U.S. patent application number 13/851003 was filed with the patent office on 2013-11-07 for breathing therapy device and method.
The applicant listed for this patent is RMX, LLC. Invention is credited to David LIGON, Amir J. TEHRANI.
Application Number | 20130296973 13/851003 |
Document ID | / |
Family ID | 34465515 |
Filed Date | 2013-11-07 |
United States Patent
Application |
20130296973 |
Kind Code |
A1 |
TEHRANI; Amir J. ; et
al. |
November 7, 2013 |
BREATHING THERAPY DEVICE AND METHOD
Abstract
A device and method is provided for electrically stimulating the
diaphragm to control breathing while inhibiting respiratory drive.
A stimulation phase is identified. The stimulation phase is it
period of time within the breathing cycle in which stimulation will
inhibit respiratory drive. The respiratory drive inhibition may be
used in a number of applications including but not limited to:
improving or remodeling the heart in heart failure patients,
treating apnea, chronic obstructive pulmonary disorder (COPD), and
hypertension.
Inventors: |
TEHRANI; Amir J.; (San
Francisco, CA) ; LIGON; David; (San Francisco,
CA) |
|
Applicant: |
Name |
City |
State |
Country |
Type |
RMX, LLC |
San Francisco |
CA |
US |
|
|
Family ID: |
34465515 |
Appl. No.: |
13/851003 |
Filed: |
March 26, 2013 |
Related U.S. Patent Documents
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Application
Number |
Filing Date |
Patent Number |
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10966474 |
Oct 15, 2004 |
8412331 |
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13851003 |
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10686891 |
Oct 15, 2003 |
8467876 |
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10966474 |
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Current U.S.
Class: |
607/62 |
Current CPC
Class: |
A61B 5/7264 20130101;
A61B 5/08 20130101; A61B 5/0488 20130101; A61N 1/3601 20130101;
A61N 1/36132 20130101; A61B 5/4818 20130101 |
Class at
Publication: |
607/62 |
International
Class: |
A61N 1/36 20060101
A61N001/36 |
Claims
1. A medical device for use in patients comprising: a stimulation
lead, said lead having at least one stimulation electrode placed
adjacent to at least one phrenic nerve of the patient; a control
unit implanted in the body of the patient, said control unit being
electrically connected said stimulation electrode; a respiration
sensor implanted in the patient, said respiration sensor being in
communication with said control unit; and a control logic
incorporated within said control unit, said control logic capable
of reading said respiration sensor, analyzing said respiration
signal and delivering stimulation pulses to maintain activation of
at least a portion of a diaphragm to said stimulation electrode at
a time proximate the transition from an inhalation phase to an
exhalation phase of a respiration, retaining air in at least one
lung and preventing exhalation of the retained air for a period of
time, and Men after the period of time has lapsed, allowing a
delayed exhalation outflow of the retained air.
2. The medical device of claim 1 further characterized by said
control logic being capable of analyzing breath and delivering
stimulation signal at the end of natural inspiration for a duration
that exceeds natural exhalation.
3. The medical device of claim 1 further comprising: at least one
sensing electrode in electrical communication with said control
unit, said sensing electrode being capable of sensing cardiac
electrical activity and transthoracic impedance.
4. The medical device of claim 1 further comprising: an implanted
motion sensor capable of sensing motion of the patient; and said
control logic being capable of sensing and analyzing motion
signals.
5. The medical device of claim 4 further characterized by said
control logic delivering phrenic nerve stimulation based on said
respiratory sensor and disabling phrenic nerve stimulation based on
said motion sensor.
6. The medical device of claim 4 wherein said motion sensor is
correlated with EMG information.
7. The medical device of claim 1 further characterized by said
control logic being capable of rejecting respiratory signals that
appear during a refractory period.
8. The medical device of claim 4 further characterized by said
control logic being capable of rejecting respiratory signals
indicative of cough, arousal and movement.
9. The medical device of claim 1 further characterized by said lead
having a plurality of stimulation electrodes.
10. The medical device of claim 1 further comprising a flow sensor
in communication with the control unit.
11. The medical device of claim 1 further comprising an EMG sensor
in communication with the control unit.
12. The medical device of claim 1 further characterized by said
lead having at least one anchoring mechanism.
13. The medical device of claim 1 further comprising an external
communications device in communication with the control unit.
14. The medical device of claim 1 further characterized by the
shape of said stimulation pulses being selected from the group
consisting of consistent amplitudes, progressively increasing
amplitudes, progressively decreasing amplitudes, and a combination
of progressively increasing amplitudes following by consistent
amplitude followed by progressively decreasing amplitude.
15.-31. (canceled)
Description
CROSS-REFERENCE TO RELATED APPLICATIONS
[0001] This application is a continuation of U.S. application Ser.
No. 10/966,474, filed Oct. 15, 2004, which is a
continuation-in-part of U.S. application Ser. No. 10/686,891 filed
Oct. 15, 2003, both of which are fully incorporated herein by
reference.
FIELD OF THE INVENTION
[0002] The invention relates to a device and method for detection,
diagnosis and treatment of breathing disorders and to the
management of pulmonary or cardiac rhythms, heart failure and other
cardiac and/or respiratory related conditions.
[0003] BACKGROUND OF THE INVENTION
[0004] Diaphragm stimulation has been used to provide breathing in
patients unable to breath on their own. Diaphragm stimulation has
also been proposed to treat sleep apnea. However, these uses of
diaphragm stimulation have not provided optimal breathing responses
or control of breathing.
[0005] Accordingly it would be desirable to provide improved
diaphragm stimulation.
[0006] Breathing is typically intrinsically controlled by complex
brain control and feedback sensing by the body. The body's
involuntary control of respiration is mediated by the brain's
respiratory center located in the brainstem, particularly in the
medulla oblongata and pons. The respiratory center regulates the
rhythmic alternating cycles of inspiration and expiration. The
dorsal respiratory group within the medulla is responsible for the
generation of respiratory rhythm through a reciprocal inhibition
with other cell groups.
[0007] In addition, various central and peripheral receptors, e.g.,
chemoreceptors and mechanoreceptors play important roles in
regulation of inspiration.
[0008] Central chemoreceptors of the central nervous system located
on the ventrolateral medullary surface, are sensitive to pH of
their environment. It is believed that these chemoreceptors act to
detect a change in pH of the cerebral spinal fluid. An increase in
carbon dioxide tension of the arteries will indirectly cause the
blood to become more acidic; the cerebral spinal fluid pH is
closely comparable to plasma pH, as carbon dioxide easily diffuses
across the blood/brain barrier. The detection of variation in the
arterial carbon dioxide tension acts as a quick response system,
useful in short term regulation. This system utilizes a negative
feedback system, therefore if the pH of the cerebral spinal fluid
is too low, then the receptor is believed in effect send an error
signal to the medulla and respiration is adjusted accordingly.
[0009] Peripheral chemoreceptors are believed most importantly to
act to detect variation of the oxygen in the arterial blood, in
addition to detecting arterial carbon dioxide and pH. These
receptors are typically referred to as aortic or carotid bodies,
and respectively are location on the arch of the aorta and on the
arch of the common carotid artery. A continuous signal is sent, via
cranial nerves from the peripheral chemoreceptors. With a decrease
in arterial oxygen tension, the signal intensities, calling for an
increase in respiration. However, increase in respiration typically
results in falling PCO2 and hydrogen ion concentration which
creates strong respiratory inhibitory effects that oppose the
excitatory effects of diminished oxygen.
[0010] Mechanoreceptors are located for example, in the airways and
parenchyma, and are responsible for a variety of reflex
responses.
[0011] Pulmonary Stretch Receptors are located in smooth muscles of
the trachea down to the terminal bronchioles. They are innervated
by large, myelinated fibers and they discharge in response to
distension of the lung. Their vagally mediated inhibition of
inspiration and promotion of expiration is believed to be sustained
as long as the lung is distended. They contribute to what is known
as the Hering-Breuer reflex which prevents over-inflation of the
lungs, by providing feedback signals that cause termination of
inspiration.
[0012] Other receptors, such as respiratory proprioreceptors
located in muscle spindle endings and tendon organs of the
respiratory muscles, are stimulated in response to rib movement or
intercostals/diaphragmatic tendon force of contraction.
[0013] In addition to involuntary control of respiration by the
respiratory center, respiration can be affected by conditions such
as, e.g., emotional state via input from the limbic system, or
temperature, via the hypothalamus. Voluntary control of the
respiration is provided via the cerebral cortex, although
chemoreceptor reflex is capable of overriding conscious
control.
[0014] Known diaphragm stimulation techniques have not interacted
with this complex respiratory control system to override, influence
or work with the system.
[0015] Accordingly improved stimulation devices and methods would
be desirable.
SUMMARY OF THE INVENTION
[0016] The invention provides a device and method for electrically
stimulating the diaphragm to control breathing while inhibiting
respiratory drive. According to the invention, a stimulation phase
is identified. The stimulation phase is a period of time within the
breathing cycle in which stimulation will inhibit respiratory drive
and most likely will occur during a first fraction of the rest
phase. Baseline breathing is sensed and stored. The length of the
rest period in a breathing cycle is identified and a stimulation
phase is determined.
[0017] The baseline is used to determine when to stimulate. The
stimulator may include a pulse generator configured to deliver
stimulating pulses. EMG or other respiratory indicators may be
sensed on a breath by breath basis or over time to determine when
to stimulate within the respiratory phase. For a given tidal volume
stimulation amplitude, duration and respiratory rate may be varied
to inhibit respiratory drive when stimulating.
[0018] The respiratory drive inhibition may be used in a number of
applications such as improving or remodeling the heart in heart
failure patients, treating apnea, chronic obstructive pulmonary
disorder (COPD), and hypertension.
DESCRIPTION OF THE DRAWINGS
[0019] FIG. 1 is an exemplary respiratory waveform with an
identified stimulation phase in accordance with the invention.
[0020] FIG. 2 is a flow showing a baseline establishment accordance
with the invention.
[0021] FIG. 3 is a flow chart showing identification of delivery
boundaries in accordance with the invention.
[0022] FIGS. 4A-4D illustrate various stimulation schemes in
accordance with the invention, for controlling breathing in
comparison to intrinsic breathing.
[0023] FIG. 5 is a table illustrating a breathing therapy scheme in
accordance with the invention.
[0024] FIG. 6 is a flow chart showing a breathing therapy scheme in
accordance with the invention.
[0025] FIG. 7 illustrates an immediate control mode of a breathing
therapy device in accordance with the invention.
[0026] FIG. 8 illustrates a gradual control scheme in accordance
with the invention.
[0027] FIG. 9 is a flow chart showing an apnea control in
accordance with the invention.
[0028] FIG. 10 illustrates treatment of apnea in accordance with
the invention.
[0029] FIG. 11 illustrates a breathing therapy mode in accordance
with the invention.
[0030] FIG. 12 illustrates a diaphragm stimulator in accordance
with the invention.
DETAILED DESCRIPTION
[0031] In accordance with the invention a diaphragm stimulation
device as shown in FIG. 12 is used. The diaphragm stimulation
device 1200 electrically stimulates the diaphragm 1290 with an
electrical signal supplied from a signal source 1260 to at least
one electrode 1220 on an implantable unit 1210. The electrode may
also sense EMG of the diaphragm which may include respiration
parameters. The sensed EMG is communicated to a processor 1280 of a
control unit 1240. The control unit also includes an input/output
device 1250 for coupling to external communications device. The
input/output device 1250 may be used to communicate to or from the
device 1210 or the processor 1280 to or from a programmer, user or
provider (e.g. via, telemetry, wireless communications or other
user/provider/programmer interface). The implantable unit 1210 also
includes a motion sensor 1230 that senses the motion of the
diaphragm 1290 to determine respiration parameters or responses to
stimulation. The motion sensor 1230 may also be used to sense
patient activity levels. The sensed signals are communicated to a
processor 1280 that stores and uses the motion and EMG signals, as
described herein, to control breathing. In addition to stimulation
of the diaphragm the phrenic nerve may be stimulated to control
breathing.
[0032] Referring to FIG. 1 an intrinsic, breathing waveform 100 is
illustrated. The waveform 100 has a total respiratory interval
length 105 that comprises an inspiration period 110, followed by an
exhalation period 120 and ending in a rest period 130. The
respiratory interval 105 begins at the beginning 101 of the
inspiration period 110 and ends at the end 160 of the rest period
130 which is the beginning of the next respiratory cycle. In
accordance with the invention as described below a time period is
identified for stimulating a diaphragm and/or phrenic nerve to
elicit a breathing response where the stimulation is believed to
capture or take over breathing control and/or inhibit breathing
driven by a subject's innate respiratory drive. The stimulation
period 170 is identified by an earliest acceptable stimulation
boundary 140 and a latest acceptable stimulation boundary 150.
[0033] In general the stimulation period 170 falls within the rest
period 130. The earliest stimulation boundary 140 may be selected
on a patient by patient basis and is the earliest time at which the
innate respiratory drive is captured by a particular stimulation.
The stimulation boundary may be determined, e.g., on a patient by
patient basis by optimizing stimulation response prior to
implanting the device. Accordingly stimulation is provided and
observed at different times near the beginning of the rest period
to identify when the respiratory drive is captured for a particular
stimulation waveform. In general, it is believed that such earliest
stimulation boundary 140 is after the end of the exhalation period
120 and at or near the beginning of the rest cycle 130. As an
alternative to optimizing on a patient by patient basis an earliest
time may be selected for example as the end of the exhalation
period 120 or a given time after the end of the exhalation cycle.
It may also be selected as a predetermined fraction of the
respiratory interval or its various components based on a baseline
respiratory interval or interval component.
[0034] The latest stimulation boundary 150 may be similarly
selected on a patient by patient basis or using a predetermined
value or a value based on a baseline. In general, in order to
capture respiration with stimulation for a subject's given minute
ventilation, according to one embodiment, the latest stimulation
boundary 150 is selected to occur at a time prior to the generation
of an inspiration signal from the dorsal respiratory group.
Accordingly, the latest stimulation boundary 150 is typically at
time substantially before the expected onset of the next breath,
before the end of the rest period. In particular, according to one
variation, the latest stimulation boundary 150 is at about 0.9 of
the total rest cycle length 130. According to another variation,
the latest stimulation boundary is a predetermined time prior to
the end of the rest cycle 160, more preferably at about 100 to 500
milliseconds prior to the end 160 of the rest cycle 130.
[0035] The identification of the inspiration cycle, exhalation
cycle rest period, tidal volume and respiratory rate may be
accomplished by sensing the respiration waveform, e.g., with a
pneumotachometer, movement sensor or using EMG. An example of such
determination is described, for example in related U.S. application
Ser. No. 10/686,891 incorporated herein by reference. Various
methods and devices that may be used to map ideal electrode
placement for a desired result or to optimize stimulation to
achieve such result are described in related U.S. application Ser.
No. 10/966,484 filed Oct. 15, 2004, now abandoned, entitled "SYSTEM
AND METHOD FOR MAPPING DIAPHRAGM ELECTRODE SITES" and is
incorporated herein by reference.
[0036] FIG. 2 is a flow chart illustrating a baseline determination
in accordance with the invention. The device identifies the phase
in which stimulation may be applied by sensing the respiratory
phase length. This may be used during patient set up to establish
patient baseline breathing. The baseline may be determined for
several tidal volume levels or for one patient tidal volume,
typically in a resting state. Baselines are established on a
patient to patient basis because, e.g., each patient may have
unique chest/lung compliance that could affect exhalation
characteristics.
[0037] In step 210, a patient is connected to a flow sensor (e.g.,
a pneumotachometer).
[0038] In step 220 a patient is instructed to breathe at a resting
respiratory rate and tidal volume. The respiration waveform is used
as a baseline. From the respiration waveform, respiration
parameters are measured, e.g., tidal volume, inspiration duration,
exhalation duration, rest period, and respiratory rate. Thus the
length of each segment of the inspiration cycle is determined, for
a given tidal volume. The minute ventilation may also be determined
from the tidal volume and respiratory rate.
[0039] At step 230 which occurs with step 220, the EMG is sensed
and the EMG is correlated with the information sensed by the
pneumotachometer in step 220. The correlation is useful when the
patient is no longer connected to the pneumotachometer. From the
EMG and measured tidal volume the tidal volume for a subsequently
observed EMG may be estimated or determined. At rest, exhalation is
correlated to tidal volume. As tidal volume increases, so does the
duration of exhalation. Thus, the exhalation phase for a given
title volume can be generally determined as the exhalation phase is
generally the same for a given tidal volume.
[0040] In step 240 which occurs with steps 220 and 230, diaphragm
motion is sensed with a motion sensor. Diaphragm motion indicates
when the lungs are inspiring, exhaling or at rest. This step is
optional but provides additional correlation information. The
motion sensor information is also correlated with EMG and
pneumotachometer information.
[0041] At step 250 the respiration parameters are stored, i.e. the
measured tidal volume and other sensed measured or calculated
parameter, and correlated EMG, pneumotachometer and motion sensor
data.
[0042] At step 260, steps 220 through 250 are repeated for a
decreased tidal volume. A patient may be coached or instructed by a
provider or programmer via telemetry to breathe at a lower tidal
volume and the same measurements are then made as were made for a
resting tidal volume.
[0043] At step 270, steps 220 through 250 are repeated for an
increased tidal volume. A patient may be coached or instructed by a
provider or programmer to breathe at a higher tidal volume and the
same measurements are then made as were made for a resting tidal
volume.
[0044] Once the initial baseline data and waveforms are stored, the
implanted device may be programmed accordingly and the device
turned on.
[0045] FIG. 3 illustrates the identification of phase boundaries
when the device is in operation.
[0046] As illustrated in step 310, the device senses EMG.
[0047] In step 320 the EMG is stored along with respiratory
parameters that may be ascertained from EMG. This includes the
inspiration period where EMG is active, the exhalation and rest
period combined where EMG is inactive.
[0048] At step 330 if a motion sensor is in use on the diaphragm,
then at step 340 the motion detector is used to differentiate
between the exhalation phase in which there is diaphragm movement
and the rest phase in which there is minimal diaphragm
movement.
[0049] At step 330, if the motion sensor is not in use on the
diaphragm, then at step 350, the data points stored in step 230 of
FIG. 2 are used to extrapolate the tidal volume for a given EMG.
For a given tidal volume, the exhalation period is generally known,
thus the rest period may be determined by subtracting the
exhalation period from the combined sensed exhalation and rest
periods.
[0050] At step 360, following either step 340 or step 350, the
stimulation delivery boundaries are determined, i.e. the earliest
stimulation boundary 140 and latest stimulation boundary 150 are
determined. The stimulation may occur in the same cycle as the EMG
or in a subsequent cycle assuming the previous cycle would be
approximately the same. In one example, the earliest stimulation
boundary is at a predetermined time after the end of the exhalation
period. The latest stimulation boundary is a predetermined time
before the end of the rest period. In another example the earliest
stimulation boundary is after a predetermined fraction of the
expected rest cycle has passed. And, the latest stimulation
boundary is before a predetermined fraction of the expected rest
cycle has passed. Other ways of determining the stimulation phase
may be used in accordance with the invention, including but not
limited to using optimization as described above with reference to
FIG. 1.
[0051] At step 370, if treatment is desirable, then at step 380,
stimulation is provided during the stimulation phase as programmed.
Subsequently, or if no treatment is required, the system resumes
monitoring EMG.
[0052] According to one aspect of the invention, stimulation is
provided that inhibits central respiratory drive for a sufficient
duration so that therapeutic stimulation and breathing control may
be applied. The therapeutic stimulation breathing is configured to
provide a therapeutic benefit at the same time that it acts to
inhibit central respiratory drive. According to one aspect the
stimulation intensity, duration and respiratory rate are
manipulated to inhibit respiratory drive while providing desired
stimulation to the diaphragm. For example, at a given respiratory
rate and tidal volume during diaphragm stimulation, extending the
inspiration or expiration duration (among other things, by
increasing stimulation duration and decreasing intensity)
effectively shortens the resting period compared to spontaneous
breathing and decreases the likelihood of a spontaneous breath
between stimulations.
[0053] One factor in inhibiting respiratory drive is to stimulate
an inspiration between the rest phase boundaries and thereby
activate the mechanoreceptors such as the stretch receptors and the
proprioreceptors to provide feed back that an individual is
actively inspiring. The stretch receptors activate when the
airways/lungs stretch and the proprioreceptors activate when
respiratory muscles of the diaphragm and/or chest wall contract.
Typically output from the respiratory center conducted by efferent
nerves to the respiratory muscles are temporarily inhibited by the
mechanoreceptor signals until the individual has exhaled.
[0054] Another factor that affects respiratory drive is the blood
oxygen concentration levels and the partial pressure of carbon
dioxide in the blood. A decrease in carbon dioxide levels tends to
create a decrease in respiratory drive whereas a decrease in oxygen
saturation levels may increase respiratory drive. These levels and
thus the chemoreceptors and respiratory drive may be influenced by
controlling minute ventilation as is described in related U.S.
patent application Ser. No. 10/966,472 filed Oct. 15, 2004, now.
U.S. Pat. No. 8,200,336, entitled "SYSTEM AND METHOD FOR DIAPHRAGM
STIMULATION" and is incorporated herein by reference. Accordingly,
parameters that effect minute ventilation e.g., tidal volume and
respiratory rate, may be manipulated to control respiratory
drive.
[0055] FIGS. 4A-4B and 4D illustrate various stimulation schemes in
accordance with the invention, for controlling breathing while
maintaining central respiratory drive inhibition. FIG. 4C
illustrates spontaneous breathing 450 with the dotted line showing
what spontaneous breathing would continue to look like without
stimulated breathing.
[0056] According to one aspect stimulation is provided within the
defined stimulation phase (See FIGS. 1 and 3) of the rest phase
before the effect of the lack of mechanoreceptor activation allows
the brain to initiate inspiration. In addition, tidal volume is
maintained which is believed to help prevent other brain receptor
functions from causing the initiation of inspiration.
[0057] As noted previously, in setting up and programming the
device for a specific patient, various stimulation responses may be
tested until a desired response (e.g., tidal volume an respiratory
rate) is obtained.
[0058] Referring to FIG. 4A a set or a series of stimulation pulses
410, 411, 412 is illustrated following a spontaneous breath 400.
Each of the series of pulses 410, 411, 412 elicit a slower rate and
more shallow breathing (e.g., flow) response 420, 421, 422 in
comparison to the spontaneous breaths 490, 496, 497, 498, while
each maintaining a tidal volume approximately the same as the tidal
volume of the spontaneous breaths 496, 497, 498 (FIG. 4C). Each of
the initiation points 402, 404, 406 fall within a stimulation phase
that is a less than or is a fraction of the spontaneous breath rest
phase 495 (FIG. 4C). The rest phases 403, 405, 407 are shorter.
Accordingly, spontaneous breathing is inhibited.
[0059] Similarly in FIG. 4B a set of a series of stimulation pulses
440, 441, 442 is illustrated following a spontaneous breath 430.
Each of the series of pulses 440, 441, 442 elicit a slower rate and
more shallow breathing response 450, 451, 452 in comparison to the
spontaneous breaths 490, 496, 497, 498, while each maintaining a
tidal volume approximately the same as the tidal volume of the
spontaneous breaths 496, 497, 498 (FIG. 4C). Each of the initiation
points 432, 434, 436 fall within a stimulation phase that is a less
than or is a traction of the spontaneous breath rest phase 495
(FIG. 4C). The rest phases 433, 435, 437 are shorter than the rest
phase 495 while somewhat longer than the rest phases 403, 405, and
407 of FIG. 4A. Accordingly, spontaneous breathing is
inhibited.
[0060] FIG. 4D illustrates a set of a series of stimulation pulses
470, 471, 472 is illustrated following a spontaneous breath 460.
Each of the series of pulses 470, 471, 472 elicit a similar
breathing response 480, 481, 482 in comparison to the spontaneous
breaths 490, 496, 497, 498,(except the rate is faster) thus each
maintaining a tidal volume approximately the same as the tidal
volume of the spontaneous breaths 490, 496, 497, 498. Each of the
initiation points 462, 464, 466 fall within a stimulation phase
that is a less than or is a fraction of the spontaneous breath rest
phase 495 (FIG. 4C). While the breathing responses 480, 481, 482
are similar or the same as those of the spontaneous breaths, 496,
497, 498, the respiration rate is increased. Accordingly,
spontaneous breathing is inhibited.
[0061] The stimulation scheme of the invention may be used in a
number of applications. In general, a patient's breathing is
captured by the stimulator and breathing stimulation is applied to
control breathing for a period of time.
[0062] In one application, breathing is stimulated to increase
oxygen saturation levels for a period of time. It is believed that
this scheme will allow positive remodeling of the heart by reducing
the load on the heart for a period of time e.g., for one or more
time intervals during sleep. Reduced contractility and cardiac
output for a period of time provides an opportunity for an
overloaded heart to rest. The oxygen saturation levels can be
increased by increasing minute ventilation. Therefore one aspect of
the invention is a device and method for treating heart failure
patients by providing breathing stimulation for periods of time
that increase oxygen saturation levels.
[0063] Examples of a breathing therapy schemes are shown in FIGS.
5-8. As shown in FIG. 5, during normal breathing tidal volume
respiratory rate and minute ventilation are observed as described
with respect to FIGS. 1-3 herein. Tidal volume is maintained at the
normal level while respiratory rate is increased, thus increasing
minute ventilation and SaO2 levels, decreasing PCO2 levels, and
therefore maintaining central respiratory drive inhibition. This
therapy mode is maintained for a programmable amount of time, e.g.,
for one or more intervals of time during the night or during the
day. After the breathing therapy mode, breathing is normalized to
allow PCO2 to slowly increase so spontaneous breathing can be
restored. This may be accomplished by returning respiratory rate
back to normal and maintaining normal tidal volume to increase PCO2
and thereby encourage the return of intrinsic breathing and
respiratory drive. If after the stimulator stimulates breathing at
a normal rate for a period of dine and spontaneous breathing has
not returned, the patient is weaned from the stimulator by further
decreasing the respiratory rate and therefore minute ventilation.
This will allow intrinsic breathing and respiratory drive to return
by allowing an increase in PCO2.
[0064] FIG. 6 is a flow chart illustrating the scheme set forth in
FIG. 5. At step 610 the breathing therapy scheme is activated, e.g.
at a programmed time.
[0065] At step 620, control of breathing is taken over either
immediately as described with respect to FIG. 7, or gradually as
described with respect to FIG. 8.
[0066] At step 630 the stimulation delivery boundaries identified
as described in FIG. 2 are recalled (which have been dynamically
observed and recorded).
[0067] At step 640 the diaphragm is stimulated at an increased
minute ventilation for a given or programmed duration.
[0068] At step 650 breathing stimulation is normalized and the
normalization mode is activated. Stimulation at a normal minute
ventilation is provided for a given duration or until spontaneous
breathing returns.
[0069] At step 660, the weaning mode is activated and minute
ventilation is decreased for a given duration or until spontaneous
breathing returns.
[0070] Referring to FIG. 7, immediate control begins after a period
of normal breathing 700 by taking over breathing at a point 705
within an identified stimulation phase. Stimulation of breathing at
the increased respiratory rate is continuously applied for the
breathing therapy portion 710. Stimulation is then normalized for a
period of normalization 720 and the patient is weaned for a period
of weaning 730. While not specifically shown in FIG. 7, stimulation
continues until the return of spontaneous breathing.
[0071] FIG. 8 illustrates a gradual control mode. In the first
portion 810 of the gradual control mode stimulated breaths 801 are
induced between spontaneous breaths 800. The effective minute
ventilation is gradually increased as the rest period 812 between
the spontaneous breath 800 and the subsequent stimulated breath 801
are shorter than the intrinsic rest period 811. Over time in this
first portion 810 of the gradual mode, SaO2 will increase and PCO2
will decrease gradually decreasing the respiratory drive. The
length of the rest period is determined, e.g., using a motion
sensor, until it reaches a critical length that has increased due
to decreased respiratory drive (e.g. at rest period 820 ending at
802). At that point breathing is controlled by the stimulator as it
has transitioned to the immediate control mode for a period of time
830. Then breathing is normalized 840 and finally the patient is
weaned 850.
[0072] Another aspect of the invention provides for breathing
therapy in treating apnea. It is believed that stimulated breathing
prior to or during apnea may stabilize the broad swings of blood
gas concentrations that occur during cycles of Cheyne-Stokes and
apnea. Further it is believed that diaphragmatic stimulation during
apnea may stimulate vagal afferent signals to the respiratory
center and thus may maintain vagal tone associated with restful
sleeping. Vagal tone has a calming effect on heart rate, blood
pressure and cardiac output during restful sleep stages.
Furthermore, diaphragmatic stimulation may prevent a fall in oxygen
saturation that would typically initiate an arousal episode during
apnea. Arousal episodes are associated with increases of
sympathetic nerve activity which increases ventilation rate, heart
rate and blood pressure. If oxygen saturation falls below a
threshold, it is believed that hyperventilation will attempt to
compensate for the falling oxygen saturation and also create
arousal. Accordingly the invention provides a device and method for
preventing apnea arousals. The invention also provides a device and
method for providing greater periods of restful sleep particularly
in patients suffering from ongoing bouts of apnea and resulting
arousal from sleep.
[0073] Referring to FIG. 9 at step 910 apnea is detected and an
episode is initiated. Apnea may be detected e.g., by a lack of EMG
for a given period of time.
[0074] At step 920, stimulation is provided. If stimulation is
provided during an apnea interval, (preferably at the beginning of
the apnea level before SaO2 levels are depleted) stimulation is
provided at a predetermined rate and tidal volume based on previous
baseline determinations. In particular stimulation is provided at
lower minute ventilation than normal. This is to gradually allow
for more oxygenation than will occur during apnea while also
allowing an increase in the PCO2 levels until the respiratory drive
increases at least above the apneac threshold, and spontaneous
breathing at a desired level returns. Cheyne-Stokes and apnea tend
to occur in repeated cycles in heart failure patients. This is
believed to occur in part due to the delay in the feedback or
chemoreceptor sensing due to circulatory delay which is common in
heart failure patients. The purpose of the apnea therapy described
herein is to stabilize the blood gas levels more gradually and to
reduce the extreme fluctuations between Cheyne-Stokes
hyperventilation and apnea.
[0075] At step 930, the stimulation rate is set and may gradually
be reduced by increasing the intervals between successive breaths
or stimulations. If no EMG 940 is sensed within interval 930 or a
sensed EMG does not meet the amplitude criterion and the interval
length has not reached a maximum length, then the stimulation is
delivered at step 920 and the cycle 930 & 940 repeated. If an
EMG is sensed 940 within the 930 interval and meets amplitude
criterion then the stimulation will be inhibited at step 950. If a
defined number of successive sensed EMGs meeting step 940 criterion
are not met then the interval is again set at step 930. If a
defined number of successive sensed EMGs meeting step 940 criterion
are met in step 960 then the episode is over and the device returns
to apnea detection mode 910.
[0076] FIG. 10 illustrates apnea treatment as described with
respect to FIG. 9. The waveform at 1000 may be a normal intrinsic
breath. At 1010 a breath with an increased amplitude may be a
precursor to Cheyne-Stokes hyperventilation that may indicate the
imminent onset of Cheyne-Stokes. At 1020 Cheyne-Stokes
hyperventilation is at a peak amplitude. At 1030 the amplitude is
decreasing indication the imminent onset of apnea. At 1040, apnea
has occurred. At 1010, 1020, or 1030, a precursor to apnea may be
sensed and stimulation may be provided to take over breathing in a
manner similar to that described with reference to FIGS. 5-8. The
stimulation may be adjusted to increase or decrease minute
ventilation to stabilize blood gas fluctuations and avoid further
episodes of Cheyne-Stokes and/or apnea. Maintaining stable blood
gas levels with stimulation may prevent Cheyne-Stokes
hyperventilation and hence avoid arousal events otherwise
associated with large swings of these gases.
[0077] If detection of apnea occurs, e.g., at point 1040, then
stimulation begins at 1050. As described with respect to FIG. 9,
stimulation is at minute ventilation that is reduced from a normal
baseline. At 1060 the intervals between stimulation cycles
increase. At 1070 an EMG is sensed but it is not at a desired level
and the stimulation continues. At 1080 an EMG is sensed and
stimulation is inhibited until an interval passes. At 1090 a set
interval has passed without spontaneous breathing and stimulation
then resumes. At 1095 spontaneous breathing has resumed and
continues for a requisite number of cycles (until point 1099 is
reached). It is then determined that the episode is over and the
system returns to apnea sensing mode.
[0078] As an alternative to detecting apnea as an episode is
occurring, precursors to apnea or to Cheyne-Stokes may be sensed
and treated. A precursor to apnea may be detected in a number of
ways, for example, by detecting Cheyne-Stokes hyperventilation or a
precursor to Cheyne-Stokes hyperventilation. Also as precursor to
apnea may be detected by detecting periodic breathing throughout a
day prior to night time. If this is the case stimulation is
delivered throughout the night, in intervals as described, with
respect to FIGS. 5-8. In addition, the device may be set to detect
actual apnea events if they occur in spite of administering
breathing therapy as described with respect to FIGS. 9 and 10
herein. Detection of precursors s described in more detail in
related U.S. Ser. No. 10/966,421 filed Oct. 15, 2004, now U.S. Pat.
No. 8,255,056, entitled: "BREATHING DISORDER AND PRECURSOR
PREDICTOR AND THERAPY DELIVERY DEVICE AND METHOD" and is
incorporated herein by reference.
[0079] In accordance with another aspect of the invention, provides
for treatment of hypertension. Studies have shown that patients
coached to breath at about 6 breaths per minute have a reduction in
blood pressure and resting oxygen saturation is improved.
[0080] FIGS. 11A-B illustrate an example of a hypertension
breathing therapy device. According to the example, capture of
breathing as described in FIGS. 5-8 may occur on a nightly basis
for specific preprogrammed durations. In addition stimulation may
also be provided during an exhalation cycle to further extend the
length of the active breathing portion (inspiration and exhalation)
of the respiration cycle. The duration of the rest period is
greatly reduced so that the central respiratory drive may remain
inhibited. The minute ventilation is maintained in accordance with
a baseline determined as described with reference to FIG. 2. The
goal is to create long slow breathing, e.g., at about 6 cycles per
minute or at another rate that provides desired therapy.
[0081] FIGS. 11A-B illustrates an example of inducing slow
controlled breathing therapy. FIG. 11A illustrates the breathing
morphology while FIG. 11B illustrates the corresponding stimulation
bursts or series of pulses. During the first period 1100
spontaneous breathing is occurring which can be used as a baseline.
During a second period 1110, breathing is captured and the
breathing rate is slowed. During period 1110, stimulation induces
an inspiration cycle with a passive exhalation and a rest period as
in spontaneous breathing.
[0082] Subsequently during period 1120 stimulation ramps up to
induce an inspiration cycle, as in period 1110, and gradually ramps
down during exhalation to extend the length of the exhalation
cycle. Thus, the normally passive exhalation phase is now
influenced with active stimulation. The increase in the duration of
the active breathing portion of the respiration cycle decreases the
rest phase duration which tends to inhibit the occurrence of
spontaneous breathing. During period 1120 minute ventilation is
approximately equal to minute ventilation during period 1110 which
is achieved by increasing the tidal volume and decreasing the rate.
In the period 1120 (the therapy cycle), the stimulation 1131
becomes longer in duration than stimulation 1130, further extending
the duration of the breaths and decreasing the rest phase, which
inhibits spontaneous breathing and maintains a decreased
respiration rate. Then the stimulation 1132 decreases in duration
and stimulation is inhibited. After breathing therapy is complete,
the stimulation is turned off or stimulation is gradually returned
to normal breathing in a manner similar to that described in
examples above. Spontaneous breathing will then resume. In
accordance with this aspect of the invention preferably the
breathing rate is reduced to 20 breaths per minute or less, more
preferably about 10 breaths per minute or less and most preferably
between about 4 and 8 breaths per minute.
[0083] The respiratory drive inhibition may also be used in
treating COPD patients. COPD patients have difficulties exhaling
CO.sub.2 and therefore typically retain high levels of CO.sub.2 in
their blood. Low levels of inspiration with high levels of
exhalation may be induced by inducing longer periods of exhalation
in a manner similar to that described with respect to FIGS. 11A-11B
where the exhalation period is extended.
[0084] While the invention has been described in detail with
reference to preferred embodiments thereof, it will be apparent to
one skilled in the art that various changes can be made, and
equivalents employed, without departing from the scope of the
invention.
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