The electrophysiology laboratory and electrophysiologic procedures





Abstract:


The speciality of electrophysiology has evoloved dramatically encompassing both detection, diagnosis, and treatment of complex cardiac arrthymias. This chapter provides the fundamentals to appreciate EP studies and apply new techniques in the EP laboratory.




Keywords:

electrophysiology, pacemaker, ICD, CRT, ablation, arrhythmia

 


During the past two decades, the dedicated electrophysiology laboratory has evolved into a highly specialized procedure room where a variety of procedures are offered, ranging from diagnostic electrophysiologic (EP) studies, curative catheter ablation procedures, implantation of loop recorders, and pacemakers, defibrillators, and resynchronization therapy devices to extraction of chronic in-dwelling leads.


The electrophysiologic study (EPS) is an invasive procedure that involves the placement of multipolar catheter electrodes at various intracardiac sites. Electrode catheters are routinely placed in the right atrium (RA), across the tricuspid valve annulus in the area of the atrioventricular (AV) node and His bundle (a special part of the conduction system), in the right ventricle (RV), in the coronary sinus, and sometimes in the left ventricle (LV; Fig. 7.1 ). The general purposes of EPS are to characterize the EP properties of the conduction system, to induce and to analyze the mechanism of arrhythmias, and to evaluate the effects of therapeutic interventions. Invasive EP techniques and procedures are routinely used in the clinical management of patients who have supraventricular and ventricular arrhythmias ( Box 7.1 ). In today’s laboratory, computer-generated electroanatomical maps are very much a part of the jargon, and even a novice must be able to recognize the color-coded activation patterns of common arrhythmias shown later in this chapter. Individuals seeking a more in-depth discussion of the procedures and concepts described should refer to the Suggested Readings section later in this chapter.




Fig. 7.1


Catheter positions for routine electrophysiologic study (EPS). Multipolar catheters are positioned in the high right atrium (RA) near the sinus node, area of the atrioventricular (AV) node and His bundle, right ventricular (RV) apex, and coronary sinus.


Box 7.1

Clinical Applications of Electrophysiologic Studies.


Diagnostic





  • Diagnose SND



  • Determine site of AV nodal block



  • Define cause of syncope of unclear origin



  • Differentiate VT from SVT in cases of wide-complex tachycardia



  • Define mechanism of SVT or VT and map site of origin of tachycardia



Therapeutic





  • Guide drug therapy for sustained VT, aborted sudden death, or SVT



  • Select appropriate candidates for cardioverter-defibrillator and antitachycardia pacing therapy



  • Test efficacy of device therapy for ventricular tachyarrhythmias



  • Select appropriate candidates for catheter ablative and surgical therapy



  • Test efficacy of ablative and surgical therapies



Interventional





  • AV nodal ablation or modification for AF



  • Ablation for atrial tachycardia and atrial flutter



  • AV nodal modification (slow-pathway or fast-pathway ablation)



  • Accessory pathway ablation in WPW syndrome



  • Ablation of VT



Prognostic





  • Risk stratification in asymptomatic WPW syndrome



  • Risk stratification in patients after myocardial infarction



  • Risk stratification in patients with nonsustained VT



AF, Atrial fibrillation; AV, atrioventricular; SVT, supraventricular tachycardia; SND, sinus node dysfunction; VT, ventricular tachycardia; WPW, Wolff-Parkinson-White.





Equipment


An EP laboratory is equipped with radiographic imaging systems, a recording and monitoring system, a stimulator, and all drugs and equipment required for advanced cardiovascular life support (ACLS) ( Fig. 7.2 ). Although a dedicated laboratory would be preferable, in many institutions, these procedures are performed in the cardiac hemodynamic-angiographic catheterization laboratory. If used for pacemaker and defibrillator implantation procedures, the room should have air filtering equivalent to that in a surgical operating room.




Fig. 7.2


General setup of the equipment used for electrophysiologic studies (EPSs). EP, Electrophysiologic.


Although expensive and elaborate equipment cannot substitute an experienced and careful operator, the use of inadequate equipment may prevent adequate amounts of data from being collected and can make all the difference between success and failure. The arrhythmia targeted determines which equipment is required. A complete evaluation of most arrhythmias that may require activation mapping necessarily involves the use of multiple catheters, several recording channels, a programmable stimulator, and sophisticated and computerized three-dimensional (3D) mapping systems. Thus, an appropriately equipped laboratory should provide all of the equipment necessary for the most detailed study.


Electrode catheters


Diagnostic catheters


The hallmark feature of an EP catheter is the presence of at least two ring electrodes that can be used for bipolar and unipolar pacing and recording of local myocardial electrical activity. The material used to construct these catheters may be of the woven Dacron variety or synthetic materials, such as plastic or polyurethane. The number of electrodes in these catheters can vary between 2 and 20, interelectrode spacing between 2 and 20 mm, and thickness between 4 F and 7 F. The shape of these catheters can vary on the basis of the structures that they are designed to map: the crista terminalis, His bundle, coronary sinus, or pulmonary vein ostium. Typical EP catheters are shown in Figure 7.3 .




Fig. 7.3


(A) Several types of multipolar catheters used in routine electrophysiologic studies (EPSs). Note the difference in the number of electrodes and in spacing between the electrodes among the various catheters. (B) Proximal end of a quadripolar electrode catheter. The number on each pin corresponds to the electrode position at the tip of the catheter, with D representing the most distal electrode.


Ablation catheters


Ablation catheters of various designs allow the operator to map and to deliver energy in a very precise manner. These catheters vary with respect to the length of the ablation/tip electrode, which can range from 3.5 to 10 mm in length. Figure 7.4 shows commonly used ablation catheters. Notice that the tip of the catheter can be deflected to allow the arrhythmogenic myocardium to be reached. Conventionally, the tip of the ablation catheter is longer than the electrode of a diagnostic catheter to prevent overheating of the ablation electrode with consequent coagulum formation. Prevention of overheating of the ablation electrode can also be achieved by actively cooling with saline irrigation.




Fig. 7.4


Specialized large-tip catheter electrodes designed for ablative procedures.


Electroanatomical mapping catheters


In the mid 1990s, a novel technology termed nonfluoroscopic electroanatomical mapping revolutionized the practice of interventional EP. Electroanatomical mapping systems integrate three functionalities: (1) nonfluoroscopic catheter localization in 3D space, (2) 3D display of activation sequences and electrogram voltage, and (3) integration of this electroanatomical information with noninvasive images of the heart (i.e., computed tomography, magnetic resonance images, or ultrasound images [image fusion]). Two leading mapping systems are available and most laboratories use one or both. They are (1) the CARTO 3 system, manufactured by Biosense Webster, Inc., and (2) the NavX system, manufactured by St. Jude Medical.


CARTO 3.


In the mid 1990s, Biosense Webster, Inc. created a catheter that has the appearance of a standard ablation catheter with a magnetic sensor within the shaft near the tip. Together with a reference sensor, it can be used to map precisely the 3D spatial location of the catheter ( Fig. 7.5 ). The electroanatomical mapping system is called the CARTO 3 system and consists of the reference and catheter sensor, an external ultra-low magnetic emitter ( Figs. 7.6 and 7.7 ), and a processing unit. The amplitude, frequency, and phase of the sensed magnetic fields contain information to solve the algebraic equations, yielding the precise locations (see Fig. 7.6 ) in three dimensions (x, y, and z axes) and orientation of the catheter tip sensor (roll, pitch, and yaw). An electrogram can also be recorded simultaneously in space, and an electroanatomical map can be generated. The catheter can also be moved without fluoroscopy, thus decreasing radiation exposure. An example of atrial tachycardia arising from a focal point that was mapped and ablated successfully with the use of the CARTO 3 system is shown in Fig. 7.7 for focal tachycardia. A left anterior oblique (LAO) view of an electroanatomical map of the right and left atria is shown as well as the coronary sinus. The activation data seen with the color scale show the arrhythmia to arise from the ostium of the coronary sinus.




Fig. 7.5


Illustration of the principles of operation of the CARTO 3 system; specifically, how catheter location is determined. The location pad, fixed beneath the patient table, is constructed of three coils that generate ultra-low magnetic fields (1, 2, and 3 kHz). The emitted fields possess well-known temporal and spatial distinguishing characteristics that code the mapping space around the patient’s chest. Sensing of the magnetic field by the location sensor (passive) enables determination of the location and orientation of the catheter in 6 degrees of freedom.



Fig. 7.6


Ultra-low external magnetic field emitter used in the CARTO 3 system. This device is placed below the patient. The system comprises a miniature passive magnetic field sensor located at the tip of the catheter, external ultra-low magnetic field emitter, and processing unit. The system uses the magnetic technology to determine accurately location and orientation of the catheter in 6 degrees of freedom (x, y, z, roll, pitch, and yaw) and simultaneously records the intracardiac local electrogram from its tip. The three-dimensional (3D) geometry of the chamber is reconstructed in real time with the electrophysiologic (EP) information, which is color-coded and superimposed on the electroanatomical map.



Fig. 7.7


Focal tachycardia image showing an electroanatomical map of right and left atria (RA; LA) along with the coronary sinus (CS) . The activation sequence pattern of an atrial tachycardia is shown. Red: sites of early activation. Blue and purple: late sites. The activation pattern shows a focal arrhythmia arising from the anterior lip of the coronary sinus ostium. Maroon dots: sites where catheter ablation was performed. LAT, Lateral.


NavX.


The NavX system uses three low-amplitude high-frequency current fields that are generated in three axes over the patient’s thorax to compute the position of an electrode in the thorax relative to a reference electrode that can be placed in the heart or on the patient’s thorax. On the basis of these measurements, the system then displays the position of any EP catheter. The advantage of this system is that multiple catheters can be displayed, and unlike the CARTO 3 system, they are not limited to the products of a single manufacturer. Figure 7.8 shows an example of an LAO cranial view of an electroanatomical map of the left atrium (LA, purple shell) along with the four pulmonary veins and the left atrial appendage (LAA, green) constructed with NavX. Also seen are the coronary sinus catheter, tip of the ablation catheter, and a circular mapping catheter. This map was performed in a patient undergoing catheter ablation of atrial fibrillation (AF).




Fig. 7.8


Example of left anterior oblique (LAO) cranial view of an electroanatomical map of the left atrium (LA, purple shell) along with the four pulmonary veins and left atrial appendage (LAA, green) constructed with NavX. Also seen are the coronary sinus catheter, the tip of the ablation catheter, and a circular mapping catheter. This map was performed in a patient undergoing catheter ablation of atrial fibrillation (AF). CS, Coronary sinus; LIPV, left interior pulmonary vein; LSPV, left superior pulmonary vein; RSPV, right superior pulmonary vein.

(EnSite, Velocity, Quartet, SJM Confirm, and St. Jude Medical are trademarks of St. Jude Medical, Inc. or its related companies. Reproduced with permission from St. Jude Medical, © 2015. All rights reserved.)


Junction box and recording apparatus


The junction box and recording apparatus consists of pairs of numbered multiple pole switches matched to each recording and stimulation channel and permits the ready selection of any pair of electrodes for stimulation or recording. Current computer junction boxes come in banks of 8 or 16. Nowadays, the signal processor (filters and amplifier), visualization screen, and recording apparatus are incorporated as a single unit in the form of a computerized system. GE Healthcare, EP Med Systems (St. Jude Medical), and Bard Electrophysiology manufacture popular systems. Eight to 14 amplifiers should be available to process surface electrocardiogram (ECG) leads simultaneously with multiple intracardiac electrograms. The number of amplifiers can be as many as 128 in some systems. Intracardiac recordings must be displayed simultaneously, with at least three surface ECG leads. Most computers allow several pages to be stored, with one page displaying a 12-lead ECG. Thus, an operator can always have a 12-lead ECG recorded simultaneously while observing intracardiac electrogram data. The amplifiers used for recording intracardiac electrograms must have the ability to have gain modification and to alter both high and low band pass filters to permit appropriate attenuation of the incoming signals. For example, the His bundle electrogram is most clearly visualized when the signal is filtered between 30 and 40 Hz (high pass) and 400 and 500 Hz (low pass; Fig. 7.9 ). In addition, assessing unipolar electrograms also requires acquiring open filters (0.05 to 500 Hz).




Fig. 7.9


Effect of filtering frequency on the His bundle electrogram. Pacing from the proximal coronary sinus is performed at a basic cycle length of 60 ms. In each of the four panels, surface leads I, II, aV F , and V 1 are shown. A recording catheter is placed in the standard position to record the His bundle electrogram; and recordings from the proximal, mid, and distal electrode pairs are displayed. (A) His bundle electrograms, where the signal is filtered between 30 Hz (high pass) and 500 Hz (low pass); (B) recording made between filter settings of 0.05 and 500 Hz; (C) recording made between 30 and 1000 Hz; (D) recording made between 100 and 500 Hz. The clearest recording of the His bundle electrogram occurs with a filtering of the signals below 30 Hz and above 500 Hz (A) .


Stimulation apparatus


Most EPSs require a complex programmable stimulator that has (1) a constant current source, (2) minimal current leakage, (3) the ability to pace at a wide range of cycle lengths (100 to 2000 ms) from at least two simultaneous sites, (4) the ability to introduce multiple extrastimuli, and (5) the ability to synchronize the stimulator to appropriate electrograms during spontaneous and paced rhythms. The stimulator is equipped with dials or switches by which the pacing intervals and coupling intervals of the extrastimuli may be adjusted ( Fig. 7.10 ). A junction box that interfaces with the recording system and stimulator facilitates changes in the pacing site without the need to disconnect catheters. The stimulator should be able to deliver variable currents that can be accurately controlled, with a range from 0.1 to 10 mA. The ability to change pulse widths is also useful. The results of programmed stimulation can be influenced by the delivered current, and for consistency and safety, stimulation is generally performed at two and a half times diastolic threshold.




Fig. 7.10


Junction box/recording apparatus and stimulation apparatus. Image shows the Prucka CardioLab EP system. Also seen within the white oval is a computerized stimulator manufactured by Micropace. The junction box interfaces with the recording system and stimulator, thus allowing us to change the pacing site without the need to disconnect catheters.


It is preferable that the stimulator, computerized data recorder, and other devices used in EP are permanently installed. Most laboratories use a stimulator and computer system that modifies all input signals and stores them in an optical disc. All equipment must be grounded, and other aspects of electrical safety must be ensured because even small amounts of leakage current can pass to the patient and potentially induce arrhythmias. A technical engineer must check the equipment so that leakage current remains <10 mA. Figure 7.2 shows an illustration of the organization of the relevant equipment required during an EPS.


Defibrillator


A functioning defibrillator should be available at the patient’s side throughout all EPSs. A backup defibrillator is optimal in case of a rare but potentially disastrous failure of one defibrillator. Defibrillators should be tested before each study and equipped with an emergency power source. Many laboratories use commercially available R2 pads, which are placed on the patient before the EPS procedure begins. One pad is placed under the right scapula and the other on the anterior chest over the LV apex and connected to the defibrillator with an adapter. In rare instances in which transthoracic defibrillation fails to convert induced ventricular fibrillation (VF), emergency defibrillation through an intracardiac electrode catheter may be effective in terminating the arrhythmia ( Fig. 7.11 ). It is our practice to have biphasic defibrillators in our laboratories.




Fig. 7.11


Diagram of intracardiac defibrillation, which may be used when ventricular fibrillation (VF) is refractory to multiple transthoracic defibrillations. During the routine electrophysiologic study (EPS) , anterior and posterior skin patches are attached by a connector to a standard defibrillator. When multiple transthoracic high-energy shocks fail to terminate VF, the anterior patch may be disconnected and the distal pole of the right ventricular (RV) catheter attached to the defibrillator. High-energy shocks are delivered from the RV catheter to the posterior patch.

(From Cohen TJ, Scheinman MM, Pullen BT, et al. Emergency intracardiac defibrillation for refractory ventricular fibrillation during routine electrophysiologic study. J Am Coll Cardiol . 1991;18:1280-1284.)


Because the physician’s attention is often focused on the stimulator and electrograms, he or she relies heavily on the nurse to monitor the patient’s condition and to communicate significant changes. The nurse usually sits between the patient and the cardioverter-defibrillator and crash cart. The nurse monitors the patient’s blood pressure, heart rate (HR), rhythm, and oxygen saturation via a pulse oximeter; administers drugs for diagnostic and therapeutic interventions during EPS; and performs cardioversion or defibrillation when an induced hemodynamically unstable arrhythmia appears. Optimally, a second nurse is available during procedures to administer medications or assist in technical aspects of the procedure.


Implantation of pacemakers, defibrillators, and resynchronization therapy devices


Pacemakers


Pacemakers, the original devices implanted for cardiac rhythm management, have the ability to provide electrical stimulation (pace) to the heart. They are indicated in patients who no longer have the intrinsic ability to provide adequate electrical stimulation to maintain a functional HR or complete conduction from the atria to the ventricles. They can be either single or dual chamber devices with a lead in the atrium, ventricle, or both, depending on the patient, pathology, and clinical scenario. Recently, a leadless pacemaker has been approved. This device is different from standard pacemakers in that the entire device is contained within the heart, which eliminates the need for a generator and a pocket, therefore reducing the risk of infection. These devices are single-chamber ventricular pacemakers implanted via the femoral vein and are an alternative for transvenous pacemakers for patients who only require ventricular pacing. ( Fig 7.12 )




Fig. 7.12


Figure from Medtronic for Micra.

(©2019 Medtronic. All rights reserved. Used with the permission of Medtronic.)


A technique that has been showing benefit in recent research is that of His bundle pacing.


RV apical pacing causes interventricular dysynchrony, which can lead to adverse hemodynamics and progression to pacing induced cardiomyopathy (PCIM) in some patients. While biventricular pacing may be an option, it introduces a nonphysiologic ventricular activation sequence. Permanent His bundle pacing is an alternative option as it directly engages the His-Purkinje system, utilizing normal physiology to maintain synchronized ventricular activation.


Implantable cardiac defibrillators


Where pacemakers are used for bradycardic indications, defibrillators are designed to treat tachyarrhythmias, specifically ventricular tachycardia (VT) and VF. These devices have all of the functions of a pacemaker, but in addition, they have the ability to defibrillate (shock) the heart. The primary difference in these devices in comparison with a pacemaker is the use of a high-voltage lead in the RV with an active “can” (pulse generator [PG]) to complete the defibrillation circuit. The lead has at least one shock coil and acts with the PG to provide a defibrillation wave front across the heart if the need arises. In addition, all current defibrillators have the ability to pace the ventricle rapidly (anti-tachycardia pacing [ATP]) to attempt to terminate ventricular tachyarrhythmias and to prevent the need for a shock.


In addition to transvenous defibrillators, there are also subcutaneous defibrillators (SICD) that have become available in recent years. With transvenous ICDs, insertion of electrodes into the central venous circulation and inside cardiac chambers can cause vascular obstruction, thrombosis, infection, and cardiac perforation. In addition, lead failure has been estimated to be up 20% in 10 years. The SICD consists of a 3-mm tripolar parasternal lead (12 F, 45 cm) connected to an electrically active pulse generator. The lead is vertically positioned in the subcutaneous tissue of the chest, parallel and 1 to 2 cm to the left sternal mid line. The pulse generator is positioned in the subcutaneous tissue of the left lateral chest. ( Fig. 7.13 ). These devices are currently only capable of defibrillation and only have postshock (subcutaneous) pacing. They are not capable of performing any other pacing function, including ATP pacing to terminate arrhythmias or bradycardia pacing.




Fig. 7.13


Diagram of external subcutaneous pacing array system.


When a patient with an implantable cardiac defibrillator (ICD) undergoes a change in his or her antiarrhythmic drug regimen, the device may need to be tested, because changes in rate of tachycardia may necessitate reprogramming the device’s rate detection criteria, and changes in the defibrillation threshold may be caused by certain medications.


Primary prevention of sudden death


The survival rate after out-of-hospital cardiac arrest is extremely low, and attention has been directed at identifying high-risk patients who may benefit from prophylactic treatment as a means of primary prevention of sudden cardiac death. Two primary prevention trials indicated that patients with coronary disease, significant LV dysfunction (left ventricular ejection fraction [LVEF] 35% to 40%), spontaneous nonsustained VT, and inducible sustained ventricular arrhythmia by EPS experienced a survival benefit from prophylactic ICD implantation. There is no evidence that EPS-guided antiarrhythmic drug therapy is effective as preventive therapy for sudden cardiac death in high-risk individuals. A primary prevention trial, which did not require spontaneous or induced ventricular arrhythmias as entry criteria, concluded that prophylactic ICD implantation benefited patients with coronary artery disease and found an LVEF of less than 30%. This study suggests that poor LV function alone is a strong predictor of subsequent sudden cardiac death. Indications for implantation of pacemakers and ICDs are listed in Table 7.1 .



Table 7.1

Indications for Pacemaker and Implantable Cardiac Defibrillator Implantation.
























































Pacemaker
SND


  • SND with documented symptomatic bradycardia, including frequent sinus pauses that produce symptoms (class I, LE C)



  • Symptomatic chronotropic incompetence (class I, LE C)



  • Symptomatic sinus bradycardia that results from required drug therapy for medical conditions (class I, LE C)



  • Minimally symptomatic patients with chronic HR <40 bpm while awake (class IIb, LE C)



  • Not indicated for SND in asymptomatic patients (class III, LE C)



  • Not indicated for SND in patients for whom symptoms suggestive of bradycardia have been clearly documented to occur in the absence of bradycardia (class III, LE C)



  • Not indicated for SND with symptomatic bradycardia resulting from nonessential drug therapy (class III, LE C)

Acquired AV block in adults


  • Third-degree and advanced second-degree AV block at any anatomic level associated with bradycardia with symptoms (including HF) or ventricular arrhythmias presumed to be due to AV block (class I, LE C)



  • Third- and advanced second-degree AV block at any anatomic level associated with arrhythmias and other medical conditions requiring drug therapy that results in symptomatic bradycardia (class I, LE C)



  • Third- and advanced second-degree AV block at any anatomic level in awake, symptom-free patients in sinus rhythm, with documented periods of asystole ≥ 3.0 s, any escape rate <40 bpm, or an escape rhythm that is below the AV node (class I, LE C)



  • Third- and advanced second-degree AV block at any anatomic level after catheter ablation of the AV junction (class I, LE C)



  • Third- and advanced second-degree AV block at any anatomic level associated with postoperative AV block that is not expected to resolve after cardiac surgery (class I, LE C)




  • Third- and advanced second-degree AV block at any anatomic level associated with neuromuscular diseases with AV block, such as myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy (limb-girdle muscular dystrophy), and peroneal muscular atrophy, with or without symptoms (class I, LV B)



  • Second-degree AV block with associated symptomatic bradycardia regardless of the type or site of block (class I, LE B)



  • Asymptomatic persistent third-degree AV block at any anatomic site with average awake ventricular rates of 40 bpm or faster if cardiomegaly or LV dysfunction is present or the site of block is below the AV node (class I, LE B)



  • Second- or third-degree AV block during exercise in the absence of myocardial ischemia (class I, LE C)



  • Persistent third-degree AV block with an escape rate >40 bpm in asymptomatic adult patients without cardiomegaly (class IIa, LE C)



  • Asymptomatic second-degree AV block at intra- or infra-His levels found at EPS (class IIa, LE B)



  • First- or second-degree AV block with symptoms similar to those of pacemaker syndrome or hemodynamic compromise (class IIa, LE B)




  • Asymptomatic type-II second-degree AV block with a narrow QRS (class IIa, LE B)



  • Neuromuscular diseases, such as myotonic muscular dystrophy, Erb dystrophy, and peroneal muscular atrophy with any degree of AV block (including first-degree AV block), with or without symptoms, because there may be unpredictable progression of AV conduction disease (class IIb, LE B)



  • AV block in the setting of drug use and/or drug toxicity when the block is expected to recur even after the drug is withdrawn (class IIB, LE B)



  • Not indicated for asymptomatic first-degree AV block (class III, LE B)



  • Not indicated for asymptomatic type I second-degree AV block at the supra-His (AV node) level or that which is not known to be intra- or infra-Hisian (class III, LE C)



  • Not indicated for AV block that is expected to resolve and is unlikely to recur (e.g., drug toxicity, Lyme disease, or transient increases in vagal tone or during hypoxia in sleep apnea syndrome in the absence of symptoms) (class III, LE B)

Chronic bifascicular block


  • Advanced second-degree AV block or intermittent third-degree AV block (class I, LE B)



  • Type II second-degree AV block (class I, LE B)



  • Alternating bundle-branch block (class I, LE C)



  • Syncope not demonstrated to be caused by AV block when other likely causes have been excluded, specifically VT (class IIa, LE B)



  • Incidental finding at EPS of a markedly prolonged H–V interval (≥ 100 ms) in asymptomatic patients (class IIa, LE B)



  • Incidental finding at EPS of pacing-induced infra-His block that is not physiologic (class IIa, LE B)



  • In the setting of neuromuscular diseases, such as myotonic muscular dystrophy, Erb dystrophy, and peroneal muscular atrophy with bifascicular block or any fascicular block, with or without symptoms (class IIb, LE C)



  • Not indicated for fascicular block without AV block or symptoms (class III, LE B)



  • Not indicated for fascicular block with first-degree AV block without symptoms (class III, LE B)

After acute phase of MI


  • Persistent second-degree AV block in the His-Purkinje system with alternating bundle-branch block or third-degree AV block within or below the His-Purkinje system after STEMI (class I, LE B)



  • Transient advanced second- or third-degree infranodal AV block and associated bundle-branch block. If block site is uncertain, an EPS may be necessary (class I, LE B)



  • Persistent and symptomatic second- or third-degree AV block (class I, LE C)



  • Persistent second- or third-degree AV block at the AV node level, even in the absence of symptoms (class IIb, LE B)



  • Not indicated for transient AV block in the absence of intraventricular conduction defects (class III, LE B)



  • Not indicated for transient AV block in the presence of isolated left anterior fascicular block (class III, LE B)



  • Not indicated in new bundle-branch block or fascicular block in the absence of AV block (class III, LE B)



  • Not indicated for persistent asymptomatic first-degree AV block in the presence of bundle-branch or fascicular block (class III, LE B)

Hypersensitive carotid sinus syndrome and neurocardiogenic syncope


  • Recurrent syncope caused by spontaneously occurring carotid sinus stimulation and carotid sinus pressure that induces ventricular asystole of >3 s (class I, LE C)



  • Syncope without clear, provocative events and with a hypersensitive cardioinhibitor response of ≥ 3 s (class IIa, LE C)



  • Significantly symptomatic neurocardiogenic syncope associated with bradycardia documented spontaneously or at the time of tilt-table testing (class IIb, LE B)



  • Not indicated for a hypersensitive cardioinhibitory response to carotid sinus stimulation without symptoms or with vague symptoms (class III, LE C)



  • Not indicated for situational vasovagal syncope in which avoidance behavior is effective and preferred (class III, LE C)

After cardiac transplantation


  • Persistent inappropriate or symptomatic bradycardia not expected to resolve and for other class I indications for permanent pacing (class I, LE C)



  • When relative bradycardia is prolonged or recurrent, which limits rehabilitation or discharge after postoperative recovery from cardiac transplantation (class IIb, LE C)



  • Syncope after cardiac transplantation even when bradyarrhythmia has not been documented (class IIb, LE C)

Recommendations for permanent pacemakers that automatically detect and pace to terminate tachycardias


  • Symptomatic recurrent SVT that is reproducibly terminated by pacing when catheter ablation and/or drugs fail to control the arrhythmia or produce intolerable side effects (class IIa, LE C)



  • Not indicated in the presence of an accessory pathway that has the capacity for rapid anterograde conduction (class III, LE C)

Pacing to prevent tachycardia


  • Sustained pause-dependent VT with or without Q–T prolongation (class I, LE C)



  • High-risk patients with congenital LQTS (class IIa, LE C)



  • For prevention of symptomatic, drug-refractory, recurrent AF in patients with coexisting SND (class IIb, LE B)



  • Not indicated for frequent or complex ventricular ectopic activity without sustained VT in the absence of LQTS (class III, LE C)



  • Not indicated for torsades de pointes VT resulting from reversible causes (class III, LE A)

Pacing to prevent AF


  • Not indicated for the prevention of AF in patients without any other indication for pacemaker implantation (class III, LE B)

Recommendations for pacing in patients with HCM


  • SND or AV block in patients with HCM as described previously in guidelines (class I, LE C)



  • Medically refractory symptomatic patients with HCM and significant resting or provoked LV outflow tract obstruction (class IIa, LE A)



  • Not indicated for patients who are asymptomatic or whose symptoms are medically controlled (class III, LE C)



  • Not indicated for symptomatic patients without evidence of LV outflow tract obstruction (class III, LE C)

Recommendations for permanent pacing in children, adolescents, and patients with congenital heart disease


  • Advanced second- or third-degree AV block associated with symptomatic bradycardia, ventricular dysfunction, or low cardiac output (class I, LE C)



  • SND with correlation of symptoms during age-inappropriate bradycardia; the definition of bradycardia varies with patient age and expected HR (class I, LE B)



  • Postoperative advanced second- or third-degree AV block that is not expected to resolve or that persists for at least 7 days after cardiac surgery (class I, LE B)



  • Congenital third-degree AV block with a wide QRS escaped rhythm, complex ventricular ectopy, or ventricular dysfunction (class I, LE B)



  • Congenital third-degree AV block in an infant with a ventricular rate <55 bpm or with congenital heart disease and a ventricular rate <70 bpm (class I, LE C)



  • Congenital heart disease and sinus bradycardia for the prevention of recurrent episodes of intraatrial reentrant tachycardia; SND may be intrinsic or secondary to antiarrhythmic treatment (class IIa, LE C)



  • Congenital third-degree AV block beyond the first year of life with an average HR <50 bpm, abrupt pauses in ventricular rate that are two or three times the basic cycle length, or association with symptoms caused by chronotropic incompetence (class IIa, LE B)



  • Sinus bradycardia with complex congenital heart disease with a resting HR <40 bpm or pauses in ventricular rate >3 s (class IIa, LE B)



  • Congenital heart disease and impaired hemodynamics caused by sinus bradycardia or loss of AV synchrony (class IIa, LE C)



  • Unexplained syncope in the patient with prior congenital heart surgery complicated by transient CHB with residual fascicular block after a careful evaluation to exclude other causes of syncope (class IIa, LE B)




  • Transient postoperative third-degree AV block that reverts to sinus rhythm with residual bifascicular block (class IIb, LE C)



  • Congenital third-degree AV block in asymptomatic children or adolescents with an acceptable rate, narrow QRS complex, and normal ventricular function (class IIb, LE B)



  • Asymptomatic sinus bradycardia after biventricular repair of congenital heart disease with a resting HR <40 bpm or pauses in ventricular rate >3 s (class IIb, LE C)




  • Not indicated for transient postoperative AV block with return of normal AV conduction in an otherwise asymptomatic patient (class III, LE B)



  • Not indicated for asymptomatic bifascicular block with or without first-degree AV block after surgery for congenital heart disease in the absence of prior transient complete AV block (class III, LE C)



  • Not indicated for asymptomatic type I second-degree AV block (class III, LE C)



  • Not indicated for asymptomatic sinus bradycardia with the longest relative risk interval <3 s and a minimum HR >40 bpm (class III, LE C)

Implantable Cardiac Defibrillator



  • Survivors of cardiac arrest caused by VF or hemodynamically unstable sustained VT after evaluation to define cause of event and exclude any completely reversible causes (class I, LE A)



  • Structural heart disease and spontaneous sustained VT, whether hemodynamically stable or unstable (class I, LE B)



  • Syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT or VF induced at EPS (class I, LE B)



  • LVEF ≤35% caused by prior MI, at least 40 days after myocardial infarction, and NYHA functional class II or III (class I, LE A)



  • Nonischemic dilated cardiomyopathy, LVEF ≤35%, and NYHA functional class II or III (class I, LE B)



  • LV dysfunction caused by prior MI or at least 40 days after myocardial infarction, LVEF ≤30%, and NYHA functional class I (class I, LE A)



  • Nonsustained VT caused by prior MI, LVEF ≤40%, and inducible VF or sustained VT at EPS (class I, LE B)



  • Unexplained syncope, significant LV dysfunction, and nonischemic dilated cardiomyopathy (class IIA, LE C)



  • Sustained VT and normal or near-normal ventricular function (class IIA, LE C)



  • HCM with one or more major risk factors for sudden cardiac death (class IIA, LE C)




  • Prevention of sudden cardiac death, with ARVC or ARVD and one or more risk factors for sudden cardiac death (class IIA, LE C)



  • Reduction of sudden cardiac death, with LQTS, syncope, and/or VT while receiving β-blockers (class IIa, LE B)



  • Nonhospitalized and awaiting transplantation (class IIA, LE C)



  • Brugada syndrome and prior syncope (class IIA, LE C)



  • Brugada syndrome and documented VT that has not resulted in cardiac arrest (class IIa, LE C)



  • Catecholaminergic polymorphic VT, syncope, and/or documented sustained VT while receiving β-blockers (class IIa, LE C)



  • Cardiac sarcoidosis, giant cell myocarditis, or Chagas disease (class IIa, LE C)



  • Nonischemic heart disease, LVEF ≤35%, NYHA functional class I (class IIb, LE C)



  • LQTS and risk factors for sudden cardiac death (class IIb, LE B)



  • Syncope and advanced structural heart disease with thorough invasive and noninvasive investigation failing to define cause (class IIb, LE C)



  • Familial cardiomyopathy associated with sudden death (class IIb, LE C)



  • LV noncompaction (class IIb, LE C)



  • Not indicated in those without reasonable expectation of survival, with acceptable functional status for at least 1 year even after meeting ICD implantation criteria specified in class I, IIa, and IIb recommendations above (class III, LE C)



  • Symptomatic sustained VT in association with congenital heart disease, with prior hemodynamic and EP evaluation; catheter ablation or surgical repair may offer possible alternatives in carefully selected patients (class I, LE C)



  • Congenital heart disease with recurrent syncope of undetermined origin in the presence of either ventricular dysfunction or inducible ventricular arrhythmias at EPS (class IIa, LE B).



  • Recurrent syncope associated with complex congenital heart disease and advanced systemic ventricular dysfunction after thorough invasive and noninvasive investigations have failed to define a cause (class IIb, LE C)


AF, Atrial fibrillation; AV, atrioventricular; AVRC, arrhythmogenic right-ventricular cardiomyopathy; AVRD, arrhythmogenic right-ventricular dysplasia; bpm, beats per minute; CHB, complete heart block; EP, electrophysiologic; EPS, electrophysiologic study; HCM, hypertrophic cardiomyopathy; HF, heart failure; HR, heart rate; ICD, implantable cardiac defibrillator; LE, level of evidence; LQTS, long QT syndrome; LV, left ventricle; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NYHA, New York Heart Association; QRS, Q, R, and S waves; SND, sinus node dysfunction; STEMI, ST-segment elevation myocardial infarction; SVT, supraventricular tachycardia; VF, ventricular fibrillation; VT, ventricular tachycardia.


Cardiac resynchronization therapy


In the mid 1990s, a new tool was developed to assist in the management of patients with systolic heart failure (HF): biventricular pacing to improve systolic function. Since that time, the use of cardiac resynchronization devices has become a mainstay of an EP practice. These devices have undergone numerous refinements with time, and as clinical trials have been published, the patient population that can benefit from such therapy has greatly expanded ( Fig. 7.14 ). This section provides a broad overview of cardiac resynchronization therapy (CRT) as a common procedure performed in the EP laboratory.




Fig. 7.14


Indications for biventricular pacing. ACCF/AHA, American College of Cardiology Foundation/American Heart Association; CRT, cardiac resynchronization therapy; CRT-D, cardiac resynchronization therapy defibrillator; GDMT, guideline-determined medical therapy; HF, heart failure; ICD, implantable cardiac defibrillator, LBBB, left bundle-branch block; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NYHA, New York Heart Association. (From Tracy CM, Epstein AE, Darbar D, et al. ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2013;61:e6-e75.)




Theory


HF remains an extensive and expensive problem in the United States, and the majority of HF patients have systolic dysfunction. As systolic dysfunction becomes progressively worse, both mechanical and electrical remodeling occurs. The electrical component manifests in the QRS duration. As QRS duration increases, morbidity and mortality levels from systolic dysfunction significantly increase. The electrical delay often leads to delayed activation of the LV. Because of this delay in activation, the septal wall is not held stable by simultaneous contraction of the LVs and RVs, leading to a less efficient contraction. This has led to the advent of cardiac resynchronization devices to allow for pacing of both chambers to resynchronize the contraction and stabilize the septum for a more effective LV contraction.


Clinical response to CRT is variable and 30% of patients are considered “nonresponders.” One of the most important correctable causes for lack of response to CRT is suboptimal coronary sinus lead position. As a result, multisite pacing (MSP) has been developed, which may be one way to improve the number of nonresponders in an appropriately selected patient population.


Implantation procedure


The primary difference in implanting a CRT device compared with standard pacemakers and defibrillators is in the placement of an LV lead in a branch of the coronary sinus. This adds an additional level of complexity to the standard implant procedure, and thus, knowledge of the coronary sinus anatomy is essential. Given that cardiac electrophysiologists routinely place catheters in the coronary sinus for EPSs, they are very experienced in the intricacies of working in this vessel and are natural implanters for these devices. The coronary sinus is often accessed via the axillary vein and a long sheath is passed into the coronary sinus to deliver the lead. LV leads are designed to be wedged into a branch vessel of the coronary sinus, and the lead tip usually has a cant or tab to help maintain the location of the lead ( Figs. 7.15 , 7.16 , and 7.17 ). Once a lead is advanced and located in a branch of the coronary sinus, the sheath is split and removed. The lead is sutured in place and can interface with a CRT defibrillator (CRT-D) or CRT pacemaker (CRT-P) PG.




Fig. 7.15


Examples of LV leads.

(Reproduced with permission of Medtronic, Inc.)



Fig. 7.16


Examples of LV leads.

(From Boston Scientific Corporation.)



Fig. 7.17


Example of an LV lead.

(EnSite, Velocity, Quartet, SJM Confirm, and St. Jude Medical are trademarks of St. Jude Medical, Inc. or its related companies. Reprinted with permission of St. Jude Medical, © 2015. All rights reserved.)


Not only is it necessary to find a branch vein of the coronary sinus to accept the lead, location of the lead is also very important. Subgroup analyses of many major trials have investigated the importance of lead location and found that patients obtain the most benefit from a basilar location on the posterior or lateral LV. Anterior placement of the lead has no benefit because of the lack of distance between LV and RV pacing (apical RV) locations, so true resynchronization does not occur. In addition, an apical placement of the lead has been shown to be harmful because patients tend to benefit less on subgroup analyses.


With the higher complexity of implanting a LV lead comes a higher level of complications from the procedure. Procedure times tend to be longer for CRT device implantation when compared with dual chamber devices. In addition, a third lead increases the risk of short-term and long-term mechanical problems. Lead dislodgement occurs at a higher rate because of the passive mechanisms used to retain the lead in place. Often, the number of possible branches available is limited in any given patient who can accept a lead, and pacing thresholds can frequently be elevated compared with acceptable thresholds for RA and RV leads. Diaphragmatic stimulation can also be a problem, because branches from the coronary sinus can traverse very near the phrenic nerve, which can allow stimulation from the LV lead. However, even with the higher level of complications, the benefit from such resynchronization therapy can be substantial and in most patients these additional risks are easily justified.


Implantable cardiac monitors


The use of implantable cardiac monitors has recently grown in popularity as the size of devices has been reduced and the implantation procedure simplified. Implantable cardiac monitors, also known as loop recorders, can record and store arrhythmias. They are implanted subcutaneously and generally have a battery life of approximately 3 years. Such devices can be useful for patients with rare symptoms, in whom traditional monitoring is unlikely to provide a diagnosis, or with patients unwilling or unable to wear traditional noninvasive monitors. A relatively new indication for these monitors has been in the area of cryptogenic stroke. A significant portion of cryptogenic strokes is caused by asymptomatic paroxysmal AF. The implantable cardiac monitor provides a method of monitoring these patients for AF. A diagnosis of this arrhythmia would change therapy for a stroke with the initiation of anticoagulation ( Figs. 7.18 and 7.19 ).


Feb 21, 2020 | Posted by in CARDIOLOGY | Comments Off on The electrophysiology laboratory and electrophysiologic procedures

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