What the Anesthesiologist Should Know before the Operative Procedure

Atrial fibrillation

Atrial fibrillation (AF) is the most common arrhythmia, with a prevalence of 0.4% to 1% in the general population, increasing to 8% in those older than 80 years. Propagation of electrical activation during AF is uncoordinated and unpredictable in its anatomic path. AF is classified as (1) paroxysmal AF (two or more episodes that terminate spontaneously within 7 days); (2) persistent AF (sustained beyond 7 days, or lasting <7 days but necessitating pharmacologic or electrical cardioversion), or (3) longstanding persistent AF (continuous AF of >1-year duration).

Rationale for ablation

Current data suggest that the benefit of achieving sinus rhythm medically is largely offset by the adverse effects of currently available antiarrhythmic drugs. Catheter ablation may not only avoid such side effects but also be superior in achieving long-lasting sinus rhythm and improving quality of life. Indications for catheter ablation of AF per the HRS/EHRA/ECAS Expert Consensus Statement (2009) are (1) symptomatic AF refractory or intolerant to at least one Class 1 or 3 antiarrhythmic medication; (2) in rare clinical situations, it may be appropriate to perform AF ablation as first-line therapy; (3) selected symptomatic patients with heart failure and/or reduced ejection fraction; and (4) presence of a left atrial (LA) thrombus is a contraindication to catheter ablation of AF.

Ablation therapy technique

Areas of automaticity within the pulmonary veins (PVs) are still the main target for catheter ablation. Recent observations that potentials can also arise from the posterior LA wall, superior vena cava, vein of Marshall, crista terminalis, interatrial septum, and coronary sinus have resulted in a wider repertoire of catheter ablative techniques. The procedure is guided by three-dimensional electroanatomic mapping, by fluoroscopy, or by intracardiac echocardiography (ICE). Successful ablation is documented by amplitude reduction within the ablated area, elimination (or dissociation) of the PV potentials recorded from mapping catheters, and/or exit block from the PV. To improve outcome, additional linear lesions are sometimes placed similar to the lesions placed in surgical maze procedures.

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Ventricular fibrillation

Sustained ventricular arrhythmias are the most common cause of sudden cardiac death. Ventricular tachycardia (VT) rarely occurs in a structurally normal heart. Predominantly, the electrophysiology and function of the myocardium are markedly altered secondary to ischemic, dilatative, or hypertrophic cardiomyopathy. Different classifications exist based on morphology (i.e., monomorphic VT [appearance of all the beats match] and polymorphic VT [beat-to-beat variations in morphology] and based on duration (e.g., nonsustained VT [arrhythmia self-terminates within 30 seconds] and sustained VT [arrhythmia lasts >30 seconds]).

As in many cases multiple reentrant circuits coexist, an ablation procedure does not always avert the risk of sudden death. As a consequence, catheter ablation of sustained monomorphic VT is an important option to control recurrent ventricular tachycardias (VTs) but must be considered adjunctive to ICD placement, especially when structural heart disease is present. Catheter ablation has a high acute success rate in eliminating clinical VT in 50% to 88% of patients (12-month follow-up).

Indications for catheter ablation for VT per the EHRA/HRS Expert Consensus Document (2009) are as follows.

In patients with structural heart disease (including prior myocardial infarction [MI], dilated cardiomyopathy, arrhythmogenic right ventricular [RV], and cardiomyopathy/dysplasis [ARVC/D]), catheter ablation of VT is recommended for (1) symptomatic sustained monomorphic VT, including VT terminated by an ICD, that recurs despite antiarrhythmic drug therapy or when antiarrhythmic drugs are not tolerated or not desired, (2) control of incessant sustained monomorphic VT or VT storm that is not due to a transient reversible cause, (3) patients with frequent premature ventricular complexes, nonsustained VTs, or VT that is presumed to cause ventricular dysfunction, (4) bundle branch reentrant or interfascicular VTs, and (5) recurrent sustained polymorphic VT and VF refractory to antiarrhythmic therapy when there is a suspected trigger that can be targeted for ablation.

Catheter ablation should be considered in (1) patients who have one or more episodes of sustained monomorphic VT despite therapy with one or more Class I or III antiarrhythmic drug, (2) patients with recurrent sustained monomorphic VT due to prior MI who have LV ejection fraction >0.30 and expectation for 1 year of survival, and is an acceptable alternative to amiodarone therapy, and (3) patients with hemodynamically tolerated sustained monomorphic VT due to prior MI who have reasonably preserved LV ejection fraction (>0.35) even if they have not failed antiarrhythmic drug therapy.

In patients without structural heart disease, catheter ablation of VT is recommended for patients with idiopathic VT with (1) monomorphic VT that is causing severe symptoms, (2) monomorphic VT when antiarrhythmic drugs are not effective, not tolerated, or not desired, and (3) recurrent sustained polymorphic VT and VF (electrical storm) refractory to antiarrhythmic therapy when there is a suspected trigger that can be targeted for ablation.

VT catheter ablation is contraindicated in the presence of (1) a mobile ventricular thrombus (epicardial ablation may be considered); (2) asymptomatic premature ventricular beats and/or nonsustained monomorphic VT that is not suspected of causing or contributing to ventricular dysfunction; and (3) VT due to transient, reversible causes, such as acute ischemia, hyperkalemia, or drug-induced torsade de pointes.

Ablation therapy technique

Mechanisms of VT can be identified by the introduction of stimuli during vulnerable period until a sustained VT develops similar to that of the spontaneous arrhythmia; then ablation is performed within a protected isthmus of reentrant circuit. Several factors complicate this approach: the underlying scar region may be large, induced VT is often not hemodynamically stable enough for adequate mapping, and multiple morphologies of inducible VTs may coexist.

New approach

Strategic ablation can be done without mapping individual reentrant circuits. Ablation is guided by three-dimensional computed mapping to identify myocardial scars whose perimeter may contribute to reentrant circuit.

Rationale for ablation

1. What is the urgency of the surgery?

What is the risk of delay in order to obtain additional preoperative information?

Both ablation for AF and ablation for ventricular fibrillation are performed as elective procedures. Thorough preoperative evaluation in this often multimorbid patient group is therefore imperative. One exception is ablation for incessant VT, which may be treated on an urgent basis.

2. Preoperative evaluation

When scheduled for ablation, an extensive preprocedural workup for cardiologic evaluation is generally available:

History and physical examination is performed to determine the presence and nature of associated symptoms, including the clinical type of AF and the presence of underlying conditions.

AF is idiopathic in approximately 15% of cases. Cardiac conditions include valvular heart disease (mitral valve disease is the most common cause in younger patients), coronary artery disease/MI, LV systolic dysfunction (the most common cause in older patients), hypertension (especially if LV hypertrophy is present), restrictive cardiomyopathy, cardiac tumors, myocarditis, post cardiac surgery, sick sinus syndrome, preexcitation syndromes, cardiac trauma, and pericarditis. Noncardiac conditions include pulmonary embolism, metabolic disorders (hyperthyroidism), toxic effects of alcohol (“holiday heart syndrome”), or drugs.

Ventricular fibrillation can be idiopathic. Cardiac conditions include, most commonly, severe structural heart disease: ischemic, dilatative, orhypertrophic cardiomyopathy. Electrophysiologic abnormalities include Brugada syndrome and long QT syndrome. Noncardiac conditions include intoxications (digitoxin, quinidine) and electrolyte disturbances.

An electrocardiographic (ECG) study is performed.

In AF, irregular oscillatory waves replacing regular P waves are seen. The ventricular response is irregular and usually rapid but this depends on the myocardial conduction properties (especially atrioventricular [AV] node), vagal and sympathetic tone, presence or absence of accessory conduction pathways, and drug actions. Regular R-R intervals are possible with AV block or ventricular or AV junctional tachycardia. Irregular, sustained wide QRS complex tachycardia can be found in AF with conduction over an accessory pathway or in AF with underlying bundle branch block.

In ventricular fibrillation, tachycardia with broad (QRS >0.12 second) monomorphic or polymorphic QRS complexes are seen. Atrial and ventricular activation is uncoordinated (AV dissociation: “capture-beat,” “fusion-systole”). At slower ventricular rates, P waves may be recognized but appear independent of ventricular activation. Signs of underlying heart disease include LV hypertrophy and prior MI.

An echocardiographic study is performed. Patients with persistent AF who are in AF at the time of ablation should have transesophageal echocardiography (TEE) performed to screen for a thrombus regardless of prior anticoagulation. The ablation catheter will be manipulated throughout the LA during an AF procedure leading to possible dislodgment of an in situ thrombus and resultant thromboembolic complication. Valvular heart disease, LA and right atrial (RA) size, signs of LV hypertrophy, LV size and function, and RV pressure (pulmonary hypertension) are noted.

Exercise testing includes cardiac exercise tolerance, adequacy of rate control, induction of exercise-induced AF, and exclusion of ischemia.

Chest radiography evaluates lung parenchyma, pulmonary vasculature, and signs of edema.

Holter monitoring is also performed.

3. What are the implications of co-existing disease on perioperative care?

b. Cardiovascular system

In addition to a physical examination, routine laboratory evaluation, and ECG, additional testing is aimed to identify coronary artery disease that may warrant revascularization. This testing is relevant, especially for VT ablation, because obstructive coronary artery disease is a common cause of myocardial fibrosis and resultant arrhythmia and because, during catheter ablation, VT may be sustained for an extended period of time to allow for activation and entrainment mapping.

c. Pulmonary

General anesthesia is used for patients at risk of airway obstruction and those with a history of sleep apnea. A thorough clinical history and, if indicated, blood gas analysis or pulmonary function testing should be aimed to identify patients at risk.

d. Renal-GI:


e. Neurologic:


f. Endocrine:


g. Additional systems/conditions which may be of concern in a patient undergoing this procedure and are relevant for the anesthetic plan (eg. musculoskeletal in orthopedic procedures, hematologic in a cancer patient)


4. What are the patient's medications and how should they be managed in the perioperative period?

Both AF and ventricular fibrillation are often a consequence of underlying, especially cardiac, disease. Patients scheduled for ablation therefore generally present with a complex medical treatment plan that includes medications for coronary artery disease, antihypertensive medications, medications for congestive heart failure, medications for metabolic syndrome, and medications for AF and associated risks.

The general treatment principles for AF according to American College of Cardiology (ACC)/American Heart Association (AHA)/ESC 2006 guidelines are as follows:

Patients with AF have an increased long-term risk of stroke, heart failure, and all-cause mortality. Treatment strategies aim at:

Anticoagulation to decrease risk of thromboembolism

Recommended for all patients except those with lone AF or contraindications

Choice of anticoagulation regimen has to balance risk of bleeding with risk of stroke: low risk, aspirin; and high risk, vitamin K antagonist, INR target depends on stroke risk.

Rate control to limit symptoms and reduce risk of tachycardia-associated cardiomyopathy

Achievement of rhythm control using currently available antiarrhythmic drugs offers no benefit over rate control. The exception may be younger patients with little underlying heart disease, who might profit more from reestablishment of sinus rhythm.

Rate control target is approximately 60 to 80/min at rest and 90 to 115/min during moderate exercise.

Recommended drugs for rate control:

Persistent or permanent AF: beta-blocker or nondihydropyridine calcium channel antagonist

Acute setting (no accessory pathway): intravenous beta-blocker or nondihydropyridine calcium channel antagonist

Acute setting (no accessory pathway, heart failure): amiodarone, digoxin

Acute setting (with accessory pathway): amiodarone

For restoration of regular rhythm (considered in paroxysmal or persistent AF): cardioversion (medical, electric), ablation, AV node ablation and implantation of pacemaker (does not recover atrial function)

The general treatment principles for ventricular arrhythmia according to ACC/AHA/ESC 2006 guidelines are as follows:

VT is the most common cause for sudden cardiac death. Treatment consists of:

Implantable cardioverter-defibrillator (ICD) implantation: improved survival with ICD therapy in high-risk patients with LV dysfunction due to ischemic and nonischemic cardiomyopathy

Antiarrhythmic drugs: Effective in suppressing ventricular ectopic beats and arrhythmias: beta-blockers (first-line choice in most cases), sotalol, amiodarone

Ablation therapy

h. Are there medications commonly seen in patients undergoing this procedure and for which should there be greater concern?

Antiarrhythmic therapy

Drugs that interfere with electrophysiologic mapping should generally be avoided perioperatively; this may require hospitalization, such as for patients with poorly tolerated VT. For idiopathic VT in the absence of structural heart disease, antiarrhythmic drugs (including beta-blockers) should be discontinued for 4 to 5 half-lives before the procedure to facilitate activation mapping during spontaneous or induced VT. After ablation of idiopathic VT, most patients can be discharged without antiarrhythmic drugs.

For VT related to significant structural heart disease, many patients have received prior Class III antiarrhythmic drugs such as sotalol or amiodarone. Class III or I antiarrhythmic drugs with short elimination half-lives should be discontinued prior to catheter ablation. Due to the very prolonged elimination half-life of amiodarone, many patients will undergo catheter ablation of VT while therapeutic effects are present.

In some cases, intravenous procainamide or amiodarone is administered to slow the rate of VT, allowing the mapping of otherwise hemodynamically unstable VT. After successful catheter ablation, amiodarone may be discontinued but is often continued at a reduced dose. In patients with structural heart disease, preexistent therapy with beta-adrenergic blockers is usually continued after ablation.

For patients with an ICD or pacemaker, most patients undergoing catheter ablation of VT either have a previously implanted ICD or will undergo device implantation after ablation. Radiofrequency (RF) ablation may affect both the myocardial VT substrate and the pacing and sensing functions of an ICD. Programmed electrical stimulation and RF current are sensed by ICDs. To prevent oversensing and unintended delivery of antitachycardia therapies, ICDs must be reprogrammed prior to the ablation procedure.

Pacemaker function in pacemaker-dependency should be programmed to an asynchronous mode before RF current is applied. Pacemaker function without pacemaker-dependency is generally programmed to asynchronous mode at a low pacing rate. Stimulation thresholds and intracardiac electrogram amplitudes should be measured before and after ablation because RF current can significantly change tissue characteristics around previously implanted leads.


Oral anticoagulation is generally stopped 4 to 5 days before the ablation procedure. Bridging therapy may be administered with heparin (either low-molecular-weight heparin or unfractionated heparin) until the day before the ablation procedure. Ablation of AF should not be performed in patients on aspirin and clopidogrel because of an increased risk of cardiac tamponade. In these cases, ablation should be postponed to a time when aspirin and clopidogrel can be safely discontinued.

i. What should be recommended with regard to continuation of medications taken chronically?


Antihypertensive therapy is generally continued, with the exception of beta-blockade. Angiotensin-converting enzyme (ACE) inhibitors are a cornerstone of therapy for congestive heart failure and are important in the therapy of hypertension and coronary artery disease. There are some indications from experimental data that these drugs may prolong the action potential, but the clinical relevance of therapeutic levels on cardiac electrophysiology is unclear.


Standard therapy is continued to ensure stable pulmonary function.


Nephrotoxic drugs such as furosemide are problematic in a setting where substantial amounts of intravenous contrast agents are administered. However, techniques such as intracardiac echocardiography and three-dimensional electroanatomical mapping have significantly reduced the amount of contrast agent needed during ablation. While adequate hydration is important to avoid renal injury, this has to be adjusted for congestive heart failure if present. During ablation procedures, relevant amounts of fluid are administered through the sheaths, and overhydration with resultant pulmonary congestion must be avoided.


See above. Continuation of antiplatelet drug therapy depends on individual patient risk factors. Antiplatelet therapy (especially IIB/IIIA glycoprotein receptor blockers and clopidogrel) should be avoided if possible. At the conclusion of the procedure, sheath removal requires withdrawal of anticoagulation for a window of time to achieve adequate hemostasis.


Interference of most psychiatric drugs with the conduction system has been reported and therefore may complicate electrophysiologic measurements. A close liaison of cardiologist and psychiatrist is needed to develop an individualized strategy for patients regularly taking such medications.

j. How To modify care for patients with known allergies –


k. Latex allergy- If the patient has a sensitivity to latex (eg. rash from gloves, underwear, etc.) versus anaphylactic reaction, prepare the operating room with latex-free products.


l. Does the patient have any antibiotic allergies? (common antibiotic allergies and alternative antibiotics)

Ablation procedures do not mandate antibiotic prophylaxis, unless foreign material is introduced permanently (e.g., pacemaker, automated ICD [AICD]) or specific patient indications exist (refer to 2007 AHA guidelines for the prevention of infective endocarditis).

m. Does the patient have a history of allergy to anesthesia?


5. What laboratory tests should be obtained and has everything been reviewed?


Intraoperative Management: What are the options for anesthetic management and how to determine the best technique?

Ablation of the thin-walled atrium, in close vicinity to regions of autonomic innervation and the esophagus, requires patients to lie motionless for extended periods. Stimuli from ablation may be painful, and therefore most of these procedures are performed under conscious sedation or general anesthesia. While patient and institutional preferences play an important role, some advantages/disadvantages of each method exist that should be discussed on an individual basis. However, current data suggest that some form of airway intervention is needed during ablation procedures in up to 40% of cases, suggesting that many of the patients are undergoing general anesthesia for at least portions of the procedure.

The final decision on the anesthetic strategy should take into account these discussion points:

Drug effect on electrophysiologic measurements

Higher doses of anesthetics have the potential for suppressing VT inducibility. General anesthesia and deeper levels of sedation should therefore be avoided in patients with catecholamine-sensitive VTs, particularly if VT was not inducible at a prior procedure.

Volatile anesthetics: There are indications that volatile agents (enflurane > isoflurane > halothane) increase refractoriness of accessory and AV pathways; this may confound electrophysiologic studies. 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 (SA) node.

Opioids: These may depress SA automatism or AV node conduction reserve.

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 SA node activity or intra-atrial conduction.

Paralytic drugs:Long-acting paralytic drugs should be avoided as these may prevent identification of the phrenic nerve by high output pacing during mapping and ablation procedures.

Duration of procedure

Complexity of the case should be discussed with the cardiologist performing the procedure.

Ablation for atrial flutter ablation is shorter in duration as it is generally due to an anatomically well-defined macroreentry circuit amenable to catheter ablation by creating a linear conduction block across tricuspid-IVC ishmus.

Ablation for AF and ventricular tachycardia are more lengthy (3 to 6 hours or longer) due to an extensive ablation strategy and/or need for more extensive electrophysiologic mapping.

Patient factors

General anesthesia is used for patients at risk of airway obstruction, those with a history of sleep apnea, and also those at increased risk of pulmonary edema.

Pulmonary hypertension may exacerbate with inadequate ventilation and resultant hypercarbia leading to right heart failure. It is important to identify these patients and ensure adequate ventilation via a secure airway and monitored expiratory CO2.

General anesthesia may be used to improve patient tolerance for the procedure.

a. General anesthesia

Benefits include airway control, continued monitoring of ventilation, patient comfort during lengthy procedure, control of patient movement and ventilation, and improved catheter stability and potentially better ablation efficacy.

Drawbacks are the potential effects of anesthetics on the conduction system.

Other issues involve qualified personnel and airway concerns due to limited airway accessibility during the procedure because of cardiologic equipment.

b. Monitored anesthesia care

Benefits include that the depth of patient sedation can be adjusted according to need, that patient feedback can be used to recognize early esophageal injury, and neurologic monitoring.

Drawbacks include a lack of airway control and that incomplete respiratory monitoring may lead to hypercarbia and pulmonary hypertension. (Inadequate oxygenation/ventilation is the most common injury in the closed claims database for non–operating-room anesthesia!) In addition, negative thoracic pressures secondary to respiratory efforts against upper airway obstruction can lead to air entrainment or shifting of intracardial structures. Also, sudden patient movements/irregular respiration are issues.

6. What is the author's preferred method of anesthesia technique and why?

Prophylactic antibiotics

Ablation procedures do not mandate antibiotic prophylaxis, unless foreign material is introduced permanently (e.g., pacemaker, ICD) or specific patient indications exist (refer to 2007 AHA guidelines for the prevention of infective endocarditis).

Intraoperative Care

Adenosine causes transient blockade of the AV node to reveal important ECG features in arrhythmias, such as atrial flutter, or latent preexcitation. Suggested is the administration of incremental doses at 1-minute intervals, starting at 0.05 mg/kg and continuing until complete AV block is induced or a maximum of 0.25 mg/kg is reached. A history of asthma is a relative contraindication. Aminophylline antagonizes and dipyridamole potentiates the effects of adenosine.


Isoprenaline (isoproterenol) is a beta-adrenergic drug that is used to increase the heart rate and, during electrophysiologic study, to facilitate the induction of supraventricular (SVT) and ventricular tachycardias (VT). The infusion of isoproterenol is required in exercise-related arrhythmias, in arrhythmogenic right ventricular cardiomyopathy, in idiopathic ventricular tachycardia and in idiopathic dilated cardiomyopathy. Incremental doses of isoproterenol infusion (1 to 3 µg/min and even up to 20 μg/min) are used.

Anticoagulation during procedure

The need for intraprocedural anticoagulation should be discussed with the cardiologist. Recommendations by the European Heart Rhythm Association 2008 (EHRA) are as follows:

Low-risk procedures: Right-side interventions (atrial tachycardias, Kent bundle, and junctional tachycardia and VT) except those performed during atrial flutter.

No anticoagulation is necessary unless other risk factors for systemic embolism are present.

Intermediate-risk procedures:Ablation for persistent common atrial flutter, left-sided interventions excluding AF and overt structural heart disease:

Intravenous sodium heparin: after arterial access bolus of 5000 U followed by 1000 U/h during the procedure. More aggressive anticoagulation regimens in individual cases such as those undergoing complex procedures, and extensive RF applications.

High-risk procedures: Ablation for atrial fibrillation, ablation of ventricular tachycardia with overt heart disease

After sheath insertion and trans-septal puncture, IV heparin bolus of 5000 to 10,000 U or 50 to 100 U/kg followed by 1000 to 1500 U/h. The lower level of anticoagulation should be maintained at an ACT of at least 300 to 350 seconds throughout the procedure. Less intense anticoagulation is associated with a high prevalence of in situ thrombus adherent to the trans-septal sheaths. If significant atrial enlargement or spontaneous echo contrast is present, a higher ACT range of 350 to 400 seconds is often targeted.

At completion of procedure, IV heparin is discontinued or reversed with protamine. If protamine is used, care should be taken in patients who have received NPH insulin or have a fish allergy who may be sensitized to protamine and are at risk for an anaphylactic reaction. Sheaths are removed when the ACT is subtherapeutic (160 seconds).

Postprocedural care

IV heparin is resumed for 12 to 24 hours at a maintenance dose of 1000 U/h without a bolus (PTT at 60 to 80 seconds or twice the baseline), followed by subcutaneous low-molecular-weight heparin after 12 to 24 hours. Oral anticoagulation is resumed the day after the procedure and continued for a minimum of 12 weeks.

In the absence of prior indication for warfarin, periprocedure anticoagulation is followed by fractionated heparin or IV heparin for 12 to 24 hours and aspirin thereafter (80 to 325 mg/d) for at least 1 month.

Common intraoperative complications

Cardiac tamponade (incidence 0% to 6%) can present clinically as an abrupt fall in blood pressure, or more insidiously, gradually. Therefore, it is imperative to be vigilant to the development of cardiac tamponade as a delay in diagnosis may be fatal. An early sign is a reduction in the excursion of the cardiac silhouette on fluoroscopy at the time of systemic blood pressure change. ICE may be helpful for earlier detection of a pericardial effusion. In the majority of 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 sac and placement of an intrapericardial catheter. Surgical drainage and repair are needed less commonly; still, catheter ablation should only be performed in the context of an adequately equipped hospital with access to emergency surgical support.

Embolism of air or thrombus (incidence 0% to 7%): The first 2 weeks after ablation are considered a high-risk period but typically thromboembolic complications occur in first 24 hours and are a major source of cerebral, coronary, or peripheral vascular compromise. The most common cause of air embolism is introduction of air into the trans-septal sheath. While this may be introduced through the infusion line, it can also occur with suction when catheters are removed.

Pulmonary edema (incidence 1.7%): Flushing of catheter sheaths and administration of cooling fluid during ablation can amount to significant fluid volumes (2 to 4 L).

Mitral valve trauma: Entrapment of the mitral valve apparatus has been reported after the curvilinear electrode mapping catheter had been inadvertently positioned intraventricularly.

Acute coronary occlusion: An uncommon complication of AF ablation is acute circumflex coronary artery occlusion following RF energy delivery to create a “mitral isthmus” linear lesion.

Patient access and monitoring

Patient access is limited during the case due to the catheter laboratory equipment. Intravenous access should be established via at least one free-flowing peripheral intravenous line. It should be kept in mind that the groin access via the catheter introducers may serve as emergency access for rapid administration of volume. Beat-to-beat blood pressure monitoring should be established via an intra-arterial line. This line also allows blood sampling for ACT monitoring during the procedure. Urine output should be monitored through a urinary catheter placed under sterile conditions at the beginning of the case. Esophageal temperature probe is often inserted to identify potentially dangerous heating of the esophagus. However, within the broad esophagus, the temperature probe may not align with the ablation electrode, giving a false impression of safety.

a. Neurologic:


b. If the patient is intubated, are there any special criteria for extubation?

The aim is an early postprocedural extubation.

c. Postoperative management

There is generally no pain associated with the procedure itself. However, patients may complain of discomfort following prolonged supine positioning. Overnight telemetry is appropriate to evaluate postprocedural rhythm abnormalities.

Complications (see also Intraoperative complications)

Esophageal injury/atrioesophageal fistula (incidence <0.25%): The esophagus is close to the posterior wall of the LA and ablation procedures here can damage esophageal wall or affect esophageal innervation or vascular supply. This typically presents 2 to 4 weeks after the ablation with fever, chills, and recurrent neurologic events or more acutely as septic shock or death. Atrioesophageal fistula has extremely high mortality, putting extra focus on very early detection and especially prevention. Various approaches have been proposed, including multidetector computed tomography, topographic tagging of the esophageal position with an electroanatomical mapping system, esophageal temperature probe to detect heating during RF energy delivery, preprocedural administration of esophageal barium paste (cave barium aspiration during conscious sedation), and intracardiac echocardiography.

Periesophageal vagal injury from thermal injury originating from the posterior LA wall can lead to acute pyloric spasm and gastric hypomotility.

Vascular complications (incidence 0% to 13%): Incidence may be higher than other catheterization procedures due to the number of catheters introduced and the anticoagulative therapy.

PV stenosis (incidence 1.3% to 3.4%): This results from thermal injury to PV musculature, but its incidence has dropped markedly with better awareness of the problem. Symptoms of PV stenosis include chest pain, dyspnea, cough, hemoptysis, recurrent lung infections, and those of pulmonary hypertension.

Phrenic nerve injury (incidence 0% to 0.48%): The right phrenic nerve is located near the right superior PV and the superior vena cava can be damaged, clinically presenting as dyspnea, hiccups, atelectasis, pleural effusion, cough, and thoracic pain.

What's the Evidence?

Fuster, V. “ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society”. Circulation. vol. 114. 2006. pp. e257-e354. (Recommendations and level of evidence by the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology and Committee for Practice Guidelines for management of patients with atrial fibrillation covering the subjects pathophysiologic considerations, pharmacologic rate control during atrial fibrillation, prevention of thromboembolism, cardioversion of atrial fibrillation, indications for catheter ablation, maintenance of sinus rhythm, indications for catheter ablation, management of atrial fibrillation in special clinical settings.)

Calkins, H. “HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation: recommendations for personnel, policy, procedures and follow-up. A report of the Heart Rhythm Society (HRS) Task Force on Catheter and Surgical Ablation of Atrial Fibrillation developed in partnership with the European Heart Rhythm Association (EHRA) and the European Cardiac Arrhythmia Society (ECAS); in collaboration with the American College of Cardiology (ACC), American Heart Association (AHA), and the Society of Thoracic Surgeons (STS). Endorsed and approved by the governing bodies of the American College of Cardiology, the American Heart Association, the European Cardiac Arrhythmia Society, the European Heart Rhythm Association, the Society of Thoracic Surgeons, and the Heart Rhythm Society”. Europace. vol. 9. 2007. pp. 335-79. (Consensus Statement of European Heart Rhythm Association (EHRA), the European Cardiac Arrhythmia Society (ECAS), in collaboration with the American College of Cardiology (ACC), American Heart Association (AHA), and the Society of Thoracic Surgeons (STS) providing a state-of-the-art review of the field of catheter and surgical ablation of atrial fibrillation.

Zipes, DP. “ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society”. Circulation. vol. 114. 2006. pp. e385-e484. (Practice Guidelines of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines. Includes recommendations on diagnostic workup and therapeutic options for different clinical settings.)

Aliot, EM. “EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a Registered Branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA)”. Heart Rhythm. vol. 6. 2009. pp. 886-933. (Developed in a partnership with the European Heart Rhythm Association (EHRA), the Heart Rhythm Society (HRS), and in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA) summarizes the foundation of knowledge for those involved with catheter ablation of VT.)

Shook, DC, Savage, RM. “Anesthesia in the cardiac catheterization laboratory and electrophysiology laboratory”. Anesthesiol Clin. vol. 27. 2009. pp. 47-56. (Summarizes the special anesthesiologic considerations regarding the work environment and patient population encountered in the cardiac catheterization laboratory and electrophysiology laboratory.)

Gaitan, BD. “Sedation and analgesia in the cardiac electrophysiology laboratory: a national survey of electrophysiologists investigating the who, how, and why?”. J Cardiothorac Vasc Anesth. vol. 25. 2011. pp. 647-59. (Recent survey on current practice of sedation and analgesia in the electrophysiology laboratory.)

Trentman, TL. “Airway interventions in the cardiac electrophysiology laboratory: a retrospective review”. J Cardiothorac Vasc Anesth. vol. 23. 2009. pp. 841-5. (Raises the issue of depth of sedation during electrophysiologic interventions with important implications for patient safety.)

Blanc, JJ. “Consensus document on antithrombotic therapy in the setting of electrophysiological procedures”. Europace. vol. 10. 2008. pp. 513-27. (A document of the Scientific Initiatives Committee of the European Heart Rhythm Association pertaining to general risks of thromboembolism or bleeding and the risks of venous or arterial access.)

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