The DDI mode of cardiac pacing.
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Biomedical subjects
Publications and source records attributed to S S Barold.
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Fifty-seven patients with implanted DDD pulse generators (23 Intermedics Cosmos and 34 Medtronic Symbios) were studied to characterize the behavior of the so-called ventricular safety pace period or nonphysiologic AV delay (ventricular triggering period) in a variety of circumstances. The pulse generators were programmed to various combinations of upper rate, lower rate, and atrioventricular (AV) intervals. We then evaluated the response of the pulse generators to a variety of signals sensed by the ventricular channel during the ventricular triggering period (VTP). In the Cosmos DDD pulse generators, the VTP lengthened from its nominal value (100 ms) whenever the sum of the atrial escape (pacemaker VA) interval and the nominal value of the VTP was shorter than the upper rate limit interval. Extension of the VTP reflected the necessary delay required to maintain constancy of the (ventricular) upper rate limit interval. In contrast, the Medtronic Symbios DDD pulse generators exhibited constancy of the VTP even when the sum of the atrial escape (pacemaker VA) interval and the duration of the nonprogrammable VTP (110 ms) was shorter than the upper rate limit interval. This response was observed only with a programmed lower rate of 90 ppm, upper rate of 100 ppm, and AV interval of 250 ms. Under these circumstances, in the presence of crosstalk or myopotentials sensed in the VTP, the Symbios DDD pulse generator violated its ventricular upper rate limit interval, but remained faithful to its separate (but equal) atrial upper rate limit interval by omitting the succeeding atrial stimulus. The behavior of the VTP of DDD pulse generators, particularly its relation to the upper rate response, must be known for the proper interpretation of pacemaker function.
This report describes two cases of double sensing of the P and QRS signals by an implanted atrial bipolar automatic burst tachycardia-terminating pulse generator (Intermedics CyberTach 60) used for the treatment of supraventricular tachycardia. Double sensing occurred during normal sinus rhythm at a rate slower than the tachycardia detection criterion and caused inappropriate delivery of burst stimulation. These observations underscore the importance of the far-field QRS signal in the detection of supraventricular tachycardia by automatic pulse generators sensing the atrial electrogram.
We studied the occurrence and characteristics of crosstalk related to the atrial sense marker function of the Intermedics Cosmos DDD pulse generator in 29 patients. Upon activation of the atrial sense markers, the pulse generator delivers a series of markers in the form of triggered atrial stimuli at 0.025 ms in duration at the programmed voltage output of the atrial channel. Under certain circumstances, these atrial sense marker stimuli may cause crosstalk when they are sensed by the ventricular sensing amplifier. This form of crosstalk may be eliminated in most cases by decreasing ventricular sensitivity and/or atrial output voltage.
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Five patients with drug-resistant paroxysmal atrial flutter received permanent burst atrial pacemakers for the treatment of tachycardia. All patients had extensive electrophysiologic evaluations to determine the safety and efficacy of atrial pacing. The absence of prolonged spontaneous or electrically induced atrial fibrillation was also documented in all patients. Three pulse generators were patient activated (nonautomatic) and two were multiprogrammable and automatic. The atrial pacemakers terminated many attacks of paroxysmal atrial flutter safely and reliably in a follow-up period ranging from 24 to 60 months (average, 42). No major complications developed. In four patients, concomitant drug therapy was necessary, although to a lesser degree, to reduce the frequency of attacks and the ventricular rate. Our study documents the long-term efficacy and low risk associated with permanent-burst atrial pacing in the treatment of drug-refractory paroxysmal atrial flutter in selected patients.
In some clinical situations, an abnormal Q wave may represent intense but reversible ischemia, but the point at which irreversible myocardial damage occurs is seldom known in the acute phase. Unfortunately, the correct diagnosis is presently too cumbersome and takes far too long by means of serial ECGs and enzyme determinations. This delay may preclude rapid therapeutic interventions such as angioplasty, thrombolysis, and emergency coronary bypass surgery to provide myocardial salvage. The remarkable progress in the treatment of unstable coronary artery disease has created the need for more reliable markers of cell death so as to exclude patients from aggressive therapy or to terminate aggressive therapy to salvage what is considered ischemic myocardium. Transient Q waves are being reported far more frequently and have assumed far greater clinical importance because of the current aggressive therapy of MI (and ischemia) with thrombolytic agents, angioplasty, and coronary bypass surgery. A Q-wave deflection associated with ST-segment elevation or depression does not invariably indicate MI. The pronouncement of myocardial death has become more complicated than in the past because Q waves are not pathognomonic of myocardial necrosis. Transient ischemic electrical silence with Q waves in the absence of MI is a rare phenomenon and affects the anterior leads much more commonly than the inferior leads. Such Q waves may appear acutely or may be present chronically with the potential of disappearing when coronary perfusion is restored. A transient intraventricular conduction disorder induced by ischemia should always be ruled out before making the diagnosis of a transient ischemic Q wave or electrical silence. Some workers believe that all transient Q waves represent an unstable intraventricular conduction disorder, but recent developments suggest that most transient Q waves in coronary artery disease are engendered by ischemia. Edema and inflammation may play a part in rendering the myocardium electrically inert, and their disappearance may explain the loss of Q waves. The presence of a small MI should not detract from the importance of associated transient Q waves due to potentially salvageable, severely ischemic myocardium, that is, the zone of so-called concussion around the area of necrosis. In evolving Q-wave MI, a new Q wave may reverse acutely if coronary perfusion is restored very early. Disappearance of Q waves several days after MI suggests return of myocardial viability and does not represent a factitious electrical change. Electrical stunning may be associated with myocardial stunning.(ABSTRACT TRUNCATED AT 400 WORDS)
The diagnosis of myocardial infarction during ventricular pacing can be made in a substantial number of patients, mostly by applying the diagnostic criteria that are useful in the presence of complete left bundle branch block. There are, however, important exceptions to this general rule during ventricular pacing, and normal depolarization patterns must be recognized to avoid the erroneous diagnosis of myocardial infarction.
Chest wall stimulation may be used diagnostically and therapeutically in the follow-up of patients with automatic tachycardia-terminating pulse generators. In this report, we present our experience with chest wall stimulation in the follow-up of five patients with implanted Intermedics CyberTach 60 automatic tachycardia-terminating pacemakers (three for supraventricular tachycardia and two for ventricular tachycardia). Chest wall stimulation delivered at a rate faster than the rate detection criterion of the pulse generator often precipitates reentry tachycardia, making it possible to perform a noninvasive electrophysiologic study. In addition, chest wall stimulation may be invaluable in the termination of reentry tachycardia which is unsensed by an implanted pulse generator either because the rate is too slow, or below the rate detection criterion, or because the intracardiac signal does not attain the sensitivity of the pulse generator.
It is well known that removal of a testing magnet from a DDD pulse generator may cause endless loop tachycardia in patients with retrograde ventriculoatrial conduction; application of the magnet then terminates the tachycardia. We have observed the opposite response to the magnet and in this report we describe the paradoxical induction of endless loop tachycardia by magnet application over a DDD pulse generator and its persistence despite repeated removal and reapplication of the magnet. This unusual behavior occurred only in the "magnet off" function and is due to magnet-induced signals sensed by the atrial channel circuitry.
This report describes the long-term follow-up of two patients who received implantable automatic burst tachycardia-terminating ventricular pacemakers for the treatment of drug-refractory sustained ventricular tachycardia. After implantation, both pulse generators continued to terminate ventricular tachycardia without any major complications. In one patient, after three years, many episodes of ventricular tachycardia were slower than the tachycardia-detection criterion rate of 137 per minute; ventricular tachycardia was then terminated by chest wall stimulation that activated the burst function of the pacemaker. In this particular patient, the pulse generator was removed after four and one-half years and replaced with a DDD system because of the pacemaker syndrome and attacks of ventricular tachycardia, often at a rate of about 100/minute. In the second patient, the pacemaker continued to terminate ventricular tachycardia for over five and one-half years as determined by the repeated activation of the flag (memory) function of the pacemaker indicating detection of tachycardia by the pulse generator and resultant delivery of burst pacing.
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An Omni Orthocor 234A special device pacemaker was implanted in nine patients for treatment of drug-resistant supraventricular tachycardia (three patients) or ventricular tachycardia (six patients). This device is activated using a special external unit, which delivers from six to 15 stimuli at preselected coupling intervals ranging from 195 to 500 ms. Serial noninvasive electrophysiology studies were performed either in the hospital or on an outpatient basis using the triggered mode, which can respond to programmed chest wall stimulation. Three patients with reciprocating supraventricular tachycardia were treated effectively by this device during an average follow-up of 2.2 years. Of the six patients with stable ventricular tachycardia amenable to pacemaker termination, only four remained successful during an average follow-up of 1.9 years. Such devices may find important use in serial noninvasive electrophysiologic testing during long-term clinical follow-up. The present form of this device is inadequate for widespread application, but may be useful for highly selected individuals.
Signals responsible for pacemaker oversensing may arise from the pacing system itself, P or T wave, concealed ventricular extrasystoles, skeletal muscle potentials, and distant electromagnetic fields. Oversensing is the most common cause of pacemaker pauses and a common clinical problem during follow-up of patients with implanted pulse generators. This article reviews the mechanisms and diagnosis of oversensing and the importance of multiprogrammability for its treatment.
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Safe and reliable DDD pacemakers with multiple programming capabilities have now been developed. Certain programmable parameters are basic, including mode, voltage (or current) output, pulse width, sensitivity and refractory periods in each chamber. Upper rate response as well as low rate settings and A-V delays are equally important. In certain models, the ability to program the blanking period has proven quite useful. The interrelationship between all these functions will assure the smooth overall performance of these sophisticated devices.
Six cases are presented in which a transient or chronic rise in the stimulation threshold of a permanently implanted unipolar pacemaker resulted in the loss of effective pacing after therapeutic defibrillation or cardioversion. Although damage to the pulse generator may still occur, leading to a loss of function as demonstrated in a seventh patient, improvements in the internal protection circuits of the present generation of pacemakers makes this less likely while possibly predisposing to endocardial burns and increased fibrosis at the electrode-endocardial interface. The theoretical explanations for this phenomenon are discussed, along with recommendations for the prospective and retrospective management of the pacemaker patient who requires defibrillation or cardioversion.
Doppler echocardiographic studies were performed in 14 patients with dual chamber pacemakers. Transmitral flow studies (12 patients) revealed absence of mitral regurgitation (MR) or no change in MR severity in 6, new development or increased MR during VVI and/or short or long AV interval lengths compared to more normal AV intervals (150-160 ms) in 5, and appearance of MR when the pacing mode was changed from VVI to DVI with a fixed AV interval of 250 ms in 1 patient. Aortic peak flow velocity measurements (7 patients) showed significant increases in stroke volume (range 9 to 25%, mean 19.5%) in all patients with DVI/VDD pacing compared to VVI pacing (4 patients) or to shortest available AV interval (3 patients). Presence of Doppler left atrial systolic flow correlated with evidence of atrial depolarization in all 7 patients in whom high quality 12-lead surface electrocardiograms were obtained. Our preliminary study demonstrates the value of Doppler echocardiography in the "fine tuning" of cardiac pacemaker parameters by assessment of presence, absence, or change in severity of MR, estimation of relative changes in stroke volume, and determination of atrial capture in different pacing modes and at various AV intervals.