Electrophysiology Laboratory

Initially, the main purpose of the EP laboratory was for diagnostic studies. However, its focus has evolved to include many therapeutic procedures such as catheter ablation and cardiac rhythm device implantation and extraction. The EP laboratory is divided into the control room, which is shielded from radiation by a glass partition and doorway, and the area where the procedure is performed, which contains the patient table and imaging equipment. While the procedure is being performed, a technician (and sometimes a second electrophysiologist) in the control room monitors the patient’s cardiac rhythm and performs various pacing maneuvers. A large amount of equipment is required (e.g., single or biplane fluoroscopy, mapping patches, electrocardiogram [ECG] leads, catheters, boom with multiple screens), limiting access to the patient during the procedure and thus complicating anesthetic care. Some laboratories also contain a magnetic catheter navigation system (e.g., Stereotaxis Inc.), which occupies even more space and introduces the logistical considerations (i.e., magnetic resonance imaging [MRI]-compatible monitors and anesthesia machine) and potential dangers of a ferromagnetic field. Because fluoroscopy is constantly used in the EP laboratory, necessary radiation safety precautions (e.g., lead aprons or shields, eye protection) must be followed. Radiation dosimeters should be worn by personnel who routinely work in this environment.

Catheter Placement and Generation of Intracardiac Electrograms

Right heart catheter placement is most often performed via the femoral vein; however, the internal jugular, subclavian, or brachial vein can be used. Multiple intravenous (IV) sheaths are placed so that catheters can be advanced into the heart to record intracardiac signals (electrograms). In contradistinction to the surface ECG, which provides summed vectors of the heart’s electrical activity, the intracardiac electrogram records a discrete local signal from a small area of the myocardium. These diagnostic catheters, some with multiple electrode pairs, are used to determine information such as signal voltage, complexity, and local activation (timing compared with a reference). The exact type and location of the catheters placed depend on the procedure being performed and physician preference.

To perform a basic EP study, several electrograms are typically obtained by placing catheters into the high right atrium (hRA), coronary sinus (CS), His bundle, and RV apex (RVa) ( Fig. 15.1 ). A variable number of surface ECGs leads are also displayed. To better visualize the signals, they are displayed at a sweep speed of 100 mm/s compared with 25 mm/s for a standard ECG. Real-time signals are viewed on one screen, and an additional screen is available for measurements and static review.

Intracardiac electrograms obtained during a standard electrophysiology study in a patient with ventricular preexcitation. This screen shot shows the intracardiac and surface electrocardiogram (ECG) recordings obtained while a high right atrial catheter was used to pace the atrium. Displayed are three surface ECG leads (I, aVF, V1), and the following intracardiac recordings: high right atrial (HRA), three His (proximal, mid, distal), five coronary sinus (CS), and a right ventricular apex (RVa). The bottom-most tracing is a stimulation channel (Stim 1), which confirms pacing is being performed. The pacing artifact seen on the surface ECG may not necessarily be seen on the anesthesia team’s monitor, and review of the stimulation channel on the screen can confirm that pacing is occurring. In this patient, the short PR interval and delta wave visible on the surface ECG leads are characteristic of ventricular preexcitation.

Catheter Mapping System

Mapping systems are used to collect and display information gathered from intracardiac recordings. A three-dimensional (3D) shell of the chamber(s) of interest is generated along with pertinent timing and voltage information. These systems reduce radiation exposure compared with fluoroscopy alone by integrating preprocedural images obtained from computed tomography (CT) or magnetic resonance (MR) or use intraprocedural ultrasound to improve anatomic relationships. During an arrhythmia, an activation map is produced by measuring the timing of different cardiac events and then using color coding or an animation to display the wavefront proceeding across the 3D map ( Fig. 15.2 ). The map helps the electrophysiologist determine the area that should be targeted for ablation by pinpointing the source of a focal tachycardia or the area of slow conduction in the case of a macroreentrant tachycardia. Voltage mapping is used in addition to or in lieu of activation mapping if an arrhythmia is noninducible and provides important information about the scar substrate responsible for reentrant rhythms.

An activation map showing typical atrial flutter with counterclockwise rotation (arrows) . The color bar (located on the left edge of the image) provides a reference for timing and color correlation. Earliest activation sites are noted by white followed by red, with purple indicating the last activated site compared to the reference time. A macroreentrant circuit is continuous; thus early and late are arbitrarily defined, but the so-called “early meets late” pattern supports the mechanism as reentry rather than a focal tachycardia. The right atrium is seen in both the right anterior oblique view (image on left) and left anterior oblique caudal view (image on right). CS, Coronary sinus; HB, His bundle; IVC, inferior vena cava; RAA, right atrial appendage; SVC, superior vena cava.

Mechanisms of Cardiac Arrhythmias

Arrhythmias are classified as slow (bradyarrhythmia) or fast (tachyarrhythmia) based on whether the heart rate is less than 60 beats/min or greater than 100 beats/min, respectively.

Tachyarrhythmias

Tachyarrhythmias are caused by one of three mechanisms ( Box 15.1 ). In the EP laboratory, the most commonly treated mechanism is reentry. A reentrant tachycardia is defined by its continuous circular path in which the wavefront of excitability returns to the site of initiation. Requirements of reentry include two adjacent pathways with differing EP properties that connect proximally and distally to form a single circuit with a nonexcitable central area. Unidirectional block is required and occurs when differences in refractory periods allow an impulse to initially conduct down one pathway but not the other. Because of slow conduction, by the time the wavefront reaches the end of the first pathway, the second pathway is no longer refractory and accepts the impulse. The impulse then continues until it returns to its origin and thus completes one cycle of tachycardia. There is often an area of slow conduction that facilitates reentry and may be targeted for ablation (e.g., the cavotricuspid isthmus in typical atrial flutter [AFL]).

Box 15.1

Tachyarrhythmia Mechanisms

• •
  

  Reentry (mechanism most commonly addressed in electrophysiology procedures)

  
  
• •
  

  Automaticity

  
  
• •
  

  Triggered

The remaining two mechanisms, automaticity and triggered activity, are abnormalities in impulse formation rather than conduction. Automaticity is spontaneous impulse formation and is normal behavior when occurring in specialized conduction tissue. Failure of automaticity may result in a bradyarrhythmia such as sinus bradycardia. Alternatively, increased automaticity in diseased or ischemic atrial or ventricular myocardial cells may result in a sustained tachyarrhythmia or induce premature beats that initiate reentry. Triggered activity requires a preceding impulse and is caused by oscillations in the cellular membrane potential called afterdepolarizations. Afterdepolarizations are further characterized as early or delayed depending on when they occur during the action potential. Clinical examples of early and delayed afterdepolarizations include torsades de pointes in long-QT syndrome and digoxin toxicity, respectively. Table 15.2 summarizes key characteristics of the different tachyarrhythmias treated in the EP laboratory.

Table 15.2

Tachyarrhythmias Treated in the Electrophysiology Laboratory

Arrhythmia	Mechanism	Ablation Target	Sedation Level Needed
AV nodal reentry	Reentry	Slow pathway	Moderate
AV reciprocating tachycardia	Reentry	Accessory pathway	Moderate
Atrial tachycardia	Reentry, triggered activity, automaticity	Origin of focal tachycardia	Moderate
Atrial flutter	Reentry	Area of slow conduction	Moderate
Atrial fibrillation	Multiple mechanisms coexist	Pulmonary vein isolation initially	Moderate to general anesthesia
PVCs	Automaticity, reentry, triggered activity	PVC focus (outflow tract most common)	Moderate
VT with a structurally normal heart	Automaticity, reentry, triggered activity	VT focus	Moderate
VT with structural heart disease	Reentry caused by fibrosis	Critical isthmus or extensive substrate modification	General anesthesia

 

AV, Atrioventricular; PVC, premature ventricular contraction; VT, ventricular tachycardia.