases or
stops hemorrhage distal the point of occlusion and increases
myocardial and cerebral perfusion by increasing central and
intracranial arterial pressure.
[0027] According to another aspect of the invention, a non-invasive
method of subdiaphragm hemorrhage control in a patient or of
enhancing cerebral and myocardial perfusion in a patient includes
positioning an inflatable device through the patient's esophagus in
a portion of the patient's stomach juxtaposed with the patient's
descending aorta. The inflatable device is inflated and a force is
applied with the inflatable device posteriorly in the direction of
the patient's descending aorta sufficient to at least partially
occlude the descending aorta. This decreases or stops hemorrhage
distal the point of occlusion and increases myocardial and cerebral
perfusion by increasing central and intracranial arterial
pressure.
[0028] A non-invasive apparatus according to an aspect of the
invention for at least partially occluding the descending aorta of
a patient includes a tubular member configured at least in part to
a patient's esophagus having a selectively moveable portion
positioned adjacent the patient's esophageal-gastric junction when
the tubular member is positioned in a patient's esophagus. The
moveable portion is moveable a sufficient distance and has a
surface of sufficient area to at least partially occlude the
patient's descending aorta. A displacement mechanism is provided
for displacing the moveable portion in the direction of the
patient's descending aorta with a force sufficient to cause at
least partial occlusion of the patient's descending aorta.
[0029] According to yet an additional aspect of the invention, a
non-invasive apparatus for at least partially occluding the
descending aorta of a patient includes an inflatable member and a
positioning device which positions the inflatable member through
the patient's esophagus in a portion of the patient's stomach
juxtaposed with the patient's descending aorta. An inflation
mechanism is provided which selectively inflates the inflatable
member. A force-producing mechanism is provided producing a force
with a surface of the inflatable member posteriorly in the
direction of the patient's descending aorta sufficient to cause at
least partial occlusion of the patient's descending aorta.
[0030] According to yet an additional aspect of the invention, a
non-invasive apparatus for at least partially occluding the
descending aorta of a patient includes an inflatable member and an
elongated member which positions the inflatable member through the
patient's esophagus either in a portion of the patient's stomach
juxtaposed with the patient's descending aorta or adjacent the
patient's esophageal-gastric junction. An inflation mechanism is
provided which selectively inflates the inflatable member. A
displacement mechanism is provided which is operable to displace
the inflatable member from the elongated member posteriorly in the
direction of the patient's descending aorta thereby producing a
force posteriorly in the direction of the patient's descending
aorta sufficient to at least partially occlude the descending
aorta.
[0031] The invention provides hemorrhage control to a trauma
patient. Additionally, by inhibiting flow of blood below the
diaphragm, perfusion to critical organs, particularly during
cardiopulmonary resuscitation, is increased. In this manner, the
present invention provides an adjunct to enhance the effectiveness
of CPR.
[0032] These and other objects, advantages and features of this
invention will become apparent upon review of the following
specification in conjunction with the drawings.
BRIEF DESCRIPTION OF THE DRAWINGS
[0033] FIG. 1 is a sectional view through the frontal plane of a
patient illustrating relationships between organs relevant to the
invention;
[0034] FIG. 2 is a sectional view taken along the lines II-II in
FIG. 1;
[0035] FIG. 3 is a sectional view taken along the lines III-III in
FIG. 1;
[0036] FIG. 4 is a sectional view taken along the lines IV-IV in
FIG. 1;
[0037] FIG. 5 is a perspective view of a non-invasive apparatus for
at least partially occluding the descending aorta of a patient
according to the invention;
[0038] FIG. 6 is the same view as FIG. 2 illustrating the apparatus
in FIG. 5 being utilized to enhance cerebral and myocardial
perfusion in a patient or treat shock in a patient;
[0039] FIG. 7 is the same view as FIG. 1 of the method and
apparatus illustrated in FIG. 6;
[0040] FIG. 8 is a sectional view taken along the lines VIII-VIII
in FIG. 7;
[0041] FIG. 9 is the same view as FIG. 1 illustrating an
alternative embodiment of a non-invasive apparatus for at least
partially occluding the descending aorta of a patient being used to
enhance cerebral and myocardial perfusion in a patient or treating
shock in a patient;
[0042] FIG. 10 is the same view as FIG. 2 of the method and
apparatus illustrated in FIG. 9;
[0043] FIG. 11 is a sectional view taken along the lines XI-XI in
FIG. 9;
[0044] FIG. 12 is an enlarged partial perspective view of another
alternative embodiment of a non-invasive apparatus for at least
partially occluding the descending aorta of a patient;
[0045] FIG. 13 is the same view as FIG. 2 illustrating the
apparatus in FIG. 12 being used to enhance cerebral and myocardial
perfusion in a patient or to treat shock in a patient;
[0046] FIG. 14 is the same view as FIG. 1 of the method illustrated
in FIG. 13;
[0047] FIG. 15 is a sectional view taken along the lines XV-XV in
FIG. 14;
[0048] FIG. 16 is the same view as FIG. 2 illustrating a
modification to the embodiment of the method and apparatus in FIGS.
12 and 13;
[0049] FIG. 17 is a perspective view of another alternative
embodiment of a non-invasive apparatus for at least partially
occluding the descending aorta of a patient;
[0050] FIG. 18 is an enlargement of each area designated
XVIII-XVIII in FIG. 17;
[0051] FIG. 19 is the same view as FIG. 2 illustrating the
apparatus in FIG. 17 used to enhance cerebral and myocardial
perfusion to treat shock in a patient;
[0052] FIG. 20 is a sectional view taken along the lines XX-XX in
FIG. 19;
[0053] FIG. 21 is an enlarged partial perspective view of another
alternative embodiment of a non-invasive apparatus for at least
partially occluding the descending aorta of a patient;
[0054] FIG. 22 is the same view as FIG. 2 illustrating the
apparatus in FIG. 21 used to enhance cerebral and myocardial
perfusion or to treat shock in a patient;
[0055] FIG. 23 is a sectional view taken along the lines
XXIII-XXIII in FIG. 22;
[0056] FIG. 24 is an enlarged partial perspective view of another
alternative embodiment of a non-invasive apparatus for at least
partially occluding the descending aorta of a patient;
[0057] FIG. 25 is the same view as FIG. 2 illustrating the
apparatus in FIG. 24 used to enhance cerebral and myocardial
perfusion or to treat shock in a patient;
[0058] FIG. 26 is a sectional view taken along the lines XXVI-XXVI
in FIG. 25;
[0059] FIG. 27 is an enlarged partial perspective view of another
alternative embodiment of a non-invasive apparatus for at least
partially occluding the descending aorta of a patient;
[0060] FIG. 28 is the same view as FIG. 2 illustrating the
apparatus in FIG. 27 used to enhance cerebral and myocardial
perfusion or to treat shock in a patient;
[0061] FIG. 29 is a sectional view taken along the lines XXIX-XXIX
in FIG. 28;
[0062] FIGS. 30 is an enlarged partial perspective view of another
alternative embodiment of a non-invasive apparatus for at least
partially occluding the descending aorta of a patient;
[0063] FIG. 31 is an enlarged partial perspective view of another
alternative embodiment of a non-invasive apparatus for at least
partially occluding the descending aorta of a patient;
[0064] FIG. 32 is an enlarged partial perspective view of yet
another alternative embodiment of a non-invasive apparatus for at
least partially occluding the descending aorta of a patient;
[0065] FIG. 33 is a diagram illustrating increases in myocardial
and perfusion pressure in a swine model treated according to the
invention; and
[0066] FIG. 34 is a diagram illustrating increases in myocardial
and cerebral perfusion pressure in a swine model treated according
to the invention.
DESCRIPTION OF THE PREFERRED EMBODIMENT
[0067] Referring now specifically to the drawings, and the
illustrative embodiments depicted therein, in U.S. Pat. No.
5,531,776 for a NON-INVASIVE AORTIC IMPINGEMENT AND CORE AND
CEREBRAL TEMPERATURE MANIPULATION METHOD, the disclosure of which
is hereby incorporated herein by reference, I disclosed a
non-invasive technique for partially or completely occluding the
descending aorta based upon the realization that the majority of
the population has the same relationship of the esophagus to the
descending aorta. The method includes positioning a device, having
an elongated tubular member, in a portion of the patient's
esophagus juxtaposed with the patient's descending aorta and
displacing with the tubular member a wall of the portion of the
esophagus posteriorly-laterally in the direction of the descending
aorta. This provides at least partial occlusion of the descending
aorta and thereby increases central and intracranial arterial
pressure without increasing central and intracranial venous
pressure. This, in turn, causes an immediate increase in myocardial
and cerebral perfusion and thereby provides an adjunct to
cardiopulmonary resuscitation (CPR). Additionally, the method may
be used during hemorrhagic shock in order to decrease blood
loss.
[0068] As can be seen by reference to FIGS. 1-4, the descending
aorta 40 is juxtaposed with the esophagus 42 throughout a
significant portion of the thoracic cavity. However, the esophagus
and descending aorta are most closely bound where they mutually
pass in close proximity through the diaphragm 44 just above the
esophageal-gastric junction 46. Below the diaphragm, the descending
aorta 40 passes posteriorly of the stomach 48 between the stomach
and vertebral spinal column 50. The present invention is based upon
a discovery that, because the descending aorta and esophagus are
tightly bound in close proximity where they pass through the
diaphragm, manipulation of a device positioned adjacent the
esophageal-gastric junction may be used to deflect or expand the
esophagus and/or stomach and thereby at least partially occlude the
aorta against the vertebral column.
[0069] To carry out such non-invasive partial or complete occlusion
of the aorta requires proper positioning both longitudinally and
radially of a surface which is moveable laterally a sufficient
distance, with a sufficient force, and having a surface of
sufficient area to at least partially occlude the patient's
descending aorta. This is accomplished in the various embodiments
of the invention in a manner which overcomes the difficulties of
proper positioning of the moveable surface notwithstanding the
great variety in the anatomy of a patient, as will be described in
more detail below.
[0070] A non-invasive apparatus 52 for at least partially occluding
the descending aorta of a patient includes a force-producing
surface, defined by an inflatable member 54, and a positioning
device, in the form of an elongated member 56, for positioning
inflatable member 54 through the patient's esophagus in a portion
of the patient's stomach 48 which is juxtaposed with the patient's
descending aorta 40. Apparatus 52 further includes an inflation
mechanism 58 which selectively inflates inflatable member 54 and a
force-producing mechanism, in the form of a handgrip 59 affixed to
a distal end of elongated member 56, which produces a force, with
the surface of inflatable member 54, posteriorly-laterally in the
direction of the patient's descending aorta sufficient to cause
either partial, or substantially complete, occlusion of the
patient's descending aorta.
[0071] With apparatus 52 positioned in the patient, as illustrated
in FIG. 6, inflation mechanism 58 is actuated in order to inflate
inflatable member 54 in the patient's stomach 48. Traction is then
applied to handgrip 59, as illustrated in FIG. 6, which applies a
force F with inflatable member 54 posteriorly-laterally in the
direction of the patient's descending aorta to partially or
completely occlude the descending aorta as illustrated in FIG.
8.
[0072] Because of its size, inflatable member 54 can only be
properly inflated in the patient's stomach. Furthermore, once
inflated in the patient's stomach, proper positioning of the
inflatable member is readily achieved by the initial movement
caused by the traction force F applied to handgrip 59 which draws
the inflatable member to the wall of the stomach at the
esophageal-gastric junction. Further traction force draws the
inflatable member upwardly arid posteriorly which is the direction
necessary to impinge the descending aorta. Substantially completely
occluding the patient's descending aorta requires extensive
movement of an extensive portion of a wall of this artery against
an extensive resistant force. The descending aorta is a main artery
of the body. As such, it is a large vessel as can be seen in FIGS.
1-4. It is pressurized by the heart to a pressure that may extend
over 200 millimeters of mercury, or approximately four pounds per
square inch. Therefore, in order to substantially completely
occlude the descending aorta, the device must overcome this
pressure. Furthermore, the aorta is a muscular structure having
muscle tone which affords rigidity to the structure. Therefore, the
descending aorta has a stiffness which resists crushing thereof.
While less than the pressure of the fluid in the descending aorta,
this muscle tone adds appreciably to the force required to
substantially completely occlude the descending aorta. In the
illustrated embodiment, force sufficient to partially or completely
occlude the aorta is achieved with inflatable member 54 being a
balloon made of a suitable medical grade material, such as PPT,
Mylar, or the like, and having a surface with a diameter preferably
of between approximately 1 and approximately 6 inches and most
preferably between approximately 2 and approximately 4 inches.
Elongated member 56 has sufficient strength to allow sufficient
force to be transmitted from handgrip 59 to inflatable member 54 to
impart sufficient force to the surface of inflatable member 54 to
partially or completely occlude the aorta.
[0073] In another embodiment of a non-invasive apparatus 60 for at
least partially occluding the descending aorta of a patient, an
inflatable member 62 is positioned in stomach 48 by a positioning
member 64 and an inflation mechanism, similar to 58, is provided in
order to inflate inflation member 62. With inflation member 62
fully inflated, a displacement mechanism 66 displaces inflatable
member 62 posteriorly in the direction of the patient's descending
aorta thereby producing a force posteriorly in the direction of the
patient's descending aorta sufficient to partially or completely
occlude the descending aorta. In this embodiment, displacement
mechanism 66 applies a force from external the patient to
inflatable member 62. Inflatable member 62 is of a sufficient size
such that the force, which is transmitted through the patient's
abdominal wall, is transmitted through the inflatable member in
order to partially or completely occlude the descending aorta as
best illustrated in FIG. 11. In the illustrated embodiment, the
displacement mechanism 66 is a strap placed around the abdomen such
that a tightening of the strap applies the force F illustrated in
FIGS. 10 and 11.
[0074] In order to properly locate displacement mechanism 66, the
lower tip of the sternum is identified and the displacement
mechanism applied to the patient in a manner which applies a force
posteriorly just below the sternum. Because the diaphragm is
attached at the sternum, applying a force F just below the sternum
will ensure that the force is applied to the stomach and thereby
transmitted posteriorly to impinge upon the aorta.
[0075] In the illustrated embodiment, inflatable member 62, when
inflated, has a diameter of between approximately 10 and
approximately 30 inches and most preferably between approximately
15 and approximately 22 inches. While displacement mechanism 66 is
illustrated as a belt, other mechanisms, including pneumatic
actuators, manual compression, and the like, can be utilized in
order to apply force F externally of the patient. Also, the force F
may be applied in synchronism with the patient's ventricular
contractions in order to counter-pulse the aorta during ventricular
diastole such as by using a pneumatic CPR device operated from the
cardiac signal in the manner described in the '776 patent. One such
CPR device is the THUMPER.RTM. resuscitator marketed by Michigan
Instruments, Inc. of Grand Rapids, Mich.
[0076] In another embodiment illustrated in FIGS. 12-15, a
non-invasive apparatus 70 for at least partially occluding the
descending aorta of a patient includes an elongated member 72 which
is configured to extend through the patient's esophagus 42 and a
moveable portion 71 defined by an inflatable member 74 displaceable
from elongated member 72 in the patient's stomach 48 by a
displacement mechanism 76 which mechanically displaces inflatable
member 74 from proximal end 78 of the elongated member.
[0077] In the illustrated embodiment, displacement mechanism 76 is
a lever which is pivoted outwardly by an actuator 79 positioned at
a distal end 80 of elongated member 72. An inflation mechanism 82
is also provided at distal end 80 of elongated member 72 in order
to selectively inflate inflatable member 72. In operation, with
inflatable member 74 in a non-inflated state and with actuator 79
not being actuated, elongated member 72 is inserted in the
patient's esophagus, nasally or orally, until proximal end 78 is
positioned within the stomach. This can be accomplished utilizing
conventional techniques for positioning nasal gastric tubes in the
patient. Namely, markings can be provided on elongated member 72
and, prior to insertion of apparatus 70 in the patient, the
apparatus can be compared with the external physiology of the
patient in order to determine the amount of insertion necessary in
order to position proximal end 78 in the patient's stomach.
[0078] After the apparatus is properly positioned, inflation
mechanism 82 is actuated in order to inflate inflatable member 74
and thereby create an enlarged surface for impingement with the
descending aorta. With the inflatable member inflated, actuator 79
is actuated by hand manipulation in order to cause displacement
member 76 to displace inflatable member 74 posteriorly with a
sufficient force to at least partially occlude the descending aorta
as illustrated in FIG. 15. In order to ensure that operation of
actuator 79 will cause displacement mechanism 76 to displace
inflatable member 74 in the proper direction, a radially
positioning device 84, which is illustrated as a pistol grip
handle, may be provided such that with the radial positioning
device in a particular orientation with respect to the patient,
displacement mechanism 76 and inflatable member 74 are oriented in
a manner which will produce the desired movement of the inflatable
mechanism upon movement of the displacement mechanism. In the
illustrated embodiment, inflatable member 74 has a diameter, when
inflated, preferably of between approximately 1.5 and approximately
10 inches and most preferably between approximately 2 and
approximately 4 inches.
[0079] A modified non-invasive apparatus 70' for at least partially
occluding the descending aorta of a patient is illustrated in FIG.
16. Apparatus 70' is similar to apparatus 70 except that it
includes an anchor member 86 to anchor elongated member 72 in a
lower portion of esophagus 42 and a device 88 on elongated member
72' located at an upper portion of esophagus 42. Anchor 86 may be,
by way of example, an inflatable cuff and is for the purpose of
imparting somewhat rigid positioning of elongated member 72' in the
esophagus in order to increase the force that inflatable member 74
is capable of providing posteriorly in order to more effectively
partially or completely occlude the patient's descending aorta.
Device 88, which may be an inflatable cuff, is to seal the
esophagus and prohibit the contents of the stomach from flowing
upwardly through the throat and to otherwise provide proper airway
management.
[0080] Another embodiment of a non-invasive apparatus 90 for at
least partially occluding the descending aorta of a patient
includes an elongated member 92 and an inflatable member 94 which
produces a force posteriorly in the direction of the patient's
descending aorta sufficient to cause partial or complete occlusion
of the patient's descending aorta (FIGS. 17-20). Inflatable member
94 is joined with an elongated member 92 at a reaction surface, or
portion, 96 of the elongated member. Reaction portion 96 provides a
stable platform against which the inflatable member 94 expands when
inflated in order to produce a force posteriorly in the direction
of the patient's descending aorta. Apparatus 90 may include another
anchor device, such as an inflatable member 104, which is
positioned within the stomach of the patient and provides an
additional anchor for reaction portion 96. In this manner, with
inflatable member 104 inflated by an inflation mechanism 106,
reaction portion 96 is stabilized to allow greater force to be
transmitted posteriorly by the impingement surface of inflatable
member 94. In this manner, when inflatable member 94 is inflated by
actuation of inflation mechanism 98, the expansion of its surface
provides a force posteriorly in the direction of the patient's
descending aorta sufficient to cause substantially complete
occlusion of the patient's descending aorta as illustrated in FIG.
20.
[0081] Apparatus 90 additionally includes an inflation mechanism 98
for selectively inflating inflatable member 94, a second inflation
mechanism 99 for selectively inflating an anchor member 86 and an
airway control device 88 and a third inflation mechanism 100 for
selectively inflating anchor 104. Apparatus 90 may further include
a radial-positioning device 102 in the form of a pistol grip, or
the like, in order to provide for radial positioning of inflatable
member 94 and an indication of the positioning thereof.
[0082] An alternative embodiment of a non-invasive apparatus 106
for at least partially occluding the descending aorta of a patient
includes a tubular member 108 having a selectively movable portion
115 which is positioned adjacent the patient's esophageal-gastric
junction when tubular member 108 is positioned in the patient's
esophagus (FIGS. 21-23). Apparatus 106 may include an anchor
balloon 112 positionable in the patient's stomach in order to
stabilize apparatus 106 within the patient. With elongated member
108 positioned within the patient's esophagus, a displacement
mechanism including a cable 114, or the like, which is selectively
actuatable causes movable portion 115 to move laterally a
sufficient distance in order to partially or completely occlude the
patient's descending aorta. In the illustrated embodiment,
selectively movable portion 115 includes a displacement surface 116
having a sufficient area to substantially completely occlude the
patient's descending aorta and a pair of parallel linkages 118
which support displacement surface 116 in a parallel relationship
with tubular member 108 as surface 116 is displaced laterally
therefrom. Apparatus 106 may additionally include a sheath 120
covering displacement surface 116.
[0083] As best seen in FIGS. 22 and 23, actuation of cable 114 by a
displacement mechanism, or actuator, similar to 79, causes moveable
portion 115 to be laterally displaced from tubular member 108 and
thereby applying a force in the direction of the patient's
descending aorta sufficient to cause partial or complete occlusion
of the patient's descending aorta. Moveable portion 115 is
laterally displaceable preferably of between approximately 1 and
approximately 4 inches and most preferably of between approximately
2 and approximately 3 inches.
[0084] Another embodiment of a non-invasive apparatus 106' for at
least partially occluding the descending aorta of a patient is
similar to apparatus 106 except that it does not include an anchor
balloon in the patient's stomach but is otherwise the same as
apparatus 106 (FIGS. 24-26).
[0085] Another alternative embodiment 140 of a non-invasive
apparatus for at least partially occluding the descending aorta of
a patient includes a tubular member 142 having a selectively
moveable portion 144 which is positioned adjacent the patient's
esophageal-gastric junction when tubular member 142 is positioned
in the patient's esophagus (FIGS. 27-29). Selectively moveable
portion is an inflatable member, such as an inflatable cuff or
balloon, which is selectively inflatable by an inflation mechanism
through a tube 146. Inflatable member 144 is preferably constructed
to inflate primarily in a posterior direction, as illustrated, but
may also be a uniform member which inflates in all directions and
thereby applies a force posteriorly in the direction of the
descending aorta.
[0086] An alternative embodiment 140'of a non-invasive apparatus
for at least partially occluding the descending aorta of a patient
is the same as apparatus 140 except that it also includes an anchor
balloon 148 positionable in the patient's stomach and an inflation
mechanism which selectively inflates the balloon through a tube
149.
[0087] Other embodiments of a non-invasive apparatus for at least
partially occluding the descending aorta of a patient will suggest
themselves to the skilled artisan. For example, in FIGS. 31 and 32,
a non-invasive apparatus 121, 121' is provided in which a
selectively moveable portion 122, 122' is in the form of a lever
which pivots about an elongated member 124, 124' by a displacement
mechanism including a cable 126, 126'. The displacement mechanism
displaces moveable portion 122, 122' in the direction of the
patient's descending aorta, when tubular member 104, 104' is
positioned in the patient's esophagus, with a force sufficient to
cause partial or complete occlusion of the patient's descending
aorta. Apparatus 121 additionally includes an anchor balloon 128
positioned in the patient's stomach for anchoring apparatus 121
when balloon 128 is inflated.
[0088] The effectiveness of a non-invasive apparatus and method
according to the invention can be demonstrated by actual studies
performed on a swine model in which fibrillation is induced.
[0089] By reference to FIG. 33, aortic arch pressure is illustrated
by graph 130 and right atrial pressure is illustrated by graph 132
after fibrillation is induced in the patient and a conventional CPR
protocol is performed. The CPR protocol pictured involves a series
of five chest compressions followed by a pause during which
ventilation occurs as can be observed in graph 130. A non-invasive
apparatus according to the invention is utilized to at least
partially occlude the descending aorta at point A which, in the
illustrated embodiment, is more than 17 minutes following
inducement of fibrillation. It can be seen that, following
application of the invention at point A, the aortic arch pressure
begins to increase, while little change occurs in the diastolic
right atrial pressure. This results in a significant increase in
coronary and cerebral perfusion pressure. Significantly, such
increase in perfusion pressure occurred more than 17 minutes after
onset of fibrillation. This is significant because, as is known in
the art, the metabolic state of the myocardium and peripheral
vascular resistance decreases with patient arrest time.
Furthermore, this observed increase after application of the
invention occurs without the use of intravenously administered
adrenergic agents such as epinephrine. Therefore, the ability to
increase perfusion pressure after a relatively long downtime is
significant.
[0090] FIG. 34 illustrates an aortic arch pressure graph 134 and
femoral artery pressure graph 136 in a swine patient in which a
non-invasive apparatus according to the invention is utilized to
occlude the descending aorta of the patient. At point B, the
occlusion of the aorta results in a substantial increase in aortic
arch pressure and a concurrent decrease in femoral artery pressure
which represents the intravascular arterial pressure distal to the
point of occlusion. This will naturally result in an increase in
myocardial and cerebral perfusion as a result of the use of an
apparatus according to the invention to perform a method according
to the invention. Had the patient been hemorrhaging in the abdomen,
activation of the device would have stopped this hemorrhaging while
simultaneously increasing cerebral and myocardial perfusion. At
point C, the apparatus is disengaged resulting in return of the
femoral artery pressure in graph 136 and a decrease in aortic arch
pressure in graph 134. This results in a lowering of myocardial and
cerebral perfusion pressure.
[0091] The actual test results illustrated in FIGS. 33 and 34
demonstrate a diversion of blood flow from the tissue bed below the
diaphragm to the myocardial and cerebral tissue beds above the
diaphragm. This diversion of blood is proportional to the degree of
occlusion of the aorta. Therefore, the increase in coronary and
cerebral perfusion can be regulated if desired.
[0092] Thus, it is seen that the present invention provides
hemorrhage control for the management of trauma and an inhibition
of flow below the diaphragm to enhance coronary and cerebral
perfusion particularly during cardiopulmonary resuscitation.
Studies have shown that, although over half of the tissue beds are
below the diaphragm, approximately two-thirds of bleeding that
leads to hemorrhagic shock occurs below the diaphragm. Therefore,
the ability to control bleeding below the diaphragm provides a
significant advantage particularly in management of trauma. This is
particularly useful in treating patients who have suffered
abdominal injuries from knives and guns, blunt trauma from falls,
explosions, motor vehicle accidents, complications due to the
delivery of babies from subdiaphragmatic hemorrhaging and other
vascular catastrophes below the diaphragm such as ruptured
abdominal aortic aneurysms. The present invention is particularly
useful in battlefield applications in which it is essential to be
able to rapidly control life-threatening hemorrhage in a
non-invasive manner in order to avoid immediate death and
complications from infections and the like until definitive repair
of injuries can take place. Additionally, the ability to perform
this procedure rapidly and effectively reduces the exposure of the
medical personnel to battlefield injuries.
[0093] Other changes and modifications in the specifically
described embodiments can be carried out without departing from the
principles of the invention. For example, electrodes can be applied
to stomach balloons for use in cardiac pacing and defibrillation.
Although balloons and cuffs may be inflated using air, other
techniques involving hydraulic fluids and mechanical actuators may
suggest themselves to those skilled in the art. Although inflatable
devices are illustrated as spherical, other shapes could be used
such as cylindrical, pill-shaped, and the like. Also, the various
elements of each illustrated embodiment of the invention can be
combined and substituted with other of the embodiments. The
embodiments are provided in order to illustrate the invention and
should not be considered limiting. Displacement in the direction of
the patient's descending aorta in order to at least partially
occlude the descending aorta can be performed in synchronism with
the patient's ventricular contractions, as disclosed in the
above-referred to '776 patent, in order to counter-pulse the aorta
during ventricular diastole utilizing the apparatus and method
disclosed herein. The method and apparatus for partially or
completely occluding the descending aorta of a patient according to
the present invention may be combined with a method of manipulating
core and cerebral temperature disclosed in the '776 patent. The
protection afforded the invention is intended to be limited only by
the scope of the appended claims, as interpreted according to the
principles of patent law including the Doctrine of Equivalents.
* * * * *