Method and apparatus for determining atrial lead disclocation and confirming diagnosis of atrial tachyarrhythimias

In a dual chamber cardiac stimulators, e.g. cardiac pacemaker or pacemaker/cardioverter/defibrillator (PCD) system, which relies upon the detection of atrial depolarizations or the stimulation of the atria in the performance of a defined function, a method and apparatus for determining the existence of an atrial pace/sense electrode(s) dislocation from an atrial site to a position inferior to the AV node of the heart thereby affecting a function, e.g. providing a false indication of atrial tachyarrhythmia. The determination of the occurrence of a dislocation of the atrial pace/sense electrode is effected by applying a test pace pulse to the atrial pace/sense electrode; detecting the immediately following ventricular depolarization from a ventricular sense electrode; measuring the interval between the delivered atrial pace pulse and the detected ventricular depolarization; comparing the measured interval to a threshold AV interval; and determining that the atrial pace/sense electrode is in contact with the right atrium if the measured interval is longer than the threshold AV interval. Preferably, the determination is effected by: providing a first signal when the measured AV interval exceeds the threshold AV interval and a second signal when the measured AV interval is less than the threshold AV interval; applying a series of M atrial pace pulses to the atrial pace/sense electrode; counting the number of first and second signals provided in response to the series of atrial pace pulses; and determining that the atrial pace/sense electrode is located in the right atrium when a number of first signals are provided in a series of delivered atrial pace pulses. Confirmation of a provisional tachyarrhythmia is also made from the number of first and second signals.

CROSS-REFERENCE TO RELATED APPLICATIONS 
Reference is hereby made to commonly assigned co-pending U.S. patent 
application Ser. No. 08/649,145 filed May 14, 1996 for PRIORITIZED RULE 
BASED METHOD AND APATUS FOR DIAGNOSIS AND TREATMENT OF ARRHYTHMIAS in 
the name of Gillberg et al. 
FIELD OF THE INVENTION 
This invention relates to dual chamber cardiac stimulators, e.g. cardiac 
pacemaker or pacemaker/cardioverter/defibrillator (PCD) systems which rely 
upon the detection of atrial depolarizations in the performance of a 
defined function, and to a method and apparatus for determining the 
existence of an atrial pace/sense electrode(s) dislocation from an atrial 
site to a position inferior to the AV node of the heart thereby affecting 
a function, e.g. providing a false indication of atrial tachyarrhythmia. 
BACKGROUND OF THE INVENTION 
Current dual chamber, multi-mode, cardiac pacemakers typically employ 
atrial and ventricular endocardial pacing leads having one or two distally 
located pace/sense electrodes that are adapted to be attached in the right 
atrium and right ventricle, respectively, and operate to sense the atrial 
and ventricular electrogram (EGM) and deliver pacing pulses to each 
chamber, depending on the operating mode. Dual chamber demand cardiac 
pacing is dependent upon the retention of the atrial pace/sense 
electrode(s) at the atrial site. The dislocation of the atrial pace/sense 
electrode(s) to a location inferior to the AV node can result in the loss 
of sensing of the atrial EGM events (principally the P-wave). However, the 
R-wave of the ventricular EGM as well as other electrical signal peaks of 
the QRST complex may be readily detected if there is good electrode-tissue 
contact or may be intermittently detected if the electrode-tissue contact 
is intermittent. The relatively high gain setting of the atrial sense 
amplifier necessary to sense the relatively low amplitude P-wave may also 
contribute to mistaken "sensing" of peaks of the QRST complex and other 
spurious signals as P-waves. As a result, the atrial and ventricular 
pacing may be inhibited (which may not be undesirable under the 
circumstances) or become erratic, which could cause a ventricular pacing 
pulse to be delivered at an undesirable time in the pacing cycle, possibly 
provoking a tachyarrhythmia. At the least, the benefits of synchronous 
dual chamber pacing in sustaining a physiologic heart rate and adequate 
cardiac output would be lost. 
In proposed dual chamber PCD systems having the capability of detecting and 
treating atrial arrhythmias with at least a limited menu of 
anti-tachyarrhythmia therapies, also referred to as supraventricular 
arrhythmias and including atrial fibrillation and atrial flutter, the 
correct diagnosis of the nature of a detected tachyarrhythmia so that an 
appropriate treatment can be delivered is crucial. Typically, in proposed 
dual chamber PCD systems, at least both atrial and ventricular pacing and 
sensing functions are provided in conjunction with tachyarrhythmia 
detection and anti-tachyarrhythmia therapy delivery in at least one of the 
chambers. Such dual chamber PCD systems may only provide atrial 
anti-tachycardia pacing therapies of the types described below or may 
include atrial cardioversion/defibrillation capabilities as further 
described below. The failure to deliver the appropriate therapy or the 
delivery of an inappropriate therapy to treat an apparent atrial 
tachyarrhythmia can progress to or trigger more serious ventricular 
tachyarrhythmia. Consequently, a great deal of effort has been undertaken 
to refine the diagnosis of the tachyarrhythmia and to define the 
appropriate therapy in response to the diagnosis. 
The article "Automatic Tachycardia Recognition" by R. Arzbaecher et al., 
E, May-June 1984, pp. 541-547 discloses an algorithm intended to be 
implemented in a microprocessor based implantable device employing both 
atrial and ventricular rate detection via separate bipolar leads in order 
to measure the intrinsic or evoked A-A and V-A, or V-V escape intervals 
and AV delay intervals in order to distinguish among various types of 
atrial and ventricular tachycardias, fibrillation or flutter. The 
Arzbaecher et al. article also discloses the concept of employing a 
premature atrial pace stimulus that is delivered to the atrial pace/sense 
electrode to distinguish 1:1 sinus tachycardia from 1:1 paroxysmal 
tachycardia. When a 1:1 sinus or paroxysmal tachycardia is determined from 
a series of A-A and V-V intervals, the atrial pace pulse is applied at a 
time in the VA interval when it would be expected to elicit a ventricular 
response, i.e., an R-wave, after an AV propagation delay interval. If the 
tachycardia is sinus in origin, the R-wave will consistently follow the 
premature atrial pace pulse within a consistent AV delay. If there is no 
conducted ventricular response, the following R-wave will appear at the 
end of the prevailing V-V interval, signifying that the tachycardia is AV 
re-entrant or ventricular in origin with VA conduction because the atrial 
premature depolarization reaches the AV node when it is refractory. 
Other proposals for employing atrial and ventricular detection and interval 
comparison are set forth in The Third Decade Of Cardiac Pacing: Advances 
in Technology in Clinical Applications, Part III, Chapter 1, "Necessity of 
Signal Processing in Tachycardia Detection" by Furman et al. (edited by S. 
Barold and J. Mugica, Futura Publications, 1982, pages 265-274) and in 
U.S. Pat. No. 4,860,749 to Lehmann. In both cases, atrial and ventricular 
rates or intervals are compared to one another in order to distinguish 
sinus and pathological tachycardias. 
A recent article, "MATIC--An Intracardiac Tachycardia Classification 
System", by Leong et al., E, Vol. 15, September 1992, Pages 1317-1331, 
discloses an automated tachycardia analysis system which employs a neural 
network for morphology analysis and which compares measured A-V intervals 
to measured V-V intervals for classification of tachycardias displaying 
1:1 correspondence between atrial and ventricular depolarizations. 
In commonly assigned, U.S. Pat. No. 5,383,910 issued to den Dulk, 
incorporated herein by reference, a method is described for distinguishing 
AV nodal reentrant tachycardias from other tachycardias which exhibit 1:1 
correspondence between atrial and ventricular rhythms. Atrial and 
ventricular cycle lengths (ACL's and VCL'S, respectively) are determined 
from the respective atrial and ventricular electrocardiograms and for 
determining whether the VCLs (and optionally the ACLs) reflect a 
ventricular and/or atrial rate exceeding a preset tachycardia rate 
threshold. 
If the ventricular rate (or optionally the atrial rate) indicates the 
presence of a tachycardia, the method determines whether closely spaced 
atrial and ventricular depolarizations, in either order, occur 
sequentially within a series of heart cycles. Such closely spaced atrial 
and ventricular depolarizations are considered to be indicative of 
reentrant AV nodal tachycardia if they are within a short, defined time 
interval less than would be expected in a sinus tachycardia which occurs 
at a rate which meets the criteria for tachycardia detection. This defined 
time interval may be, for example, up to 50-100 ms, with intervals of 80 
msec or less preferred. A series of a predetermined number of successive 
closely spaced atrial and ventricular depolarizations satisfying this 
criteria results in a diagnosis of AV nodal reentrant tachycardia and the 
delivery of a therapy particularly adapted to terminate such an 
arrhythmia, e.g. the therapies described in the above-incorporated '910 
patent. 
In some of these proposed dual chamber PCD systems (and in existing single 
chamber PCD systems), one or two basic strategies are generally followed. 
A first strategy is to identify heart events, event intervals or event 
rates as they occur as indicative of the likelihood of the occurrence of 
specific types of arrhythmias, with each arrhythmia having a preset group 
of criteria which must be met as precedent to detection or classification. 
As events progress, the criteria for identifying the various arrhythmias 
are all monitored simultaneously, with the first set of criteria to be met 
resulting in detection and diagnosis of the arrhythmia. A second strategy 
is to define a set of criteria for events, event intervals and event rates 
which is generally indicative of a group of arrhythmias, and following 
those criteria being met, analyzing preceding or subsequent events to 
determine which specific arrhythmia is present. In the Medtronic Model 
7219 devices, an arrhythmia detection and classification system generally 
as disclosed in U.S. Pat. No. 5,342,402, issued to Olson et al., 
incorporated herein by reference in its entirety, is employed, which uses 
both strategies together. 
In the above-referenced Gilberg et al application, an arrhythmia detection 
and classification system is described wherein a prioritized set of 
inter-related rules for arrhythmia detection and discrimination are 
employed. Each rule contains a set of one or more "clauses" which must be 
satisfied (criteria which must be met). While all clauses of a rule are 
satisfied, the rule is indicated to be met (referred to as the rule 
"firing"). It is possible for multiple rules to be "firing" at the same 
time, with the highest priority rule taking precedence. Some rules trigger 
delivery of therapy when firing, whereas other rules inhibit delivery of 
therapy when firing. The highest priority rule firing at any specific time 
controls the behavior of the device. For example, the firing of a rule 
which triggers therapy is superseded by the firing of higher priority 
rules preventing delivery of therapy. Rules cease firing when their 
clauses cease to be satisfied, whether or not a therapy is triggered by 
the rule. 
Each rule includes a set of clauses or criteria which, when satisfied, 
indicate the likely occurrence of a specified type of heart rhythm, 
including various tachyarrhythmias, sinus tachycardia and normal sinus 
rhythm. A specific rhythm or tachyarrhythmia may have more than one 
associated rule. The rules are interrelated, such that progress toward 
meeting the requirements of a clause of one role may also be the subject 
matter of a clause of a different role. 
The specific criteria set forth by the clauses of the various rules as 
disclosed include a number of known criteria for evaluating heart rhythm, 
including the entire arrhythmia detection and classification system 
employed in the presently available Medtronic 7219 pacemaker cardioverter 
defibrillators, as well as criteria disclosed in U.S. Pat. No. 5,330,508, 
issued to Gunderson. In addition, a number of new evaluation criteria are 
included within the clauses of various rules disclosed in the Gilberg et 
al application. One such new detection methodology is based upon the 
classification of the events occurring associated with the sequence of two 
ventricular depolarizations into a limited number of event patterns, based 
upon the number and times of occurrences of atrial events, preceding the 
two most recent ventricular events. An event pattern is developed for each 
individual ventricular event, so that successive event patterns overlap 
one another. Certain sequences of event patterns are strongly indicative 
of specific types of heart rhythms. For heart rhythms of which this is 
true, a defined set of indicative event pattern sequences or a "grammar" 
is defined. Adherence of the heart rhythm to the grammars associated with 
various heart rhythms is determined by simultaneously operating continuous 
recognition machines, the outputs of which form the subject matter of one 
or more clauses, within the hierarchy of rules. 
In a preferred embodiment of the invention disclosed in the Gilberg et al 
application, the device is provided with rules which when satisfied 
indicate the presence of sustained atrial fibrillation and sustained 
atrial flutter and in response to detection thereof delivers anti-atrial 
fibrillation or anti-atrial tachycardia therapies. These rules include a 
set of various new classification criteria, including an atrial 
fibrillation/atrial tachycardia evidence counter which is incremented and 
decremented on a beat by beat basis and compared with a defined threshold 
count or counts taken as indicative of atrial fibrillation or atrial 
tachycardia. The atrial rate and regularity is also monitored and atrial 
fibrillation or atrial tachycardia is preliminarily detected when the 
evidence counter is at or above such a threshold and the atrial rhythm 
meets defined rate zone criteria associated with atrial fibrillation or 
atrial tachycardia. When both the evidence count and the rate zone 
criteria are met, the arrhythmia underway is preliminarily determined to 
be atrial fibrillation or atrial tachycardia, depending on which rate zone 
criteria are met. A sustained atrial fibrillation/atrial tachycardia 
duration timer is then initiated and continues to time until termination 
of atrial tachyarrhythmia is detected. The time duration since the 
provisional detection of an atrial tachyarrhythmia is continually compared 
to one or more minimum duration values associated with the atrial 
tachyarrhythmia determined to presently be underway and/or the next 
scheduled therapy for such arrhythmia. If the time duration since 
provisional detection of atrial arrhythmia meets or exceeds the applicable 
minimum duration value, and other associated criteria are also met, the 
next scheduled anti-atrial arrhythmia therapy is delivered. 
Additional associated criteria which must be met as a prerequisite to 
delivery of atrial anti-tachyarrhythmia therapies may include expiration 
of a minimum interval from the most recently delivered therapy not 
followed by a detected termination of atrial tachyarrhythmia, confirmation 
that the most recent heart cycles do not indicate a return to sinus 
rhythm, time duration since provisional detection of atrial 
tachyarrhythmia being less than a maximum duration value, time of day 
corresponding to a pre-defined time range and/or less than a preset number 
of atrial anti-arrhythmia therapies having been delivered in a preceding 
time period. 
In such complex arrhythmia determination and discrimination systems as 
described above, it is assumed that the atrial pace/sense electrodes are 
fixed in the right atrial heart chamber superior to the AV node. For 
example, such a presumption prevails in the method of distinguishing 1:1 
sinus tachycardia from 1:1 paroxysmal tachycardia proposed by Arzbaecher 
et al. as described above. In the vast majority of implantations, unipolar 
or bipolar atrial pace/sense electrodes are introduced into the right 
atrium and typically lodged in the right atrial appendage or wall where 
they remain in place. Fixation of the electrode(s) is effected either with 
a passive fixation mechanism, e.g. soft pliant tines that engage in the 
trabecular structure of the right atrial appendage, or an active fixation 
mechanism, e.g. a helical coil distal tip electrode that is screwed into a 
relatively thick portion of the right atrial wall. Despite the efforts to 
maintain fixation, the atrial pace/sense electrode(s) can, on rare 
occasion, become dislodged and migrate through the tricuspid valve into 
the right ventricle at some time after implantation and medical discharge 
of the patient. 
In such a dislocation position, the electrogram signals that are processed 
as atrial sense events may actually reflect the activity of the atria and 
the ventricles or just the ventricles or reflect oversensing due to 
intermittent contact of the electrode(s) with the endocardium and the gain 
setting of the atrial sense amplifier. The resulting sequences of event 
patterns derived from the ventricular and atrial sense amplifiers can be 
erroneously interpreted by the algorithm as representing an atrial 
tachyarrhythmia, and the device can trigger delivery of a programmed 
therapy for that tachyarrhythmia. 
In this regard, the dual chamber PCD systems under development and 
described in the above-referenced patents typically provide a programmable 
menu of therapies including a variety of atrial anti-tachycardia pacing 
and cardioversion/defibrillation shock therapies. The delivery of a 
cardioversion/defibrillation therapy may be confined to atrial 
cardioversion/defibrillation electrodes and timed to a ventricular sense 
event to help ensure against provoking a ventricular arrhythmia, 
particularly ventricular fibrillation. Atrial anti-tachycardia single 
pulse and pulse train therapies are also typically delivered in timed 
relation to the atrial sense events to avoid accelerating the atrial rate 
or arrhythmia or triggering a ventricular arrhythmia. If the atrial sense 
amplifier is not sensing atrial events because of the dislocation of the 
atrial pace/sense electrode(s), the delivery of these atrial 
tachyarrhythmia therapies may provoke a life threatening ventricular 
fibrillation episode. Although a dual chamber PCD system with ventricular 
anti-tachyarrhythmia therapy capabilities may be prepared to respond to 
the device triggered ventricular fibrillation, the episode and shock 
delivered to the patient is upsetting at the least. And recourse to such a 
fail-safe ventricular shock therapy is absent from PCD systems or 
anti-tachyarrhythmia pacing therapy devices only having atrial 
anti-tachyarrhythmia therapy capabilities. 
Moreover, in such dual chamber PCD systems, the mis-diagnosis of an atrial 
tachyarrhythmia due to the dislocation of the atrial pace/sense 
electrode(s) may mask a more serious ventricular tachyarrhythmia and 
either prevent or delay delivery of an appropriate ventricular 
cardioversion/defibrillation therapy. 
SUMMARY OF THE INVENTION 
Consequently, it is a primary object of the present invention to determine, 
in implantable systems of the types described above that the atrial 
pace/sense electrode(s) are properly located in the right atrium and not 
dislocated into a location inferior to the AV node and/or in the right 
ventricle. 
It is a further object of the present invention to determine, in dual 
chamber or atrial chamber only PCD systems that the provisional 
determination of an atrial tachyarrhythmia is correct and not resulting 
from displacement of the atrial pace/sense electrode(s) into a location 
inferior to the AV node and/or into the right ventricle. 
In accordance with the present invention, the determination of the 
occurrence of a dislocation of the atrial pace/sense electrode(s) in a 
system of the types described above is effected through the means of and 
steps for: applying a pace pulse to an atrial pace electrode(s); detecting 
the immediately following ventricular depolarization from a ventricular 
sense electrode(s); measuring the interval between the delivered atrial 
pace pulse and the detected ventricular depolarization; comparing the 
measured interval to a threshold AV interval; and determining that the 
atrial pace electrode(s) is in contact with the right atrium if the 
measured interval is longer than the threshold AV interval. 
Preferably, the determination further comprises the means for and steps of: 
providing a first signal when the measured AV interval exceeds the 
threshold AV interval and a second signal when the measured AV interval is 
less than the threshold AV interval; applying a series of atrial pace 
pulses to the atrial pace electrode(s); counting the number of first and 
second signals provided in response to the series of atrial pace pulses; 
and determining that the atrial sense electrode(s) of the atrial lead are 
located in the right atrium when a series of first signals are 
consistently provided as a result of the series of atrial pace pulses. 
In addition, the inventive method and apparatus further comprises the steps 
of and means for determining that the atrial sense electrode(s) of the 
atrial lead are located in the right ventricle when a series of second 
signals are consistently provided as a result of the series of atrial pace 
pulses. 
The threshold AV interval is selected to be a fraction of a normal AV 
conduction time for the prevailing sensed V-V interval. The series of 
atrial pace pulses are delivered after a VA interval that is also a 
fraction of the prevailing sensed V-V interval calculated to avoid 
delivering the atrial pace pulse in the T-wave of a preceding ventricular 
depolarization to avoid provoking a ventricular tachyarrhythmia if the 
atrial pace/sense electrode(s) is in the right ventricle. 
The atrial lead test apparatus and method of the present invention may be 
automatically caused to operate in response to a triggering event, e.g. at 
a particular time of day or number of system operations or may be 
triggered to operate by an action, e.g. a programmed in command from an 
external programmer. 
In a further preferred embodiment of the present invention with particular 
application to dual chamber PCD systems, the atrial lead test apparatus 
and method of the present invention may be triggered to operate in 
response to a provisional determination of an atrial tachyarrhythmia. 
Moreover, in this context, the appropriateness of the provisional 
determination may be tested by the apparatus and method of the present 
invention whereby the provisonally determined atrial tachyarrhythmia is 
confirmed as a result of the determination of the location of the atrial 
pace/sense electrode(s) in the right atrium or not confirmed as a result 
of the determination of the location of the atrial pace/sense electrode(s) 
outside the right atrium. 
More specifically, the provisionally diagnosed atrial tachyarrhythmia is 
confirmed and the selected therapy delivered when the first signal is 
provided from the comparison (i.e., when the sensed AV interval exceeds 
the threshold AV interval), and preferably when a series of the first 
signals are provided. Conversely, the provisionally diagnosed atrial 
tachyarrhythmia is not confirmed and the selected therapy is not delivered 
when the second signal is provided from the comparison (i.e., when the 
sensed AV interval is less than the threshold AV interval), and preferably 
when a series of the second signals are provided. Moreover, when a series 
of both first and second signals are provided in a single test, this 
factor is used to confirm or bias the determination that the atrial 
tachyarrhythmia is atrial fibrillation or flutter. 
The method and apparatus of the present invention provides a simple 
mechanism to confirm the location of the atrial pace/sense electrode(s) in 
systems of the type described above. In dual chamber PCD systems of the 
type described above, potential injury to the patient is avoided when an 
atrial anti-tachyarrhythmia therapy is not delivered that would provoke a 
more serious ventricular tachyarrhythmia or a ventricular 
anti-tachyarrhythmia therapy is delivered when it is required.

DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENTS 
FIGS. 1-3 illustrate a PCD implantable pulse generator (IPG) 10 and lead 
set in which the present invention may be implemented. FIG. 3 is a 
functional schematic diagram of the circuitry of a dual chamber, 
implantable PCD IPG 10 in which the present invention may usefully be 
practiced. Certain of the pace/sense and cardioversion/defibrillation 
functions and associated leads and electrodes may be disabled or not 
provided to configure the PCD system to operate in accordance with the 
preferred embodiments and variations described below. FIG. 3 should be 
taken as exemplary of the circuitry of the type of single chamber or dual 
chamber PCD IPG in which the invention may be embodied, and not as 
limiting, as it is believed that the invention may usefully be practiced 
in a wide variety of device implementations, as long as the operating mode 
or configuration involves use of an atrial sensing lead and atrial sense 
functions that may be adversely affected by dislocation of the atrial 
pace/sense electrode(s) from the intended site in the right atrium. In 
this regard, the present invention may have application in any dual 
chamber pacemaker without the capability of determining the existence of 
and responding to a tachyarrhythmia. The flow charts of FIGS. 4-6 
illustrate these possible applications and embodiments of the present 
invention. 
Turning first to the description of the leads illustrated in FIGS. 1 and 2, 
the right ventricular (RV) lead includes an elongated insulated lead body 
16, carrying three concentric coiled wire conductors, separated from one 
another by tubular insulated sheaths. Located adjacent the distal end of 
the RV lead are a ring electrode 24, an extendible helix electrode 26, 
mounted retractably within an insulated electrode head 28, and an 
elongated, exposed coil, cardioversion/defibrillation electrode 20. Each 
of the electrodes is coupled to one of the coiled conductors within the 
lead body 16. Electrodes 24 and 26 are employed for cardiac pacing and for 
sensing ventricular depolarizations. At the proximal end of the lead is a 
bifurcated connector 14 which carries three electrical connectors, each 
coupled to one of the coiled conductors, that are fitted into a high 
voltage and a low voltage receptacle of the connector block assembly 12 of 
the PCD IPG 10. The RV cardioversion/defibrillation electrode 20 may be 
fabricated from platinum, platinum alloy or other materials known to be 
usable in implantable defibrillation electrodes and may be about 5 cm in 
length. 
The right atrium-superior vena cava (RA/SVC) lead includes an elongated 
insulated lead body 15, carrying three concentric coiled conductors, 
separated from one another by tubular insulated sheaths, corresponding to 
the structure of the ventricular lead. Located adjacent the J-shaped 
distal end of the lead are a ring electrode 21 and an extendible helix 
electrode 17, mounted retractably within an insulated electrode head 19. 
Each of these pace/sense electrodes 17, 21 is coupled to one of the coiled 
conductors within the lead body 15. Pace/sense electrodes 17 and 21 are 
employed for atrial pacing and for sensing atrial depolarizations. An 
elongated RA/SVC cardioversion/defibrillation electrode 23 is optionally 
provided, extending proximally with respect to ring pace/sense electrode 
21 and is coupled to the third conductor within the RA/SVC lead body 15. 
Electrode 23 preferably is 10 cm in length or greater and is intended to 
extend from the SVC toward the tricuspid valve in the normal fixation 
location depicted in FIG. 1. A bifurcated connector 13 is located at the 
proximal end of RA/SVC lead body 15 and carries three electrical 
connectors, each coupled to one of the coiled conductors, that are 
inserted into a high voltage receptacle and a low voltage receptacle of 
the connector block assembly 12 of the PCD IPG 10. 
The coronary sinus (CS) lead includes an elongated insulated lead body 6, 
carrying one coiled conductor, coupled to an elongated, exposed coil, 
cardioversion/defibrillation CS electrode 8. Electrode 8, illustrated in 
broken outline, is located within the coronary sinus and great vein of the 
heart. At the proximal end of the lead is a connector plug 4 which carries 
an electrical connector, coupled to the coiled conductor. The coronary 
sinus/great vein electrode 8 may be about 5 cm in length. 
A PCD implantable pulse generator (IPG) 10 is shown in combination with the 
leads, with the lead connectors 4, 13 and 14 inserted into the receptacles 
of the connector block assemblies 12. Optionally, insulation of the 
outward facing portion of the housing 11 of the PCD IPG 10 may be provided 
using a plastic coating, for example parylene or silicone rubber, as is 
currently employed in some unipolar cardiac pacemakers. However, the 
outward facing portion may instead be left uninsulated, or some other 
division between insulated and uninsulated portions may be employed. The 
uninsulated portion of the housing or can 11 optionally serves as a 
subcutaneous defibrillation "CAN" electrode, used to defibrillate either 
the atria or ventricles. Other lead configurations and electrode locations 
may of course be substituted for the lead set illustrated. For example, 
atrial defibrillation and sensing electrodes might be added to either the 
coronary sinus lead or the right ventricular lead instead of being located 
on a separate atrial lead, allowing for a two-lead system. 
In FIG. 1, the atrial pace/sense electrodes 17, 21 are shown lodged into 
the right atrial appendage in the intended position of fixation. The 
distal tip, pace/sense electrode 17 in the illustrated case is formed of 
an active fixation helix that is screwed into the myocardium. It will be 
understood that the fixation mechanism may be a passive fixation mechanism 
as described above. At times, the fixation mechanism fails to retain the 
distal tip pace/sense electrode in the intended position, and, if the 
patient is not pacemaker dependent, the loss of atrial contact may not be 
noticeable to the patient. FIG. 2 illustrates the slippage of the RA/SVC 
lead further into the right ventricle. The distal tip and ring pace/sense 
electrodes may bear against the right ventricular endocardial surface and 
make continuous or intermittent contact. In this dislocated position, the 
ability to detect atrial depolarizations between the atrial pace/sense 
electrodes 17, 21 may be lost due to the location below the AV node of the 
heart and the relatively low amplitude P-wave in that location. However, 
the R-wave of ventricular depolarizations as well as other signals may be 
readily detected if there is good electrode-tissue contact or may be 
intermittently detected if the electrode-tissue contact is intermittent. 
The relatively high gain of the atrial sense amplifier in PCD IPG 10 may 
also contribute to mistaken sensing of other spurious signals as P-waves. 
FIG. 3 is a functional schematic diagram of an implantable PCD IPG in which 
the present invention may usefully be practiced. This diagram should be 
taken as exemplary and inclusive of the major components of the type of 
device in which the invention may be embodied, and not as limiting, as it 
is believed that the invention may usefully be practiced in a wide variety 
of device implementations, including devices providing therapies for 
treating atrial tachyarrhythmias instead of or in addition to ventricular 
tachyarrhythmias, cardioverters and defibrillators which do not provide 
anti-tachycardia pacing therapies, anti-tachycardia pacers which do not 
provide cardioversion or defibrillation therapies, and devices which 
deliver different forms of anti-tachyarrhythmia therapies such as nerve 
stimulation or drug administration. Moreover, the invention may be 
practiced in a dual chamber pacemaker employing atrial and ventricular 
sense electrode(s) and having only bradycardia sensing, determination and 
pacing capabilities in one or both heart chambers. 
The PCD IPG of FIG. 3 is intended to be provided with a lead system 
including pace/sense electrodes, which may be as illustrated in FIGS. 1 
and 2, although alternative lead systems may of course be used with it, as 
long as an atrial lead and atrial pace/sense electrode is in the system. 
If the electrode configuration of FIGS. 1 and 2 is employed, the 
correspondence of the illustrated electrodes to the illustrated connector 
terminals is as follows. 
Terminal 311 is adapted to be coupled with CAN electrode 11 when the CAN 
electrode 11 is used in the system. High voltage terminals 318, 320 and 
310 are adapted to be coupled with RA/SVC cardioversion/defibrillation 
electrode 18, RV cardioversion/defibrillation electrode 20, and CS 
cardioversion/defibrillation electrode 8, respectively. Terminals 311, 
318, 320 and 310 are coupled to the outputs of the high voltage output 
circuit 234. In alternative PCD IPG embodiments of the invention, only two 
or three high voltage terminals and associated electrodes may be provided. 
In other pacing only embodiments, the high voltage terminals and 
associated leads and illustrated components of FIG. 3 (described below) 
may be eliminated from the system. 
Low voltage terminals 324 and 326 are adapted to be coupled with RV 
pace/sense electrodes 24 and 26, and are used for conducting ventricular 
sense events and pace pulses from and to the right ventricle. Low voltage 
terminals 317 and 321 are adapted to be coupled with RA pace/sense 
electrodes 17 and 21, and are used for conducting atrial sense events and 
pace pulses from and to the right atrium (when the atrial lead is in the 
normal position of FIG. 1). Terminals 324 and 326 are coupled to the 
R-wave amplifier 200, which preferably takes the form of an automatic gain 
controlled amplifier providing an adjustable sensing threshold as a 
function of the measured R-wave amplitude. A signal is generated on R-out 
line 202 whenever the signal sensed between terminals 324 and 326 exceeds 
the programmed sensing threshold. Terminals 317 and 321 are coupled to the 
P-wave amplifier 204 which preferably also takes the form of an automatic 
gain controlled amplifier providing an adjustable sensing threshold as a 
function of the measured P-wave amplitude. A signal is generated on P-out 
line 206 whenever the signal sensed between electrodes 317 and 321 exceeds 
the programmed sensing threshold. The general operation of the R-wave and 
P-wave amplifiers 200 and 204 may correspond to that disclosed in U.S. 
Pat. No. 5,117,824, by Keimel, et al., incorporated herein by reference in 
its entirety. In any of the various embodiments of the present invention, 
at least the atrial and ventricular pace/sense electrode(s) and sense 
amplifiers 204, 200 must be present. 
Switch matrix 208 is used to select which of the available terminals and 
associated electrodes are coupled to wide band (0.5-200 Hz) amplifier 210 
for use in digital EGM signal analysis. Selection of electrodes is 
controlled by the microprocessor 224 via data/address bus 218, which 
selections may be varied as desired. Signals from the electrodes selected 
for coupling to bandpass amplifier 210 are provided to multiplexor 220, 
and thereafter converted to multi-bit digital signals by A/D converter 
222, for storage in random access memory 226 under control of direct 
memory access circuit 228. Microprocessor 224 may employ digital signal 
analysis techniques to characterize the digitized signals stored in random 
access memory 226 to recognize and classify the patient's heart rhythm 
employing any of the numerous signal processing methodologies known to the 
art. 
The remainder of the IPG circuitry is dedicated to the diagnosis of a 
bradycardia or tachyarrhythmia and the provision of cardiac pacing, 
cardioversion and defibrillation therapies, and, for purposes of the 
present invention may correspond to circuitry known in the prior art, as 
well as the performance of the functions and determinations of the various 
embodiments of the present invention illustrated in FIGS. 4-7. 
The pacer timing/control circuitry 212 includes programmable digital 
counters which control the basic time intervals associated with DDD, VVI, 
DVI, VDD, AAI, DDI and other modes of single and dual chamber pacing well 
known to the art. Circuitry 212 also controls escape intervals associated 
with anti-tachyarrhythmia pacing in both the atrium and the ventricle, 
employing, any anti-tachyarrhythmia pacing therapies known to the art. 
Intervals defined by pacing circuitry 212 include atrial and ventricular 
pacing escape intervals, the refractory periods during which sensed 
P-waves and R-waves are ineffective to restart timing of the escape 
intervals and the pulse widths of the pacing pulses. The durations of 
these intervals are determined by microprocessor 224, in response to 
stored data in memory 226 and are communicated to the pacing circuitry 212 
via address/data bus 218. Pacer circuitry 212 also determines the 
amplitude of the cardiac pacing pulses under control of microprocessor 
224. 
During pacing, the escape interval counters within pacer timing/control 
circuitry 212 are reset upon sensing of R-waves and P-waves as indicated 
by R-OUT and P-OUT signals on lines 202 and 206, and in accordance with 
the selected pacing mode, on time-out trigger generation of pacing pulses 
by pacer output circuits 214 and 216. The escape interval counters are 
also reset on generation of pacing pulses, and thereby control the basic 
timing of cardiac pacing functions, including anti-tachyarrhythmia pacing. 
The durations of the intervals defined by the escape interval counters are 
determined by microprocessor 224, via data/address bus 218. The value of 
the count present in the escape interval counters when reset by sensed 
R-waves and P-waves may be used to measure the durations of V-V intervals, 
A-A intervals, AV intervals and V-A intervals, which measurements are 
stored in memory 226 and used in conjunction with the present invention to 
diagnose the occurrence of a variety of tachyarrhythmias and the 
dislocation of the atrial pace/sense electrode(s), as discussed in more 
detail below. 
Microprocessor 224 operates as an interrupt driven device, and is 
responsive to interrupts from pacer timing/control circuitry 212 received 
via data/address bus 218 and corresponding to the occurrences of P-OUT and 
R-OUT signals generated by sense amplifiers 204 and 200 and corresponding 
to the generation of A-E and V-E cardiac pacing pulses by pacing 
pulse generators 214 and 216. Any necessary mathematical calculations to 
be performed by microprocessor 224 and any updating of the values or 
intervals controlled by pacer timing/control circuitry 212 take place 
following such interrupts. A portion of the memory 226 (FIG. 4) may be 
configured as a plurality of recirculating buffers, capable of holding 
several series of measured V-V, V-A, A-A and A-V intervals, which may be 
analyzed in response to the occurrence of a predetermined count of pace or 
sense interrupts to determine whether the patient's heart is presently 
exhibiting atrial or ventricular tachyarrhythmia. The intervals may be 
compared with various threshold intervals employed in tachyarrhythmia 
analysis and determination and in the practice of the present invention as 
described in detail below. The threshold intervals may be programmed into 
memory or calculated by the microprocessor and stored in memory for use in 
such determinations. Also counters may be configured to store counts of 
events and the results of comparisons during the determination of the 
tachyarrhythmia and the location of the atrial pace/sense electrodes The 
arrhythmia detection method of the present invention may include prior art 
tachyarrhythmia detection algorithms of the types described and referenced 
above in the Background of the Invention section in alternative 
embodiments of the invention. 
The overall context for the determination of a tachyarrhythmia is set forth 
in FIG. 4 which is taken from the above-incorporated '910 patent. At step 
400 the microprocessor 224 is in the standby mode to conserve battery 
power. It will be assumed that a run of high rate atrial and ventricular 
depolarizations are occurring such that bradycardia pacing modes are 
suppressed in both chambers. As in the bradycardia operating modes, when 
an atrial or ventricular sense event interrupt (P-OUT or R-OUT) is 
received from the respective sense amplifier, the microprocessor 224 
awakens in step 402 to compute and store the V-A, and A-A intervals or the 
V-V and AV intervals, respectively. The most recent series of intervals, 
extending over the preceding several minutes are stored in memory on a 
FIFO basis, as depicted in step 404. In the event that a predetermined 
number of short intervals less than an atrial or ventricular tachycardia 
detection interval (TDI) or fibrillation detection interval (FDI) occurs 
during a predetermined time interval or a preceding series of heart 
cycles, or other criteria are satisfied, a tachycardia is provisionally 
determined at step 406. The main diagnostic routine for determining the 
type of tachycardia or other tachyarrhythmia is then entered in step S408. 
Preferably, the algorithms set forth in the above-referenced Gilberg et al 
application or the above-incorporated '910 patent are invoked at this 
point to provisionally identify and then confirm a specific 
tachyarrhythmia and invoke a therapy or series of therapies as described 
below. 
In the event that an atrial or ventricular tachycardia is so determined, 
and an anti-tachycardia pacing regimen is programmed, appropriate timing 
intervals for controlling generation of anti-tachycardia pacing therapies 
are loaded from microprocessor 224 into the pacer timing and control 
circuitry 212, to control the operation of the escape interval counters 
therein and to define refractory periods during which detection of R-waves 
and P-waves is ineffective to restart the escape interval counters. 
Circuitry may be used for controlling the timing and generation of 
anti-tachycardia pacing pulses as described in U.S. Pat. No. 4,577,633, 
issued to Berkovits et al., incorporated herein by reference. 
In the event that generation of a cardioversion or defibrillation shock is 
programmed, microprocessor 224 employs an escape interval counter to 
control timing of such cardioversion and defibrillation shocks, as well as 
associated refractory periods. In response to the detection of atrial or 
ventricular fibrillation or tachyarrhythmia necessitating a cardioversion 
shock, microprocessor 224 activates cardioversion/defibrillation control 
circuitry 230, which initiates charging of the high voltage capacitors 
246, 248 via charging circuit 236, under control of high voltage charging 
control line 240. The voltage on the high voltage capacitors is monitored 
via VCAP line 244, which is passed through multiplexor 220 and, in 
response to reaching a predetermined value set by microprocessor 224, 
results in generation of a logic signal on Cap Full (CF) line 254, 
terminating charging. Thereafter, timing of the delivery of the 
defibrillation or cardioversion shock is controlled by pacer 
timing/control circuitry 212. Following delivery of the fibrillation or 
tachycardia therapy, the microprocessor 224 then returns device operation 
to bradycardia cardiac pacing and awaits the next successive interrupt due 
to pacing or the occurrence of a sensed atrial or ventricular 
depolarization. 
One embodiment of an appropriate system for delivery and synchronization of 
ventricular cardioversion and defibrillation shocks and for controlling 
the timing functions related to them is disclosed in more detail in 
commonly assigned U.S. Pat. No. 5,188,105 by Keimel, and incorporated 
herein by reference in its entirety. If atrial 
cardioversion/defibrillation capabilities are included in the IPG, 
appropriate systems for delivery and synchronization of atrial 
cardioversion and defibrillation therapies and for controlling the timing 
functions related to them may be found in PCT patent application No. 
W092/18198 by Adams et al., and in U.S. Pat. No. 4,316,472 by Mirowski et 
al., both incorporated herein by reference in their entireties. 
In addition, high frequency pacing pulse bursts may be delivered to the 
atrial or ventricular pace/sense electrode pairs 19, 21 or 24, 26 to 
terminate atrial or ventricular tachyarrhythmias, as described in PCT 
Patent Publication No. WO95/28987, filed by Duffin et al., and PCT Patent 
Publication No. WO95/28988, filed by Mehra et al., both incorporated 
herein by reference in their entireties. 
In the illustrated PCD IPG of FIG. 3, delivery of the cardioversion or 
defibrillation shocks is accomplished by output circuit 234, under control 
of control circuitry 230 via control bus 238. Output circuit 234 
determines whether a monophasic or biphasic pulse is delivered, whether 
the housing 11 serves as cathode or anode, and which electrodes are 
involved in delivery of the pulse. Examples of circuitry which may be used 
to control delivery of monophasic or biphasic cardioversion shocks are set 
forth in commonly assigned U.S. Pat. No. 5,163,427 issued to Keimel, and 
U.S. Pat. No. 4,953,551, issued to Mehra et al., respectively, both 
incorporated herein by reference. 
In modern PCD IPGs, the particular therapies are programmed into memory 
ahead of time by the physician, and a menu of such therapies is typically 
provided. For example, on initial detection of an atrial or ventricular 
tachycardia, an anti-tachycardia pacing therapy may be selected and 
delivered to the chamber in which the tachycardia is diagnosed or to both 
chambers. On re-detection of tachycardia, a more aggressive 
anti-tachycardia pacing therapy may be scheduled. If repeated attempts at 
anti-tachycardia pacing therapies fail, a higher energy cardioversion 
shock may be selected thereafter. Therapies for tachycardia termination 
may also vary with the rate of the detected tachycardia, with the 
therapies increasing in aggressiveness as the rate of the detected 
tachycardia increases. For example, fewer attempts at anti-tachycardia 
pacing may be undertaken prior to delivery of cardioversion shocks if the 
rate of the detected tachycardia is above or accelerates above a preset 
threshold. 
In the event that fibrillation is identified either initially or through 
progression from a tachycardia, a high frequency burst of pacing pulses 
may be employed as the initial attempted therapy. Subsequent therapies may 
be delivery of high amplitude defibrillation shocks, typically in excess 
of 5 joules. Lower energy levels may be employed for synchronized 
cardioversion shocks delivered in synchronization with an R-wave. It is 
envisioned that the amplitude of the defibrillation shock may be 
incremented in response to failure of an initial shock or shocks to 
terminate fibrillation. 
These various types of anti-tachyarrhythmia therapies that may be employed 
in the PCD IPG system are merely illustrative and do not affect the 
present invention. However, it is recognized that the delivery of an 
inappropriate therapy in response to an erroneous determination of the 
nature of an atrial or ventricular tachyarrhythmia may have serious 
consequences to the patient. As described above, dislocation of the atrial 
pace/sense electrode(s) into the ventricle or tricuspid valve can cause 
such an erroneous determination due to the delivery of P-OUT signals in 
rapid succession in response to a variety of signal sources. The present 
invention is directed in this context and in other contexts to making a 
determination as to when an atrial lead is dislocated such that the atrial 
pace/sense electrode is positioned in the ventricle (e.g. the RA/SVC lead 
position depicted in FIG. 2), and the purported atrial sense events (the 
P-OUT signals of sense amplifier 204 of FIG. 3, for example) are not to be 
relied on or may be used to bias a determination. The electrode 
dislocation determination may be made in an atrial pace test sequence 
initiated at a given time of day or by a programmed in command during a 
patient work-up or upon determination of a tachyarrhythmia dependent upon 
the P-OUT signals. The test sequences and the determinations made from the 
test sequences are conducted as follows. 
Referring to FIG. 5, it depicts the initial steps of testing for the 
location of the atrial pace/sense electrode(s) starting either from an 
initiating event including a provisional determination of an atrial 
tachyarrhythmia following the steps of FIG. 4 or periodically or in 
response to a programmed in command. FIG. 6 illustrates a first embodiment 
of the further steps for making the determination of the location of the 
atrial pace/sense electrodes, and FIG. 7 illustrates a second embodiment 
of the further steps for confirming or denying a determination of an 
atrial tachyarrhythmia made in the steps of FIG. 4. 
In FIG. 5, step 502 illustrates the provisional determination of an atrial 
tachyarrhythmia (which may take place in step 408 of FIG. 4) following any 
of the methodologies described in the prior art, e.g. those disclosed in 
the above-incorporated '910 patent and the above-referenced Gilberg et al 
application. 
At this point, it should be noted that step 502 may be replaced by a 
substitute or additional step of simply triggering the remaining steps of 
the algorithm of FIG. 5 and continuing with the steps of FIG. 6 at a 
specific time of day or in response to a programmed in command or in 
response to any other trigger event or action. 
Regardless of the triggering action or event, it will be presumed that the 
ventricular heart rate as evidenced by the prevailing stored V-V intervals 
(VCLs) does not evidence a ventricular tachyarrhythmia tracking or 
independent of the atrial tachyarrhythmia so that the ventricles can be 
paced at a rate exceeding the current intrinsic ventricular rate. In 
practice, the algorithm used in step 502 would not, in any case, 
provisionally determine an atrial tachyarrhythmia under such 
circumstances. This same condition must prevail at the time of invoking 
the test atrial pacing mode at a given time of day or by a programmed in 
command in the absence of any provisionally determined atrial 
tachyarrhythmia. 
In step 504, the test atrial pace parameters are defined. Specifically, a 
V-A escape interval is defined as a percentage of the prevailing V-V 
escape interval and an AV threshold value is defined. A useful test V-A 
interval may be on the order of 80% of the prevailing V-V interval. No 
test V-A interval should be shorter than about 350 msec to avoid 
proarrhythmia that may be caused by pacing on a T-wave. Normal AV 
conduction times vary with the intrinsic V-V escape interval in a range of 
80-150 msec, for example. When an atrial pace pulse is delivered into the 
ventricle at a site that is superior to the ventricular apex,, e.g. the 
site shown in FIG. 2, and is timed at a time that evokes a ventricular 
depolarization, the delay until the depolarization wave is detected at the 
ventricular sense electrode(s) is on the order of 40-50 msec. Therefore, 
an AV threshold (AVT) value of 80 msec is a useful value for the normal 
range of ventricular rates. The sum of the test V-A interval and the AVT 
must be less than the prevailing intrinsic V-V interval. 
The V-A test pace interval is timed out in step 506 and monitored in step 
508. When it is timed out, the A-E test pulse is delivered in step 510 
and an A-T--R-OUT timer is started in step 512. When the R-OUT is 
generated in step 514, the test A-T--R-OUT interval (TAV) is measured 
and stored in steps 516 and 518. If no R-OUT occurs within a further 
maximum AV delay, e.g. 150 msec (possibly longer if the patient has 
abnormally long AV conduction delays), then the test atrial pace pulse may 
be incremented in energy or the test V-A interval may be varied. 
The test count of a test counter is incremented in step 520, and the test 
count is compared to a test count threshold, M (e.g. 8 or 16) in step 522. 
If the test count does not equal M, the next atrial test pulse sequence is 
conducted by repeating steps 506-522 upon sensing the next intrinsic 
R-wave generating a R-OUT. 
When the test count is equal to M in step 522, the stored TAV intervals are 
compared to the threshold AVT interval in step 526. If the stored TAV 
interval is longer than the threshold AVT interval, then a normal atrial 
lead position (NALP) count is incremented in step 528. Similarly, if the 
stored TAV interval is shorter than the threshold AVT interval, then a 
dislodged atrial lead position (DALP) count is incremented in step 530. 
If at least N of the M counts (N=6 and M=8, for example) indicate a lead 
dislodgement, i.e., the DALP counter is .gtoreq. to N after M test pulses 
are delivered, then there is a significant probability that the atrial 
lead has dislodged into the ventricle. Steps 524-530 can alternatively be 
conducted each time that the test counter is incremented in step 522 so 
that a quicker determination of the trend can be made. For example, if 
each succeeding comparison increments the DALP count as the test pace 
count approaches N, then the atrial pace test mode may be prematurely 
terminated and other action taken. For example, the AVT may be shortened 
to try to find the actual A-V interval between the delivered test A-E 
and the evoked R-OUT. 
At least two determinations may be made from the results of the NALP and 
DALP counts that may be used in different contexts. In FIG. 6, a 
determination is simply made that the atrial pace/sense electrode(s) is 
dislocated which may be of use in the context of a dual chamber 
bradycardia pacemaker, for example. FIG. 6 is to be interpreted in 
conjunction with step 502 taking any of the above-described forms. In FIG. 
7, the algorithm proceeds to use the correct location or dislocation 
determination to confirm the presence or declare the absence of an atrial 
tachyarrhythmia despite the apparent rapid atrial heart rate so that an 
improper atrial anti-tachyarrhythmia therapy is not delivered. 
In FIGS. 6 and 7, the NALP and DALP counts are compared to counter 
thresholds N1 and N2 at step 532 and comparison results are declared in 
steps 534 and 538 in each case. In FIG. 6, if NALP is determined to be 
greater than or equal to N1 in step 534, then the atrial pace/sense 
electrode(s) are declared in step 540 to be apparently not dislodged and 
in the proper position superior to the AV node of the heart and the 
current rhythm is normal sinus rhythm, based on the prevailing duration of 
the measured AV intervals. If DALP is greater than or equal to N2, then 
the atrial pace/sense electrode(s) are declared in step 542 to be 
apparently dislodged and not in the proper position superior to the AV 
node of the heart, based on the prevailing duration of the measured AV 
intervals. However, if neither NALP nor DALP are greater than or equal to 
their respective counter thresholds, the results of the test are ambiguous 
and may be indicative of proper atrial lead position with the underlying 
rhythm being atrial fibrillation, or lead dislodgement with intermittent 
pacing capture. A number of possible actions may be taken in block 544, 
e.g. simply date stamping and storing the test results, increasing pacing 
output to improve capture, initiating a further test sequence with an 
incremented or decremented TAV interval, initiating a further diagnostic 
test etc. In the context of a dual chamber bradycardia pacemaker, these 
test results are preferably date stamped and stored in memory with or 
without other data that can read out by a physician and be used at a later 
date to diagnose the reasons why the ambiguous results were obtained at 
the time of the test. 
In FIG. 7, steps 550-556 are substituted for steps 540-546 of FIG. 6. When 
NALP is greater than or equal to N1 in step 534, the atrial 
tachyarrhythmia determination is confirmed or declared valid in step 550 
and the test atrial pace mode is stopped in step 556. If the NALP is not 
greater than or equal to N1 in step 534, and if DALP is greater than or 
equal to N2 as determined in step 538, then the provisional determination 
of the atrial tachyarrhythmia made in step 408 is declared invalid in step 
552 and the algorithm is stopped in step 544. In this instance, there is 
sufficient evidence that the TAV intervals are shorter than the AVT, 
indicating that the atrial pace/sense electrode(s) is dislodged and that 
the provisional determination is unreliable. Consequently, the atrial 
anti-tachyarrhythmia therapies scheduled to be delivered are not 
delivered. If for some reason there is an error in the comparisons of the 
TAV intervals to the AVT threshold, and the patient is experiencing an 
atrial fibrillation or flutter, he/she will feel the affects of the 
arrhythmia and contact medical personnel to determine why no therapy was 
delivered. The physician may determine whether or not the atrial 
pace/sense electrode(s) is actually dislodged by a variety of other tests 
and observations made when the patient is present. In the meantime, the 
delivery of a potentially harmful therapy that could trigger a more 
serious ventricular tachyarrhythmia is avoided. 
In episodes of atrial fibrillation, it is typically the case that long and 
short AV delay intervals shorter and longer than the AVT are spontaneously 
detected from the chaotic atrial electrogram. In this algorithm, if 
neither DALP nor NALP is greater than or equal to their respective 
thresholds N1 and N2, then a provisional determination of atrial 
fibrillation may be confirmed, or a factor may be provided that is weighed 
with the other factors employed in the algorithm to provisionally 
determine the presence of atrial fibrillation to effect the confirmation 
in step 554 of FIG. 7. In other words, the step of making a "provisional 
diagnosis" may be incomplete at step 502, that is, an atrial 
tachyarrhythmia may be suggested by the atrial rate without concluding 
even a provisional diagnosis, and the atrial pace test algorithm may be 
initiated so that the results may be used as a weight or factor to include 
in making the diagnosis. In this particular case, the factor of erratic 
measured AV intervals may be used to thereby "confirm" atrial fibrillation 
in step 554. For example, in preferred embodiments of the above-referenced 
Gillberg et al application, additional prerequisite criteria for delivery 
of anti-atrial tachyarrhythmia therapies may be included. For example, 
confirmation that a sinus rhythm has not resumed may also be required as a 
prerequisite to delivery of AF/AT therapy. An AF/AT Therapy Confirmation 
Criterion will prevent the initiation of atrial therapy when sinus rhythm 
has returned but AF/AT episode termination has not yet been detected. The 
AF/AT Therapy Confirmation Criterion may be satisfied for the current 
ventricular interval if either the number of atrial events in the current 
ventricular interval is greater than two, or the number of atrial events 
in the current ventricular interval is two and the atrial interval for 
both events is either less than the ATDI if AT detection is ON or AFDI if 
AT detection is OFF or if the confirmation of atrial fibrillation in step 
554 of FIG. 7 is achieved. 
While there has been shown what are considered to be the preferred 
embodiments of the invention, it will be manifest that many changes and 
modifications may be made therein without departing from the essential 
spirit of the invention. It is intended, therefore, in the following 
claims to cover all such changes and modifications as may fall within the 
true scope of the invention.