**5. Management**

Therapy for atrial flutter has two goals: management of the arrhythmia itself with either rate control or rhythm control and management of the complications of the arrhythmia with stroke prophylaxis [12].

#### **5.1. Non-invasive management**

#### *5.1.1. Rate control*

Rate control is generally reserved for patients who are in permanent atrial flutter and have no or minimal symptoms and cannot achieve rhythm control due to co-morbidities or are not willing to undergo procedures or take medications. There is debate in the literature about what exactly is adequate rate control; this however pertains to atrial fibrillation as it has not been specifically studied in atrial flutter. The same parameters however could generally be applied as the goal is to avoid tachycardia-induced cardiomyopathy whilst preserving exercise capacity. Typically, the aim is an average 24-hour heart rate over 24 hours of 80 bpm and a maximum of less than 130 bpm [13]. An emerging data however shows that less strict control such as heart rates less than an average 24-hour heart rate of less than 110 bpm is adequate [13, 14]. Various pharmacological agents which are used in non-invasive management are pre‐ sented in Table 2.

Rate control of atrial flutter can be very difficult to achieve pharmacologically. It is important to understand that atrial flutter ablation has a high success rate unlike atrial fibrillation, and extreme methods of rate control such as pacemaker implantation and AV nodal ablation are rarely used as a management strategy.


**Table 2.** Pharmacological management therapies

#### *5.1.2. Rhythm control*

recent reports have characterised the substrate as showing wide scarred areas with low voltage

Atrial flutter can be paroxysmal or persistent. When atrial flutter is associated with an increased ventricular response, it can result in palpitations, shortness of breath, chest pain, fatigue or pre-syncope. If a patient presents with atrial flutter and a rapid ventricular rate, stroke, tachycardia-induced cardiomyopathy and rarely myocardial infarction are complica‐ tions that can be encountered. Syncope in the setting of atrial flutter is rare if there is no significant cardiac history [11]. When presenting because of a more prolonged episode, increased symptoms of heart failure may be evident. Occasionally, atrial flutter is an incidental

Therapy for atrial flutter has two goals: management of the arrhythmia itself with either rate control or rhythm control and management of the complications of the arrhythmia with stroke

Rate control is generally reserved for patients who are in permanent atrial flutter and have no or minimal symptoms and cannot achieve rhythm control due to co-morbidities or are not willing to undergo procedures or take medications. There is debate in the literature about what exactly is adequate rate control; this however pertains to atrial fibrillation as it has not been specifically studied in atrial flutter. The same parameters however could generally be applied as the goal is to avoid tachycardia-induced cardiomyopathy whilst preserving exercise capacity. Typically, the aim is an average 24-hour heart rate over 24 hours of 80 bpm and a maximum of less than 130 bpm [13]. An emerging data however shows that less strict control such as heart rates less than an average 24-hour heart rate of less than 110 bpm is adequate [13, 14]. Various pharmacological agents which are used in non-invasive management are pre‐

Rate control of atrial flutter can be very difficult to achieve pharmacologically. It is important to understand that atrial flutter ablation has a high success rate unlike atrial fibrillation, and extreme methods of rate control such as pacemaker implantation and AV nodal ablation are

finding on ECG with patients who are completely asymptomatic.

or absent electrograms [10].

8 Abnormal Heart Rhythms

**4. Clinical presentation**

**5. Management**

prophylaxis [12].

*5.1.1. Rate control*

sented in Table 2.

rarely used as a management strategy.

**5.1. Non-invasive management**

In an acute setting, atrial flutter with hemodynamic compromise or rarely significant cardiac symptoms (i.e. severe chest pain), synchronised direct current cardioversion is indicated to revert patients to sinus rhythm. Previously, lower defibrillator outputs such as 50 J were employed to prevent pain, but the current recommendation is 200 J biphasic with either anteroposterior or midline and lateral defibrillation pad positioning. There is no difference in pain and potential of ventricular fibrillation induction with lower energy levels.

In clinically stable atrial flutter, the various non-invasive management therapies include cardioversion (electrical or pharmacological) and rate control with pharmacotherapy to slow down AV nodal conduction (see Table 2) or if an atrial pacing lead is in situ rapid atrial pacing for overdrive termination. This is commonly burst pacing to depolarise tissue in the macroreentrant circuit into which the activation front of the arrhythmia is depolarising to terminate the tachycardia. The pacing is typically for three to five seconds at rate approximately 20 ms less than flutter wave cycle length; though this also has the potential to cause atrial fibrillation.

For a list of antiarrhythmic drugs for cardioversion of atrial flutter, refer to Table 2. Classes Ia and Ic can result in slowing the rate of atrial flutter which can facilitate 1:1 conduction of atrial flutter via AV node and cause a rapid ventricular rate. Thus, it is recommended to have concurrent AV blocking agents to control the ventricular response. These antiarrhythmic agents are not very well studied in atrial flutter patient population. The data about their efficacy is derived from clinical trials where atrial flutter was grouped with atrial fibrillation. In terms of prevention of atrial flutter recurrence, flecainide and dofetilide have a long-term efficacy of 50 % and 70 %, respectively [15, 16].

#### **5.2. Stroke prevention**

Anticoagulation is key to preventing ischemic cerebrovascular events [17]. It is extremely important when either above-mentioned management option is considered. Even though the evidence for anticoagulation in the atrial flutter patient population is not as robust as for atrial fibrillation, it is felt that the risks are similar especially for typical cavo-tricuspid isthmusdependent atrial flutter. Thromboembolic prophylaxis is indicated in the management of chronic atrial flutter similar to atrial fibrillation. In our clinical practice, we use CHA2DS-VASc score which has superseded the older CHADS2 score to calculate the annual risk of cerebral thromboembolic event [18]. For oral anticoagulants that are used to prevent stroke, refer to Table 2. Patients who have atrial flutter and undergo DC cardioversion should be on novel anticoagulation or on warfarin with therapeutic international normalised ratio (INR) (>2) for a minimum period of three weeks prior to the DCCV and for a minimum of one month later. The new oral anticoagulants do not have as much data for direct-current cardioversion as warfarin therapy, and some clinicians perform trans-oesophageal echocardiograph prior to direct-current cardioversion [19]. There is no role for aspirin in stroke prophylaxis as the risks of bleeding are greater than the benefit of stroke reduction.

#### **5.3. Invasive strategy**

#### *5.3.1. Typical cavo-tricuspid-dependent atrial flutter*

A standard electrophysiological (EP) case for typical CTI-dependent atrial flutter most often requires the use of three catheters; these include the ablation catheter, a multipolar coronary sinus catheter and a right atrial (RA) mapping catheter. The RA mapping catheter can be either a decapolar or duodecapolar catheter (sometimes referred to as orbital catheter) and is placed along the lateral RA wall anterior to the crista terminalis with the tip down to the lateral inferior RA and tricuspid annulus. Some operators also prefer to additionally use a His and/or right ventricular catheter (Figure 3). Radio-frequency ablation (RFA) is the most commonly used ablation modality in treatment of atrial flutter.

**Figure 3.** Fluoroscopic image of catheters used for a typical atrial flutter study with duodecapolar catheter in the right atrium, ablation catheter at the cavo-tricuspid isthmus and decapolar catheter in the coronary sinus (courtesy of PA hospital EP Lab)

A similar catheter configuration may be used for an atypical or non-CTI-dependent atrial flutter although a 3D mapping system for these arrhythmias is highly beneficial and can negate the need for other electrogram-based mapping catheters. The mapping system can be utilised to define the entire macro-reentrant circuit by identifying the anatomical boundaries and the ablation target which is generally the area of slow conduction. A line of block is achieved by making a linear ablation line between areas of conduction block (discussed under Radio-Frequency Ablation).

### **5.4. Electrophysiological study**

anticoagulation or on warfarin with therapeutic international normalised ratio (INR) (>2) for a minimum period of three weeks prior to the DCCV and for a minimum of one month later. The new oral anticoagulants do not have as much data for direct-current cardioversion as warfarin therapy, and some clinicians perform trans-oesophageal echocardiograph prior to direct-current cardioversion [19]. There is no role for aspirin in stroke prophylaxis as the risks

A standard electrophysiological (EP) case for typical CTI-dependent atrial flutter most often requires the use of three catheters; these include the ablation catheter, a multipolar coronary sinus catheter and a right atrial (RA) mapping catheter. The RA mapping catheter can be either a decapolar or duodecapolar catheter (sometimes referred to as orbital catheter) and is placed along the lateral RA wall anterior to the crista terminalis with the tip down to the lateral inferior RA and tricuspid annulus. Some operators also prefer to additionally use a His and/or right ventricular catheter (Figure 3). Radio-frequency ablation (RFA) is the most commonly used

**Figure 3.** Fluoroscopic image of catheters used for a typical atrial flutter study with duodecapolar catheter in the right atrium, ablation catheter at the cavo-tricuspid isthmus and decapolar catheter in the coronary sinus (courtesy of PA

of bleeding are greater than the benefit of stroke reduction.

*5.3.1. Typical cavo-tricuspid-dependent atrial flutter*

ablation modality in treatment of atrial flutter.

**5.3. Invasive strategy**

10 Abnormal Heart Rhythms

hospital EP Lab)

Generally with cavo-tricuspid isthmus-dependent ablation, there is little electrophysiological study performed as the target of ablation and arrhythmia circuit are known. However, manoeuvres such as entrainment (discussed below) can still be used to confirm cavo-tricuspid isthmus dependence. In atypical atrial flutter ablation, entrainment manoeuvres can be used to localise the arrhythmia circuit. However, with the advent of non-fluoroscopic mapping, entrainment is being employed less frequently to confirm isthmus dependence.

Entrainment is used to determine if a specific anatomical site is a part of the re-entrant circuit [20]. To confirm that atrial flutter is typical and cavo-tricuspid isthmus dependant (not a bystander), entrainment from the CTI and/or another site such as the proximal coronary sinus is performed. By entraining in the atria at a cycle length approximately 10 to 20 ms faster than the tachycardia cycle length and then measuring the post-pacing interval (PPI) (return cycle length), one can determine if CTI (or pacing site) is a part of the re-entrant circuit (Figures 4). The post-pacing interval is the time between the last pacing stimulus that entrained the tachycardia and the next recorded electrogram at the pacing site. The pacing site is considered to be a part of the circuit if the post-pacing interval (PPI) is equal or within 30 ms of tachycardia cycle length.

If entrainment from the isthmus does not demonstrate isthmus involvement, further thought needs to be carried out regarding treatment options, as the tachycardia is likely to be atypical and 3D mapping may be more appropriate.

### **5.5. Radio-Frequency Ablation (RFA)**

Ablation therapy for typical atrial flutter targets the cavo-tricuspid isthmus (CTI). It is a narrow point of the circuit and the slow conduction part of the circuit between two nonconductive boundaries; anteriorly this is bounded by the tricuspid annulus and posteriorly by IVC. It is easily accessible percutaneously and distant from the AV node. Conventionally, atrial flutter ablation involved delivering RF energy in a linear ablative line across the entire isthmus to create bidirectional block. Ablation is started on or near the tricuspid annulus and the catheter brought (dragged) back along the isthmus towards the IVC. Ablation can be performed in both atrial flutter and during atrial pacing (empirically) from the coronary sinus but can equally be performed with pacing from the lower right atrium.

11

Figure 4: Entrainment of typical CTI ablation demonstrating that pacing site (ablation catheter) is within the circuit of the tachycardia. PPI − TCL = 7 ms. Note also the unidirectional activation of the lateral RA wall superiorly (RA 9,10) to inferiorly (RA 1,2) **Figure 4.** Entrainment of typical CTI ablation demonstrating that pacing site (ablation catheter) is within the circuit of the tachycardia. PPI − TCL = 7 ms. Note also the unidirectional activation of the lateral RA wall superiorly (RA 9,10) to inferiorly (RA 1,2) (courtesy of PAH EP Lab)

#### Bidirectional Block **6. Post-ablation bidirectional electrophysiological study**

Post-Ablation Bidirectional Electrophysiological Study

#### This is the electrophysiological endpoint of ablation of the isthmus in CTI-dependent atrial **6.1. Bidirectional block**

(courtesy of PAH EP Lab)

flutter [21]. Activation mapping to measure the trans-isthmus conduction time, differential pacing and online double potentials are the three commonly used techniques that can be employed to determine if the ablation has been successful and bidirectional block has been achieved. Activation Mapping This is the electrophysiological endpoint of ablation of the isthmus in CTI-dependent atrial flutter [21]. Activation mapping to measure the trans-isthmus conduction time, differential pacing and online double potentials are the three commonly used techniques that can be employed to determine if the ablation has been successful and bidirectional block has been achieved.

#### Activation mapping involves pacing from either side of the ablation line (proximal CS pacing low lateral RA are commonly used). With incomplete CTI ablation, the wavefront along the **6.2. Activation mapping**

RA mapping catheter will be fused as conducts in different directions as depicted in Figure 5 and 6. Activation mapping involves pacing from either side of the ablation line (proximal CS pacing low lateral RA are commonly used). With incomplete CTI ablation, the wavefront along the RA mapping catheter will be fused as conducts in different directions as depicted in Figure 5 and 6.

12

**Figure 5.** Pacing site from proximal coronary sinus.

7 and 8).

Figure 5: Pacing site from proximal coronary sinus.

11

Figure 4: Entrainment of typical CTI ablation demonstrating that pacing site (ablation catheter) is within the circuit of the tachycardia. PPI − TCL = 7 ms. Note also the unidirectional activation of the lateral RA wall superiorly (RA 9,10) to inferiorly (RA 1,2)

**Figure 4.** Entrainment of typical CTI ablation demonstrating that pacing site (ablation catheter) is within the circuit of the tachycardia. PPI − TCL = 7 ms. Note also the unidirectional activation of the lateral RA wall superiorly (RA 9,10) to

PPI (313ms) -TCL (306ms) = 7ms

This is the electrophysiological endpoint of ablation of the isthmus in CTI-dependent atrial flutter [21]. Activation mapping to measure the trans-isthmus conduction time, differential pacing and online double potentials are the three commonly used techniques that can be employed to determine if the ablation has been successful and bidirectional block has been

This is the electrophysiological endpoint of ablation of the isthmus in CTI-dependent atrial flutter [21]. Activation mapping to measure the trans-isthmus conduction time, differential pacing and online double potentials are the three commonly used techniques that can be employed to determine if the ablation has been successful and bidirectional block has been

Activation mapping involves pacing from either side of the ablation line (proximal CS pacing low lateral RA are commonly used). With incomplete CTI ablation, the wavefront along the RA mapping catheter will be fused as conducts in different directions as depicted in Figure 5

Activation mapping involves pacing from either side of the ablation line (proximal CS pacing low lateral RA are commonly used). With incomplete CTI ablation, the wavefront along the RA mapping catheter will be fused as conducts in different directions as depicted in Figure 5

(courtesy of PAH EP Lab)

inferiorly (RA 1,2) (courtesy of PAH EP Lab)

Bidirectional Block

12 Abnormal Heart Rhythms

**6.1. Bidirectional block**

Activation Mapping

**6.2. Activation mapping**

achieved.

and 6.

and 6.

achieved.

Post-Ablation Bidirectional Electrophysiological Study

**6. Post-ablation bidirectional electrophysiological study**

Figure 6: Prior to CTI ablation depicting activation pattern in the right atrium. It is chevron shaped due to persistent conduction through the isthmus and fusion of wavefront in the right atrium **Figure 6.** Prior to CTI ablation depicting activation pattern in the right atrium. It is chevron shaped due to persistent conduction through the isthmus and fusion of wavefront in the right atrium

With successful bidirectional block, the activation along the RA catheter is uniform (Figures

With successful bidirectional block, the activation along the RA catheter is uniform (Figures 7 and 8). 13

Figure 7: Bidirectional block demonstrated by activation; A, indicates proximal CS pacing and sequential activation around the RA from proximal to distal RA catheter; B, pacing from distal RA with sequential activation from distal to proximal RA – both showing conduction **Figure 7.** Bidirectional block demonstrated by activation; A, indicates proximal CS pacing and sequential activation around the RA from proximal to distal RA catheter; B, pacing from distal RA with sequential activation from distal to proximal RA – both showing conduction block over the cavo-tricuspid isthmus region (Courtesy of PAH EP Lab)

block over the cavo-tricuspid isthmus region (Courtesy of PAH EP Lab)

**Figure 8.** Pacing from proximal sinus and from RA lateral/anterior wall respectively

### **6.3. Trans-isthmus conduction time**

With successful bidirectional block, the activation along the RA catheter is uniform (Figures

Figure 7: Bidirectional block demonstrated by activation; A, indicates proximal CS pacing and sequential activation around the RA from proximal to distal RA catheter; B, pacing from distal RA with sequential activation from distal to proximal RA – both showing conduction

**Figure 7.** Bidirectional block demonstrated by activation; A, indicates proximal CS pacing and sequential activation around the RA from proximal to distal RA catheter; B, pacing from distal RA with sequential activation from distal to proximal RA – both showing conduction block over the cavo-tricuspid isthmus region (Courtesy of PAH EP Lab)

block over the cavo-tricuspid isthmus region (Courtesy of PAH EP Lab)

**Figure 8.** Pacing from proximal sinus and from RA lateral/anterior wall respectively

13

7 and 8).

14 Abnormal Heart Rhythms

During the flutter circuit, the isthmus conduction time accounts for ~33 % of the cycle time, and the RA cycle accounts for ~66 % of the cycle length [22]. The isthmus conduction time is measured from the pacing site to the signal arising on the other side of the cavo-tricuspid isthmus.

At baseline, if the patient is in sinus rhythm, pacing from proximal CS, the measurement would be to low in RA and vice versa. When there is no damage to the isthmus, conduction time should be <90 ms. Post-successful CTI ablation trans-isthmus conduction time increases by 50 % [23] or from <90 ms to >140 ms.

#### **6.4. Differential pacing**

One important manoeuvre to establish bidirectional block is to perform differential pacing [24]. Differential pacing is most useful when there is a very slow conduction across CTI with long conduction time, leaving it difficult to confirm bidirectional block with trans-isthmus time measurements and activation mapping. It involves pacing at two different sites on the lateral side of the CTI line (along the lateral wall of the RA).

During differential pacing, the wavefront conducts in two directions, counterclockwise towards the isthmus line and clockwise around the right atria towards the septal border of the CTI line (or the CS ostium). When isthmus block has been achieved, moving the catheter further away from the CTI line should result in a decreased clockwise activation time from lateral pacing site to the CS ostium. It can also be performed the other way by pacing from a standard site (CS ostium) and then positioning the mapping catheter in two sites on the lateral side of the CTI line.

#### **6.5. Online double potentials**

Online double potentials represent an area of local conduction block at the line of ablation. A 110 ms separation of signals has been identified as a 100 % positive predictor value for isthmus block [25]. The early first signal results from the initial wavefront from the pacing stimulus reaching the line, which then encounters block. The second delayed signal results from activation entering the opposite side of the line of ablation.

The online double potential technique is an assistance guide to determining bidirectional block and should be used in conjunction with other methods.

#### **6.6. Atypical atrial flutter**

An isthmus for atypical flutter can be formed by a number of anatomical barriers, including the tricuspid or mitral annuluses, superior or inferior vena cava, pulmonary veins or the CS ostium. It can also form a circuit secondary to scars which can occur after infarction, myocar‐ ditis or congenital or valvular surgery. Electrically, the isthmus can be represented by low amplitude or fractionated signals, areas of slow conduction and/or double potentials. Double

15

Figure 9: Differential pacing with pacing from RA 11, 12 of a duodecapolar catheter (lateral) and then more laterally from site RA 3,4 of the duodecapolar catheter (courtesy of PA EP **Figure 9.** Differential pacing with pacing from RA 11, 12 of a duodecapolar catheter (lateral) and then more laterally from site RA 3,4 of the duodecapolar catheter (courtesy of PA EP Lab)

potential indicates line of block and fragmented potentials and mid-diastolic potentials indicate critical zones of slow conduction. Lab) Online Double Potentials

Atypical atrial flutter can be very difficult to assess and treat. The use of anatomical and 3D mapping systems has an important role in identification and successful ablation of atypical atrial flutter. Online double potentials represent an area of local conduction block at the line of ablation. A 110 ms separation of signals has been identified as a 100 % positive predictor value for isthmus block [25]. The early first signal results from the initial wavefront from the pacing stimulus reaching the line, which then encounters block. The second delayed signal results

#### **6.7. 2D mapping and electrophysiology**

To assist with 2D and signal mapping, it is very important to know the chamber the flutter is originating from. The online double potential technique is an assistance guide to determining bidirectional block and should be used in conjunction with other methods.

#### *6.7.1. Localising atypical flutter to the right atrium*

from activation entering the opposite side of the line of ablation.

Activation of the coronary sinus from proximal to distal is the first clue that the flutter is most likely to be originating from the RA. Other clues include RA activation time accounting for

**Figure 10.** Online double potentials; an immediate signal post-ablation site (medial side of isthmus line) and a signal out later (lateral side of the isthmus line)

more than 50 % of the tachycardia cycle length, entrainment at multiple sites in the RA and post-pacing interval of equal or less than 30 ms including CTI and right free wall but not RA septum. Variability in LA cycle length with relatively fixed RA cycle length is also a clue that atypical flutter is localised to the right atrium.

#### *6.7.2. Localising Atypical Flutter to the Left Atrium*

Electrogram activation is usually, but not exclusively, distal to proximal on the CS catheter with passive RA conduction, or early septal RA activation, indicating breakthrough to the RA from the LA. Entrainment within the RA at multiple sites should elicit a PPI − TCL response of more than 30 ms.

#### **6.8. 3D or non-fluoroscopic mapping**

potential indicates line of block and fragmented potentials and mid-diastolic potentials

Figure 9: Differential pacing with pacing from RA 11, 12 of a duodecapolar catheter (lateral) and then more laterally from site RA 3,4 of the duodecapolar catheter (courtesy of PA EP

**Figure 9.** Differential pacing with pacing from RA 11, 12 of a duodecapolar catheter (lateral) and then more laterally

A B

15

Atypical atrial flutter can be very difficult to assess and treat. The use of anatomical and 3D mapping systems has an important role in identification and successful ablation of atypical

Online double potentials represent an area of local conduction block at the line of ablation. A 110 ms separation of signals has been identified as a 100 % positive predictor value for isthmus block [25]. The early first signal results from the initial wavefront from the pacing stimulus reaching the line, which then encounters block. The second delayed signal results

To assist with 2D and signal mapping, it is very important to know the chamber the flutter is

The online double potential technique is an assistance guide to determining bidirectional

Activation of the coronary sinus from proximal to distal is the first clue that the flutter is most likely to be originating from the RA. Other clues include RA activation time accounting for

indicate critical zones of slow conduction.

from site RA 3,4 of the duodecapolar catheter (courtesy of PA EP Lab)

Online Double Potentials

**6.7. 2D mapping and electrophysiology**

*6.7.1. Localising atypical flutter to the right atrium*

from activation entering the opposite side of the line of ablation.

block and should be used in conjunction with other methods.

atrial flutter.

Lab)

16 Abnormal Heart Rhythms

originating from.

Mapping atypical flutter with a 3D mapping system (CARTO and NavX) allows direct visualisation of the re-entrant circuit [26]. When mapping the flutter, it is important to get high resolution and to cover as much as the cycle length as possible (Figure 11). Analysing up to 80–100 points increases accuracy, and covering >90 % of the circuit allows for the whole circuit to be covered. 3D mapping can be used to demonstrate the typical activation pattern. Scar can be determined by areas of signals less than 0.5 mV or inability to pace capture at 20 mA.

**Figure 11.** Figure 11: A 3-dimensional CARTO map of cavo-tricuspid isthmus-dependant atrial flutter in a patient with a history of congenital heart disease (tetralogy of Fallot, s/p repair) and symptomatic typical atrial flutter. Right anteri‐ or oblique (RAO) view and inferior view of RA demonstrating the macro-reentrant mechanism and the ablation sites

**Figure 12.** Activation sequence in upper-loop re-entry compared to lower-loop re-entry. Lower-loop re-entry is classi‐ fied in the same group as typical atrial flutter because the circuit is dependent on CTI

#### *6.8.1. Upper-loop re-entry atrial flutter*

This atypical flutter has clockwise activation sequence around the SVC and breaks out through the crista terminalis (Figure 12). This type of flutter is typically seen in patients with hyper‐ tension or some structural heart disease. Entrainment should be performed between the fossa ovalis and the superior vena cava (SVC) in the atrial septum. The targeted ablation site is at the excitable gap in the crista terminalis.

#### *6.8.2. RA free wall atrial flutter*

This atrial flutter is seen in patients with no structural heart disease, who develop scar in the right atria and in postsurgical patients with a scar caused by an atriotomy procedure. When mapping for the scar relating to the flutter, online double potentials will be present, and fractionation at the end of the line denotes the pivot point for the flutter. The ablative strategy for this flutter is to create a linear line from the lateral RA (at the end of the line) to the IVC or to create a line of block between the scar and the crista terminalis. It is also recommended that the cavo-tricuspid isthmus line be performed. It is important to pace in the right atrium at the proposed ablation point to avoid phrenic nerve injury.

#### *6.8.3. LA atrial flutter*

**Figure 11.** Figure 11: A 3-dimensional CARTO map of cavo-tricuspid isthmus-dependant atrial flutter in a patient with a history of congenital heart disease (tetralogy of Fallot, s/p repair) and symptomatic typical atrial flutter. Right anteri‐ or oblique (RAO) view and inferior view of RA demonstrating the macro-reentrant mechanism and the ablation sites

**Figure 12.** Activation sequence in upper-loop re-entry compared to lower-loop re-entry. Lower-loop re-entry is classi‐

This atypical flutter has clockwise activation sequence around the SVC and breaks out through the crista terminalis (Figure 12). This type of flutter is typically seen in patients with hyper‐

fied in the same group as typical atrial flutter because the circuit is dependent on CTI

*6.8.1. Upper-loop re-entry atrial flutter*

18 Abnormal Heart Rhythms

Flutter arising from the left atria is almost certainly related to the patient having some sort of structural heart disease. It is most likely to arise from the mitral annulus, the pulmonary veins or a spontaneous scar. The target ablation site for left atrial flutters depends on the circuit of the flutter and the position of the anatomical block. A new class of left atrial flutter has arisen in the recent past which is idiopathic in origin, post-pulmonary vein isolation and left atrial ablation for atrial fibrillation. This form of atrial flutter occurs between ablation lines per‐ formed to isolate and compartmentalise the left atrium to modify the burden of atrial fibrilla‐ tion in patients. It has rapidly become a very common form of left atrial flutter, perhaps the most common.
