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Demystifying the EP Laboratory

Anesthetic Considerations for Electrophysiology Procedures

Cheruku, Sreekanth, MD*; Boud, Travis J., MD*; Kulkarni, Nitin, MD; Lynch, Isaac P., MD

International Anesthesiology Clinics: October 2018 - Volume 56 - Issue 4 - p 98–119
doi: 10.1097/AIA.0000000000000201
Review Articles

*Department of Anesthesiology and Pain Management, UT Southwestern, Dallas, Texas

Division of Cardiology, UT Southwestern and VA North Texas Health Care System, Dallas, Texas

Department of Anesthesiology and Pain Management, UT Southwestern, Dallas, Texas

The authors declare that they have nothing to disclose.

Address Correspondence to: Isaac P. Lynch, MD, Department of Anesthesiology and Pain Management, UT Southwestern Medical Group, 5323 Harry Hines Blvd., Dallas, TX 75390. E-mail: isaac.lynch@utsouthwestern.edu

Abnormalities of heart rhythm have been recognized since the ancient Egyptians first described the examination of the peripheral pulse in 1700 BCE. It was not, however, until 1887, that a more developed understanding of both cardiovascular physiology and electromagnetism culminated in the development of the electrocardiogram (ECG) by August Waller. Practical improvements to the ECG by a contemporary of Waller, Willem Einthoven, enabled the widespread evaluation of rhythm abnormalities. These developments paved the way for the exploration of early antiarryhthmic therapies, starting in the early 20th century with Karel Wenckebach, who successfully used quinine to treat a patient with atrial fibrillation (AF). Over the next several decades, a spectrum of antiarrhythmic drugs was developed to alter each phase of the cardiac action potential, and classified by Miles Vaughan Williams (Table 1). This new understanding of cardiac electrical currents opened the door to transvenous catheter technologies that could pace the heart and to the first external pacemaker device, developed by Paul Zoll in 1951, to treat a patient with heart block. By the 1980s, implantable pacemakers and defibrillator devices were available and, by the end of the 20th century, intracardiac recordings of electric potentials were possible. This ability to “visualize” the cardiac circuitry of the heart led to devices that could map and ablate arrhythmogenic foci and signaled the birth of modern cardiac ablative therapy for arrhythmias.

Table 1

Table 1

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Arrhythmias

The normal cardiac impulse originates from the sinoatrial (SA) node, depolarizes the atria, and proceeds through different pathways to the atrioventricular (AV) node. It is then conducted to the bundle of His, runs down each of the 2 bundle branches, and depolarizes the ventricles (Fig. 1). Any disturbance in this pattern of conduction is termed an arrhythmia. The broad definition of arrhythmia includes premature atrial contractions (PACs) and premature ventricular contractions (PVCs), which are very common and do not have acute hemodynamic consequences. PVCs can be symptomatic, and patients with a high burden can experience deterioration of left ventricular ejection fraction.1,2 Hemodynamically significant arrhythmias include bradyarrhythmias, supraventricular tachycardias (SVTs), AF, atrial flutter (AFl), and ventricular arrhythmias (VA). Common presenting arrhythmias in patients presenting for electrophysiology (EP) procedures are discussed here.

Figure 1

Figure 1

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Bradyarrhythmias

Bradyarrhythmias are arrhythmias that result in a slow ventricular rate (<60 beats/min) because of abnormalities in impulse formation or impulse conduction. Sinus node dysfunction, a disorder of impulse formation, can result in bradyarrhythmias by interfering with the generation of the initial cardiac action potential. A multitude of etiologies can precipitate sinus node dysfunction including ischemia, infection, medications, autonomic dysfunction, and the most common etiology, degenerative fibrosis. When sinus node dysfunction results in clinical symptoms such as dizziness or syncope, it is referred to as sick sinus syndrome. Ambulatory ECG monitoring is useful in making the diagnosis of sick sinus syndrome by correlating symptoms with episodes of bradycardia and is also useful for the identification of other arrhythmias, most commonly AF. Symptomatic patients with intrinsic sinus node dysfunction should undergo implantation of a permanent pacemaker.

AV block, a disorder of impulse conduction, also has a multifactorial etiology and results in slowed impulse transmission through the AV node. This slowing is clinically measured by evaluating the relationship between the P-wave and QRS complexes on the ECG. A fixed, prolonged PR interval (>200 ms) is diagnostic for first-degree heart block and frequently does not result in clinical symptoms. Second-degree AV block involves pathology of the AV node or the His-Purkinje system and is further subdivided into Mobitz type 1 and type 2. Mobitz type 1 block results from AV node pathology above the level of the His bundle, and manifests as a progressively lengthening PR interval, followed by a nonconducted P-wave. Mobitz type 2 block is because of pathology in the infra-Hisian conduction system and results in nonconducted P-waves that occur without predictable increases in the PR interval. Third-degree AV block denotes a complete failure in the transmission of SA nodal impulses to the ventricles and has a significant association with ischemic and structural heart disease. Although patients with lower degree AV block—first-degree and Mobitz type 1—can be managed conservatively, those with higher degree AV block—Mobitz type 2 and third-degree AV block—require the placement of a permanent pacemaker.

A junctional rhythm can serve as an escape rhythm in the setting of complete heart block, and is a result of the AV node generating the primary cardiac impulse. It can also be seen in patients with metabolic derangements such as hypokalemia, after myocardial infarction, or as a complication of cardiac surgery. The AV nodal rate can be between 40 and 60 beats per minute and does not necessarily result in clinical symptoms. Because the impulse is being formed at the level of or above the His bundle, the ECG often shows a regular, narrow QRS complex (<120 ms) with dissociated P-waves. If no reversible etiology is found and no evidence of AV nodal recovery is seen, patients may require permanent pacemaker implantation. It is noteworthy that patients can develop a junctional rhythm faster than the intrinsic sinus rate, termed junctional ectopic tachycardia, which is often seen after congenital cardiac surgery.3 The presence of a junctional rhythm in the setting of AV dissociation should not be mistaken for complete heart block, and careful assessment of the junctional and sinus rates should be performed for the correct diagnosis. An irregularity of the ventricular rhythm should prompt an evaluation for whether atrial impulses are intermittently being conducted across the AV node, which is seen in AV dissociation.

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Supraventricular Tachycardias

The 3 most common causes of SVT are atrioventricular nodal re-entry tachycardia (AVNRT), atrioventricular re-entrant tachycardia (AVRT), and atrial tachycardia. The most common cause of SVT, AVNRT, occurs in patients with dual AV node physiology, in which there exists, within the AV node, a slow conducting pathway with a short refractory period and a fast conducting pathway with a longer refractory period. Whereas a sinus impulse travels through both pathways simultaneously and does not result in arrhythmia, a PAC can result in anterograde block in the fast pathway, setting up the milieu for re-entry: conduction travels anterograde through the slow pathway and then retrograde through the fast pathway, resulting in a tachycardia with near-simultaneous activation of the atria and the ventricles. Symptomatic patients present with palpitations, particularly in response to physiological stress such as exercise. Vagal maneuvers and the AV nodal blocking agent adenosine can be used to terminate acute episodes, whereas beta blockers and calcium channel blockers can be used for chronic therapy. Patients who are unresponsive to medical therapy can be considered for catheter ablation of the re-entrant circuit as a curative therapy.4

AVRT is a re-entrant tachycardia utilizing the AV node and His bundle as one limb of the circuit and an accessory pathway as the second limb of the circuit. Wolff-Parkinson-White (WPW) syndrome is a genetic disorder resulting in one or more anterograde conducting accessory pathways electrically connecting the atria and ventricles, independent of the AV node. This can lead to antidromic AVRT, which is characterized by anterograde impulse transmission through an accessory pathway to the ventricles and retrograde transmission through the AV node back to the atria. The ECG in these patients shows a short PR interval reflecting the much faster transmission of the impulse through the accessory pathway and an upstroke of the QRS complex (delta wave) resulting from ventricular preexcitation. However, patients without WPW can also develop AVRT. Patients with an accessory pathway that can only conduct in a retrograde manner (termed “concealed” accessory pathway) can develop AVRT in which an anterograde impulse conducts over the His bundle Purkinje system to activate the ventricles, followed by retrograde conduction over the accessory pathway to activate the atria. Treatment of symptomatic patients with WPW begins with reduction of environmental stressors and avoidance of stimulants such as caffeine. Radiofrequency (RF) ablation of one or more accessory pathways is often required to prevent recurrence of symptoms.5

Atrial tachycardia occurs when one or more foci in the atrium compete with the SA node to determine the ventricular rate. When tachycardia originates from a single focus, the condition is termed unifocal atrial tachycardia and typically results from excessive sympathetic discharge, inotropic medications, congenital heart disease, and areas of atrial scar, either from previous surgical incisions6 or previous ablations.7 Multifocal atrial tachycardia (MAT) has a strong association with pulmonary diseases such as chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA). MAT is believed to result from chronic hypoxia and hypercapnia and the increase in global sympathetic activity associated with pulmonary disease. Unlike unifocal atrial tachycardia, MAT is defined by the presence of 3 or more morphologically distinct P-waves on ECG. Treatment of the underlying cause of atrial tachycardia is the first-line therapy. The ventricular rate can be controlled using calcium channel-blocking and beta-blocking medications. Ablation of the ectopic focus is a curative option for patients with sustained MAT.8

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Atrial Fibrillation and Atrial Flutter

AF is the most common arrhythmia in the elderly, with an estimated current prevalence of 3 to 6 million patients in the United States. This number is expected to increase to 12 million by 2030.9 Risk factors for AF besides advanced age include ischemic heart disease, valve disease, hypertension, diabetes, alcohol use, and chronic lung disease. The pathophysiology of AF is considered to require 3 components—atrial tissue capable of rapid ectopic conduction, a trigger to stimulate this ectopic activity, and pathways in the atrium capable of propagating waves of ectopic impulses.10 EP studies have localized atrial ectopic tissue involved with AF to muscular bands adjacent to the pulmonary veins in the left atrium and the cavo-atrial junctions of the right atrium. In response to triggers such as sympathetic stimulation or inflammation after cardiac surgery, these arrhythmogenic foci rapidly fire impulses that are likely propagated by re-entrant mechanisms. The result is chaotic, fibrillatory activation of the atria and a ventricular response that depends on the refractoriness of the AV node. Patients who are asymptomatic when in AF can be managed with a rate control strategy, along with systemic anticoagulation for stroke prophylaxis. Symptomatic patients require a rhythm control strategy with the use of antiarrhythmic agents such as flecainide, propafenone, and dofetilide. Those patients who are refractory to or intolerant of medical therapy should be referred for catheter ablation of AF.11 Currently, the 2 most widely accepted strategies for AF ablation are point-by-point RF application for wide circumferential pulmonary vein isolation (PVI) and single-step cryoballoon application for each pulmonary vein. A recently published major randomized clinical trial showed no major differences between efficacy or safety between these 2 techniques.12 Although current guidelines only recommend AF ablation for symptom management, recent trials have shown an improvement in ejection fraction and mortality in patients with AF and left ventricular dysfunction.13–15 Whether these benefits can be seen in a less sick population is uncertain and is being studied by the ongoing CABANA trial.16

AFl is an atrial dysrhythmia propagated by an atrial macro re-entrant circuit and commonly originates from ectopic tissue between the inferior vena cava and the tricuspid annulus. The AV node serves to block the transmission of a fixed ratio of these flutter waves to the ventricle—for example, 2:1 or 3:1. The diagnosis of AFl can be made by performing vagal maneuvers or administering adenosine to increase the ratio of flutter waves blocked by the AV node, making flutter waves more easily visible on ECG. Medical therapy for hemodynamically stable patients begins with controlling the ventricular rate with beta blockers and calcium channel blockers. Both electrical cardioversion and pharmacologic cardioversion with antiarrhythmics such as ibutilide can be used to restore sinus conduction in patients with new-onset AFl. Like patients with AF, those who remain in AFl are at risk for thrombus formation in the left atrium and should be anticoagulated. RF ablation is the first line of treatment for patients with typical AFl, given the high rate of success (>95%), the relatively low risk of major complications, and the possibility of avoiding antiarrhythmic medications or long-term anticoagulation in patients with successful outcomes. In patients who are deemed to be at high risk from an anesthetic standpoint, medical therapy can be considered.

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Ventricular Arrhythmias

VA result from re-entry circuits or abnormal depolarizations in the ventricle and are commonly associated with myocardial infarction and scarring, congenital heart disease, electrolyte disturbances, and drug effects. Monomorphic ventricular tachycardia (VT) originates from a single ventricular focus or re-entrant circuit, whereas polymorphic VT results from multiple foci, and often occurs in the setting of a prolonged QTc interval or coronary ischemia. Patients with VT in the presence of structural heart disease should undergo placement of an implantable cardioverter defibrillator for sudden cardiac death protection. Chronic medical therapy for these patients includes beta blockers and antiarrhythmics such as amiodarone. Catheter ablation should be considered for patients experiencing frequent implantable cardioverter defibrillator shocks because of VT.17 A subset of patients who develop VA have no evidence of structural heart disease, termed “idiopathic VT.” These arrhythmias are often benign and the indication for catheter ablation is driven by the severity of symptoms.18

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Catheter Ablation Techniques

Although medical therapy is a cornerstone of tachyarrhythmia management, catheter ablation is increasingly being utilized as an adjunctive, if not first line, therapy in a wide variety of clinical settings. In addition, patients with heart failure and other medical comorbidities poorly tolerate antiarrhythmic medications, many of which are myocardial depressants and have other systemic adverse effects. To address this growing therapeutic gap, there has been an exponential increase in the number of interventional procedures performed in the EP laboratory over recent decades.

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Electroanatomic Mapping (EAM)

The simplest form of cardiac mapping requires the use of a single electrode catheter to generate an electrogram consistent with an arrhythmogenic focus combined with fluoroscopy to locate the position of the catheter within the heart. To allow mapping of complex arrhythmias and the ablation of multiple targets, multiple electrode catheters and EAM were developed. EAM relies on generating a magnetic or an impedance-based field around the patient to triangulate the location of the catheter. Electrograms measured by the catheter are integrated with magnetic or impedance data to generate a color-coded, 3-dimensional model of the cardiac chambers (Fig. 2). The 2 commercially available EAM systems include EnSite (St. Jude Medical, St Paul, MN), which utilizes magnetic and impedance-based patches placed on the patient’s chest, and CARTO (Biosense, Diamond Bar, CA), which relies on magnets below the patient. The use of EAM has been shown to improve procedural success and reduce fluoroscopic time.19,20

Figure 2

Figure 2

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RF Catheter Ablation

The first intracardiac catheter ablation was performed in the 1980s using direct current from an external defibrillator.21 RF ablation was later adopted to enable more precise targeting with minimal damage to the surrounding tissue. The ablation targets for common arrhythmias are listed in Table 2. The components of a modern RF ablation include an external generator and an intracardiac catheter with an electrode and a thermistor. After mapping has been performed and targets of interest have been identified, the RF ablation catheter is advanced into the heart through the venous system, with the femoral vein being the favored conduit. The left atrium is most frequently accessed from the right side by trans-septal puncture, but ablation of the left ventricle requires a retro-aortic approach through femoral arterial access. After contact with the ablation site is confirmed, RF energy is delivered for 30 to 60 seconds, targeting a tissue temperature of 50 to 60°C. Arrhythmia induction is often attempted after ablation to ensure that the substrate for the tachycardia has been eliminated.

Table 2

Table 2

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Anesthesia for EP Procedures

The vast numbers of patients presenting for EP procedures were typically sedated by qualified nursing personnel supervised by the cardiologist performing the procedure. An increase in the number of patients with advanced cardiac and pulmonary disease has led to anesthesiologists being consulted frequently to manage patients in the EP laboratory. Some of these patients may require general anesthesia (GA) and/or invasive hemodynamic monitoring. A 2011 survey of major EP programs reported that the majority used a combination of anesthesiologist-led teams and qualified nursing staff to provide care for these patients.22 Providing leadership in this role requires the anesthesiologist be familiar with the environment of the EP laboratory, the pathophysiology of arrhythmias, the procedural details of catheter-based interventions, and the management of patients with significant comorbidities.

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The EP Laboratory Environment

In many institutions, the EP laboratory is physically and logistically isolated from the main operating room (OR) suite and shares some of the limitations and challenges of nonoperating room anesthesia (NORA) locations. EP laboratories are primarily designed to house the specialized equipment required for cardiac mapping and fluoroscopic procedures and to provide optimal ergonomics for the EP team. The fluoroscopic C-arm and the bed are frequently controlled by the electrophysiologist and can dislodge monitors, intravenous lines, and the airway circuit when moving. Lines and tubing should be extended and secured out of the anticipated path of the C-arm before the procedure. The C-arm can also impede visualization of the patient’s face and airway during the procedure. Communication with the EP team is necessary to allow access to these structures, particularly when the C-arm is pressing against the patient and when emergent conversion to GA is necessary. The built-in monitors in the EP laboratory are frequently not designed to be shared with the anesthesia team. As a result, invasive hemodynamic monitoring data may be unavailable to the anesthesiologist.

The infrequent presence of the anesthesia team in the EP laboratory can result in barriers to communication between the anesthesiologist and the electrophysiologist. Team introductions before commencement of each case are a necessary first step in establishing rapport. Having enough knowledge of the scheduled EP procedure to converse with the electrophysiologist about the anesthetic implications, expected course, and potential complications is also important and establishes the anesthesiologist as a consultant rather than a proceduralist.

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Preoperative Evaluation

Patients presenting for EP procedures may not follow the same pathway for outpatient preanesthetic evaluation as surgical patients for a multitude of organizational reasons. They frequently present as outpatients to the preoperative holding area on the same day as their scheduled procedure.23 Nonetheless, the preoperative evaluation should be performed with the usual rigor and focus on the patient’s presenting arrhythmia and any comorbidities.

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Cardiovascular

A detailed evaluation of the patient’s cardiac function is necessary to ensure that they are optimized for the procedure. Arrhythmias requiring intervention in the EP laboratory can be isolated phenomena in young individuals, but are more likely accompanied by coronary artery or structural heart disease. AF, for example, is associated strongly with congestive heart failure and valve disease.24 It is reasonable to expect that these patients will already have an ECG available. The ECG should be examined for the presence of preexisting conduction abnormalities, such as left bundle branch block, as these patients have a higher risk of complete heart block during the procedure. Transthoracic echocardiography (TTE) is also performed frequently on these patients and should be used to evaluate ventricular function and valvular pathology. Patients with coronary disease may not tolerate rapid pacing or pharmacologic chronotropes such as isoproterenol and their anticipated use should be discussed with the electrophysiologist.

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Respiratory

Pulmonary disease is also associated with tachyarrhythmias, likely mediated by the effect of chronic hypoxia and hypercarbia on the autonomic system. MAT is associated classically with COPD, but other SVTs are also observed in these patients. Patients presenting with COPD should be optimized medically as COPD exacerbation is associated with increased frequency of MAT.25 Pulmonary function tests should be reviewed in patients with severe lung disease and high-risk patients may be managed optimally without endotracheal intubation. Both inhaled beta-agonists such as albuterol and oral agents such as theophylline can precipitate SVTs and VTs. Patients with pulmonary disease should also be evaluated for their ability to lay flat for the EP procedure. An inability to do so, even with oxygen supplementation, may necessitate GA with endotracheal intubation.

OSA is commonly associated with AF, likely because of left atrial stretch because of volume overload and long-term atrial remodeling from chronic hypoxic and hypercapnic episodes.26 Because patients presenting with new-onset AF may have undiagnosed OSA, we recommend screening all patients presenting for EP procedures with a validated test such as the STOP-Bang questionnaire (Fig. 3).27 Patients with OSA often show sensitivity to opioids, resulting in respiratory depression, and may benefit from postoperative continuous positive airway pressure.

Figure 3

Figure 3

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Medications

A review of the patient’s medications and assessing compliance can mitigate potential complications. Patients presenting with AF are anticoagulated with warfarin or a direct oral anticoagulant such as apixaban for at least 3 weeks before the procedure (Table 3). There is significant variation between institutions as to whether and when to stop these agents before the EP procedure and it should be ensured that the patient followed these guidelines.

Table 3

Table 3

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Selection of Anesthesia

The choice of anesthetic modality, monitored anesthesia care (MAC) or GA, should be made on the basis of the patient’s risk factors and procedural concerns. MAC does not signify the depth of anesthesia, which can range from anxiolysis to deep sedation, but simply denotes the presence of a dedicated anesthesia team caring for an arousable patient. In patients who can lie flat without anxiety or arterial desaturation and who are undergoing ablative procedures for simple arrhythmias or pacemaker placement, MAC should be strongly considered. Common infusions for MAC include midazolam, propofol, and dexmedetomidine, with the last having a lower incidence of respiratory depression. A combination of the sedative infusion with a regimen that includes local anesthetic infiltration of the vascular access site, opioids, benzodiazepines, and nonsteroidal anti-inflammatory drugs will ensure patient comfort and stability.

When determining the anesthetic plan for patients undergoing AF ablation, the complexity of the ablation and expected duration should be discussed with the electrophysiologist. Although MAC anesthesia is used most frequently, GA may be preferable in prolonged, complex cases, such as those requiring transeptal access, and when the patient has significant comorbid conditions.28 In addition, in a randomized-controlled trial, the use of GA for AF ablation was associated with better procedural success and a decreased incidence of pulmonary vein reconnection seen on subsequent ablations.29 In patients undergoing an EP study to induce SVTs, MAC with light sedation is preferred to increase the likelihood of success. Once the SVT foci have been identified, deeper sedation or GA can be used for the ablation. GA is the preferred modality for scar-related VT ablation because the procedures tend to be longer, there is a higher likelihood of hemodynamic instability, and because GA has not been found to interfere with VT induction. In a retrospective review of 226 patients, Nof and colleagues showed no difference in VT inducibility or ablation between patients who received GA versus those who received sedation.30

Specific anesthetic considerations should be noted for patients undergoing PVC ablation. Sedation can decrease the PVC burden because of alterations in sympathetic and parasympathetic tone. This situation can make mapping the PVC origin challenging, and may even reduce the likelihood of a successful ablation. Communication with the EP team of the anesthetic plan is crucial for these cases as short-acting agents are often preferable to allow the patient to become more arousable.

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Monitors

Irrespective of the anesthetic technique utilized, standard monitors to measure oxygenation, ventilation, perfusion, and temperature are required. Capnography, even when used in spontaneously ventilating patients, can rapidly detect apnea and act as a crude monitor of cardiac output. The proximity of the esophagus to the left atrium makes it especially vulnerable to heat-induced injury and atrio-esophageal fistula during AF ablation. The use of GA for AF ablation has been associated with an increased risk of esophageal injury compared with patients receiving fentanyl-midazolam sedation in a small, single-center randomized-controlled trial.31 The proposed mechanism for this injury was reduced esophageal motility and impaired pain-induced swallowing because of a deeper plane of anesthesia. The electrophysiologist should be notified when esophageal temperature reaches the institutional threshold—typically between 38.5 and 40°C—or if the temperature increases at least 1°C above the patient’s baseline.32 It is important to note that because of variable contact between the temperature probe and the esophageal wall and variability in the distance between the thermistor and the ablation target, this method of detecting heat transfer to the esophagus is not sensitive.

The use of invasive hemodynamic monitors has the potential for redundancy and their placement should be discussed with the EP team. In high-risk patients who need an arterial line for hemodynamic monitoring, sharing the electrophysiologist’s arterial access may not be appropriate when the planned approach involves retrograde ablation through the femoral artery. Insertion of the large bore ablation catheter in these cases can lead to occlusion of the vessel and dampening of the transduced pressure. If the arterial line is needed intermittently for serial laboratory tests such as activated clotting time, it is then appropriate to share this access. If there is a need for continuous monitoring of central venous pressure or large bore venous access, it is imperative to establish this access independent of the electrophysiologist’s femoral venous puncture site.

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Intraoperative Management

Monitored Anesthesia Care

When MAC anesthesia is selected for EP procedures, a multitude of intravenous agents can accomplish the goals of providing adequate sedation, maintaining hemodynamic stability, and supporting spontaneous ventilation. The use of midazolam, fentanyl, and propofol to provide deep sedation for AF ablation has been studied extensively and found to be safe.33 Propofol, however, has been reported to suppress SVT in human34 and animal35 studies, and its use in these cases should be limited. The use of dexmedetomidine in the EP laboratory has increased in recent years because it is associated with less respiratory depression. In a randomized-controlled trial during AF ablation, the combination of dexmedetomidine and remifentanil provided deeper procedural sedation and anxiolysis with less arterial desaturation than midazolam-remifentanil.36 Dexmedetomidine has been shown to reduce the incidence of arrhythmias in postcardiac surgery patients,37 raising the question of whether it can complicate arrhythmia induction. However, this has not been reported to be the case in large series of patients undergoing AF38 or SVT ablation.39 Ketamine, which is frequently used with midazolam to prevent emergence delirium, can be used in atrial arrhythmias that are difficult to induce because it shortens atrial conduction time and increases sympathetic outflow.40

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General Anesthesia

In patients undergoing GA for ablation procedures, induction of anesthesia should be performed with short-acting intravenous agents such as propofol. Propofol has no direct effect on SA node function, AV node conduction, or accessory pathway conduction.41 Etomidate is a suitable alternative in patients with cardiac comorbidities as it has a negligible effect on myocardial contractility. During cryoablation for AF, phrenic nerve pacing is utilized during ablation of the right pulmonary veins to monitor for impending phrenic nerve injury. Therefore, neuromuscular blockade use should not be extended beyond the induction period in these cases. No single volatile agent is more likely than others to promote arrhythmia inducibility or increase procedural success. Intravenous anesthetics, however, should be considered in patients under GA in AVNRT and other SVT ablations as all volatile agents suppress these arrhythmias.42

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Mechanical Ventilation

Patient immobility and controlled mechanical ventilation generally lead to better catheter stability under GA. Nevertheless, positive pressure ventilation creates fluctuations in atrial pressure and volume, which can dislodge the ablation catheter. To improve procedural conditions, a variety of ventilation strategies have been described in the literature. Low tidal volume ventilation, apneic oxygenation, and high-frequency jet ventilation can all be used to decrease cardiac movement during catheter ablation. Goode and colleagues found that the use of high-frequency jet ventilation in PVI resulted in fewer ablative lesions because of less frequent electrode dislodgement.43 With each of these hypoventilation strategies, there is a risk of hypercarbia, atelectasis, and decreased delivery of volatile anesthetics. The use of a depth of anesthesia monitor, such as the bispectral index (Medtronic, Fridley, MN), to detect inadequate anesthesia, supplementation with intravenous anesthetic agents, and resumption of conventional ventilation with positive end-expiratory pressure after each ablation cycle may mitigate these adverse effects.

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Anticoagulation

When large cannulae are placed into the arterial system or the left heart, systemic anticoagulation is mandatory to reduce the risk of thrombus formation and consequent stroke. In AF ablation, unfractionated heparin should be administered before trans-septal puncture. The activated clotting time should be checked periodically and maintained above 300 seconds. Protamine sulfate should be used to reverse heparin in most patients toward the end of the procedure, once catheters have been pulled back into the right heart.

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Arrhythmia-inducing Medications

Both when mapping arrhythmogenic foci and to evaluate success after ablation, the primary approach is to rapidly pace the patient using an intracardiac catheter. Atrial pacing is most commonly utilized, but ventricular pacing may also elicit tachycardia that is conducted through retrograde and accessory pathways. When pacing fails to induce tachycardia, isoproterenol, a nonselective β-adrenergic agonist with predominantly chronotropic and inotropic properties, can be used for arrhythmia induction. Isoproterenol decreases systemic vascular resistance and the mean arterial pressure, and may require concurrent administration of a vasoconstrictor. The associated tachycardia can also induce myocardial ischemia in vulnerable patients. Adenosine, an ultra–short-acting purine nucleoside, is used to evaluate for dormant conduction through the pulmonary veins after a PVI procedure. Any such conduction pathway is a candidate for subsequent ablation. Adenosine can result in nausea, dyspnea, chest discomfort, and hypotension in lightly sedated patients.

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Volume Status

The patient’s volume status should be assessed carefully over the course of any EP procedure involving RF ablation, particularly when using open irrigation ablation catheters. These catheters use cool saline to reduce the temperature at the tip of the catheter and minimize tissue damage. In one large series, the mean volume of saline infused into patients using these catheters was >4 L.44 When central venous pressure monitoring is not available to the anesthesiologist, venous and intracardiac pressures measured by the EP team can be used to diagnose fluid overload. Patients with heart failure may develop pulmonary and peripheral edema from these volumes. The administration of a single dose of a diuretic is appropriate toward the end of the procedure to reduce postoperative morbidity and patient discomfort.

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Complications

Ablation procedures in the EP laboratory are generally safe, but can result in a range of complications requiring prompt diagnosis and management (Table 4). The femoral venous access site is susceptible to injury and hematoma formation, particularly in obese, elderly, and anticoagulated patients. After the access sheath is withdrawn, manual pressure should be applied to ensure hemostasis. Cannulation of the femoral artery with an access sheath, as is necessary when performing ablation in the left ventricle, can be complicated by retroperitoneal hemorrhage and pseudoaneurysm formation. Avoidance of forceful coughing at the time of extubation is prudent. An awake patient with retroperitoneal hemorrhage may present with lower abdominal or back pain, before characteristic flank bruising is evident. A pseudoaneurysm results from blood escaping from the lumen to the walls of the artery and can occur from inadequate hemostasis after removing an arterial sheath. Identification of the arterial leak with ultrasound and its compression may result in resolution. In severe cases, a separate surgical procedure for endovascular exclusion of the pseudoaneurysm may be necessary.

Table 4

Table 4

Arrhythmias are a frequent and expected complication in the cohort of patients undergoing ablation in the EP suite. Prolonged arrhythmias can decrease cardiac output and result in hypoperfusion. The anesthesiology team should be prepared to cardiovert or defibrillate patients with unstable rhythms and provide hemodynamic support with inotropes and vasopressors. AV block of variable severity and duration can occur, particularly when the ablative focus is the AV node or adjacent to the interatrial septum. Patients with preexisting left bundle branch block are at a higher risk for complete heart block. When AV block is suspected, further ablation should be aborted as conduction abnormalities are generally transient and resolve with time. The placement of a temporary or a permanent pacemaker may be necessary to provide hemodynamic support.

Cardiac perforation and tamponade are rare and dreaded complications associated with catheter manipulation and ablation within the thin-walled atria. Persistent hypotension requiring escalating doses of vasopressors or a sudden drop in blood pressure any time after insertion of the ablation catheter should prompt clinical suspicion of tamponade. TTE is readily available in most EP laboratories and can be used to make a definitive diagnosis. Once the diagnosis is confirmed, anticoagulation should be reversed and percutaneous placement of a drainage catheter into the pericardium should be performed by the electrophysiologist. In most cases, the perforation is small enough to heal spontaneously and will not require surgery. Catheter-associated injury to the cardiac valves can also occur. Injury to the mitral valve is most common and results from catheter entanglement in the subvalvular apparatus when the ablation catheter is inserted retrograde through the aorta. If the catheter cannot be retrieved, surgical repair may be necessary.

Esophageal injuries can result from the transmission of thermal energy to the esophageal mucosa during RF ablation of the left atrium. The degree of injury ranges from mucosal erythema, which is most common, to esophageal ulceration, atrioesophageal fistula formation, and esophageal perforation. Strategies to prevent esophageal injuries include monitoring esophageal temperature, monitoring the left atrium using TTE, and limiting the power and duration of RF ablation. The presenting symptoms in patients with postprocedural esophageal injury include dysphagia, odynophagia, and retrosternal chest pain. These patients should be promptly referred to the gastroenterology service for further evaluation and esophagoscopy. Mucosal erythema and ulceration is often treated conservatively with proton-pump inhibitors and sucralfate. Esophageal perforation and atrioesophageal fistulae are rare, associated with significant mortality, and require prompt surgical intervention.

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Postoperative Care

Postoperative care after uncomplicated procedures in the EP laboratory is similar to recovery after other NORA procedures. Much of the pain after these procedures is associated with the puncture site and a multimodal pain management strategy is recommended to treat this. The patient’s volume status should be assessed before leaving the EP suite. Large volume infusions of fluid through the ablation catheter can result in volume overload and dyspnea, whereas diuretic administration can lead to dehydration and hemodynamic instability.

Nursing personnel involved in the care of these patients should be familiar with potential postprocedural complications. The patient should lie flat to avoid bleeding complications associated with femoral puncture sites. The bandages should be inspected for bleeding and lower extremity compartments should be evaluated for hematoma. Hemodynamic instability and arrhythmias can occur postoperatively and the EP team should be alerted early to diagnose and treat these conditions. The patient’s anticoagulation requirements vary depending on institutional preference and the type of ablation procedure performed. After AF ablation, most patients require at least 2 months of systemic anticoagulation with either warfarin or a direct oral anticoagulant. After demonstrating hemodynamic stability and adequate oxygenation and ventilation, most patients after EP procedures are admitted to the hospital overnight for observation and discharged home within 24 hours of the procedure.

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Future Directions

There has been a groundswell of attention and progress made in the areas of EP mapping and intervention; work is being carried out that will advance the field even further. Improvements in computational modeling will yield high-fidelity models of cardiac EP function, which will spur the development of new antiarrhythmic drugs and ablative therapies.45 Improvements in steerable catheters will improve the efficiency and success of interventions, and leadless cardiac pacemakers will decrease lead-related and pocket-related complications and expand treatment options for patients with cardiac conduction disease.46

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Conclusions

EP as a specialty was born out of a modern and nuanced understanding of the cardiac conduction system and has resulted in a myriad of new therapeutic options for treating and eliminating arrhythmias. Despite years of experimentation and study of medical approaches for cardiac dysrhythmias, in many instances cure with medicine alone is not feasible and may be more dangerous than the disease itself. Because of this limited success of medical therapy alone and an increasing disease burden in the aging population, ablative procedures are becoming increasingly common.

Given the specialized technologies required to administer cardiac ablative therapy, it is important for the anesthesia practitioner to have a basic understanding of the underlying pathologies and the procedural considerations when caring for patients undergoing these procedures.

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