The paced 12-lead electrocardiogram should no longer be neglected in pacemaker follow-up.
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Biomedical subjects
Publications and source records attributed to S S Barold.
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This report describes the development of an unusual pacemaker tachycardia in a patient with a conventional dual chamber pacemaker used for biventricular pacing in the VVIR mode. The atrial channel was connected to the left ventricle and the ventricular channel to the right ventricle. The tachycardia was sustained by sensing of the T wave by the "atrial channel" which triggered pacing by the "ventricular channel. " This "cross-ventricular" endless loop tachycardia is a reentrant pacemaker tachycardia like classic endless loop tachycardia and can be prevented by appropriate programming of the pacemaker.
2:1 AV block can occur in either the AV node or the His-Purkinje system and cannot be classified into type I or type II second-degree AV block because there is only one PR interval to examine before the blocked P wave. It is inappropriate to use terms such as 2:1 or 3:1 type I or type II AV block because this characterization violates the accepted traditional definitions of type I and type II block based on electrocardiographic patterns and not on the anatomical site of block. Type I and type II second-degree AV block can progress to 2:1 AV block, and 2:1 AV block can regress to type I or type II block. Consequently, the site of the lesion in 2:1 block can often be determined by seeking the company 2:1 AV block keeps. An association with type I block and a narrow QRS complex almost always reflects AV nodal block but type I block with a wide QRS complex occurs more commonly in the His-Purkinje system than the AV node. Type II block, if correctly defined, is always infranodal. Outside of acute myocardial infarction, sustained 2:1 and 3:1 AV block with a wide QRS complex occurs in the His-Purkinje system in 80% of cases and 20% in the AV node. Administration of atropine in patients with His-Purkinje disease may increase the degree of AV block.
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In this review, we discuss the various forms and causes of second-degree atrioventricular (AV) block and the reasons they remain poorly understood. Both type I and type II block characterize block of a single sinus P wave. Type I block describes visible, differing, and generally decremental AV conduction. Type II block describes what appears to be an all-or-none conduction without visible changes in the AV conduction time before and after the blocked impulse. Although the diagnosis of type II block is possible with an increasing sinus rate, absence of sinus slowing is an important criterion of type II block because a vagal surge (generally a benign condition) can cause simultaneous sinus slowing and AV nodal block, which can superficially resemble type II block. The diagnosis of type II block cannot be established if the first postblock P wave is followed by a shortened PR interval or is not discernible. A pattern resembling a narrow QRS type II block in association with an obvious type I structure in the same recording (e.g., Holter) effectively rules out type II block because the coexistence of both types of narrow QRS block is exceedingly rare. Concealed His bundle or ventricular extrasystoles confined to the specialized conduction system without myocardial penetration and depolarization can produce electrocardiographic patterns that mimic type I and/or type II block (pseudo-AV block). All correctly defined type II blocks are infranodal. A narrow QRS type I block is almost always AV nodal, whereas a type I block with bundle branch block barring acute myocardial infarction is infranodal in 60% to 70% of cases. A 2:1 AV block cannot be classified in terms of type I or type II block, but it can be nodal or infranodal. Infranodal blocks require pacing regardless of form or symptoms. The widespread use of numerous disparate definitions of type II block appears primarily responsible for many of the problems surrounding second-degree AV block. Adherence to the correct definitions provides a logical and simple framework for clinical evaluation.
This report describes the occurrence of a repetitive nonreentrant ventriculoatrial (VA) synchronous rhythm precipitated by the noncompetitive atrial pacing algorithm of a Medtronic DDDR pacemaker. This algorithm delivers an atrial stimulus 300 ms after the detection of an atrial signal in the postventricular atrial refractory period of the pacemaker. In our patient, the atrial stimulus released by the algorithm was ineffectual because it encountered prolonged refractoriness of the atrial myocardium. This situation produced a repetitive nonreentrant VAl synchronous rhythm in the setting of retrograde VA conduction.
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It is possible to characterize some of the sensing functions of new multisite pacing systems by resurrecting the split format in the third position of the standard pacemaker code. This approach permits accurate representation of the horizontal and vertical triggering functions of multisite dual-chamber pacemakers without creating a new code.
This report describes the development of atrioventricular block by programmed stimulation of the right ventricular (RV) outflow tract in a patient with undiagnosed syncope. Burst pacing from the RV apex and outflow tract and programmed stimulation from the RV apex were unsuccessful. The observations were consistent with the fatigue phenomenon of the His-Purkinje system and illustrate the importance of an appropriate stimulation protocol in the electrophysiological evaluation of syncope.
This report describes a patient with type I second-degree atrioventricular block and sequences consistent with type II block according to widely accepted criteria. The electrocardiograms illustrate the importance of deductive reasoning and the clinical context in the diagnostic evaluation of perplexing forms of second-degree AV block.
Paradoxical shortening of the paced AV delay (atrial paced-ventricular paced or Ap-Vp interval) was observed at rest in the DDD and DDDR modes in three patients with implanted CPI Vigor DR pacemakers programmed with a long AV delay and a relatively narrow difference between the lower and upper rates. This behavior is related to the VA extension algorithm designed to prevent the sensor-driven atrial pacing rate from exceeding the programmed upper rate whenever a sensed conducted QRS complex continually follows an atrial stimulus. We found that this algorithm also becomes manifest at rest and may cause shortening of the Ap-Vp intervals. The VA extension algorithm is best conceptualized in terms of a separate atrial upper rate that functions on exercise and at rest. The atrial and ventricular upper rates are equal but the atrial upper rate is initiated by an atrial-paced or sensed event and the ventricular upper rate is initiated by a paced or sensed ventricular event. Under certain circumstances delay in the release of the atrial stimulus Ap to conform to the atrial upper rate interval produces variable abbreviation of the paced AV (Ap-Vp) delays with resultant variation in the duration of the atrial escape intervals despite fundamental ventricular-based lower rate timing.
In a patient with severe congestive heart failure and ischemic disease, frequent episodes of ventricular tachycardia were completely suppressed by an implantable cardioverter defibrillator with biventricular pacing.
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