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A great deal of information exists regarding the influence of the autonomic nervous system on the electrical properties of the myocardium and on the genesis of a variety of cardiac arrhythmias. The purpose of this presentation is not to review this vast literature, but to present new information we have developed over the past several years. Specifically, in this manuscript, we will discuss the effects of the autonomic nervous system on recovery properties in the endocardium and the epicardium of the canine left ventricle (1, 2); the effects of the autonomic nervous system on myocardial activation during acute myocardial ischemia in the dog (3); and new models in which to study the effects of ischemia, including vascularized hamster cardiac allographs (4); and rodent myocardium damaged by epinephrine (5).

In 1965, we reported data from a series of studies designed to investigate the electrophysiologic features of functional bundle branch block in the intact canine heart [1]. We did not record electrical activity from the bundle branches and therefore did not document the activation sequences directly. Subsequently, we [2] reinvestigated this problem in a canine preparation in which we stimulated and recorded from the free-running false tendon in vivo. These studies provided some additional data. Most recently, we [3] recorded the activation sequence with electrodes placed on the bundle branches and have confirmed many of our initial conclusions that were based on deductive reasoning. The purpose of this report is to review some of our earlier findings, and extend them with data from our most recent study.

Patients we consider as candidates to undergo electrophysiologic testing to define drug therapy are those who have supraventricular tachycardia (SVT) that is drug-resistant, that produces severe symptoms and those patients who have Wolff-Parkinson-White syndrome and a very rapid ventricular response during atrial fibrillation. Regarding patients who have ventricular tachycardia, we would evaluate those patients who are symptomatic during the ventricular tachycardia, and whose ventricular tachycardia is drug-resistant, occurs infrequently, and is more likely to be inducible electrophysiologically, such as those patients who have sustained ventricular tachycardia on the basis of coronary artery disease. Patients who are resuscitated from ventricular fibrillation should also be considered as candidates for an electrophysiologic study.

Atrioventricular nodal Wenckebach periodicity (Mobitz type 1 AV block) is a pattern of AV transmission in which successive P-R intervals increase by decreasing increments until transmission failure occurs, whereupon temporary restitution of conductivity in the AV node initiates a new cycle.

The sino atrial pacemaker dominates subsidiary pacemakers through the process of overdrive suppression. Subsidiary pacemakers that demonstrate spontaneous diastolic depolarization are located in specialized atrial and ventricular fibers. Diastolic depolarization is normally absent in ordinary atrial and ventricular fibers, although under certain experimental conditions, considered by Surawicz [l], these fibers may develop diastolic depolarization and spontaneous automaticity. The purpose of this chapter is to review the mechanisms responsible for diastolic depolarization and spontaneous automaticity in cardiac Purkinje fibers, with particular emphasis on the effects that pharmacologic agents exert on automaticity that occur at high and low levels of transmembrane potential.

Hodgkin and Katz[l] 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 Huxley [2] 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.

Within the past ten years, the concept has emerged that the ionic currents underlying the cardiac action potential involve 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 of the pathogenesis of some arrhythmias.

Tachyarrhythmias result from disorders of impulse formation, impulse conduction or combinations of both mechanisms. Since cells dependent on the slow inward current possess the properties of impulse formation and conduction [1], it is quite plausible to consider that the slow inward current may serve as an important ionic substrate in fibers responsible for, or at least participating in, the genesis and maintenance of various supraventricular tachyarrhythmias that occur clinically. Such ionic characterization can be made on experimental preparations and ample evidence, reviewed in other chapters of this book, supports the role of the slow inward current in the generation of action potentials from of the slow inward current in the generation of action potentials from normal and abnormal fibers in the atrium. For example, the data strongly indicate that the normal sinus and atrioventricular (AV) nodes are slow-channel dependent. In addition, other atrial fibers, some made abnormal by a variety of methods, may be slow-channel dependent. However, our present diagnostic tools do not permit for most clinically occurring tachyarrhythmias, i.e., reentry or automaticity, and certainly do not allow convincing differentiation into which arrhythmias may be slow-channel dependent. Nevertheless, extrapolating from experimental animal observations, from in vitro studies on human atrial tissues, and from the response of arrhythmias to the clinically available slow-channel blocker, verapamil[2], in this chapter we will consider the evidence supporting the possible participation of the slow inward current in the genesis of supraventricular tachycardia (SVT).

Transvenous electrical cardioversion refers to the reversion of cardiac arrhythmia by delivery of synchronized electrical shock to the endocardial surface of the heart through a transvenous catheter. The application of a catheter system for transvenous intracardiac cardioversion represents a logical extension of the techniques and concepts of electrical cardioversion and defibrillation. The concept of delivering electrical shocks directly to the heart through a catheter has been advanced by the work of investigative teams lead by Mirowski et al [1, 2]. They demonstrated the feasibility and safety of such an approach with work that has progressed to the development of an implantable defibrillation system. With this background, it was further reasoned that synchronized shocks delivered through a catheter electrode system would successfully cardiovert ventricular tachycardia using very low energies.

The purpose of this chapter is to discuss the influence of the autonomic nervous system on various electrophysiologic characteristics of the ventricle and to present a variety of experimental and clinical situations in which important cardiac arrhythmias occur and in which the autonomic nervous system is thought to play a significant role. Several important reviews [1–4] have presented recently an extensive update on cardiac aspects of the autonomic nervous system.