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.

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.

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.

Thoracic skeletal abnormalities in idiopathic mitral valve prolapse.

Idiopathic prolapse of the mitral valve is a common disorder, but many cases are clinically subtle. Thoracic skeletal abnormalities, reported recently to accompany the syndrome, may serve as an easily identifiable clinical indicator. The prevalence of these abnormalities was defined in 24 patients with proved prolapse of the mitral valve. The valvular syndrome was defined clinically, by echocardiography and, in seven cases, by left ventricular angiography. The skeletal deformities were defined clinically and radiographically. Pectus excavatum was present in 62 percent of the patients, "straight back" in 17 percent and severe scoliosis in 8 percent. Eighteen of the 24 patients (75 percent) had a definite thoracic skeletal deformity. The association of idiopathic prolapse of the mitral valve with these skeletal deformities may represent a forme fruste of Marfan's syndrome. Patients with "straight back" and pectus excavatum should be examined clinically and perhaps by echocardiography to exclude idiopathic prolapse of the mitral valve; when murmurs are present, a diagnosis of "pseudoheart disease" should not be made before mitral valve prolapse has been excluded.

Familial cardiac myxoma: emphasis on unusual clinical manifestations.

This report describes familial cardiac myxoma involving parent and child. The familial occurrence of this condition, previously reported in four other families, underscores the necessity of screening all direct members of the family by echocardiography once the diagnosis of cardiac myxoma is made. Each patient presented with unusual clinical manifestations. The father, who had a right atrial myxoma associated with an atrial septal defect and mitral valve prolapse, presented with findings highly suggestive of paradoxical embolism. The daughter, who had an infected right ventricular myxoma, was initially treated for valvular subacute bacterial endocarditis before the diagnosis was made.

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)

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.

Oversensing by single-chamber pacemakers: mechanisms, diagnosis, and treatment.

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.

Characterization of pacemaker arrhythmias due to normally functioning AV demand (DVI) pulse generators.

Normally functioning DVI pulse generators with different electronic characteristics may cause complex cardiac arrhythmias that must not be interpreted as pacemaker malfunction. When there is no refractory period after the atrial output, a DVI pulse generator may deliver atrial pacemaker impulses at irregularly shortened intervals and produce an increase in the atrial pacemaker rate compared with the programmed free-running AV sequential rate. Theoretically this variation of the atrial cycle length can occur only within a well-defined range that represents the difference between the ventricular and atrial output escape intervals. In reality, the interplay of the spontaneous sinus rate, duration of AV conduction, time of sensing the ventricular electrogram in relation to the surface QRS complex, and the programmed AV sequential time all influence the atrial pacemaker rate. DVI pulse generators may also create interesting arrhythmias such as pseudopseudofusion beats (delivery of an atrial spike within the QRS complex), double pseudofusion beats, and double pacemaker impulses within the QRS complex according to the electrophysiologic circumstances and specifications of the pulse generator.

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.

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.