Download System and method of AV interval selection in an implantable

USOO8498705B2
(12) United States Patent
(10) Patent N0.:
Chirife et a].
(54)
(45) Date of Patent:
SYSTEM AND METHOD OF AV INTERVAL
(56)
U.S. PATENT DOCUMENTS
(75) Inventors: Raul Chirife, Acassuso (AR); William
-
~
~
4 485 813 A
12/1984 And
5,154,171 A
5,179,949 A
5,267,560 A
10/1992 Chirife
1/1993 Chirife
12/1993 Cohen
5,330,511 A
7/1994 Boute
437193921 A
J. Combs, Mlnnetonka, MN (US);
Russell R. Lundstrom, Coon Rapids,
MN (US)
.
*Jul. 30, 2013
References Cited
SELECTION IN AN IMPLANTABLE
MEDICAL DEVICE
~
US 8,498,705 B2
t l.
M988 Chirfgon e a
5,334,222 A
8/1994
Salo et al.
(73) Ass1gnee. Medtronlc, Inc., MInneapohs, MN (US)
2002/0151938 A1
(*)
2003/0028222 A1
200% Stahmann
FOREIGN PATENT DOCUMENTS
Notice:
Subject to any disclaimer, the term of this
patent is extended or adjusted under 35
This patent is subject to a terminal dis-
EP
10/2002 Corbucci
607951
Clalmer'
7/1994
OTHER PUBLICATIONS
(21) Appl- NO-I 13/037,780
International Search Report, PCT?JSZOO6/041247, Sep. 2, 2007, 7
(22)
p g
a cs.
Filed:
Mar. 1, 2011
(65)
Prior Publication Data
Us 2011/0152964 A1
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Primary Examiner * Kennedy Schaetzle
23 2011
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Assistant Examiner * Erica Lee
(74) Attorney, Agent, or Firm * Reed A. Duthler
Related US. Application Data
(62)
Division of application No. 11/257,643, ?led on Oct.
25 2005
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ABSTRACT
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An Implantable med1ca1 deVIce prOVIdes ventr1cu1ar pac1ng
capabilities and optimizesAV intervals for multiple purposes.
In general, intrinsic conduction is promoted by determining
When electromechanical systole (EMS) ends and setting an
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AV interval accordingly. EMS is determined utilizing various
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USPC .................. .. 607/9, 17, 18, 25; 600/509, 513,
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See application ?le for complete search history.
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1
2
SYSTEM AND METHOD OF AV INTERVAL
SELECTION IN AN IMPLANTABLE
MEDICAL DEVICE
tioned at the right ventricular apex. Assuming a given patient
had no intrinsic rhythm and fully relied upon the pacemaker,
This application is a divisional of US. patent application
Ser. No. 11/257,643, ?led Oct. 25, 2005 entitled “SYSTEM
the rate would always be the device’s escape interval which
de?nes an A-A interval. This interval may be varied by the
device based upon sensor input to provide rate responsive
(RR) pacing. An AVI or AV interval is programmed and may
be varied by the device depending upon rate or other factors.
AV synchrony is maintained in that a ventricular paced event
AND METHOD OF AV INTERVAL SELECTION IN AN
IMPLANTABLE MEDICAL DEVICE”, US. Pat. No.
DDD pacemaker may operate in this manner.
RELATED APPLICATION
(VP) will always follow an atrial paced event (AP). A typical
7,899,533, issued Mar. 1, 2011 herein incorporated by refer
While the present discussion is overtly super?cial both in
terms of the cardiac cycle and operation of a pacemaker,
ence in its entirety.
several fundamental aspects have been illustrated that are
FIELD OF THE INVENTION
currently being questioned. The ?rst is that ventricularpacing
in the right ventricular apex may not be hemodynamically
optimal for all patients. The second is that a programmed AV
The present invention relates to implantable medical
devices. More speci?cally, the present invention relates to
implantable medical devices that are capable of delivering
interval that more or less assures ventricular pacing, even to
maintain synchrony, is not necessarily optimal in all patients.
pacing stimuli.
20
DESCRIPTION OF THE RELATED ART
At a super?cial level, the mechanical aspects of the cardiac
cycle of the human heart are fundamentally simple. The heart
has four chambers. Deoxygenated blood is returned from the
Implanting leads into the right atrium and right ventricle is
signi?cantly easier than implanting leads to pace the left
25
body to the right atrium. The right atrium (RA) ?lls the right
ventricle (RV), which, upon contraction, pumps blood to the
lungs. Oxygenated blood from the lungs ?lls the left atrium
(LA), which in turn ?lls the left ventricle (LV). The contrac
tion of the left ventricle then delivers oxygenated blood
throughout the body. Thus, the atrial chambers serve the
trodes within the left atrium or left ventricle as this could
30
cycle are also fundamentally simple, at a super?cial level. The
35
Ventricular pacing from the right ventricular apex causes
40
been recognition that intrinsic conduction is preferable to
pacing in most cases. That is, even if the AV delay is longer
than “normal,” it is preferable to wait for the intrinsically
ventricular (V) events. Thus, the activation of the SA node is
45
tricles depolarize. There is a delay and the process is repeated.
Thus, normal timing is A-V-A-V, etc. For purposes of under
standing the physiology as well as for programming various
conducted beat than to pace. This is, of course, at odds with
standard DDD (or similar) modes, which will provide a ven
tricular pace after a predetermined interval (AVI), which is
pacemakers, this simple understanding provides several com
50
will be used herein for explanatory purposes). The time
usually short enough that it precludes intrinsic conduction.
Certain patients who are pacemaker dependant, e.g., those
that have complete heart block, will require and bene?t from
such ventricular pacing. Other patients may have pacemakers
implanted for other reasons and have intact conduction or
may have intermittent block. For those patients, intrinsic con
between the atrial event and the ventricular event is the AV
interval and not surprisingly, the time between the ventricular
event and the subsequent atrial event is the VA interval.
As rate is increased, the A-A interval decreases in duration.
The AV node modi?es the delay imparted, thus the AV inter
val is also reduced. The mechanical actions involved (con
of the left ventricle with respect to the right ventricle is
skewed electrically and mechanically. Recently, there has
depolarizing and contracting the ventricles.
The cardiac cycle is often described by atrial (A) events and
mon variables. The rate of the heart is de?ned by a complete
cycle and may either be an A-A interval or V-V interval (A-A
norm. When dual chamber pacemakers are so implanted, the
device is typically programmed to operate in a DDD mode or
VDD for a single chamber, ventricular pacemaker. Such set
tings restore rhythm, but ensure that pacing occurs in a high
the depolarization wave to travel a rather unnatural path and
while it will cause the left ventricle to depolarize, the timing
chambers respond to the depolarization by engaging in a
an intrinsic atrial depolarization. Some time later, the ven
promote clotting that results in a thrombus. Thus, right side
implantation of single or dual chamber pacemakers is the
percentage of cardiac cycles.
and initiates electrical depolarization of the heart at a prede
termined rate, based upon physiologic need. The SA node is
located in the right atrium and upon activation, the atrial
muscular contraction. The depolarization wavefront eventu
ally reaches the AV node, where a delay is imparted before
atrium or left ventricle, as leads on the left side are preferably
implanted epicardially or within the veins of the heart proxi
mate, but external to the relevant left sided chamber. That is,
there is a general medical bias against placing leads or elec
purpose of ?lling their respective ventricular chambers.
Similarly, the electrical and timing aspects of the cardiac
sinoatrial node (SA node) is the heart’s natural pacemaker
Finally, the entirety of the above discussion was in terms of
RA to RV electrical timing, which while common parlance
tends to ignore a great many aspects of the cardiac cycle.
55
duction is often if not always possible and is typically pre
cluded by standard DDD mode settings.
Again referencing a device having leads in the right atrium
and/or right ventricle, the timing relied upon both for pro
gramming/discussion purposes as well as what is sensed by
traction of a chamber; ejection of a ?uid) may occur more
quickly, but there is a limit or minimal time required for
the implanted device is based upon right side electrical tim
ing. The use of right side timing will tend to ignore the delays
e?icacious operation.
This highly simpli?ed overview can actually provide for
of pacing. In a normal, healthy heart the SA node will depo
many of the key programming parameters in a given dual
chamber pacemaker. Typically, a dual chamber pacemaker
will have an atrial lead (and electrode) positioned within the
right atrium and a ventricular lead (and electrode) positioned
within the right ventricle, generally with the electrode posi
in left sided response that occur naturally and/ or as the result
larize and generate a wavefront along an atrial conduction
pathway that eventually reaches the left atrium causing it to
65
depolarize and contract. The wavefront also reaches the AV
node and progresses along the Bundle of His. The left sided
pathway propagates somewhat faster than the right, but
US 8,498,705 B2
3
4
because the right ventricle is smaller the wavefront leads to a
FIGS. 14-16 are ?owcharts illustrating processes utilizing
embodiments consistent with the teachings of the present
invention.
generally synchronized mechanical contraction of both ven
tricles.
When atrial pacing is introduced, the electrode is typically
offset from the SA node, commonly in the right atrial append
age, and different conduction (and possibly less e?icient)
DETAILED DESCRIPTION
FIG. 1 is schematic, sectional diagram illustrating the
pathways are taken. See US. Pat. No. 5,179,949, issued to
anatomy of a human heart 10. Blood returning from the
venous system ?ows into the right atrium 20 from the superior
(SVC) 50 and inferior vena cava. In a normal, healthy heart
Chirife, which is herein incorporated by reference in its
entirety. The net result is that there is an interatrial conduction
delay (IACD) that is imposed. That is, the left atrium will
10, the sinoatrial (SA) node 22 produces an action potential
that is responsible for the automaticity of the cardiac conduc
tion process. A depolarization wavefront is generated and
depolarize and then contract after a longer interval from the
pacing pulse than would occur intrinsically, i.e., after the SA
node initiates depolarization. Thus, if the remainder of the
conduction pathway were intact, this would skew the results
for ventricular sensing. That is, an A pace occurs and after
some interval, ventricular depolarization is sensed in the right
ventricle by the pacemaker. This duration is determined to be
the AV interval. However, the left atrium did not depolarize
simultaneously with the A pace, nor within the normal physi
progress through the right atrium (RA) 20 along the atrial
conduction pathway 26 to the atrioventricular (AV) node 24.
At the same time, the depolarization wavefront propagates
from the SA node 22 into the left atrium (LA) 40 along the RA
to LA conduction pathway 30. The depolarization wavefront,
generally referred to as the P wave triggers a subsequent
20
muscular contraction as it propagates. That is, the electrically
detected wavefront, i.e., an EKG, is not identically synchro
nized with the mechanical contraction.
As blood is ?lling the RA 20, the LA 40 is similarly being
25
ventricle (RV) 46 and the left ventricle (LV) 54 are being
ologic window. Thus, the left sided AV (LAV) interval is
shorter than the sensed right sided (RAV) interval. That is,
LAVIRAV—IACD.
?lled via the pulmonary veins. During this time, the right
Another left sided variation to timing occurs when right
sided ventricular pacing, particularly at the right ventricular
apex is provided. As indicated, normal ventricular conduction
passively ?lled with blood ?owing through the tricuspid valve
52 and the mitral valve 56, respectively. When the atrial
chambers mechanically contract, they force an additional
volume of blood into the ventricles, causing the ventricles to
begins at the AV node and more or less simultaneously propa
gates along a left and right side of the Bundle of His and
spreads around each ventricle. With right sided pacing, the
normal conduction pathway is not necessarily activated and
30
When the atrial electrical wavefront reaches the AV node
rate. In addition, the wavefront propagates from the apex
retrograde along the Bundle of His, then down the left side
pathway eventually depolarizing the left ventricle. The delay
imparted from the ventricular pace to contraction of the left
35
ventricle is referred to herein as the interventricular conduc
tion delay (IVCD).
Yet another offset is the difference between an event, e.g.,
an atrial depolarization, and the time at which that event is
sensed by the pacemaker. This delay is referred to as the P
40
These various delays are biased towards right side events.
That is, failing to account for such delays may have the most
consequence on left side activity, which is generally more
45
BRIEF DESCRIPTION OF THE DRAWINGS
FIG. 1 is schematic, partially sectional view of a human
heart.
50
heart progressing through a cardiac cycle.
FIG. 3 is illustrates a correspondence between depolariza
tion events occurring throughout a heart and how those events
55
FIG. 4 is a graph illustrating correlations between a surface
the period of isovolumic relaxation, where all valves (AV and
semilunar) are again closed. As diastole continues (FIG. 2D),
FIG. 6 is a block diagram of a ?rst embodiment of the
60
FIG. 7 is a block diagram of a second embodiment of the
present invention.
ther ?ll the ventricles. The process then returns to FIG. 2A and
repeats.
present invention.
corresponding EKG data.
passive ventricular ?lling occurs as the pressure within the
atrial chambers causes the AV valves 100 to open. During
active ?lling (FIG. 2E), the atrial chambers contract and fur
FIG. 8 is a block diagram of a third embodiment of the
FIG. 9 is a graph illustrating device rate limits.
FIGS. 10-13 illustrate stylized pressure waveforms and
isovolumic contraction. The AV valves 100 (mitral and tri
cuspid) and semilunar valves 110 (aortic and pulmonic) are
closed at this point. In FIG. 2B, systole continues with the
period of ej ection where the out?ow of blood opens the semi
lunar valves 110. FIG. 2C illustrates the onset of diastole and
EKG, pressure data, volume data and heart sounds.
FIG. 5 is a series of stylized EKG tracings.
present invention.
pid valve 52 and mitral valve 56 to close. The continued
contraction ejects a large percentage of the ?uid from the
ventricles in a coordinated action. After cardiac cells depo
larize, they are refractory for a period of time. The contracted
chambers relax and the process repeats.
FIG. 2 illustrates some of the mechanical and ?uid ?ow
characteristics generated during the cardiac cycle. In FIG.
2A, the heart 10 is entering systole and is in the period of
FIGS. 2A-2E illustrate the mechanical contractions of a
generate a composite EKG tracing.
24, a delay is imparted. This delay provides time for the atrial
chambers to contract and fully ?ll the ventricles, prior to
ventricular contraction. After this delay (the PR interval), the
depolarization wavefront progresses downward through the
ventricular septal wall along the Bundle of His 32 and splits
into the left bundle branch (LBB) 35 and right bundle branch
(RBB) 36. The bundle branches diverge proximate the apex
42 of the heart 10 and propagate along the Purkinje ?bers 41
surrounding the ventricles. Due to the atrial kick, the ven
tricles are expanded or stretched somewhat. As the muscular
contraction occurs in response to depolarization, the ?uid
pressure within the ventricles increases and causes the tricus
wave sense offset (PSO).
important to hemodynamic performance.
stretch somewhat. This is referred to as atrial kick and
improves overall cardiac output.
instead propagation from cell to cell may occur at a slower
65
In describing the cardiac cycle, both electrical and
mechanical reference points have been described. Typically,
the cardiac cycle is represented electrically and most accu
US 8,498,705 B2
6
5
Cycle length (CL), as used herein is simply the length of a
rately in that context by a surface EKG. Electrodes on the
surface of the skin detect, over multiple vectors, the electrical
signals generated as depolarization occurs. A complete car
diac cycle includes a P wave indicative of atrial depolariza
given cycle (e.g., T1 to T10) and may vary on a beat to beat
basis due to physiologic demand for an intrinsic rate or con
trolled by a pacemaker based upon programmed parameters
and various sensory input. As cycle length decreases, the AV
interval (T1 to T3) is able to slightly decrease. Similarly,
tion, a QRS complex indicative of ventricular depolarization,
and a T wave indicative of ventricular repolarization. FIG. 3
illustrates the potential along the conduction pathways and
how each portion contributes to the overall represented cycle.
ventricular diastole may be shortened.
Of note, the electrical representation does not indicate any
mechanical effect. That is, there is a difference between the
onset of electrical activity and mechanical contraction. Like
within certain parameters. The present invention relates to
Such variation based upon dynamic cycle lengths is normal
promoting intrinsic conduction without permitting these
variations from exceeding those normal parameters. As illus
trated in FIG. 4, ventricular systole occurs from time T5 with
isovolumic contraction and ends at time T8, when isovolumic
relaxation begins. This is the time period during which the left
ventricle is actually contracting. As used herein, the term
wise, the electrical signals do not represent either the strength
of ef?cacy of a given contraction. Finally, the representative
EKG signal is a summation of electrical activity and does not
readily allow for differentiation of certain components.
FIG. 4 is a timing diagram that illustrates the correlation in
time of an idealized EKG tracing A, pressure graph B, ven
tricular volume graph C, and heart sound graph D. The pres
sure graph B includes left atrial pressure P1, left ventricular
pressure P2 and aortic pressure P3. At time T1, the surface
EKG indicates initiation of the P wave (atrial depolarization);
however, there is a delay until LA contraction occurs and
begins to increase atrial pressure P1 at time T2. Prior to this
point, the LV has been passively ?lled and with the LA con
traction beginning at time T2, a maximum or end diastolic
volume is reached at time T5.
electromechanical systole (EMS) begins with either the pac
ing pulse or R wave depending upon the embodiment, and
ends when passive left ventricular ?lling begins at time T9. In
other words, EMS includes a time period initiated by the
20
ends at time T8 or at a time between T8 and T9, as described
herein.
FIG. 5 illustrates three timing diagrams, schematically
25
Ventricular depolarization begins with the initiation of the
QRS complex at time T3. Isovolumic contraction of the LV
begins after a delay at time T5 and the pressure within the LV
causes the mitral valve to close. Pressure P2 within the LV
period of ejection occurs between time T6 and T8 and LV
volume (graph C) falls as blood is ejected from the LV into the
arterial system. The T wave, or repolarization, begins during
the period of ejection, as illustrated.
When the falling LV pressure P2 is exceeded by aortic
pressure P3, the semilunar valves close at time T8. The time
illustrating selected events at various times for different heart
rates. In each scenario, the AV interval is constant. In scenario
A, the heart rate is assumed to be 70 beats per minute (BPM).
At time T1, an atrial pace is delivered with an R wave occur
30
ring at time T2. The EMS is illustrated through time T3 and a
second atrial pace is delivered at time T4. The time difference
between T3 and T4 is suf?cient for ventricular passive ?lling
increases but the semilunar valves remain closed until this
pressure exceeds that within the aorta P3 at time T6. When the
LV pressure P2 exceeds aortic pressure P3, the semilunar
valves open at time T6. LV pressure P2 continues to increase
until approximately time T7 and then begins to drop. The
pacing pulse (or sensed R wave), mechanical systole, and the
period of isovolumic relaxation. In some embodiments, EMS
(see FIG. 4). In scenario B, the heart rate is 90 BPM; thus, the
A-A interval is shorter than in scenario A. Here, the secondA
pace is delivered at time T4, very close in time to the end of
35
40
EMS at time T3. This will overlap the period of passive
ventricular ?lling with active ?lling due to left atrial contrac
tion. Finally, in scenario C, the heart rate is at 110 bpm. As
such, the atrial pace is delivered (T3) during the EMS which
ends at T4, causing truncation of active atrial ?ow.
There are two undesired results that may occur as an atrial
event encroaches the EMS. The ?rst is that the period for
period referred to as isovolumic relaxation occurs between
active ?lling overlaps with passive ?lling rendering left atrial
times T8 ad T9. During this time, LV pressure P2 is falling
rapidly, but is still in excess of LA pressure; thus keeping the
mitral valve closed. At time T9, the LV pressure P2 falls
tion occurs (in full or in part) during the EMS. During this
time, the ventricular pressure is higher than the atrial pres
contraction less ef?cacious. The second is that atrial contrac
45
below the LA pressure P1 and the mitral valve opens. This
sure. Thus, even with atrial contraction, insuf?cient pressure
begins the period of passive ventricular ?lling that occurs up
is generated to open the AV valves; thus, ?uid ?ow is pre
until time T11.
A second cardiac cycle is illustrated with the initiation of
the P wave at time T10, initiation of active LV ?lling at T11,
start of the QRS complex at time T13, R wave at time T14 and
isovolumic contraction from T15-T16. The T wave begins at
time T17 and isovolumic relaxation begins at time T18. Thus,
one complete cardiac cycle may be de?ned from a ?rst P wave
at time T1 to a second P wave at time T10. Similarly, the cycle
cluded to the ventricles but does occur retrograde into the
pulmonary veins and pulmonary capillary vessels. Mean pul
50
monary venous pressure will increase and may result in ?uid
passing from the veins into the pulmonary tissue, impeding
normal gas exchange. Symptoms similar to that of heart fail
ure may occur or preexisting pulmonary edema may worsen.
The condition may be referred to as pacemaker syndrome or
55
pseudo-pacemaker syndrome if no pacemaker is implanted.
may be de?ned by a ?rst R wave at time T4 to a second R wave
at time T14. The surface EKG illustrates the intition of a P
As illustrated, in FIG. 5, this occurs at a higher atrial rate
with a constant AV More accurately, the AV interval (or PR
wave at time T1. It should be appreciated that for a variety of
interval) is too long for scenario C; thus leading to the second
A pace occurring during the EMS. It should be appreciated,
reasons, an implanted device might not sense this same P
wave at time T1. Rather, the implanted device will sense the
P wave at time T1+PSO, where PS0 is a P-wave sense offset.
60
Depending upon lead placement and location, sensed activa
tion is not necessarily the earliest actual activation. While this
does not change the times at which the other events occur, it
does change how the electrical representation or at least a
portion thereof would be shifted with respect to the actual
occurrence of these other events.
65
that abnormally long AV intervals may result in the same or
similar symptoms even in the absence of atrial pacing.
This situation is commonly averted through the use of a
pacemaker operating in a traditional DDD mode. A simple
solution is to utilize the standard DDD pacing mode with
relatively short AV interval to avoid encroachment; however,
as previously mentioned, intrinsic conduction is highly pref
erable to ventricular pacing when possible. The scenarios