A novice in a busy electrophysiology (EP) laboratory will generally learn to recognize the common arrhythmias in a relatively short time. It requires considerably more seasoning to recognize the variants and unusual mechanisms, or to “hit the curve ball.” It is hoped that the following commentary assists in providing structure and focus to the EP study and facilitates analysis of the case studies to follow.

The EP study is an extension of the electrocardiogram (ECG) with the addition of intracardiac recording and programmed electrical stimulation. Insightful interpretation of the ECG allows for prospectively considering additional catheters, stimulation sequences, or maneuvers appropriate for the postulated arrhythmia. This limits the diagnostic possibilities and avoids unnecessary steps (Fig. 1–1). The fundamentals of ECG interpretation of an arrhythmia include identification of P waves, determining the atrioventricular (AV) relationship, and analyzing the QRS morphology (Table 1–1). For confusing problems, it is useful to create a “written” list of all potential hypotheses and to plan for specific interventions that will test them. As data are accumulated during the EP study, the facts supporting or refuting the hypotheses can be tabulated. The hypotheses can be represented by schematic drawings for complicated scenarios. This method is illustrated at the end of this chapter.

There are those gifted, intuitive individuals who leap to the correct diagnosis and apparently bypass all the rational, systematic steps. Most of us, however, are better served by a consistent, methodical approach that does not cut corners. A sample protocol for an unknown supraventricular tachycardia (SVT) is shown in Table 1–2. When used routinely, such a protocol will usually result in induction of clinically relevant tachycardia and provide an assessment of the pertinent EP of the heart. Determining the functional properties of the atria, ventricles, and AV conduction system in an individual elucidates the potential arrhythmia mechanisms and limits the diagnostic possibilities for the observed arrhythmia. For example, it is difficult to imagine AV reentrant tachycardia occurring in the total absence of retrograde conduction, even realizing the relatively rare occurrence of conduction over an accessory pathway (AP) only in the presence of isoproterenol. It is also important to display the data channels in a consistent sequence to provide an orderly and familiar framework that facilitates analysis. This point is underscored by the fact that even experienced electrophysiologists require a period of adjustment when looking at data from other laboratories. Of course, other nonconventional recording sites can be added to facilitate diagnosis in selected cases. For example, recording from the left bundle branch can be useful when confirming the diagnosis of bundle branch reentrant tachycardia.

A thorough diagnostic study need not be time consuming and pays dividends both intellectually and clinically. The temptation to ablate an obvious AP without study will not be productive if the patient’s symptoms are not related to any tachycardia, the patient’s tachycardia is not related to the pathway, or the “culprit” AP is a different pathway (Fig. 1–2). The study also provides information regarding other potential rhythm problems that may be unrecognized during the clinical assessment and allows consideration of alternative approaches such as slow pathway ablation in a patient with AV reentrant tachycardia that can only occur with anterograde conduction over the slow AV node pathway. Radio-frequency ablation itself is an important diagnostic tool. Cases involving multiple tachycardia mechanisms can be very confusing. In such situations, at least one of the tachycardia mechanisms is frequently obvious and successful ablation of the tachycardia generally simplifies the diagnosis of the remaining mechanism(s).

Fishermen have long appreciated that the majority of the fish are caught in a relatively small area of the lake. Similarly, the correct diagnosis may not be apparent from the copious EP records during stable tachycardia. Although the electrograms may have a certain temporal sequence, there is no indication of cause and effect in the sequence of electrograms. Is the atrium driving the ventricle or vice versa? Is the preexcited QRS an active participant in the tachycardia circuit or merely a bystander camouflaging another mechanism? The “hot spots” that frequently yield the answer are the zones of transition. The zones include the onset of tachycardia, the termination of tachycardia, change to an alternate QRS morphology, irregularities in cycle length (CL), and ectopic cycles (Table 1–3). The onset reveals the conditions necessary to initiate the tachycardia. Does it require block in an AP, critical prolongation of the atrio-His (AH) interval, or conduction delay in the His–Purkinje system? Does a SVT consistently terminate spontaneously with an atrial electrogram? The latter strongly suggests that the tachycardia mechanism obligates AV node conduction. Does a change from normal QRS to bundle branch block alter any of the conduction intervals or tachycardia CL, suggesting the bundle branch is a critical component of the tachycardia circuit? Careful attention to the zones of transition is often rewarding as is illustrated.

The EP study provides an opportunity to disturb an arrhythmia with pacing, extrastimuli, autonomic maneuvers, physical maneuvers, and drugs. Single, or multiple, atrial or ventricular extrastimuli are programmed into the cardiac cycle and made progressively more premature to loss of capture. This invariably provides the zone of transition that clarifies the requirement of atrium or ventricle in the mechanism or alters the tachycardia in a manner that clarifies the problem. In other words, if the tachycardia mechanism is not perfectly obvious, overdrive pacing or programming extrastimuli will almost invariably clarify it. A long-standing “inverse rule” may be useful to trainees—initially introduce premature atrial extrasystoles into a wide QRS tachycardia and ventricular extrasystoles into a narrow QRS tachycardia. Changes in posture cause autonomic adjustments and alter cardiac filling. Agents such as adenosine usually affect specific tissues and mechanisms, and can be invaluable. Isoproterenol is useful for mimicking states of catecholamine excess or altering specific EP properties to allow induction of tachycardia.

Although many pacing and extrastimulation maneuvers have been described, it is useful to understand the basic underlying principles by which they function. The overriding principle underpinning most pacing interventions is illustrated schematically in Fig. 1–3. In essence, the ability of pacing to influence or “reset” a tachycardia is dependent on two key variables.

The first is distance from the pacing site to the tachycardia mechanism. (Note that this distance may also be “electrophysiologic” as well as geographic in that the pacing site may be “far” from the tachycardia mechanism if there is conduction block adjacent to pacing site requiring a roundabout access to the mechanism.)

The second is access to the circuit. A large reentrant circuit with a large excitable gap is more penetrable by pacing than a “focal” arrhythmia source. In essence, preexcitation of the subsequent A by a premature ventricular complex (PVC) during SVT occurs much more readily with a large AV reentrant circuit close to the pacing site rather than the much smaller and most distant circuit of AV node reentry. Similarly, capture of a SVT by ventricular pacing also depends on the same factors. The postpacing interval (PPI) and the difference of ventriculoatrial (VA) during tachycardia compared with VA during pacing clearly depend on these. In fact, the PVC that resets the A during SVT is just capture for one cycle and all the useful postpacing data also apply to the single PVC that resets tachycardia as will become evident in some of the exercises.