REVIEW ARTICLES Paul G. Barash, MD Giovanni Landoni, MD Section Editors

Anesthesia for Catheter Ablation Procedures Alina Nicoara, MD, FASE,* Fredrik Holmquist, MD, PhD, FESC,† Chad Raggains, MSN, CRNA,* and Joseph P. Mathew, MD, MHSc*

D

RIVEN BY TECHNOLOGIC ADVANCES, the practice of interventional cardiology has evolved rapidly and expanded in recent years. Procedures that traditionally were possible only through surgical intervention have become minimally invasive. Catheter ablation procedures for arrhythmias, especially atrial fibrillation, now commonly are performed at most large medical centers throughout the world. In the United States, catheter ablation for atrial fibrillation has increased 15% per year from 1990 to 2005.1 To provide a perspective of the potential growth in this arena, estimates of the prevalence of atrial fibrillation in the United States ranged from 2.7 to 6.1 million in 2010, but will rise to between 5.6 and 12 million in 2050 as the population continues to age.2 Many patients undergoing catheter ablation procedures may require anesthetic care due to the presence of major comorbidities, need for invasive monitoring, or need for deep sedation or general anesthesia. The anesthesiologist’s knowledge of the technical aspects of catheter ablation procedures and the specific impact of the anesthetic techniques on these procedures is, therefore, paramount to providing high-quality medical care. CARE PROVIDERS IN THE ELECTROPHYSIOLOGY SUITE

The complexity of electrophysiology (EP) interventional procedures, combined with the greater medical acuity of the patients undergoing these interventions, make the EP environment unique when compared with other procedures not performed in the operating room, and has accelerated the demand for anesthesiology services in this setting. In many institutions, procedures under sedation, especially with propofol, still are performed by non-anesthesiologists for convenience and economic reasons. However, there is a fine line between sedation and general anesthesia, and propofol doses used for mild sedation often overlap unpredictably with doses that achieve or maintain general anesthesia with potential harm to patients. In a retrospective analysis of proceduralist-directed, nurseadministered propofol sedation for implantable cardioverterdefibrillator procedures, there was a 10% rate of adverse events defined as unexpected transfer to an intensive care unit, respiratory failure requiring intubation/bag-mask ventilation, or hypotension requiring vasoconstrictor/inotrope support.3 In a prospective study of patients undergoing atrial fibrillation ablation at 2 European centers, 650 consecutive patients received deep sedation with propofol from an EP nurse under the supervision of an electrophysiologist.4 An oxygen saturation o85% was seen in 1.5% of patients, and arterial systolic pressure o70 mmHg occurred in 2.3%, but the investigators reported no complications related to deep sedation, and no patient required endotracheal intubation. It is difficult to

ascertain whether the findings of this study can be applied widely, because the patients in this study were American Society of Anesthesiologists (ASA) classes 1-3 and had a mean left ventricular ejection fraction of 60% and a mean body mass index (BMI) of 28. Procedures outside the operating room may deviate from the standards of anesthesia practice and guidelines, partially accounting for an increased incidence of adverse outcomes.5 Twenty-five percent of ASA closed malpractice claims in locations remote from the operating room are from cardiac catheterization and EP laboratories and are associated with nearly double the proportion of deaths compared with claims in the operating room. Inadequate oxygenation and/or ventilation represent the most common mechanisms of these injuries.6 In a retrospective chart review of patients undergoing cardiac EP procedures, 40% of patients receiving monitored anesthesia care required airway intervention ranging from nasal airway insertion to endotracheal intubation.7 The ASA recommends that a designated individual be present to monitor the patient throughout procedures performed under sedation and analgesia and that this individual have no other responsibilities if the patient is under deep sedation or receiving propofol, regardless of the level of sedation. These providers should have basic life support skills and be able to rescue patients from any level of anesthesia. Furthermore, the ASA recommends that an individual with advanced airway skills be available immediately (within 5 minutes) for moderate sedation and in the procedure room for deep sedation.8 In reality, a recent survey of cardiologists involved in procedures in the EP laboratory of academic electrophysiology programs in the United States revealed that an anesthesiologist exclusively provided deep sedation in only 16% of cases. Approximately one quarter of the respondents answered that patient and/or case complexity in the EP laboratory justify the involvement of anesthesia professionals all or most of the time; however, scheduling difficulties and perceived economic implications, such as increased turnover time and decreased operating room efficiency, were the main reasons cited for

From the *Division of Cardiothoracic Anesthesiology and Critical Care Medicine, Department of Anesthesiology; and †Department of Cardiology, Duke University Medical Center, Durham, NC. Address reprint requests to Alina Nicoara, MD, FASE, Department of Anesthesiology, Duke University, 2301 Erwin Road, DUMC 3094, Durham, NC 27710. E-mail: [email protected] © 2014 Elsevier Inc. All rights reserved. 1053-0770/2601-0001$36.00/0 http://dx.doi.org/10.1053/j.jvca.2014.05.030 Keywords: anesthesia, electrophysiology, catheter ablation, arrhythmia

Journal of Cardiothoracic and Vascular Anesthesia, Vol 28, No 6 (December), 2014: pp 1589–1603

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having registered nurse-administered sedation.9 A dedicated anesthesiology team covering multiple locations in the EP suite would overcome all of these obstacles. As stated in a recent editorial,10 while it may be possible for the non-anesthesiologist to walk the tightrope between deep sedation and general anesthesia, prospective randomized trials have not been conducted to compare methods of anesthesia care in patients undergoing complex EP procedures. Furthermore, given the complexity and duration of cardiac EP procedures, it cannot be extrapolated from the experience of other subspecialties, such as gastroenterology, with regard to the administration of propofol by non-anesthesiologists.10 ENVIRONMENT OF THE ELECTROPHYSIOLOGY LABORATORY

Electrophysiology and cardiac catheterization laboratories are commonly “off-site” at a location remote from the operating rooms, where anesthesia providers have been called only to provide airway support in emergency situations. Although true for any anesthetic plan, thorough preparation and a clear plan for summoning backup resources is even more important in the electrophysiology laboratory given the remoteness of the location, complexity of cases, and acuity of patients. In times of crisis or after hours, assistance from the perioperative staff may not arrive in a timely fashion due to unfamiliarity with the location. Inadequate preparation, and delays in delivery of necessary equipment, blood products, medications, and other resources, could prove disastrous for the patient. Layout and Design The EP laboratory traditionally has been designed by and for the cardiology team who will perform the procedures. Thus, anesthesia personnel and equipment frequently are positioned according to the preferences of the electrophysiologist and the location of the EP equipment, eg, fluoroscope and echocardiograph. Airway circuits, intravenous and arterial lines, and monitoring cables are likely to require extensions due to field-avoidance and the greater distance between the patient and anesthesiology equipment. These extensions may become damaged during manipulation of laboratory equipment, and back-up supplies should be readily available. Access to the patient is likely to be challenging during any part of the anesthetic, but is especially difficult after the procedure has begun with the patient positioned, sterilely draped, and surrounded by equipment. Some procedures require mild sedation during initial EP mapping, followed by a general anesthetic for the ablation. Securing the patient’s airway will be substantially more challenging in this scenario because the anesthesiologist and anesthesia machine may be located far from the patient’s head, while the fluoroscopy Carm limits the space needed for optimal airway management. Design of the EP laboratory of the future must include the needs of the anesthesiology care team. Radiation Safety During the management of anesthesia in the EP laboratory, radiation exposure during fluoroscopy is a continuous risk factor for the anesthesia provider. As the percutaneous

minimally invasive techniques have evolved, the dependence on fluoroscopy has grown exponentially. It is estimated that the annual radiation exposure per person is about 2 to 3 times higher for interventional cardiologists compared with radiologists, and the exposure has increased steadily over the past 2 decades.11,12 The level of exposure for the laboratory personnel is variable and depends on the procedure and their proximity to the patient during fluoroscopy, because scatter radiation tends to emanate from the patient in all directions. The International Commission on Radiological Protection recommends that annual occupational exposure to ionizing radiation be confined to o20 milliSievert (mSv) of effective dose averaged over a period of 5 years (100 mSv/5 years), and that it not exceed 50 mSv in any single year.13 One of the fundamental principles regulating the use of radiation in the United States is As Low As Reasonably Achievable, which emphasizes that there is no specific amount of radiation that can be considered safe and makes reduction of radiation exposure an ethical issue.14 In addition to the risk of radiation exposure, the staff of the EP procedure room is exposed to regular use of heavy lead aprons and other protective gear, often with poor ergonomic design, leading to a predisposition to orthopedic injuries, especially to the neck, spine, and hip.12,15 A tendency to avoid using personal protective gear increases the risk of exposure to ionizing radiation.12,16 In 2003, Macle et al compared radiation exposure associated with more complex procedures, such as ablation for atrial fibrillation, to exposure during ablation for atrial flutter or accessory pathway ablation. They found that radiofrequency ablation for paroxysmal atrial fibrillation was associated with a 2-fold increase in radiation exposure to both patient and physician compared with other ablation procedures. The radiation exposure remained, however, below the upper recommended annual dose limit if an operator performed o300 procedures/year.17 The advent of complex ablation procedures and concerns over long-term radiation exposure for both patients and operators has stimulated the development of new technologies for catheter navigation. The introduction of nonfluoroscopic 3D mapping systems, such as the CARTO system (Biosense Webster, Inc, Diamond Bar, CA), EnSite NavX system (St. Jude Medical, Inc, St. Paul, MN), and MediGuide TM technology (St. Jude Medical Inc, St. Paul, MN), has reduced significantly the fluoroscopy exposure times, especially in patients undergoing atrial flutter ablation or complex atrial fibrillation procedures.18–20 Despite advancements in technology and effective procedure protocols, radiation exposure is inevitable in the electrophysiology laboratory. Therefore, personal radiation protection devices should be used, including a 2-piece lead apron with wrap-around back coverage to prevent exposure to scatter radiation, a thyroid shield, and leaded glasses with built-in temple shields. Other protective equipment includes lead sidedrapes, rolling shields, and hanging/ceiling-mounted shields.21 A recent study evaluated the impact of a comprehensive safety program on patient and operator radiation exposure during pulmonary vein isolation. This program included the use of nonfluoroscopic 3D mapping and catheter navigation. The study found that the mean operator exposure time was reduced

ANESTHESIA FOR CATHETER ABLATION PROCEDURES

by 50%, and the mean patient skin dose was reduced by 3 to 10 times.22 CARDIAC ABLATION PROCEDURES

Arrhythmias: Etiology and Classifications The etiology of cardiac arrhythmias usually falls into 1 of 3 categories: (1) disorders related to impulse formation (automaticity or triggered activity), (2) impulse conduction (reentry), or (3) a combination of these anomalies.23 Automaticity and triggered activity involve the ability of a cell to initiate an impulse. Under normal circumstances, automaticity is confined to the myocardial cells in the atria, the atrioventricular (AV) node, and the His-Purkinje system. Under physiologic conditions, the rate of spontaneous discharge is highest in the sinus node, which controls the normal cardiac rhythm. However, pathologic conditions, such as myocardial infarction, can result in abnormal automaticity and thus give rise to arrhythmia, eg, atrial tachycardia or ventricular tachycardia. Triggered activity relates to additional depolarizations that occur during or immediately after a cardiac depolarization, and may cause a sustained arrhythmia.23 This phenomenon typically is rate-dependent, and is thought to be involved in the initiation of “torsades de pointes” in long QT syndrome. Reentry occurs when a propagating action potential does not terminate, but continues to circulate around areas of block (Fig 1). Reentry currently is thought to be the mechanism of most recurrent clinical arrhythmias and is considered to be either anatomic (the underlying structure defines the pathway) or functional (without clearly defined anatomic borders). Typically, a reentry requires a central area of block (anatomic or functional), unidirectional conduction block, and areas of

Fig 1. A schematic illustration of the mechanism behind reentry. Instead of terminating, the propagating wavefront continues to circle around the central area of block (which could be anatomic or functional) as long as there is fully recovered (ie, excitable) tissue ahead of the wavefront. The fully recovered and the partly recovered tissue together make up the so-called excitable gap.

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slow conduction. In addition, an initiating trigger is required, commonly a premature impulse that could be due to abnormal automaticity or triggered activation. Two common examples of anatomic reentry are isthmusdependent atrial flutter (circus movement in the right atrium around the tricuspid annulus) and AV reentrant tachycardia (circus movement involving the atria, AV node, ventricle(s), and the accessory pathway). Functional reentry is not limited to anatomically defined structures, and usually consists of smaller, often fluctuating, reentrant circuits defined by the electrophysiologic properties of the tissue.23 Arrhythmias thought to be associated with functional reentry include atrial and ventricular fibrillation, as well as some forms of ventricular tachycardia.23 Arrhythmias also can be classified by rate (brady- or tachycardia) or site of origin, such as atrial, junctional, or ventricular. Two of the most common arrhythmias encountered in the EP laboratory for catheter ablation procedures are atrial fibrillation and ventricular tachycardia. The initiation and maintenance of atrial fibrillation may result from (1) multiple random propagation wavelets, (2) focal electrical discharges, and (3) localized reentrant activity with fibrillatory conduction. According to the multiple random wavelets hypothesis, atrial fibrillation results from independent wavelets that occur simultaneously and propagate through the right and left atria. A minimum number of wavelets is required to initiate atrial fibrillation, and certain conditions, such as slowed conduction, increased atrial mass, and shortened refractory periods, favor the perpetuation of atrial fibrillation.24 In a subset of patients, focal triggers commonly located in the cardiac tissue sleeves around the pulmonary veins, may initiate atrial fibrillation. Maintenance of atrial fibrillation depends on atrial size, pressure, and wall stress, extent of atrial wall fibrosis, autonomic tone, inflammation, and genetics.25 Different types of atrial fibrillation are summarized in Table 1. Ventricular tachycardia (VT) is defined as a cardiac arrhythmia of 3 or more consecutive complexes emanating from the ventricles at a rate 4100 bpm.26 VT can be idiopathic or related to structural heart disease. Ventricular tachycardia also can be classified according to (1) the morphology of the electrocardiogram (monomorphic or polymorphic), (2) duration of arrhythmia (nonsustained [with a duration o30 ms], or sustained), or (3) underlying etiology (reentry, enhanced automaticity, or triggered automaticity). Idiopathic VT most commonly has a left bundle-branch block electrocardiographic pattern and arises from the right ventricular outflow tract or, less frequently, from the tricuspid annulus. Although less common, idiopathic VT can arise from the left side (left ventricular outflow tract, aortic cusps, or septum) and have a variable electrocardiographic pattern. Ventricular tachycardia in the presence of structural disease, such as prior myocardial infarction, dilated cardiomyopathy, or arrhythmogenic right ventricular dysplasia, may result from multiple reentrant circuits or from large reentrant circuits originating deep in the myocardium and may, therefore, be more difficult to ablate.27 Common indications for ventricular tachycardia ablation, based on the 2009 recommendations of

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Table 1. Classifications of Atrial Fibrillation Classification

Definition

Episode AF Paroxysmal AF

AF with a duration of at least 30 seconds documented by ECG monitoring Recurrent AF (Z2 episodes) that terminates spontaneously within 7 days, or episodes of AF r48 hours, terminated with electrical or pharmacologic cardioversion. Continuous AF that is sustained beyond 7 days, or episodes of AF that are terminated by electrical or pharmacologic cardioversion after 48 hours but before 7 days of onset Continuous AF for more than 12 months Refers to a group of patients for whom the decision has been made not to restore or maintain sinus rhythm by any means, including surgical or catheter ablation.

Persistent AF Longstanding persistent AF Permanent AF

Adapted from Calkins et al: HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation. Heart Rhythm 9:632-696, 2012.24 Abbreviations: AF, atrial fibrillation; ECG, electrocardiogram.

the European Heart Rhythm Association and Heart Rhythm Society, are presented in Table 2.27 Technical Aspects of Catheter Ablation The ablation procedure generally is performed in the following sequence: (1) achieve vascular access, (2) induce the arrhythmia to confirm the diagnosis, (3) locate the source by mapping, (4) perform ablation, and (5) test to confirm the results of ablation.

The specific catheter setup depends on the areas of interest and on the specific patient procedural management needs (Table 3). However, a typical setup includes multipolar recording electrode catheters placed in the coronary sinus, right atrium, right ventricle, and close to the His-bundle (Fig 2). When pulmonary vein isolation is performed in patients with atrial fibrillation, a decapolar circular-shaped catheter typically is placed in the pulmonary vein via a transseptal puncture to confirm electrical isolation of the pulmonary veins (Figs 3 and 4).

Placement of Catheters Electrode catheters are used to record and pace during electrophysiologic procedures. To introduce catheters, the percutaneous approach is used almost exclusively. The catheters are inserted most commonly via a femoral vein, but the jugular veins occasionally may be used, eg, to facilitate coronary sinus access or in subjects with abnormal cardiovascular anatomy. Arterial access sometimes is required for mapping the left ventricle, although the left heart also could be accessed via the venous system using a transseptal approach. On rare occasions, access to the pericardial space is required for an epicardial approach to ablate arrhythmias such as specific forms of ventricular tachycardia. In a recent survey of tertiary centers that perform ventricular tachycardia ablation, respondents reported that only 17% of procedures involved epicardial mapping.28

Fluoroscopy, 3D-Mapping Systems, and Echocardiography Conventionally, fluoroscopy is used to guide the intracardiac positioning of the catheters, and standard frontal and/ or oblique projections typically are used. In recent years, advanced electroanatomic mapping systems have become available and, increasingly, are used in the clinical routine. These systems allow chamber reconstruction and tagging of important anatomic landmarks and can display activation and voltage maps. To improve visualization even further, these systems allow integration of the catheter-derived electrical information, with imported radiographic images. The use of electroanatomic systems has not influenced significantly the procedural time or success rate, but has led to a decrease in fluoroscopy exposure. In fact, in selected

Table 2. Indications for Catheter Ablation of Ventricular Tachycardia Patients with structural heart disease Catheter ablation recommended

Symptomatic sustained monomorphic VT (SMVT), including VT terminated by an ICD, that recurs despite antiarrhythmic drug therapy or when antiarrhythmic drugs are not tolerated or desired For control of incessant SMVT or VT storm that is not due to a transient reversible cause For patients with frequent PVC, NSVT, or VT that is presumed to cause ventricular dysfunction For bundle-branch reentrant or interfascicular VT For recurrent sustained polymorphic VT and VF that is refractory to antiarrhythmic therapy and when there is a suspected trigger that can be targeted for ablation

Patients without structural heart disease Catheter ablation recommended for For monomorphic VT that is causing severe symptoms patients with idiopathic VT For monomorphic VT when antiarrhythmic drugs are not effective, not tolerated, or not desired For recurrent sustained polymorphic VT and VF (electrical storm) that is refractory to antiarrhythmic therapy and when there is a suspected trigger that can be targeted for ablation. Adapted from Aliot et al: EHRA/HRS expert consensus on catheter ablation of ventricular arrhythmias Europace 11:771-817, 2009.27 Abbreviations: VT, ventricular tachycardia; SMVT, sustained monomorphic ventricular tachycardia; ICD, implantable cardioverter-defibrillator; NSVT, nonsustained ventricular tachycardia; PVC, premature ventricular contraction; VF, ventricular fibrillation.

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Table 3. Typical Catheter Setups for Various Electrophysiologic Procedures Typical Catheter Setup

Procedure

RA

His

CS

RV

Diagnostic procedure AVNRT AVRT Atrial flutter Atrial fibrillation

X X X

X X X

X X X X X

X X X X X

Multipolar RA Catheter (eg, Halo, Radia, or Livewire)

Circular, Multipolar Catheter (eg, Lasso NAV, Orbiter PV, or Inquiry, Optima)

X X

Abbreviations: RA, right atrium; His, His-bundle; CS, coronary sinus; RV, right ventricle; AVNRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentrant tachycardia.

patients, a near-zero fluoroscopic exposure has been achieved by using an electroanatomic mapping system instead of fluoroscopy for the duration of the procedure.29 Currently, 2 different mapping systems dominate the field: The CARTO advanced mapping system (Biosense Webster, Diamond Bar, CA) and the Ensite NavX mapping system (Endocardial Solutions, St. Jude Medical, St. Paul, MN). The CARTO system uses a magnetic field for catheter navigation (magnetic-based measurements), and only proprietary catheters can be used (Fig 5). In contrast, NavX uses an electrical field for catheter navigation (impedance-based measurements), and any catheters can be used.20 The CARTO system uses a point-to-point contact activation mapping algorithm, and requires multiple positions of the magnetic tip to create a complete picture of cardiac geometry. The NavX technology uses both contact and noncontact mapping systems, and simultaneously can display 3D positions of many catheters. Intracardiac echocardiography (ICE) is used at some centers to improve the imaging of intracardiac anatomy. This may be particularly useful when performing a transseptal puncture. In addition to its utility during transseptal puncture, ICE imaging during pulmonary vein ablation provides direct visualization of the pulmonary veins and the atrial-venal junction, and ensures that the ablation catheter tip is within the pulmonary vein antrum.30 Currently, 2 modalities of ICE are available: the mechanical ultrasound catheter radial imaging system, which provides circumferential real-time imaging (Ultra ICE Catheter, Boston Scientific, Natick, MA), and the phased-array catheter sector imaging system (ACUSON AcuNav Catheter, Siemens, Malvern, PA; ViewFlex ICE Catheter, St. Jude Medical, St. Paul, MN).31 The current consensus statement on catheter and surgical ablation of atrial fibrillation shows that the use of ICE varies substantially among centers. Indeed, only 50% of task force members routinely use ICE to facilitate the transseptal procedure and/or to guide catheter ablation.24 Transesophageal echocardiography (TEE) use has been described during ablation procedures; however, it is limited due to interference with fluoroscopy imaging and the added thermal injury to the esophagus. TEE does allow for exclusion of intracardiac thrombi, guidance of transseptal puncture, and the safe and precise positioning of the guidewire in the left atrium, minimizing the risk for left atrial appendage damage. TEE also has been described during cryoballoon pulmonary vein isolation. It confirms the presence of the balloon in the antrum of the pulmonary vein, and the complete occlusion of the pulmonary vein by color-flow Doppler after balloon inflation.32 More

recently, three-dimensional (3D) TEE has been reported to provide better visualization of catheter placement and, especially, of the catheter tip, better visualization of the entire contour of the ostia “enface” of the pulmonary veins, and continuous monitoring of the catheter contact and stability (Fig 6).33 Induction of the Tachyarrhythmia and Arrhythmia Mapping Induction of the arrhythmia and subsequent mapping are performed to help position the ablation catheter at the proper site. Before induction of tachyarrhythmia, the intrinsic properties of the conduction system are evaluated. The following intervals are measured: (1) intraatrial (beginning of P-wave to atrial deflection in His), (2) AV-nodal (atrial deflection to His deflection), and (3) His-bundle to ventricular (His deflection to earliest recorded ventricular activation) (Fig 7). Mapping refers to correlation of anatomic locations and electrophysiologic phenomena (electrogram voltage, timing of

Fig 2. Fluoroscopic image (left anterior oblique view) of a basic catheter set-up during a diagnostic electrophysiologic procedure in a patient with cardiomegaly (note the presence of the mitral valve ring, coronary artery graft locators, and sternal wires). In this case, the catheters have been introduced through the left subclavian vein (image courtesy of Dr. Brett D. Atwater). Abbreviations: RA, right atrium; CS, coronary sinus; RV, right ventricle.

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Fig 3. Transseptal puncture using only fluoroscopy (left anterior oblique view). (A) The transseptal assembly (sheath, dilator, and needle) has been positioned at the atrial septum. (B) The puncture has been made, and the guidewire is advanced into the left atrium.

electrical activation, and surface electrocardiogram morphology). Several mapping techniques can be used—activation mapping, pacing mapping, and entrainment mapping—depending on the nature of the arrhythmia that must be triggered. Activation mapping refers to maneuvering the catheter to a site where the tip records electrical activity generated earlier than at any other endocardial site. The rationale for this approach is that the site of earliest activation is likely to be the origin of the tachyarrhythmia. This method of mapping then is used to identify the source of atrial tachycardias, atypical atrial flutter, and ventricular tachycardia. For pacing mapping, the mapping catheter is manipulated to the site of origin of a focal arrhythmia, most commonly ventricular tachycardia (VT). Pacing at this site using the same cycle length as the VT should generate QRS complexes that resemble those during VT. Entrainment mapping is a technique proposed for identifying slow conduction in patients with macroreentrant VT or atypical atrial flutter. Like pacing mapping, the QRS complexes during entrainment, ie, the time the heart rhythm is controlled via pacing, should be similar to the QRS complexes during the tachycardia. The response of the tachycardia after cessation of pacing provides important clues regarding the etiology and site of arrhythmia. Depending on the nature of the arrhythmia, drugs that influence the electrophysiologic properties of the heart, such as adenosine, caffeine, atropine, or isoproterenol, may be needed to induce and sustain the arrhythmia.

Various types of energy can be applied, but radiofrequency (RF) energy most frequently is used, as it is effective and relatively simple.24 When RF is applied, the ablation catheter heats the tissue through direct resistive heating, and also through a secondary process of heat conduction to the surrounding myocardium. Irreversible coagulation necrosis occurs, which evolves into a scar. The size of the scar depends on a number of factors

Catheter Ablation Catheter ablation is used to treat a variety of arrhythmias, most commonly supraventricular tachycardias, atrial fibrillation (AF), atrial flutter, and VT. The ablation is performed by applying energy to the cardiac tissue via an ablation catheter, thereby creating transmural lesions in the myocardial wall.

Fig 4. A fluoroscopic image (left anterior oblique view) during pulmonary vein isolation for atrial fibrillation ablation. Two transseptal sheaths have been introduced in the left atrium. A circular, multipolar catheter is used to trace pulmonary vein activity during and after the ablation. A temperature probe has been placed in the esophagus to avoid thermal injury to the esophagus.

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Fig 5. Posterior-anterior view of the left atrium during pulmonary vein isolation of atrial fibrillation. The CARTO advanced mapping system (Biosense Webster, Diamond Bar, CA) is being used. A virtual map of the left atrium (fast anatomic map) has been created and important anatomic landmarks are tagged (eg, ablation points in the current map). As seen from the red ablation points, the pulmonary veins have been encircled. A decapolar, circle-shaped catheter is placed in the left upper pulmonary vein with the ablation catheter located nearby.

including tissue contact, pulse energy and duration, convective cooling by the blood, and size of the electrode.34 In certain instances, the catheter tip must be cooled to apply sufficient energy to create a lesion that is large enough to be

therapeutic, without significantly increasing the temperature in the adjacent tissues. This usually is achieved by flushing saline through openings in the electrode (external open irrigation) or by circulating 5% dextrose within the electrode (internal closed

Fig 6. Three-dimensional transesophageal echocardiographic image showing the ostium of the left superior pulmonary vein and the ablation catheter tip at the middle portion of the ligament of Marshall (from Mackensen et al: Real-time 3-dimensional transesophageal echocardiography during left atrial radiofrequency catheter ablation for atrial fibrillation. Circ Cardiovasc Imaging 1:85-86, 200870). Abbreviations: LSPV, left superior pulmonary vein; CATH, ablation catheter; LOM, ligament of Marshall; LAA, left atrial appendage; MV, mitral valve.

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Fig 7. A typical baseline setup with 4 standard 12-lead ECG leads (aVL, III, V1, and V6), 2 His-bundle recordings (distal and proximal; HISd and HISp), and 5 bipolar recordings from the coronary sinus (CS1-2 through CS9-10), with CS9-10 the most proximal, and finally a recording from the right ventricle (RVd). The atrial signal can be seen in the proximal His-bundle recording (A) as well as in the CS leads. During normal activation, the most proximal CS lead is activated first, and the most distal last (the blue dashed line in the figure). The His-bundle activation can be seen most clearly in the distal His-bundle recording (H), and the ventricular activation (V) is seen in both His-leads as well as in CS9-10 (left ventricular branch) and RV-lead. Abbreviations: AH, time interval from atrial activation to His-bundle activation; HV, time interval from Hisbundle activation to ventricular activation; PR, time interval from onset of P-wave to onset of R-wave; RR, time interval between 2 consecutive R waves.

irrigation).34 To date, no trials have compared open irrigation with closed irrigation;27 however, external irrigation may result in more effective cooling of the catheter and a lower risk for thrombus formation. Of note, external irrigation does require intravascular saline administration amounting to a median of 1 L of saline, which may cause pulmonary edema.35 The use of irrigated tip versus conventional RF electrodes increases efficacy and decreases procedure duration of atrial flutter ablation.36 There is no definitive proof of similar benefits when using these catheters in AF ablation.24 Cryoablation, either point-to-point or balloon-based, has emerged as an alternative to an energy source. Cryoablation works by delivering liquid nitrous oxide under pressure through the catheter tip or within the balloon, where it changes to the gaseous state. This freezes the tissues, disrupts cell membranes, and ultimately causes cell death. In a recent systematic review, cryoballoon pulmonary vein isolation had an acute procedural success rate 498%. For patients with paroxysmal AF, the 1-year freedom from recurrent AF without antiarrhythmic drug therapy compared favorably with results reported in the global RF literature.37 For persistent AF, more extensive catheter ablation beyond pulmonary vein isolation with cryoballoon ablation may be required.37

Other energy types, such as high-intensity focused ultrasound, laser, or microwave, are in various stages of development or clinical investigation.24 Electrical isolation of the pulmonary veins now is recognized as the cornerstone of AF ablation.18 The goal of pulmonary vein isolation is complete block of conduction out of the vein (exit block), and block of conduction into the vein (entrance block) (Fig 8). Pulmonary vein isolation is achieved by creating a series of point-by-point RF lesions that encircle the 2 left and 2 right pulmonary veins. Additional linear ablation lesions can be created between the lesions encircling the left and right pulmonary veins (“roof line”), between the lesion encircling the left pulmonary veins and the mitral valve (“mitral isthmus”), between ipsilateral superior and inferior pulmonary veins and encircling the superior vena cava38 (Fig 9). More recently, investigators have observed that potentials can arise from the posterior left atrial wall, ligament of Marshall, crista terminalis, interatrial septum, and coronary sinus. This has led to an increase in the gamut of catheter ablation techniques.39 Catheter ablation for VT can be performed in an endocardial or epicardial fashion. Endocardial catheter ablation can be curative in cases of idiopathic VT; however, in patients with structural heart disease, adequate tissue ablation is more

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Fig 8. The surface ECG leads (I, aVF, and V1), the signals from a circular multipolar catheter (Ls 1,2 through Ls 19,20) located within the PV, and coronary sinus catheter (CSd and CS3,4) during ablation. The artifact on the signal from the ablation catheter is caused by the ongoing ablation. The first 2 atrial sinus beats are conducted (with delay) to the pulmonary veins, but the final 2 are not conducted, illustrating entrance block into the PVs (Ls 9,10 and 11, 12). Abbreviations: A, atrial activation; PV, pulmonary vein activation; V, ventricular activation.

difficult to achieve due to the location of the reentrant circuits. In these patients, the cornerstone of therapy for ventricular arrhythmias is placement of an implantable cardioverterdefibrillator (ICD). However, adjunct therapy with catheter ablation in patients with frequent ICD shocks for VT may improve symptoms and quality of life.35 For VT originating from the left ventricle, access to the left ventricle commonly is achieved in a retrograde fashion through the aortic valve. Damage to the aortic valve or the coronary arteries ostia is possible but rare. Epicardial ablation is performed when VT originates from a deep intramural or epicardial source. The pericardial space is accessed under fluoroscopic imaging with contrast injection followed by placement of a guidewire and introducer sheath40 (Fig 10).

ANESTHETIC CONCERNS SPECIFIC TO CATHETER ABLATION PROCEDURES

General Considerations The patient population requiring EP procedures can vary from healthy young patients who present for ablation of an AV-nodal reentry tachycardia to patients with left ventricular assist devices for end-stage heart failure and multiple comorbidities who present for VT ablation. Understanding the complexity of the patient population and documenting a thorough patient history will significantly improve administration, efficacy, and safety of the anesthesia. Patients presenting for AF and other atrial-related procedures frequently are obese with obstructive sleep apnea,41 pulmonary hypertension, and/or chronic anticoagulation. Prolonged supine positioning after removal of femoral venous and

Fig 9. Schematic of common lesion sets used in atrial fibrillation ablation. (A) Circumferential ablation lesions around the left and right pulmonary veins. (B) Additional ablation lines: “Roof line” connecting the lesions encircling the pulmonary veins, and an anterior ablation line connecting the “roof line” to the mitral annulus anteriorly. (C) Additional ablation lines between the superior and inferior pulmonary veins and encircling the superior vena cava (from Dewire J, Caulikins H: State-of-the-art and emerging technologies for atrial fibrillation ablation Nat Rev Cardiol 7:129-138, 201038 ).

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Fig 10. Fluoroscopic image during epicardial ablation (right anterior oblique view). A catheter has been placed in the right ventricular outflow tract (RVOT) using a long sheath to improve stability. Simultaneously, another catheter is placed in the epicardial space. An angiogram typically is performed to avoid accidental ablation too close to the coronary arteries.

arterial sheaths also can aggravate respiratory disease and may necessitate invasive or noninvasive postoperative ventilation. Because the intraoperative interruption of EP procedures can be detrimental to the patient’s safety and to operative efficacy, the need for specific venous access and invasive monitoring must be discussed adequately before the start of the case. As the cardiologist commonly obtains femoral venous and/or arterial access, it must be clear when, and if, the anesthesiologists will have access to such lines, whether such access will be adequate for the needs of both the cardiology and anesthesiology care teams, and whether these lines will remain in situ or be removed postoperatively. Surgically placed femoral arterial access can be shared with the anesthesia provider, but can become obstructed by the large operating catheters required for mapping and/or ablation. Therefore, separate radial artery access is preferred. Similarly, femoral venous access can be shared, but jugular or subclavian venous access should be considered if separate central pressure monitoring is essential or if peripheral venous access is inadequate. The electrophysiology and anesthesia care teams also should discuss the electrophysiologic effects of anesthetic agents, the potential need for vasopressors or inotropes, plans for anticoagulation, and postprocedural disposition of the patient. The amount of fluid administered intravascularly for cooling of the ablation catheter by external irrigation should be discussed and included in the overall patient’s fluid balance. Esophageal Temperature Monitoring During RF ablation, esophageal temperature should be monitored for conductive heat transfer to the esophagus, which

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may cause esophageal injury and possible transmural tissue necrosis, mediastinitis, and a fistulous connection between the esophageal lumen and the left atrium (atrio-esophageal fistula). Rapid elevation of esophageal luminal temperature (40.051C0.11C/second) may indicate efficient transfer of heat to the esophagus due to a combination of catheter orientation, catheter contact, and minimal or absent intervening connective tissue between the left atrium and the esophagus. Although thresholds of 38.51C to 401C have been cited in the literature,42,43 the authors terminate energy delivery for temperature increases of 0.51C to 11C above baseline. Another consideration is the observed temperature rise after cessation of energy delivery. Some patients continue to have a temperature rise of 11C to 21C even after the burn is terminated. Thus, a burn frequently will be terminated after a rise of 0.21C-0.41C with the knowledge that the temperature likely will continue to rise above the preferred maximum limit. Although still the most common strategy to minimize esophageal injury, monitoring esophageal intraluminal temperature is limited by the variability in esophageal wall and left atrial wall thickness, extent of periesophageal connective tissue, adequate contact between the temperature probe and the esophageal wall, and orientation, positioning and distance of the temperature probe in relation to the region of ablation.44 In addition to monitoring intraluminal temperature, other methods used to minimize esophageal injury are limiting the ablation pulse to o20 seconds, moving the ablation lines, energy titration, or using alternate ablation modalities.45 Systemic Anticoagulation During the procedure, patients may be anticoagulated, depending on the location of the ablation and the need for transseptal puncture. Right heart procedures that do not involve placement of catheters in the left ventricle or left atrium do not require systemic anticoagulation with heparin unless there are factors that may increase the risk for thromboembolization, ie, prior venous emboli, risk factors for thrombosis (factor V Leiden), extensive ablation, or use of multiple venous catheters. Left heart procedures require systemic anticoagulation with heparin. For patients undergoing AF ablation, heparin is administered before or immediately after the transseptal puncture as an initial bolus followed by a continuous infusion. Heparin is administered regardless of systemic anticoagulation with warfarin prior to the procedure.24 For patients who undergo VT ablation, intravenous heparin commonly is administered as an initial bolus followed by a continuous infusion or intermittent boluses. Greater degrees of anticoagulation may be considered if long vascular sheaths are inserted into the ventricle by retrograde aortic or transseptal approaches.27 Most common dosing regimens for heparin in left heart procedures are summarized in Table 4. Anticoagulation guidelines that pertain to cardioversion of AF should be followed for patients presenting for AF ablation.24 Historically, patients who are systemically anticoagulated with warfarin before the procedure have been “bridged” with intravenous or low-molecular-weight heparin prior to ablation. However, this approach has led to a high incidence of bleeding complications, especially at the site of vascular access.24,46 Therefore, the more recent trend is to perform AF

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Table 4. Dosing Regimens for Heparin Administration for Left Heart Procedures Procedure

Atrial fibrillation24 Ventricular tachycardia27

Heparin Bolus Dose

Heparin Infusion Dose

Target ACT

140 U/kg 50-100 U/kg or 5,000-10,000 U

2,000-2,500 U/h 1,000-1,500 U/h

ACT ¼ 300-400 sec ACT Z250 sec

ablation in patients who are continuously therapeutically anticoagulated with warfarin.24 The same regimen of heparin administration described above is used in these patients, except that the initial bolus dose is reduced by 20% in patients who present with a supratherapeutic international normalized ratio (INR) (ie, INR 42.2) or who have a high baseline ACT (150200 milliseconds). A more recent preprocedural strategy for systemic anticoagulation in patients with AF involves the use of a thrombin inhibitor (dabigatran) or a factor Xa inhibitor (rivaroxaban, apixaban). Although clinical periprocedural experience with these novel agents is limited, there is growing evidence that, in these patients, a standard intraprocedural heparin protocol results in delayed and lower levels of anticoagulation, according to ACT measurements.47,48 Data are conflicting regarding whether lower levels of intraprocedural anticoagulation translate into a higher risk for thromboembolic complications.47,49 In patients anticoagulated with novel agents, an initial heparin bolus of 160 U/kg to 180 U/kg is administered followed by an infusion of 4,000 U/h to 5,000 U/h to maintain the targeted ACT. At the end of the procedure, heparin is reversed by administering protamine, preferably before removing the vascular sheaths, to a target ACT at baseline or 20 to 30 points above baseline. Removal of venous sheaths 10-Fr or smaller requires 10 minutes of direct pressure before reassessing the site for bleeding. Removal of venous sheaths larger than 10-Fr initially may require 15 minutes. Removal of arterial sheaths requires 15-20 minutes of direct pressure. Percutaneous closure devices may be used for patients considered high risk for protamine-related complications. Patients also are required to lie flat for 4 hours and are discouraged from lifting their head without assistance because this can increase intra-abdominal pressure and lead to rebleeding at the femoral site. If rebleeding occurs, direct pressure will be applied until hemostasis is achieved, after which the patient must lie flat for an additional 4 hours. Types of Anesthesia and Associated Modalities of Ventilation Ventilation practices during cardiac ablation can range from conventional to extremely unconventional. Because pulmonary vein isolation and ablation for AF require sustained contact between the ablation catheter and the cardiac tissue for up to a minute, ventilation can reduce catheter stability due to changes in the length of the path of the catheter and variations in the dimensions of the left atrium and pulmonary veins. Realistic expectations regarding safety and efficacy of various ventilation modes must be discussed clearly and agreed upon before the start of the case. Catheter ablation can be performed under deep sedation or general anesthesia. Several studies attest to the safety of performing catheter ablation under deep sedation with

spontaneous ventilation; however, complex ablations for AF tend to be long, painful, and uncomfortable procedures. Patient movement and variable diaphragmatic motion during spontaneous ventilation may result in disturbances of the electroanatomic mapping system, may interfere with precise catheter placement, causing mapping or ablation inaccuracies, and may even increase the procedure time. In a prospective study of 650 patients undergoing AF ablation under deep sedation with propofol, no complications related to deep sedation were reported, and no patient required endotracheal intubation. However, in 1.5% of patients, saturation fell below 85%, requiring bag mask ventilation, chin lift, increase in oxygen flow, and/or a decrease in the propofol infusion rate.4 If deep sedation with spontaneous ventilation is desired, airway obstruction can lead not only to inadequate oxygenation or ventilation, but also to exaggerated chest wall and diaphragmatic movements. Noninvasive positive-pressure ventilation, via continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BPAP), prevents airway obstruction and can ensure smooth, safe sedation anesthesia. CPAP delivers the same level of positive pressure during all phases of ventilation, and BPAP provides lower levels of pressure during expiration and higher levels during inspiration. Lower levels of positive pressure delivered during the expiratory phase of ventilation may improve patient comfort and compliance and minimize the risk for gastric insufflation during anesthesia sedation. General anesthesia avoids the issues of undersedation, which include patient movement due to back pain and oversedation, which may result in airway obstruction and exaggerated chest wall excursions. In a recent randomized study of patients undergoing radiofrequency ablation for AF, general anesthesia appeared to produce superior results compared with sedation: Shorter fluoroscopy time (53 minutes v 84 minutes), more patients with freedom from arrhythmia at 17 months (88% v 69%), and fewer patients with recovered pulmonary vein conduction (19% v 42%). Patients in the general anesthesia group also had significantly shorter fluoroscopy time and procedure time.50 However, tidal volume during mechanical ventilation also can disrupt the stability of the ablation catheter. Also, the electrophysiologist may require long periods of breath-holding during transseptal puncture, mapping, and ablation, which may not be well tolerated due to obesity or underlying lung disease. High-frequency jet ventilation (HFJV) may overcome these shortcomings of mechanical ventilation.51,52 In a retrospective study of patients undergoing atrial ablation procedures, Goode et al found that procedure duration was decreased and fewer ablation lesions were required to obtain pulmonary vein isolation when HFJV was used versus conventional controlled mechanical ventilation.53 Because of difficulty in delivering inhalation anesthetics, maintenance of

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anesthesia during HFJV is achieved through a total intravenous anesthetic technique with a short-acting anesthetic, such as propofol, remifentanil, or dexmedetomidine, with or without muscle relaxants.51,52 An alternative to HFJV is low-flow low-volume ventilation using conventional ventilators with unconventional settings: High respiratory rate (30-40 breaths/minute), low tidal volume (200-300 mL), positive end-expiratory pressures of 5-10 cm H2O, and I:E ratio of 1:1. These settings may facilitate adequate gas exchange while providing more procedural field quiescence during critical periods of ablation. It is important to alternate low-flow/low-volume ventilation with more conventional mechanical ventilation to prevent hypercarbia and atelectasis. Anesthetic Considerations Data on the role of individual anesthetics in EP procedures are limited because patients generally receive a combination of drugs. Anxiolytics, such as midazolam, and opioids, such as fentanyl, are used to facilitate sedation. Intravenous anesthetics (eg, propofol, ketamine, etomidate, and dexmedetomidine) can be used for induction or maintenance of general anesthesia. Volatile anesthetics may alter cardiac conduction. Enflurane, isoflurane, and halothane increase refractoriness of accessory and AV pathways and enhance automaticity of secondary atrial pacemakers relative to the sinoatrial node, which accounts for the occurrence of ectopic atrial rhythms.54 In contrast, sevoflurane seems to have no effect on the electrophysiologic nature of the normal AV or accessory pathway, and no clinically important effect on the sinoatrial node.55 Isoflurane, sevoflurane, and desflurane prolong the heart rate-corrected QT interval.56 Neuromuscular relaxants modulate autonomic tone via ganglionic stimulation or blockade, act directly at sympathetic terminals, or cause vasodilation and reflex tachycardia by releasing histamine. Succinylcholine can precipitate both bradyand tachyarrhythmias; pancuronium is vagolytic and may increase heart rate; and vecuronium may be associated with bradycardia. Based on small studies in humans and on isolated heart preparation in animals, rocuronium is not associated with a significant change in heart rate.57,58 Certain ablation techniques may require the electrophysiologist to use high-frequency phrenic/diaphragm pacing during the procedure, to evaluate for potential ablation-related phrenic nerve damage. If phrenic pacing is required, neuromuscular blockade should not be used, or the neuromuscular blockade should be reversed. Opioids also may have a central vagotonic effect with depression of sinoatrial automatism or AV node conduction. This results in bradycardia, especially when high doses of opioid are used. In an animal study, remifentanil administered as a bolus (1 μg/kg) followed by an infusion (0.5 μg/kg/min) depressed sinus node automaticity and AV conduction,59 a possible explanation for clinical observations of remifentanilrelated bradyarrhythmias. Of note, the doses administered above are greater than the doses used in clinical practice, which may vary from 0.02 μg/kg/min for patients undergoing sedation to 0.2 μg/kg/min in patients undergoing general anesthesia.

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Propofol has no clinically significant effect on the electrophysiologic expression of the accessory pathway and the refractoriness of the normal AV conduction system. In addition, propofol has no direct effect on sinoatrial node activity or intra-atrial conduction.60 Dexmedetomidine, an α2-adrenergic receptor agonist, decreases central sympathetic outflow with resultant decreases in heart rate and blood pressure. Severe bradycardia and refractory cardiac arrest associated with administration of dexmedetomidine have been described in case reports.61,62 Small animal studies have shown that ketamine has minimal effect on AV conduction and atrial refractoriness, but may slow atrial and ventricular conduction and prolong ventricular refractoriness without inducing arrhythmias.63,64 In a recent study, patients undergoing supraventricular tachycardia ablation with deep sedation received ketamine or propofol. Heart rate, systolic and diastolic blood pressure, and atrial conduction time were increased significantly with ketamine versus propofol.65 Therefore, the stimulatory effects of ketamine may be beneficial in patients with pre-existing bradycardia and hypotension. For easy titration and timely emergence, the authors generally use a combination of shortacting anesthetics such as remifentanil (in doses ranging from 0.02-0.2 μg/kg/min) and propofol, with vecuronium for neuromuscular blockade. Table 5 summarizes some of the cardiac electrophysiologic effects of the commonly used anesthetics. Vasoactive drugs may be necessary during induction of arrhythmias and cardiac mapping. Isoprenaline (isoproterenol),

Table 5. Common Anesthetic Medications and Their Electrophysiologic Effects Drug

Enflurane, Isoflurane, Halothane

Sevoflurane Desflurane Succinylcholine Pancuronium

Vecuronium Opioids Propofol

Ketamine

Dexmedetomidine

Electrophysiologic Effects

Increases refractoriness of AV node Increases refractoriness of accessory pathways Increases automaticity of secondary atrial pacemakers Prolongs QT interval54 No effect on AV or accessory pathways No effect on the SA node55 Prolongs QTc interval 56 Stimulates muscarinic receptors in the SA node71 Vagolytic action Peripheral release of norepinephrine Inhibition of norepinephrine uptake57 Minimal effect on automaticity Minimal effect on refractoriness72 Prolongation of AV node conduction Depressant effect of the SA node73 Decreases P-wave dispersion No effect on AV node conduction No effect on accessory pathways conduction74 Minimal effect on atrial refractoriness Minimal effect on AV conduction May slow intra-atrial conduction May slow intraventricular conduction May prolong ventricular refractoriness Decreases central sympathetic outflow

Abbreviations: AV, atrioventricular; SA, sinoatrial.

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a beta-adrenergic drug, is used to increase the heart rate to facilitate the induction of supraventricular tachycardia and ventricular tachycardia, and to test the results of ablation. Incremental doses of isoproterenol infusion from 1 to 3 μg/min, and even up to 20 μg/min, are used. Atropine typically is used in standard doses from 0.25 to 1 mg if necessary. Caffeine rarely is used, but may be useful for patients with a history of caffeine-triggered tachyarrhythmia; dosing of caffeine sodium benzoate may range from 2 to 3 mg/kg. Complications Cardiac tamponade occurs in approximately 1% of pulmonary vein isolation procedures, and 6% of linear ablations.66 Clinically, it can present abruptly as a fall in blood pressure, or the hemodynamic instability can occur more gradually. Therefore, it is imperative to be vigilant for the development of cardiac tamponade, as a delay in diagnosis may be fatal. In most cases, cardiac tamponade can be managed by immediate percutaneous drainage and reversal of anticoagulation with protamine. This is best achieved by subxiphoid puncture of the pericardial space and placement of an intrapericardial catheter. Surgical drainage and repair usually are not required. Still, catheter ablation should be performed only in the context of an adequately equipped hospital with access to emergency surgical support. Other major complications have been reported in approximately 6% of catheter ablation procedures, and include pulmonary vein stenosis, thromboembolism, and atrioesophageal fistula formation. The risk for embolic strokes during catheter ablation for AF can be up to 5%, but this can be reduced by maintaining an activated clotting time 4300 seconds during the procedure.39 Atrioesophageal fistula formation is estimated to occur in 0.03% to 0.5% of cases.67 Although it is a rare complication, atrioesophageal fistula is associated with mortality in excess of 75%. In a series of 9 patients with this diagnosis, all patients died, and the diagnosis

of atrioesophageal fistula was considered in only 4 of these patients before death.68,69 The presentation of the atrioesophageal fistula may be catastrophic with exsanguination through upper esophageal bleeding, or may be more insidious with neurologic deficit, due to cerebral air embolism, and sepsis, due to esophageal contents entering the heart chambers. Pneumomediastinum on chest computed tomography (CT) and extensive ischemic changes on brain CT verify the diagnosis.67 TEE is contraindicated in these cases as it may lead to an increase in fistula size and air embolism. The hypothetical precursor of atrioesophageal fistula formation is esophageal ulceration due to thermal injury/damage. Esophageal ulcerations have been reported to occur in 6% to 26% of patients undergoing catheter ablation for atrial fibrillation even when conducted with luminal esophageal temperature monitoring.44 Pulmonary edema or decompensation of heart failure may occur due to intravascular volume administered for external irrigation and cooling of the ablation catheters, particularly in patients with preexistent depressed ventricular function and heart failure. Careful attention to fluid balance and diuresis is warranted when external irrigation of the ablation catheters is used.35 SUMMARY

Over the past decade, the role of the anesthesiologist has evolved continuously into a sine qua non component of the EP team, having intimate knowledge of the complex interventional procedures and the specific demands of the EP environment. With emphasis on coordination of care, resource optimization, and implementation of a climate of teamwork and collaboration, the anesthesiologist very likely will assume an even more enhanced role in the future. Future design of the EP suite ergonomics must take into account the needs of the anesthesia team to improve procedural workflow and maintain the focus on the patient.

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28. Sacher F, Roberts-Thomson K, Maury P, et al: Epicardial ventricular tachycardia ablation a multicenter safety study. J Am Coll Cardiol 55:2366-2372, 2010 29. Casella M, Pelargonio G, Dello Russo A, et al: “Near-zero” fluoroscopic exposure in supraventricular arrhythmia ablation using the EnSite NavX mapping system: Personal experience and review of the literature. J Interv Card Electrophysiol 31:109-118, 2011 30. Morton JB, Kalman JM: Intracardiac echocardiographic anatomy for the interventional electrophysiologist. J Interv Card Electrophysiol 1 (suppl):11-16, 2005 31. Banchs JE, Patel P, Naccarelli GV, et al: Intracardiac echocardiography in complex cardiac catheter ablation procedures. J Interv Card Electrophysiol 28:167-184, 2010 32. Siklódy CH, Minners J, Allgeier M, et al: Cryoballoon pulmonary vein isolation guided by transesophageal echocardiography: Novel aspects on an emerging ablation technique. J Cardiovasc Electrophysiol 20:1197-1202, 2009 33. Faletra FF, Regoli F, Acena M, et al: Value of real-time transesophageal 3-dimensional echocardiography in guiding ablation of isthmus-dependent atrial flutter and pulmonary vein isolation. Circ J 76:5-14, 2012 34. Wittkampf FH, Nakagawa H: RF catheter ablation: Lessons on lesions. Pacing Clin Electrophysiol 29:1285-1297, 2006 35. Stevenson WG, Wilber DJ, Natale A, et al: Irrigated radiofrequency catheter ablation guided by electroanatomic mapping for recurrent ventricular tachycardia after myocardial infarction: The multicenter thermocool ventricular tachycardia ablation trial. Circulation 118:2773-2782, 2008 36. Schreieck J, Zrenner B, Kumpmann J, et al: Prospective randomized comparison of closed cooled-tip versus 8-mm-tip catheters for radiofrequency ablation of typical atrial flutter. J Cardiovasc Electrophysiol 13:980-985, 2002 37. Andrade JG, Khairy P, Guerra PG, et al: Efficacy and safety of cryoballoon ablation for atrial fibrillation: A systematic review of published studies. Heart Rhythm 8:1444-1451, 2011 38. Dewire J, Calkins H: State-of-the-art and emerging technologies for atrial fibrillation ablation. Nat Rev Cardiol 7:129-138, 2010 39. Chikwe J, Raikhelkar J, Filsoufi F, et al: Current concepts in ablation of atrial fibrillation. Semin Cardiothorac Vasc Anesth 13:215-224, 2009 40. Stevenson WG, Soejima K: Catheter ablation for ventricular tachycardia. Circulation 115:2750-2760, 2007 41. Gami AS, Hodge DO, Herges RM, et al: Obstructive sleep apnea, obesity, and the risk of incident atrial fibrillation. J Am Coll Cardiol 49: 565-571, 2007 42. Sause A, Tutdibi O, Pomsel K, et al: Limiting esophageal temperature in radiofrequency ablation of left atrial tachyarrhythmias results in low incidence of thermal esophageal lesions. BMC Cardiovasc Disord 10:52, 2010 43. Singh SM, d'Avila A, Doshi SK, et al: Esophageal injury and temperature monitoring during atrial fibrillation ablation. Circ Arrhythm Electrophysiol 1:162-168, 2008 44. Liu E, Shehata M, Liu T, et al: Prevention of esophageal thermal injury during radiofrequency ablation for atrial fibrillation. J Interv Card Electrophysiol 35:35-44, 2012 45. Bahnson TD: Strategies to minimize the risk of esophageal injury during catheter ablation for atrial fibrillation. Pacing Clin Electrophysiol 32:248-260, 2009 46. Abhishek F, Heist EK, Barrett C, et al: Effectiveness of a strategy to reduce major vascular complications from catheter ablation of atrial fibrillation. J Interv Card Electrophysiol 30:211-215, 2011 47. Bassiouny M, Saliba W, Rickard J, et al: Use of dabigatran for periprocedural anticoagulation in patients undergoing catheter ablation for atrial fibrillation. Circ Arrhythm Electrophysiol 6:460-466, 2013

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