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Anesthesia for Cardioversion and Electrophysiologic Procedures
Key Points
- 1.
Tachyarrhythmias result from one of three mechanisms (reentry, automaticity, and triggered activity), with reentry being the mechanism most commonly treated in the electrophysiology (EP) laboratory.
- 2.
Anesthetic agents influence cardiac conduction and arrhythmogenesis and can adversely affect EP procedures.
- 3.
Opioids may have an antiarrhythmic effect in the setting of myocardial ischemia.
- 4.
While the arrhythmic properties of volatile anesthetics are controversial, overall they have an antifibrillatory effect.
- 5.
Two new, more minimally invasive cardiac implantable electrical devices include the subcutaneous implantable cardioverter-defibrillator and leadless pacemaker.
- 6.
General anesthesia is becoming increasingly preferred for atrial fibrillation ablation because of the longer procedure time and predictable thoracic excursion with mechanical ventilation.
- 7.
Atrial fibrillation is responsible for more than 35% of ischemic strokes, with the left atrial appendage being the most common place for thrombus formation.
- 8.
Complications of procedures performed in the EP laboratory are secondary to vascular access, thromboembolism, arrhythmias, pericardial effusions, air embolism, pulmonary vein stenosis, atrioesophageal fistula formation, and phrenic nerve injury.
Cardiac arrhythmias cause significant morbidity and mortality. In the United States, cardiac arrhythmias account for nearly 400,000 deaths annually. Since the implantation of the first cardiac pacemaker in 1958, clinical electrophysiology (EP) has become increasingly complex and now includes a variety of sophisticated therapeutic and diagnostic procedures. Although sedation for many EP cases has historically been performed by a nurse under the direction of the proceduralist, because of a number of factors (complexity of many of these cases, long procedural times, potential significant hemodynamic instability, and significant patient comorbidities often present), an anesthesia provider is now frequently integral to providing safe and effective EP care. Understanding the basic principles of how these procedures are performed, the mechanisms of cardiac arrhythmias, and the impact that anesthetic agents have on the cardiac conduction system is paramount for anesthesia providers working in this environment.
This chapter provides an overview of clinical EP for anesthesia providers. It discusses the effects of the most commonly used anesthetic agents in the EP laboratory on cardiac conduction. It reviews the salient details and anesthetic considerations of each of the main EP procedures as well as the associated complications that might arise during the periprocedural period. See Table 15.1 for commonly used abbreviations in clinical EP.
Table 15.1
Commonly Used Abbreviations in Clinical Electrophysiology
| AF | Atrial fibrillation |
| AFL | Atrial flutter |
| AT | Atrial tachycardia |
| AVNRT | Atrioventricular nodal reentrant tachycardia |
| AVRT | Atrioventricular reciprocating tachycardia |
| CARTO | Navigation system produced by Biosense Webster |
| CIED | Cardiovascular implantable electronic device |
| CS | Coronary sinus |
| EC | Electrical cardioversion |
| EP | Electrophysiology |
| EGM | Electrogram (generally intracardiac) |
| hRA | High right atrium |
| ICD | Implantable cardioverter-defibrillator |
| ICE | Intracardiac echocardiogram |
| LAA | Left atrial appendage |
| NavX | Navigation system (St. Jude Medical) |
| PDNA | Proceduralist-directed nurse-administered |
| PSVT | Paroxysmal supraventricular tachycardia |
| PVC | Premature ventricular contraction |
| PVI | Pulmonary vein isolation |
| SVT | Supraventricular tachycardia |
| TdP | Torsades de pointes |
| VF | Ventricular fibrillation |
| VT | Ventricular tachycardia |
Overview of Electrophysiology Procedures
Electrophysiology Laboratory
Initially, the main purpose of the EP laboratory was for diagnostic studies. However, its focus has evolved to include many therapeutic procedures such as catheter ablation and cardiac rhythm device implantation and extraction. The EP laboratory is divided into the control room, which is shielded from radiation by a glass partition and doorway, and the area where the procedure is performed, which contains the patient table and imaging equipment. While the procedure is being performed, a technician (and sometimes a second electrophysiologist) in the control room monitors the patient's cardiac rhythm and performs various pacing maneuvers. A large amount of equipment is required (e.g., single or biplane fluoroscopy, mapping patches, electrocardiogram [ECG] leads, catheters, boom with multiple screens), limiting access to the patient during the procedure and thus complicating anesthetic care. Some laboratories also contain a magnetic catheter navigation system (e.g., Stereotaxis Inc.), which occupies even more space and introduces the logistical considerations (i.e., magnetic resonance imaging [MRI]-compatible monitors and anesthesia machine) and potential dangers of a ferromagnetic field. Because fluoroscopy is constantly used in the EP laboratory, necessary radiation safety precautions (e.g., lead aprons or shields, eye protection) must be followed. Radiation dosimeters should be worn by personnel who routinely work in this environment.
Catheter Placement and Generation of Intracardiac Electrograms
Right heart catheter placement is most often performed via the femoral vein; however, the internal jugular, subclavian, or brachial vein can be used. Multiple intravenous (IV) sheaths are placed so that catheters can be advanced into the heart to record intracardiac signals (electrograms). In contradistinction to the surface ECG, which provides summed vectors of the heart's electrical activity, the intracardiac electrogram records a discrete local signal from a small area of the myocardium. These diagnostic catheters, some with multiple electrode pairs, are used to determine information such as signal voltage, complexity, and local activation (timing compared with a reference). The exact type and location of the catheters placed depend on the procedure being performed and physician preference.
To perform a basic EP study, several electrograms are typically obtained by placing catheters into the high right atrium (hRA), coronary sinus (CS), His bundle, and RV apex (RVa) ( Fig. 15.1 ). A variable number of surface ECGs leads are also displayed. To better visualize the signals, they are displayed at a sweep speed of 100 mm/s compared with 25 mm/s for a standard ECG. Real-time signals are viewed on one screen, and an additional screen is available for measurements and static review.
Catheter Mapping System
Mapping systems are used to collect and display information gathered from intracardiac recordings. A three-dimensional (3D) shell of the chamber(s) of interest is generated along with pertinent timing and voltage information. These systems reduce radiation exposure compared with fluoroscopy alone by integrating preprocedural images obtained from computed tomography (CT) or magnetic resonance (MR) or use intraprocedural ultrasound to improve anatomic relationships. During an arrhythmia, an activation map is produced by measuring the timing of different cardiac events and then using color coding or an animation to display the wavefront proceeding across the 3D map ( Fig. 15.2 ). The map helps the electrophysiologist determine the area that should be targeted for ablation by pinpointing the source of a focal tachycardia or the area of slow conduction in the case of a macroreentrant tachycardia. Voltage mapping is used in addition to or in lieu of activation mapping if an arrhythmia is noninducible and provides important information about the scar substrate responsible for reentrant rhythms.
Mechanisms of Cardiac Arrhythmias
Arrhythmias are classified as slow (bradyarrhythmia) or fast (tachyarrhythmia) based on whether the heart rate is less than 60 beats/min or greater than 100 beats/min, respectively.
Bradyarrhythmias
A bradyarrhythmia results from failure of impulse formation or conduction. The most commonly treated bradyarrhythmia in the EP laboratory is sinus node (SN) dysfunction, which occurs when impulse formation is impaired within the SN. Conduction system disease is most often from advanced age or underlying cardiovascular disease and results in three main forms of atrioventricular (AV) block—first, second, or third degree.
First-degree AV block is actually a misnomer because in this condition conduction through the AV node is simply slowed, which results in a prolonged PR interval on the ECG and requires no treatment. Second-degree AV block is subdivided into types I and II; these conditions partially impair but do not entirely block impulses from conducting to the ventricles. On the ECG, type I is diagnosed by progressive PR prolongation until a dropped ventricular beat occurs. In contrast, type II is characterized by intermittent nonconducted P-waves without progressive PR prolongation. Type II is important to identify because it indicates infranodal conduction disease, can progress to third-degree heart block, and might warrant pacemaker implantation. In third-degree heart block, there is complete AV dissociation, which requires a junctional or ventricular escape rhythm to maintain perfusion.
Tachyarrhythmias
Tachyarrhythmias are caused by one of three mechanisms ( Box 15.1 ). In the EP laboratory, the most commonly treated mechanism is reentry. A reentrant tachycardia is defined by its continuous circular path in which the wavefront of excitability returns to the site of initiation. Requirements of reentry include two adjacent pathways with differing EP properties that connect proximally and distally to form a single circuit with a nonexcitable central area. Unidirectional block is required and occurs when differences in refractory periods allow an impulse to initially conduct down one pathway but not the other. Because of slow conduction, by the time the wavefront reaches the end of the first pathway, the second pathway is no longer refractory and accepts the impulse. The impulse then continues until it returns to its origin and thus completes one cycle of tachycardia. There is often an area of slow conduction that facilitates reentry and may be targeted for ablation (e.g., the cavotricuspid isthmus in typical atrial flutter [AFL]).
Box 15.1
Tachyarrhythmia Mechanisms
-
Reentry (mechanism most commonly addressed in electrophysiology procedures)
-
Automaticity
-
Triggered
The remaining two mechanisms, automaticity and triggered activity, are abnormalities in impulse formation rather than conduction. Automaticity is spontaneous impulse formation and is normal behavior when occurring in specialized conduction tissue. Failure of automaticity may result in a bradyarrhythmia such as sinus bradycardia. Alternatively, increased automaticity in diseased or ischemic atrial or ventricular myocardial cells may result in a sustained tachyarrhythmia or induce premature beats that initiate reentry. Triggered activity requires a preceding impulse and is caused by oscillations in the cellular membrane potential called afterdepolarizations. Afterdepolarizations are further characterized as early or delayed depending on when they occur during the action potential. Clinical examples of early and delayed afterdepolarizations include torsades de pointes in long-QT syndrome and digoxin toxicity, respectively. Table 15.2 summarizes key characteristics of the different tachyarrhythmias treated in the EP laboratory.
Table 15.2
Tachyarrhythmias Treated in the Electrophysiology Laboratory
| Arrhythmia | Mechanism | Ablation Target | Sedation Level Needed |
|---|---|---|---|
| AV nodal reentry | Reentry | Slow pathway | Moderate |
| AV reciprocating tachycardia | Reentry | Accessory pathway | Moderate |
| Atrial tachycardia | Reentry, triggered activity, automaticity | Origin of focal tachycardia | Moderate |
| Atrial flutter | Reentry | Area of slow conduction | Moderate |
| Atrial fibrillation | Multiple mechanisms coexist | Pulmonary vein isolation initially | Moderate to general anesthesia |
| PVCs | Automaticity, reentry, triggered activity | PVC focus (outflow tract most common) | Moderate |
| VT with a structurally normal heart | Automaticity, reentry, triggered activity | VT focus | Moderate |
| VT with structural heart disease | Reentry caused by fibrosis | Critical isthmus or extensive substrate modification | General anesthesia |
AV, Atrioventricular; PVC, premature ventricular contraction; VT, ventricular tachycardia.
Anesthetic Agents and Cardiac Conduction
Many anesthetic agents influence cardiac conduction and arrhythmogenesis and thus have the propensity to adversely impact the efficacy of the diagnostic and therapeutic procedures performed in the EP laboratory. The most commonly used sedative and anesthetic agents along with a description of their varying effects on the cardiac conduction system are provided next. A summary of this information is also contained in Table 15.3 .
Table 15.3
Summary of Anesthetic Agent Effects on Cardiac Conduction and Electrical Properties
| Agent | Antiarrhythmic Properties | Proarrhythmic Properties | Acceptable for Use in Cardioversion | Effect on P-R Interval | Effect on QTc Interval | Benefits | Adverse Effects |
|---|---|---|---|---|---|---|---|
| Propofol | May terminate SVT May convert AF May terminate VT |
Bradycardia Lengthens SA node interval Slows AVN conduction/prolongs AVN effective refractory period Slows atrial rate Case reports of TdP |
Yes | May shorten | Varying reports: Primarily prolongs May shorten |
Rapid onset and recovery | Vasodilation Dose-dependent decrease in blood pressure Possible P-wave dispersion |
| Etomidate | None | None | Yes | NR | NR | Minimal cardiac depressive effects | Adrenocortical suppression |
| Midazolam | NR | NR | Yes | NR | None | Amnesia Minimal HD effects |
Mild venous dilation but no significant impact on contractility |
| Dexmedetomidine | Bradycardic effect has been used in SVT, VT, AFL, junctional ectopic tachycardia | SA node interval lengthening in some reports Slows AVN conduction or blockade |
Yes | Prolongs | Prolongs | Rapid onset/clearance | Use with caution in heart block, bradycardia, and heart transplant Caution when coadministered with β-blockade |
| Sevoflurane | Antifibrillatory | Atrial ectopy in pediatric reports Slowing of AVN conduction time |
Yes | NR | Prolongs | Not noxious to airways | Dose-dependent vasodilation |
| Desflurane | Antifibrillatory | Slowing of AVN conduction time | Yes | NR | Prolongs | Lowest blood:gas solubility of the three listed volatile agents | Dose-dependent vasodilation |
| Isoflurane | Antifibrillatory | Slowing of AVN conduction time APERP prolongation in preexcitation syndromes |
Yes | NR | Prolongs | Inexpensive | Dose-dependent vasodilation |
| Fentanyl | Antifibrillatory; elongates the sinus node recovery time | Bradycardia | Yes | NR | None | Inexpensive | No amnestic effect Ventilation depressant May affect accuracy of atrial mapping during EP procedures |
| Morphine | Decreases the occurrence of reperfusion-induced arrhythmias Antifibrillatory |
Bradycardia | Yes | NR | None | Inexpensive | Vasodilation secondary to histamine release |
| Remifentanil | NR | Bradycardia Slows SA node function Slows AVN conduction and prolongs AVN ERP |
Yes | NR | None; may attenuate QTc prolongation in hypertensive patients | Ultrarapid onset and recovery | No amnesia Ventilation depressant Hypotension Bradycardia Caution with β-blockade |
AF, Atrial fibrillation; AFL, atrial flutter; APERP, accessory pathway effective refractory period in pre-excitation syndromes; AVN, atrioventricular node; EP, electrophysiology; ERP, effective refractory period; HD, hemodynamic; NR, none reported; SA, sinoatrial; SVT, supraventricular tachycardia; TdP, torsades de pointes; VT, ventricular tachycardia.
Propofol
Propofol (2,6-di-isopropylphenol) is perhaps the most commonly used anesthetic agent because of its efficacy, potency, rapid titratability, and short duration of action. Because propofol induces a profound level of sedation or even general anesthesia, it is postulated to indirectly modify atrial electrical activity and AV conduction. It also inhibits vagal tone in a dose-dependent manner. Because it decreases P-wave dispersion (i.e., the difference between the widest and narrowest P-wave duration), it might be partially responsible for the conversion of atrial fibrillation (AF) to sinus rhythm.
The magnitude and significance of propofol's aforementioned indirect effects on cardiac conduction are controversial. However, its proarrhythmic and antiarrhythmic effects are thought to be dose dependent. Typically, low doses have minimal effects on cardiac conduction; the impact of larger doses might be more significant. Propofol does not directly affect sinoatrial (SA) node activity or atrial electrical conduction. Despite its potential to indirectly affect conduction, the impact is likely modest at best, and available data (albeit limited) support the use of propofol for these procedures.
Antiarrhythmic Qualities
Propofol can inhibit cardiac conduction and has been demonstrated to convert supraventricular and ventricular tachycardias. The mechanism for its conduction effects is not fully elucidated but likely involves a combination of cardiomyocyte ion channels (inward and outward ion currents (I Na , I Ca , I KR , I KS ), the autonomic nervous system, and cardiac cell gap junctions (intercellular channels that electrically and metabolically connect cardiomyocytes). Propofol shortens the cardiac action potential duration and suppresses both sympathetic and parasympathetic tone. The aggregate of these effects leads to both the antiarrhythmic and proarrhythmic properties of propofol.
Propofol has been shown to shorten the PR interval associated with Wolff-Parkinson-White syndrome, as well as shorten the QT interval, and prevent episodes of ventricular tachycardia (VT). Propofol also inhibits arrhythmias associated with ischemia-reperfusion injuries after episodes of myocardial ischemia.
Proarrhythmic Qualities
In a dose-dependent manner, propofol has been demonstrated to impede various components of the cardiac conduction system, including lengthening of the SA interval, inhibition of atrioventricular node (AVN) activity, slowing of atrial rates, and prolongation of the stimulus-to-His bundle interval length. Importantly, there are reports of clinically significant bradycardia associated with high-dose propofol including polymorphic VT and Brugada type 1 ECG pattern (upward concave ST elevation in leads V 1 –V 3 ).
Etomidate
Etomidate, a carboxylated imidazole compound that acts as a γ-aminobutyric acid type A (GABA A ) receptor agonist, is primarily used as an anesthetic induction agent. There is no evidence that etomidate possesses significant antiarrhythmogenic or proarrhythmogenic effects, and it specifically does not impact the duration of repolarization of cardiac conduction tissue.
Opioids
Opioids are primarily vagotonic; thus they can cause bradycardia and a concomitant decrease in cardiac metabolic demand. In animal studies, opioids have been shown to attenuate the excitatory influence of the sympathetic nervous system. In the setting of myocardial ischemia, they might have an antiarrhythmic effect. Opioids have had no effect on VT inducibility. The most frequently used opioids include fentanyl, morphine, hydromorphone, and remifentanil.
Fentanyl
Fentanyl, a synthetic µ-opioid receptor agonist, enhances vagal tone and has been reported to be associated with sinus tachycardia, hypertension, hypotension, arrhythmias, vasodilation, bradycardia, and bigeminy. Fentanyl indirectly raises the ventricular fibrillation (VF) threshold because of its sympatholytic effects, not by activation of vagal efferent pathways. Compared with morphine, fentanyl produces more profound bradycardia.
In pediatric patients, fentanyl has been shown to significantly elongate the SN recovery time, but not SA conduction time. Fentanyl's effect on SA function parallels that of propranolol by affecting automaticity but not SA conduction times. The clinical implication of this effect is that during EP procedures in certain patients, enhanced vagal tone may facilitate the generation of paroxysmal supraventricular tachycardia (PSVT) through its effect on refractoriness of the slow and fast AV nodal conduction pathways. Moreover, autonomic nervous system imbalances during an EP study may attenuate PSVT heart rates compared with spontaneous PSVT, and these fentanyl-induced changes in autonomic nervous system function may ultimately affect the accuracy of an EP study.
Morphine
Morphine, a µ-opioid receptor agonist, increases parasympathetic and reduces sympathetic activity. It has minimal direct cardiac conduction effects. Primarily vagally mediated, it has been reported to be associated with tachycardia, AF, hypertension, hypotension, and bradycardia. Morphine has been thought to raise the VF threshold because of its effect on altering autonomic tone.
In animal models, morphine reduces ischemia-induced membrane depolarization, attenuates myocardial ischemia-related decreases in action potential amplitude, decreases the occurrence of conduction block related to myocardial ischemia, and decreases the occurrence of reperfusion-induced arrhythmias.
Remifentanil
Remifentanil is a selective µ-opioid receptor agonist. Metabolism involves rapid hydrolysis by nonspecific tissue and plasma esterases, which leads to a very rapid onset and short duration of action that provide intense analgesia without prolonged respiratory depression.
Remifentanil has been associated with bradyarrhythmias and asystole both in children and adults. Bradycardia and hypotension have been reported and are likely caused by a centrally mediated increase in vagal nerve activity. EP studies demonstrate that remifentanil is associated with a dose-dependent slowing of SA and AV node function, causing a prolongation of SN recovery time, SA conduction time, and Wenckebach cycle length. Hence, remifentanil should be used cautiously in patients at risk for bradyarrhythmias.
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