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Biomedical subjects

M D Falkoff

Publications and source records attributed to M D Falkoff.

At least 19 recordsLinked to original sources
PubMed1988

Magnet unresponsive pacemaker endless loop tachycardia.

Endless loop tachycardia is a well-known complication of DDD pacing and is almost invariably terminated by conversion to the asynchronous DOO mode upon application of a magnet over the pulse generator. Occasionally magnet application is ineffectual because the ventriculoatrial (VA) synchrony of endless loop tachycardia is converted directly or indirectly to an atrioventricular (AV) desynchronization arrhythmia, another form of VA synchrony. This occurs when a paced ventricular beat engenders an unsensed retrograde P wave and the continual delivery of an ineffectual atrial stimulus during the atrial myocardial refractory period creates self-perpetuating VA synchrony. Upon magnet removal, AV desynchronization arrhythmia reverts immediately to endless loop tachycardia. In the absence of access to programmers, magnet unresponsive endless loop tachycardia can be easily and reliably terminated by chest wall stimulation through inhibition of the ventricular channel of the DDD pulse generator.

Cardiac Pacing, Artificial↗
PubMed1988

Termination of ventricular tachycardia by chest wall stimulation during DDD pacing. A report of two cases.

This report describes the use of chest wall stimulation (CWS) for the termination of ventricular tachycardia in two patients with dual chamber pulse generators functioning in the DDD mode. Rapid CWS induced burst ventricular pacing when CWS was selectively sensed by the atrial channel, whereupon the pulse generator triggered its ventricular output. In this way, by programming the pulse generators to the maximum upper rate, this CWS technique produced burst ventricular pacing at a rate of 175 to 180/minute that successfully terminated ventricular tachycardia in both patients. The same CWS technique also initiated ventricular tachycardia by burst ventricular pacing. This CWS technique may be useful for the termination of relatively slow ventricular tachycardia in patients with DDD pulse generators when the maximum rate of ventricular pacing cannot be otherwise increased.

Aged↗
PubMed1988

Pacemaker endless loop tachycardia: termination by simple techniques other than magnet application.

PURPOSE: Pacemaker endless loop (or reentrant) tachycardia (ELT) is often terminated by conversion to the asynchronous mode of pacing by simply placing a magnet over the implanted atrial tracking (DDD or VDD) pacemaker. We investigated three other simple methods of ELT termination--chest wall stimulation (CWS), provocation of myopotential oversensing, and chest thumping--that may be useful when the arrhythmia is unresponsive to magnet application or a magnet is unavailable. PATIENTS AND METHODS: A modified CWS technique using an external pulse generator (pulse width = 40 msec) ordinarily used for transcutaneous cardiac pacing was tested in 74 patients (40 with unipolar and 34 with bipolar DDD devices). CWS inhibited the ventricular channel of all DDD pacemakers easily and reliably. CWS was then applied during ELT in 20 patients (10 with unipolar and 10 with bipolar DDD devices). Provocation of myopotential oversensing by the ventricular channel was attempted during ELT in 10 patients with unipolar DDD pacemakers. Chest thumping was tried during ELT in six patients. RESULTS: CWS by the modified technique terminated ELT in all patients in whom the arrhythmia was induced. Myopotential oversensing resulted in successful ELT termination in six of the 10 patients. ELT was successfully terminated by chest thumping in four of six patients. CONCLUSION: These simple techniques provide effective ways of ELT termination other than magnet application, and may be easily applied by physicians unfamiliar with the complexities of contemporary DDD pacemakers and their programmers.

Cardiac Pacing, Artificial↗
PubMed1988

Resetting of DDD pulse generators due to cold exposure.

We encountered resetting of three DDD pulse generators to the VVI mode, one at the time of implantation and two others just before implantation, and we believe this resulted from cold exposure during shipment. Consequently we analyzed the effect of cold exposure on five lithium-powered DDD pulse generators from different manufacturers. Cold exposure caused resetting of three of the five DDD pulse generators to the VVI mode. Only one of the reset pulse generators responded to application of the magnet by conversion to the asynchronous (VOO) mode, while the other two remained in the VVI mode. All DDD pulse generators should be routinely interrogated before implantation. If found to be reset, the likelihood of cold exposure is very high and the pulse generator can generally be reprogrammed to the DDD mode. The absence of a magnet response in reset DDD pulse generators appropriately inhibited and functioning in the VVI mode should not be interpreted as component failure when no output is observed.

Cold Temperature↗
PubMed1987

Cephalic vein guide wire technique for implantation of permanent pacemakers.

This report describes a modified cephalic vein guide wire technique for the implantation of permanent pacemakers. The procedure was attempted in 11 patients only when pacing leads could not be passed directly into the exposed cephalic vein. Eight bipolar DDD (two leads), two unipolar DDD, and one bipolar VVI (one lead) pulse generators were implanted successfully, with only one relatively minor complication. The cephalic vein guide wire technique provides easy access to the subclavian vein and may allow implantation of most single- and dual-chamber pacemakers with only a cephalic vein cutdown.

Aged↗
PubMed1987

Hyperkalemia-induced failure of atrial capture during dual-chamber cardiac pacing.

This report describes hyperkalemia-induced failure of atrial capture associated with preservation of ventricular pacing in a patient with a dual-chamber (DDD) pacemaker. This differential effect on atrial and ventricular excitability during cardiac pacing correlates with the well known clinical and experimental observation that the atrial myocardium is more sensitive to hyperkalemia than is the ventricular myocardium.

Aged↗
PubMed1987

Double sensing by atrial automatic tachycardia-terminating pulse generator.

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.

Adult↗
PubMed1987

Crosstalk due to activation of atrial sense marker function of DDD pulse generators.

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.

Atrioventricular Node↗
PubMed1987

Implanted atrial pacemakers for paroxysmal atrial flutter. Long-term efficacy.

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.

Adult↗
PubMed1987

Significance of transient electrocardiographic Q waves in coronary artery disease.

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)

Coronary Artery Bypass↗
PubMed1987

Electrocardiographic diagnosis of myocardial infarction during ventricular pacing.

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.

Electrocardiography↗
PubMed1986

Clinical usefulness of chest wall stimulation in patients with automatic tachycardia-terminating pacemakers.

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.

Electric Stimulation↗
PubMed1986

Paradoxical induction of endless loop tachycardia by magnet application over a DDD pacemaker.

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.

Adams-Stokes Syndrome↗
PubMed1986

Long-term management of ventricular tachycardia by implantable automatic burst tachycardia-terminating pacemakers.

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.

Aged↗