Accelerated cardiac escape rhythms caused by ouabain intoxication

Although triggered activity has been identified in isolated atrial tissue with the use of cellular electrophysiologic techniques, there has been no identification of triggered atrial arrhythmias in situ. Moreover, it is unclear whether triggered rhythms of different causes and sites of origin in the heart exhibit uniform responses to pacing that might aid in their identification. We therefore studied arrhythmias induced by overdrive pacing in three canine preparations, and based the analysis of our results on guidelines derived from microelectrode studies. We studied ventricular tachycardias induced by ouabain or by anterior wall myocardial infarction and atrial (coronary sinus) arrhythmias induced by the infusion of epinephrine into the great cardiac vein. In the ouabain and postinfarction preparations, right ventricular epicardial pacing induced ventricular premature beats or tachycardias whose recovery intervals after cessation ofpacing shortened and showed overdrive acceleration as pacing rate increased. The first postpacing beat displayed progressive fusion with the paced beats but transient entrainment could not be induced. In the coronary sinus, the recovery intervals of impulses induced by epinephrine and pacing decreased as the drive rate increased, and inducibility of the paced rhythms increased at faster drive rates. Thus, the recovery intervals of triggered activity induced in the coronary sinus are phenomenologically similar to those of infarct-and digitalis-induced triggered rhythms. This is the first demonstration of consistent behavior in response to pacing of diverse types of triggered activity. Considered in light of the failure to induce transient entrainment, the results emphasize the potential utility of pacing in clinical identification of triggered rhythms and their differentiation from reentry. Circulation 77, No. 5, 113977, No. 5, -114877, No. 5, , 1988 ALTHOUGH much has been done to characterize delayed afterdepolarization-induced triggered rhythms in isolated cardiac tissues`8 and in intact animals,9' 10 it remains difficult to identify triggered arrhythmias clinically and to distinguish them from reentry. 11-16 The cellular electrophysiologic "rules" that have been applied to the identification of triggered rhythms in the intact heart are derived largely from studies of digitalistoxic Purkinje fibers.

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

The response to overdrive pacing of triggered atrial and ventricular arrhythmias in the canine heart.

Malfatto

Rosen

1988

“…One such area of interest involves the recent in vivo and in vitro demonstration of rather specific digitalis-induced arrhythmias, which exhibit overdrive acceleration rather than overdrive suppression, in response to rapid stimulation. [22][23][24][47][48][49] The mechanism responsible for this overdrive acceleration is unknown, but clearly sets these arrhythmias apart from normal automaticity which exhibits overdrive suppression. Recently, similar arrhythmias have been created with barium and strontium.…”

Section: Automaticitymentioning

confidence: 99%

Role of the slow current in cardiac electrophysiology.

Zipes¹,

Besch²,

Watanabe³

1975

MayAN OFFICIAL JOlURNAL ofthe AMERICAN JEART ASSOCIATION NO. 5 1975 EDITORIALRole of the Slow Current in Cardiac Electrophysiology OVER THE PAST TEN YEARS, the concept has emerged that the ionic currents underlying the cardiac action potential include calcium as well as sodium and potassium. The purpose of this communication is to review the development of this concept and attempt to relate it to our understanding of clinical electrophysiology and the pathogenesis of certain arrhythmias. Basic Electrophysiologic ConceptsTwenty-six years ago, Hodgkin and Katz' demonstrated that a large and relatively specific increase in the membrane permeability to sodium ions accounted for the amplitude and rate of voltage change of the depolarization phase of squid nerve action potentials. Using the voltage-clamp technique, Hodgkin and Huxley2 analyzed the currents underlying the nerve action potential. They described two constituents -an inward sodium flow followed by an outward potassium flow -and formulated equations to describe how these currents vary with transmembrane voltage potential and time.In the ensuing years, cardiac electrophysiologists, assuming that exclusively sodium and potassium movements were involved, applied the Hodgkin-

“…In so doing, we were aware of the limitations inherent in attempting to extrapolate from any given model to the intact heart but were nevertheless encouraged by the results of a similar approach used to quantify rhythms induced by digitalis toxicity.' [22][23][24][25] We have found that there are some similarities between the triggered rhythms induced by catecholamines in atrial fibers of the coronary sinus and those caused by digitalis in Purkinje fibers, but there are important differences as well. These must be considered carefully in attempting to define the behavior of triggered activity in experimental animals and in the clinic.…”

mentioning

confidence: 99%

Characteristics of initiation and termination of catecholamine-induced triggered activity in atrial fibers of the coronary sinus.

Johnson¹,

Danilo²,

Wit³

et al. 1986

We studied epinephrine-induced delayed afterdepolarizations and triggered activity in atrial fibers from the canine coronary sinus to determine whether their responses to cardiac pacing would aid in formulating a uniform set of guidelines for differentiating this triggered activity from other arrhythmogenic mechanisms. We used standard microelectrode techniques and compared the delayed afterdepolarizations and triggered activity with those occurring in ouabain-superfused Purkinje fibers. Like Purkinje fibers, the frequency of triggering in the coronary sinus and the coupling interval of the first triggered beat were related directly to the basic drive cycle length, and the delayed afterdepolarization amplitude and frequency of triggering were related to the coupling interval of premature stimuli (S2). However, unlike Purkinje fibers, the coupling interval of the delayed afterdepolarization and of the first triggered beat were independent of the S2. Once initiated, triggered activity in the coronary sinus followed one of four rhythm patterns: in all four, the minimum and equilibrium cycle lengths were independent of the initiating cycle length. Triggered activity was terminated by overdrive and S2 pacing, especially by long episodes of overdrive at short cycle length. The first escape beat after overdrive was linearly related to the overdrive cycle length, resulting in overdrive acceleration. The return cycle length after S2 was linearly related to the S2 coupling interval. Because delayed afterdepolarizations and triggered activity in the coronary sinus respond differently to pacing from those in ouabain-superfused Purkinje fibers, triggered activity in general may not be identified by a uniform set of guidelines.