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Electrophysiology Study and Ablation of Atrial Flutter

Editor: Edward Kim Updated: 7/8/2023 11:34:25 PM


The most important recent advancement in electrophysiology has been the rapid progression of transcatheter ablation techniques. Cardiac arrhythmias previously treated with potentially hazardous medications or surgery can now be routinely managed in the electrophysiology (EP) laboratory.[1]

Atrial flutter (AFL) is a macro-reentrant arrhythmia. The reentrant circuit must include an anatomic or functional barrier that creates a unidirectional block. The reentrant circuit must also have an area of slow conduction; this can result in the tissue recovering and becoming excitable again. Ablation of AFL will differ with the type of flutter. Transcatheter ablation entails applying energy via an intracardiac catheter to create a precise local scar. This scarred area can disrupt the propagation pathway of the arrhythmia circuit and terminate the flutter.

Anatomy and Physiology

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Anatomy and Physiology

Atrial flutter may be classified as typical or atypical. Typical atrial flutter involves a circuit spanning the cavotricuspid isthmus (CTI). 

Counterclockwise CTI-dependent Atrial Flutter

Counterclockwise CTI-dependent AFL is the most common atrial flutter variant. This dysrhythmia is a macroreentrant counterclockwise circuit within the right atrium. The electrical activity propagates via a slow conduction zone between the tricuspid valve annulus and the coronary sinus (CS). It then moves upwards towards the interatrial septum and depolarizes the posterior right atrium. The signal then crosses the roof of the right atrium and descends inferiorly and laterally. There it travels between the tricuspid valve and the crista terminalis. The signal is funneled into the narrow isthmus channel between the tricuspid valve annulus and the inferior vena cava, the cavotricuspid isthmus. The electrical activity then flows back through the slow conduction zone between the tricuspid valve annulus and the CS. A line of functional block can be observed along the crista terminals, precisely at the point where the ascending and descending signals collide.[2]

On surface electrocardiogram (ECG) recordings, the P waves exhibit a sawtooth inverted pattern in the inferior leads, an inverted pattern in the high lateral leads, and an upright pattern in V1. Via catheter electrograms, the wavefront is initially detected by the proximal CS catheter, followed by the His catheter, and subsequently by the poles of the multipolar catheter located in the high, lateral, and low right atrium. Moreover, CS activation occurs from the proximal to the distal sites, with the distal CS exhibiting a significantly delayed activation. The wavefront also experiences a marked delay between its progression through the low right atrium and its arrival at the His location, during which it traverses the region of slow conduction in the isthmus.

Clockwise CTI-dependent Atrial Flutter

The most common variations among typical flutters seem to be clockwise CTI-dependent AFL. The cycle length is similar to that of a typical flutter, and intracardiac electrograms indicate that the reentrant circuit follows the same path but in the opposite direction. Clockwise CTI-dependent AFL can be detected on the surface ECG by observing P waves that are notched and upright in the inferior leads and inverted in lead V1. Recognizing this arrhythmia is important; similar to a typical counterclockwise flutter, the arrhythmia relies on the isthmus of tissue between the tricuspid valve annulus and the inferior vena cava. Hence, it can be treated with ablation of this isthmus.

Atypical Flutter

Some types of atrial flutter are considered atypical, even though they involve a macroreentrant mechanism. In these cases, the reentrant circuits follow pathways different than the cavotricuspid isthmus. The most prevalent causes of non-CTI flutters are a history of ablation for atrial fibrillation (AF), prior cardiac surgery, particularly surgeries to correct congenital malformations or heart valve disease, and the presence of scar tissue within the atria that could have resulted from a prior atriotomy, atrial patch, or baffle.[3]

ECG presentations of true atypical flutter are diverse. It is common for atypical flutter to transition to and from AF, and mapping studies have indicated that a range of circuits is feasible. Atypical flutters can occur in the right or left atrium. More common atypical flutters include non-CTI-dependent right atrial flutter, peri-mitral flutter, roof-dependent left atrial flutter, and left atrial anterior wall flutter.

In all cases of atrial flutter, the activation patterns observed during flutter are essential for making an accurate diagnosis. This is particularly important in left atrial patterns, which can be observed in the electrograms of the distal coronary sinus. Electrophysiologists depend on these electrograms as an initial step when performing procedures for any type of atrial flutter.

Site of Origin

Intracardiac electrode activation sequences can indicate the site of origin of the AFL.

When the His electrode records the earliest activation, an origin in the anteroseptal region of the right atrium is suggested. However, if the proximal coronary sinus shows early activation, this suggests a posteroseptal right atrial origin.

If the high and low right atrial electrograms have similar early activation times, an origin elsewhere in the right atrium is more likely.

If the earliest recorded activation is in the distal CS, an origin within the lateral left atrium is suggested. However, if all the CS electrodes are activated simultaneously, it suggests an origin from the high left atrium. If activation occurs in the high right atrial electrodes prior to the CS electrodes, an origin near the right superior pulmonary vein is more likely.


In 2015, the American College of Cardiology, American Heart Association, and the Heart Rhythm Society released their Guidelines for the Management of Adult Patients With Supraventricular Tachycardia.[1] The 2015 ACC/AHA/HRS Guidelines are as follows:

Class I Indications

  • Catheter ablation of the CTI is useful in patients with AFL that is either symptomatic or refractory to pharmacological rate control.
  • Catheter ablation is useful in patients with recurrent symptomatic non–CTI-dependent AFL after the failure of at least one antiarrhythmic agent. 

Class IIa Indications

  • Catheter ablation is reasonable in patients with CTI-dependent AFL that occurs as the result of flecainide, propafenone, or amiodarone used to treat AF.
  • Catheter ablation of the CTI is reasonable in patients undergoing catheter ablation of AF who also have a documented history of clinical or induced CTI-dependent AFL.
  • Catheter ablation is reasonable in patients with recurrent symptomatic non–CTI-dependent AFL as primary therapy, before therapeutic trials of antiarrhythmic drugs, after carefully weighing treatment options' potential risks and benefits.

Class IIb Indications

  • Catheter ablation may be reasonable for asymptomatic patients with recurrent AFL. 


While there are no absolute contraindications for catheter ablation, the relative contraindications of bleeding diatheses, coagulopathy, deep venous thrombosis that may limit vascular access, and the presence of intracardiac thrombi with resultant increased risk of thromboembolic disease should be considered.[4] 


 A fully equipped electrophysiology (EP) laboratory comprises the following components:

  • C-arm fluoroscopy system with a radiographic table and an image intensifier
  • Cardiac stimulator and an electrophysiologic data acquisition and monitoring system
  • Introducer needles
  • Various EP catheters for diagnostic, mapping, and ablation procedures
  • An equipment interface
  • Radiofrequency energy generator
  • External defibrillator
  • Temporary pacing system
  • Hemodynamic monitoring equipment
  • Intravenous infusion systems with various fluids and necessary pharmaceuticals
  • Resuscitation cart including suction, airways, endotracheal tubes, and emergency drugs

The following standby equipment, facilities, and personnel are recommended:

  • Anesthesia  team
  • Cardiac intensive care capabilities
  • Echocardiography
  • Pericardiocentesis kit
  • Percutaneous coronary intervention
  • Cardiac surgery


  • Cardiac electrophysiologist
  • Cardiac electrophysiology laboratory technician
  • Clinical nursing staff
  • Anesthesia team (for complex cases)
  • Radiographers


Informed Consent

The patient should be informed about the purpose, advantages, risks, and alternatives of the AFL ablation procedure.

Patient Preparation

Most antiarrhythmic medications are typically recommended to be discontinued prior to most EP procedures, although exceptions may exist. Medications should be discontinued for 3 to 5 half-lives; for most medications, this is equivalent to 2 to 3 days. EP studies are invasive procedures, and it may be necessary to discontinue anticoagulant therapy and adjust or interrupt hypoglycemic drug regimens.

Patients are required to fast before the procedure for at least 6 hours. 

Intravenous access should be established, usually accomplished before arrival in the EP lab. Surface electrodes are applied to obtain a routine 12-lead surface ECG, and a noninvasive blood pressure cuff should be attached unless invasive monitoring will be utilized. If sedative drugs are going to be administered, continuous pulse oximetry should be performed. To allow defibrillation with minimal disruption and without compromising the sterile field, the placement of remote defibrillation pads may be necessary. Lastly, an indifferent skin electrode plate is placed when ablation is intended.

Sedation and Anesthesia

The approach to premedication, sedation, and anesthesia during EP procedures varies among different institutions. One approach is to administer premedication or titrated conscious sedation utilizing a combination of an opiate and a benzodiazepine, along with an antiemetic. Another approach is to administer general anesthesia; this is most necessary in cases that are expected to require extensive ablation, cases where external cardioversion may be needed, or for psychological reasons, such as in young adults and children.

Technique or Treatment

Catheter Ablation of CTI-dependent Atrial Flutter

The elimination of macroreentrant circuits requires the creation of a line of block within the path of the circuit. In typical atrial flutter, the circuit travels through the CTI, which provides several advantages as an ablation target; conduction through the CTI is a necessary pathway for the circuit, so the flutter wavefront cannot bypass it. Also, creating a line of block of limited length, approximately 2 to 3 cm, can usually interrupt conduction across the CTI. In addition, the CTI is relatively safe to ablate; the risk of damaging the atrioventricular (AV) node or perforating the free right atrial wall at the CTI is low. 

A diagnosis of CTI-dependent atrial flutter must be confirmed with an EP study. This study may require a multi-electrode catheter to be inserted into the right atrium, with the tip of the catheter positioned in the CTI and its proximal poles placed anterior to the crista terminalis. Additional catheters are positioned in the conventional His and CS locations.

The diagnosis may be confirmed in one of 3 ways. Firstly, during the AFL, the activation of the CS should happen from the proximal end to the distal end. The flutter may originate in the left atrium if the activation is not clearly occurring from proximal to distal. Secondly, pacing from the CTI slightly faster than the tachycardia cycle length should entrain the flutter with concealed entrainment, and the post-pacing interval (PPI) should match the tachycardia cycle length (TCL) within 10 to 30 msec.[5] Thirdly, if 3-D electrical-anatomic mapping is used, it should reveal rotation around the right atrium. For instance, in a counterclockwise flutter, 3-D electroanatomic activation appears as a broad wavefront that exits from the CTI medially, moves up the septum, and proceeds to flow down the lateral right atrial wall. 

To form a line of block at the isthmus, insert the ablation catheter into the femoral vein and guide it into the right atrium and through the tricuspid valve. The line of block should be initiated at a point on the ventricular side of the tricuspid annulus, where the atrial electrogram disappears while a ventricular electrogram is still visible.[6] Gradually withdraw the catheter back towards the atrial side of the annulus, creating a series of lesions along its path, and then back towards the inferior vena cava until the electrogram is no longer visible. Successful ablation can be achieved towards the posterior end of the tricuspid annulus, lateral to 6 o'clock on the left anterior oblique view, or towards the anterior end near the coronary sinus ostium. More septal lesions, however, risk injury to the right coronary artery and increase the risk of damage to the AV node causing inadvertent complete heart block.[7][8]

The decision on where to create a line of block is usually based on practical factors that affect the ease of the ablation procedure. The pectinate muscle ridges in the isthmus region can make the endocardial surface uneven, making it difficult to establish electrode contact in some areas. Creating a transmural lesion using a standard catheter can be challenging in places where the tissue is thick.[9] However, the exact location is not crucial as long as the line is uninterrupted. 

A successful isthmus ablation requires achieving a conduction block in both directions across the isthmus; it is not sufficient to only make the AFL non-inducible. Once a bidirectional conduction block is achieved, the chance of CTI-dependent flutter recurring is minimal. It is also crucial to ensure that the achieved block is a complete block; an incomplete block can lead to delayed conduction and reentry, which can be pro-arrhythmic. Confirming complete blockage across the CTI is typically simple; various assessment methods exist.

To confirm a complete block, some practitioners use 2 multi-pole catheters in the coronary sinus and the lateral right atrium to confirm complete block during coronary sinus pacing. Using a multi-pole catheter makes a CTI block easier to observe during ablation, as the sequence of activation changes as the isthmus is ablated. Block is confirmed when the multipolar catheter within the right atrium activates from proximal to the distal poles while being paced from the CS, and the last area activated is the closest to the line of the block. Delayed conduction through the isthmus is noted when the distal electrodes on the multipolar catheter are not activated last, indicating an incomplete block. Pacing should be performed from both sides of the isthmus because the block must be bidirectional. The duration of the electrical signal traveling from the right lateral atrium to the coronary sinus should be equivalent to the duration of the electrical signal traveling from the coronary sinus to the right atrium during pacing. Using multi-pole catheters can facilitate the identification of CTI block, but they are not obligatory and have been recently found to be less reliable.[10]

The detection of polarity reversal in bipolar electrograms recorded slightly anterior to the isthmus block line during coronary sinus pacing following AFL ablation is a straightforward and reliable indication of a complete isthmus block.

Another technique for evaluating a complete block is differential pacing using pacing at different distances from the line of block while recording from the opposite side of the block. This approach is typically performed by pacing on the lateral right atrial wall and moving the pacing site from superior to inferior, with a corresponding increase in the time to the recording in the coronary sinus if a complete block is present.

Yet another method is the use of double potentials, which are observed from the isthmus and are usually spaced ≥110 msec apart in a complete block.[11] An incomplete block is probable if the potentials are spaced <90 msec apart. Another valuable method for checking for a complete block across the isthmus is to use incremental pacing and assess for a change in the double potential by >20 msec during slow (600 msec) and fast (250 msec) pacing lateral to the line of block. A complete block has been achieved if the double potential change is <20 msec.[12]  Also, a significant increase of at least 50% in the trans-isthmus interval, usually to an interval of more than 150 msec, in both clockwise and counterclockwise directions is linked to high specificity and negative predictive value in identifying a complete bidirectional trans-isthmus block.[13] 

For the most part, however, relying on the results of one technique is insufficient for confirmation, and the use of multiple techniques is necessary to identify that a complete block has been achieved definitively. 

Catheter Ablation of Non–CTI-dependent Right Atrial Flutter

Atrial flutters in the right atrium that do not involve the CTI are typically observed in patients with a history of heart surgery.[14] Reentry can be caused by the suture line in the right atrium or by scar tissue from atrial dilation. In some rare cases, atrial cardiomyopathy can also be responsible for macroreentrant arrhythmia in the right atrium. Anticipating the most likely pathways for reentry is important when performing ablation on non-CTI-dependent right AFL. The location of the flutter circuit typically depends on the location of a scar, which frequently appears in one of two areas, the right atrial free wall or around a central obstacle within the superior vena cava.

Identifying these isthmuses is critical as they are potential ablation targets. The two ECG features that may indicate non-CTI-dependent right atrial flutter, while not conclusive, are a negative flutter wave in lead V1 and isoelectric periods in between the flutter waves. In the case of intracardiac electrodes, the right atrial flutter should show activation of the CS from proximal to distal poles. A multi-pole right atrial catheter should show the earliest signals from the lateral wall that move both superiorly and inferiorly. 

A stable electrode is needed to map the arrhythmia as a reference; this is usually provided by a lead in the coronary sinus catheter with a large atrial signal. A 3-D map is often used for electrical and anatomic mapping. The map should encompass over 90% of the cycle length if the tachycardia is within the right atrium.

The ablation catheter can be used to record points in the right atrium. In right atrial flutters after surgery, low-voltage areas are often found in the lateral or posterolateral right atrium. These areas are typically where early and late activation are close together and should be viewed in the 3-D map if the macroreentrant tachycardia is located within the right atrium. Low-voltage fractionated electrograms are frequently observed from the catheter tip at these locations, which are considered potential ablation sites. Attempting entrainment from these areas is beneficial. If the catheter is placed in a critical isthmus, pacing 20 to 30 msec faster than the tachycardia cycle length will cause entrainment and concealed fusion. The PPI should equal the TCL within 30 msec. If no fusion is observed or the PPI is longer than the tachycardia cycle length, the catheter is not situated in a critical isthmus within the tachycardia.

Before performing ablation in the lateral right atrial wall, particularly in the superior right atrium, pacing with 10 mA or higher is necessary to detect any phrenic nerve stimulation. If the diaphragm is stimulated, phrenic capture is present, and ablation at this site should be avoided entirely to avoid diaphragmatic paralysis. An anatomical marker can be placed on the 3-D map to indicate sites where phrenic nerve capture was detected.

In cases with right atrial scar regions, there could be a critical isthmus between the scar and a close anatomical boundary like the superior vena cava, crista terminalis, or tricuspid annulus. Creating a complete linear lesion across this isthmus usually results in the elimination of the flutter.

After successfully terminating the flutter with ablation at a critical isthmus in the right atrium, it is recommended to perform additional ablation in the same area as a precaution. Ablating macroreentrant flutter in the right atrium not only slows down conduction but creates boundaries that favor the development of CTI-dependent flutter. Therefore, it is advisable to perform CTI ablation if it has not been done previously. Once ablation is completed, checking for the re-induction of the arrhythmia with programmed stimulation and burst pacing is essential. Also, if linear ablation lesions were created, ensuring a complete block across both sides of the line is prudent. Double potentials that are widely spaced, and differential pacing or recording from any side of the ablation line, indicate a successful block.

Catheter Ablation of Left Atrial Flutter

Left atrial flutter has become more common due to increased AF ablation. When a patient presents with new AFL after an ablation procedure, left atrial flutter should be suspected, especially if the AFL occurs in the first weeks or months after the initial procedure. Left AFL can be difficult to control and is usually poorly tolerated. Although a surface ECG is not a definitive diagnostic tool for left AFL, the presence of discordant flutter waves with positive waves in lead V1, negative waves in leads I, aVL, and V6, and isoelectric periods between the waves indicate a left atrial origin.[15] It is essential to consider the possibility of left AFL before commencing with an ablative procedure; maneuvering in the left atrium requires transseptal puncture and often requires more extensive ablation. Transseptal puncture and extensive ablation increase procedure-related risk.

Observation of the activation pattern of the coronary sinus, which wraps around the mitral annulus posteriorly, is important when placing intracardiac catheters. The activation pattern provides information about left atrial activation and should be examined first. If the coronary sinus activation is simultaneous or occurs distally to proximally, this proves a left atrial origin of the flutter. However, proximal to distal coronary sinus activation is not definitive for a right atrial origin; peri-mitral flutter, which occurs in the counterclockwise direction, can also have this activation pattern. To differentiate, pacing from the CTI and the right atrium should be used to confirm entrainment with fusion and assess the PPI.[16]

After evaluating the activation patterns of the coronary sinus, the next step is to rule out atrial tachycardia or flutter that depends on the pulmonary veins. It is common for the pulmonary vein isolation to fail after ablation of AF, resulting in conduction gaps that can act as an anchor point for microreentry or allow for pulmonary vein tachycardia to enter into the left atrium. If there is left atrial tachycardia or flutter with pulmonary vein reconnection, the initial intervention is usually to attempt reisolation of the pulmonary veins. If the procedure results in pulmonary vein isolation but the tachycardia persists, the subsequent intervention involves detecting variability in the cycle length of the atrial tachycardia. If the variation in cycle length is more than 15%, or the tachycardia exhibits an abrupt start-stop pattern, then a focal atrial tachycardia is probable. If the variation in cycle length is less than 15%, the diagnosis is likely to be macroreentry.[17] 

If that macroreentry is confirmed, the search for an ablation target for left atrial macroreentrant flutter can commence. This search involves identifying the most common circuits, including peri-mitral flutter, roof-dependent flutter, anterior wall reentry through an area of scar tissue, intraseptal reentry, or atrial appendage reentry; intraseptal and atrial appendage reentry are less common. It is crucial to assess coronary sinus activation during the arrhythmia to distinguish among these various possibilities. 

Peri-mitral Flutter Ablation

Similar to CTI-dependent flutter, peri-mitral flutter can occur clockwise or counterclockwise. The examination of coronary sinus activation patterns helps diagnose peri-mitral flutter. If the activation occurs either distally to proximally in a clockwise direction or proximally to distally in a counterclockwise direction, it may indicate peri-mitral reentry. However, coronary sinus activation only reflects activation in the posterior wall. To assess activation of the anterior wall of the left atrium, signals from locations at the left inter-atrial anterior septum and the lateral wall should be recorded. Those signals can confirm the rotation of the peri-mitral flutter.

In a clockwise peri-mitral flutter, the signal from the anterior inter-atrial septum should occur before that of the anterior lateral wall, and the reverse is true for a counterclockwise flutter. If the activation pattern shows signs of peri-mitral reentry, the next step is to conduct pacing maneuvers to detect concealed entrainment. Pacing at a rate 20 to 30 msec faster than the cycle length in the distal coronary sinus or the mitral isthmus can result in the tachycardia becoming entrained with concealed fusion. The PPI should be similar to the TCL, within 10 to 30 msec range. The same procedure can be performed from the anterior septal sites situated along the mitral annulus.[18][19]

After establishing the diagnosis, a linear ablation lesion can be created to terminate the circuit. To create this lesion, ablation of the isthmus between the left inferior pulmonary vein and the mitral annulus is utilized. Although the tachycardia cycle length should be slowed during the ablation, changes in the tachycardia activation sequence may be seen. Peri-mitral tachycardia can transition to roof-dependent tachycardia during ablation. Also, in some instances, the fibers in the mitral isthmus can be located in the epicardium, which may require ablation in the coronary sinus for a successful block. 

A proposed alternative approach to peri-mitral flutter involves creating a linear ablation that extends from the mitral annulus across the anterior wall, which is located anterior to the left atrial appendage, to the right superior pulmonary vein, and an already-formed roof line. This approach, known as the anterior line, reduces the risk of tamponade but increases the likelihood of isolating the left atrial appendage and the risk of a left atrial anterior wall flutter.

Although it is encouraging when peri-mitral flutter resolves during the ablation procedure, this should not be the sole focus of ablation. Similar to CTI-dependent flutter, verifying mitral isthmus block during peri-mitral flutter ablation is essential. Confirmation may be obtained by observing activation sequence change while pacing from the left atrial appendage, resulting in a complete reversal of the coronary sinus activation, or by using differential pacing, which involves performing successive pacing from the proximal to the distal coronary sinus. As the pacing site gets closer to the distal coronary sinus, the activation time recorded in the left atrial appendage should increase.  

Catheter Ablation of Roof-dependent Left Atrial Flutter

Roof-dependent atrial flutter is frequently observed after ablation for AF.[20] A crucial diagnostic feature is the occurrence of concurrent activation in the coronary sinus, where neither distal-to-proximal nor proximal-to-distal activation is observed. Although other arrhythmias can exhibit this activation pattern, roof-dependent macroreentry is the most prevalent. The diagnosis of this tachycardia can be confirmed using simple mapping techniques.

To determine the direction of activation relative to a reference channel, recordings are taken from the ablation catheter low in the anterior wall close to the mitral annulus and then close to the anterior roof. This same process is repeated in the posterior wall. The activation pattern should move in opposite directions on the posterior and anterior walls. If the activation direction is similar on both walls, the roof is not part of the reentrant circuit but a bystander. While 3-D mapping systems are helpful, they are not necessary to verify this activation pattern. Confirming roof-dependent AFL can be achieved by entrainment. The ablation catheter is placed on the roof, and the pacing is done at 20 to 30 msec faster than the tachycardia cycle length. This will lead to entrainment of the tachycardia with concealed fusion, and the PPI should be approximately equal to the tachycardia cycle length.[21]

Using a 3-D mapping system can assist with ablating the roof. Ablation involves forming a linear lesion connecting the left superior pulmonary vein with the right superior pulmonary vein across the atrial roof. Atrial electrograms will show a reduction in amplitude, indicating the formation of an electrical block on the roof. The flutter may terminate or change its morphology before the line of block is complete. However, it is essential to continue creating the line of block even after the flutter terminates and confirm the block is complete using differential pacing on both sides. To confirm a block in this case, pacing can be performed from the left atrial appendage while recording from the posterior wall. Activation should occur the latest closest to the line within the superior posterior left atrium; with a roof block, signals move down the anterior wall, then around the floor of the left atrium, and upwards across the posterior wall.

Catheter Ablation of Left Atrial Anterior Wall Flutter

Patients with persistent or long-standing AF, typically older females, are more prone to left atrial anterior wall flutter. Usually, ablation procedures for AF do not involve targeting the left atrial anterior wall. Nevertheless, this region can contain zones with fibrotic tissue and decreased voltage, which may act as obstacles for reentry. While such circuits may occur absent prior cardiac intervention, they are typically observed in patients with previous linear ablation along the mitral isthmus or the left atrial roof. The use of 3-D mapping is not essential for the ablation of these circuits. The key characteristics of these arrhythmias are fragmented potentials and low voltage in the anterior wall, with some cases showing the entire tachycardia circuit located in this area. Pacing maneuvers can prove concealed entrainment, and the PPI will approximately match the tachycardia cycle length in these regions.[22]

To ablate this AFL, attempts can be made to target a specific critical isthmus with focal ablation. Creating an anterior line between the mitral isthmus and the right superior pulmonary vein can be an option. Focusing on a focal area for ablation can be problematic because scar formation can create a new barrier, causing flutter recurrence. However, creating anterior lines of block can also lead to complications, such as left atrial appendage isolation or compromised left atrial contractility, which can increase the risk of thrombus formation. Also, ablation in the anterior wall can cause activation of the left atrial appendage after the QRS complex, which can delay left atrial activation and compromise the systolic atrial contribution to cardiac output. There is no clear consensus regarding the best technique for ablating these flutters.


Radiofrequency (RF) ablation carries risks similar to those associated with a standard EP study and additional risks specific to the ablation procedure itself. The risks of a standard EP study encompass those typically associated with any cardiac catheterization procedure, including hemorrhage, thromboembolism, phlebitis, infection, and cardiac perforation. However, these risks are considerably lower compared to a standard cardiac catheterization; most electrophysiology studies do not involve arterial puncture and cause less damage to the arterial tree. The overall risk of these complications is below 1%. This does not include the risks associated with intraprocedural radiation exposure, which can be prolonged in complex cases.

The primary risks associated with RF ablation are the potential for inadvertent complete heart block, which typically occurs when ablating near the normal conduction system, as well as the risk of cardiac perforation and tamponade, commonly observed during ablation procedures performed in the atria, coronary sinus, or right ventricle.[8] The incidence of these complications is less than 2%.

There are also exceptionally rare complications that may arise, including the development of arrhythmogenic foci, damage to the valvular apparatus resulting in the introduction of mitral or tricuspid regurgitation, systemic embolization during manipulation within the left-sided chambers, pulmonary vein stenosis, and the formation of stenotic lesions within the coronary arteries, particularly the right coronary artery. This complication warrants considerable attention, particularly when ablating within the right ventricular outflow tract, coronary sinus, or cardiac veins.[23] Severe, life-threatening irreversible complications are extremely uncommon; the overall risk of death, myocardial infarction, or stroke is usually less than 0.5%. 

Clinical Significance

In general, the risks associated with RF ablation are minimal. RF ablation procedures become a highly favorable option when dealing with life-threatening or highly symptomatic arrhythmias that have a high likelihood of successful treatment through RF ablation. RF ablation is now the mainstay treatment of most arrhythmias and can offer an excellent success rate for treating AFL, making it a reasonable alternative to daily antiarrhythmic drug therapy.

Enhancing Healthcare Team Outcomes

RF ablation has emerged as the primary treatment for most patients with AFL.[1] A specialized interprofessional team is required to perform the ablation procedure. One operator, typically the electrophysiologist, is responsible for the invasive procedure, while another, usually the cardiac electrophysiology laboratory technician, operates the recording system and external stimulator. The clinical nursing staff assumes patient care responsibility, including vital sign monitoring and intravenous medication administration. Nurses also play an important role in the early diagnosis and management of complications and are valuable in postprocedural care. An anesthesiologist may also participate in patient care before and during the procedure to provide sedation and pain control. Internists, primary care providers, and advanced practice providers can manage postoperative monitoring and follow-up.

To achieve optimal outcomes in postoperative care, it is essential to have an interprofessional team that adopts a comprehensive and coordinated approach. Effective collaboration, shared decision-making, and open communication are vital components for achieving the desired positive outcomes. Interprofessional care to the patient should adhere to an integrated care pathway and be based on evidence-based practices when planning and assessing joint activities. Also, early recognition of complications is paramount, enhancing the prognosis and overall result.



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Level 3 (low-level) evidence


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Level 2 (mid-level) evidence


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Level 2 (mid-level) evidence


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Level 3 (low-level) evidence