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| United States Patent | 5836976 |
| Link to this page | http://www.wikipatents.com/5836976.html |
| Inventor(s) | Min; Xiaoyi (Plymouth, MN);
Wang; Li (White Bear Township, MN);
Mehra; Rahul (Stillwater, MN);
DeGroot; Paul J. (Brooklyn Park, MN);
Olson; Walter H. (North Oaks, MN);
Mongeon; Luc R. (Minneapolis, MN);
Hill; Michael R. S. (Minneapolis, MN) |
| Abstract | In an implantable pacemaker/cardioverter/defibrillator, a system for
correlating the delivery of a cardioversion therapy to an optimum point or
phase of the respiratory cycle of the patient to effect delivery of the
therapy when the impedance between the cardioversion electrodes is
minimized. In a first application for use with cardioversion electrodes
located substantially in contact with the heart chamber, the optimum point
or phase is at the end of inspiration. In a second application for use
with at least one cardioversion electrode located remotely from the heart
chamber, the optimum point or phase is at end expiration or beginning of
inspiration. The cardioversion therapy is delivered in synchrony with a
ventricular sense event, if present. If the optimum point or phase of the
respiratory cycle cannot be determined during a therapy time, a pre-shock
may be delivered to elicit a respiration cycle through a stimulated
contraction of the diaphragm. |
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Title Information  |
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Drawing from US Patent 5836976 |
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Cardioversion energy reduction system |
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| Publication Date |
November 17, 1998 |
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| Filing Date |
April 30, 1997 |
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Title Information |
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Description |
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CROSS-REFERENCE TO RELATED APPLICATIONS
Reference is hereby made to commonly assigned, co-pending U.S. patent
application Ser. Nos. 08/230,578 filed Apr. 21, 1994 now abandoned, for
TREATMENT OF ATRIAL FIBRILLATION by Luc R. Mongeon et al.; 08/495,251
filed Jun. 27, 1995, now U.S. Pat. No. 5,713,924 for DEFIBRILLATION
THRESHOLD REDUCTION PACING SYSTEM by Xiaoyi Min et al.; Ser. No.
08/230,577 filed Apr. 21, 1994 now U.S. Pat. No. 5,562,708 for METHOD AND
APPARATUS FOR TREATMENT OF ATRIAL FIBRILLATION by William J. Combs et al.;
Ser. No. 08/640,046 filed Apr. 30, 1996 now U.S. Pat. No. 5,683,429 for
ATRIAL FIBRILLATION PREVENTION PACING SYSTEM by Rahul Mehra; and
08/846,938 filed on even date herewith for CARDIOVERSION ENERGY REDUCTION
SYSTEM by Luc Mongeon et al., all of which deal with related subject
matter.
FIELD OF THE INVENTION
The present invention generally relates to implantable
cardioverter-defibrillators and, more specifically to a system for
correlating the delivery of a cardioversion therapy to an optimum phase of
the respiratory cycle of the patient to effect delivery of the therapy
when the impedance between the cardioversion electrodes is minimized.
BACKGROUND OF THE INVENTION
By way of definition, in the field of automatic implantable arrhythmia
control devices, the term "cardioversion" or "cardioverter" refers to the
process of and device for discharging relatively high energy electrical
shocks in excess of 1.0 Joule into or across cardiac tissue to arrest or
"cardiovert" a tachyarrhythmia of a cardiac chamber. Delivery of
cardioversion shocks may or may not be synchronized with a cardiac
depolarization or rhythm and may be applied to arrest a malignant atrial
or ventricular tachycardia or fibrillation with a selectable or
programmable pulse energy. The termination of high rate tachycardias with
lesser energy electrical pulses or bursts has also been referred to as
"cardioversion" The arrest of atrial or ventricular fibrillation by higher
energy shocks is referred to as "defibrillation", and defibrillation has
been characterized in the past as a form of cardioversion. Products have
been described and sold as "implantable cardioverter/defibrillator" (ICD)
systems for providing synchronized cardioversion shocks or and
unsynchronized defibrillation shocks and as
"pacemaker/cardioverter/defibrillator" (PCD) systems for providing
additional staged therapies of anti-tachyarrhythmia pacing, synchronized
cardioversion shocks and unsynchronized defibrillation shocks. In the
following description and claims, it is to be assumed that the terms
"cardioversion" and "defibrillation" and variants thereof are
interchangeable, and that use of one term is inclusive of the other device
or operation, unless specific distinctions are drawn between them in the
context of the use. For convenience, the term "cardioversion" or
"cardioversion/defibrillation" will be used unless a form of
defibrillation therapy is specifically referred to.
Tachyarrhythmias are episodes of high rate cardiac depolarizations,
typically occurring in one chamber of the heart but which may be
propagated from one chamber to the other, and are distinguished from sinus
tachycardias that physiologically accompany exercise to provide adequate
cardiac output. Tachyarrhythmias that are sufficiently high in rate and
chaotic compromise cardiac output from the affected chamber(s), leading to
loss of consciousness and death, in the case of ventricular fibrillation,
or weakness and dizziness, in the case of atrial fibrillation or flutter
and non-sinus atrial and ventricular tachycardias. Atrial fibrillation and
flutter are debilitating, due to the loss of atrial cardiac output
contribution and interference with ventricular filling, but not
immediately life threatening unless it leads to ventricular fibrillation.
High rate atrial and ventricular tachycardias may exhibit a more organized
rhythm but also may disable the patient and can lead to fibrillation if
untreated.
Fibrillation has generally been treated by means of high energy
cardioversion/defibrillation shocks, which, in the context of implantable
anti-arrhythmia devices, are applied by means of large surface area
cardioversion electrodes, including an electrode on or in the chamber to
be defibrillated. The battery life of an ICD or PCD device depends on the
amount of energy expended in delivering a therapy and the delivery
frequency. The high energy level employed in order to defibrillate
consumes considerable energy in the range of 1.0-30.0 Joules per delivered
shock. The high energy level is employed in order to simultaneously
depolarize the bulk of the heart chamber to be defibrillated, which will
include tissues in all stages of the depolarization-repolarization cycle
at the time the pulse is delivered.
For patients experiencing ventricular fibrillation, the delivered
cardioversion/defibrillation shock energy is necessary to save the
patient's life and is usually not perceived by the patient because of the
loss of consciousness shortly following onset of the arrhythmia. Accuracy
of diagnosis and delivery of a cardioversion shock having sufficient
energy to cardiovert the rhythm as quickly as possible are paramount
concerns because the efficacy of the shock decreases with time lapse from
onset of the symptoms.
Patients experiencing high rate atrial tachycardias and atrial
fibrillation/flutter typically do not lose consciousness, and the
condition is usually not life threatening. The intentional or inadvertent
delivery of the cardioversion shock therapy by an ICD or PCD device is
startling and painful to a degree that is assumed to be proportional to
the shock energy level.
It was recognized early in the development of external ventricular
defibrillators that a lower energy synchronous cardioversion shock could
be employed to interrupt a high rate ventricular tachycardia, if the shock
delivery was synchronized to a ventricular depolarization event, i.e. the
R-wave. The lower energy threshold is attributed to the assumption that
more of the ventricular muscle mass is intrinsically depolarized at this
time, thereby requiring less cardioversion energy to depolarize the
remaining ventricular muscle mass. If synchronization to a ventricular
depolarization can be achieved, staged therapy ICD and PCD devices deliver
somewhat lower energy cardioversion shocks to the affected chamber.
Ventricular synchronized atrial cardioversion and defibrillation is
employed to ensure that the cardioversion/defibrillation pulse is
delivered before the "vulnerable period" associated with the
re-polarization of the heart.
Episodes of atrial tachyarrhythmias occur frequently and are debilitating
to the patient, if not life threatening. Unfortunately, the quantity of
electrical energy required to cardiovert or defibrillate the atria is
sufficient, in most cases, to cause a sudden, propagated pain in the
patient's chest area or to stun the patient. Typically reported
defibrillation thresholds (in humans) of 2-3 Joules are required between
transvenous lead bearing electrodes placed to provide atrial cardioversion
pathways between the right atrium (RA) and the coronary sinus (CS) or the
superior vena cava (SVC) and the CS. Other atrial electrode systems may
require up to 4.0-10 Joules (in humans) to reliably cardiovert.
Significant discomfort and often intolerable pain is associated with such
atrial cardioversion/defibrillation shock therapies in this range,
resulting in sedation of some patients and refusal to accept the therapy
by other patients. Moreover, there is concern that the attempt to
defibrillate the atria will itself induce ventricular fibrillation leading
to the death of the patient. In the hospital setting, the patient is
carefully monitored, and induced ventricular fibrillation may be
defibrillated. However, the clinical procedure still entails enough risk
that drug therapies are preferred, and atrial defibrillation is used only
after other therapies fail.
The same concerns have delayed the development of implantable atrial
defibrillators so that patients prone to bouts of atrial fibrillation or
flutter could remain ambulatory. One possible approach that has been
widely published is to combine the atrial and ventricular fibrillation
detection and cardioversion/defibrillation capabilities in a single
implantable system so that induced ventricular fibrillation could be
terminated. Such a device is disclosed in U.S. Pat. No. 5,549,642, issued
to Min et al. The Incontrol Metrix TM atrial defibrillator, currently in
clinical evaluation, does not provide the capability of treating induced
ventricular tachyarrhythmias and therefore relies upon shock delivery
criteria to avoid induction of ventricular tachyarrhythmias. In the
context of atrial cardioversion, a proposed pacemaker/defibrillator is
disclosed in PCT Publication No. WO 92/18198 by Adams et al. where the
synchronization of the high voltage atrial cardioversion shock is to the
R-wave in an effort to avoid inducing ventricular tachycardia or
fibrillation. In either case, synchronization to an R-wave in a high rate,
irregular EGM has proven to be difficult to accomplish and not always
effective to avoid inducing ventricular fibrillation.
Faced with these difficulties, attempts have been made to first make the
cardiac rhythm more regular so that the P-wave or R-wave may be detected
and to then apply the synchronous cardioversion therapy. In commonly
assigned U.S. Pat. No. 5,193,536, a PCD system is described where the high
atrial or ventricular rate is made more regular by delivering overdrive
pacing pulses to capture the heart and by using the last overdrive pulse
delivered as a synchronization event to time the delivery of the
cardioversion shock. Another method is disclosed in U.S. Pat. No.
5,074,301 where a single pacing pulse is delivered to the atrium to allow
the cardioversion shock to be delivered in the atrial refractory period.
It is not suggested that the overdrive pacing pulses affect the
cardioversion threshold.
In U.S. Pat. Nos. 5,314,448 and 5,366,485, an ICD is described having a set
of cardioversion electrodes arranged around the patient's heart. When
fibrillation is detected, the high output capacitors begin to be charged.
As they are charged or after full charge is achieved, a "pre-treatment" of
the fibrillating heart muscle is commenced through the generation of a
train of pulses from the voltage on the output capacitors and delivery of
the pulses across the cardioversion electrodes. The capacitors are
recharged and at the end of the recharge time period, the high energy
cardioversion pulse is delivered across the cardioversion electrodes. It
is stated that the pre-treatment pulses begin the process of organizing
the chaotically contracting myocardial cells and result in a reduction of
cardioversion threshold and the total energy expended. It is emphasized
that the pre-treatment pulse voltages are well in excess of pacing level
voltages and that the same cardioversion electrodes are employed to
deliver the energy to the same myocardial cells as will be defibrillated
by the cardioversion pulse. In this manner, the pre-treatment pulses are
delivered into the high current density regions of the current pathways in
the heart chamber between the spaced apart cardioversion electrodes.
In the above-referenced '251 application, a method and apparatus for
terminating fibrillation is disclosed using a burst of pacing energy, high
frequency pulses applied into a low current density region of the cardiac
tissue in the chamber in fibrillation prior to the delivery of one or more
cardioversion energy pulses. The burst of pacing energy pulses is
delivered between the pace/sense electrodes located in the low current
density region of the cardioversion pathway around and through the heart
chamber defined by the cardioversion energy distributed between the spaced
apart cardioversion electrodes. The burst of pacing energy pulses injected
into the low current density region results in the lowering of the
cardioversion threshold, and the decreased energy cardioversion pulse
effectively terminates the fibrillation episode. The burst of pacing
energy pulses appears to develop a refractory island in the low energy
region of the heart chamber that may itself lower the cardioversion
energy, and also appears to prevent ectopic beats originating in the low
energy region from re-fibrillating the heart.
Recently, the theoretical possibility of employing low energy pacing level
pulses (i.e. less than 0.05 joules) to terminate atrial fibrillation has
been explored. For example, in the recent article "Regional Control of
Atrial Fibrillation by Rapid Pacing in Conscious Dogs", by Allessie et al,
published in Circulation, Volume 84, No. 4, October 1991, pages 1689-1697,
the ability of pacing pulses to capture a small area of fibrillating
atrial tissue, if applied during a specified time interval synchronized to
the sensed depolarization waveform at the pacing electrode site, is
reported. However, the depolarization wavefront created by such pulses
does not propagate through the entire chamber due to the varying
polarization states of the tissue surrounding the stimulation site.
Consequently, it has not been demonstrated that this approach can
defibrillate a heart chamber actually in fibrillation.
It is generally believed that the delivery of pacing pulse bursts to the
atrium can induce atrial fibrillation, unless the delivery is synchronized
to P-waves to assure that the pulse bursts occur within the refractory
period of the atrium. This effect is discussed in U.S. Pat. No. 5,334,221
which discloses a device which provides pulse bursts, synchronized to a
P-wave, to the SA nodal fat pad in the atrium to reduce the sinus rate of
patients who suffer from angina.
Despite this general belief, it has also been proposed to avoid
synchronizing the delivered pacing pulse or burst | | |
