Atrial flutter is characterised by rapid but regular atrial depolarisations with a consistent ECG morphology. In the most common form the inferior leads on the ECG show a p wave with a gradual down-slope followed by a rapid upstroke. This is described as a “saw-tooth” appearance and is easily recognised (Fig 1).
There are less common forms of flutter where the p waves look different (see “less common flutters”). The atrial rate in flutter is usually around 300 bpm. Clearly it would not be desirable for all these impulses to be conducted to the ventricles, so the AV node comes to the rescue by only conducting a proportion. If the node conducts every other impulse the resulting ventricular rate is 150 bpm. This is described as flutter with 2:1 conduction. 3:1 conduction results in a ventricular rate of 100 bpm, 4:1 conduction in a rate of 75 bpm.
Because of this the heart rare trend in 24 hr tapes of patients with flutter often show abrupt step-wise changes in rate rather than the gradual changes the sinus node produces. Patients are symptomatic when the rate steps up. Atrial fibrillation may sometimes mimic atrial flutter but in AF the p wave morphology varies over time and gives rise to a disorganised ventricular rhythm. Occasionally flutter is conducted in a 1:1 fashion resulting in a very rapid ventricular response which may cause syncope (Fig 2). This usually occurs where the atrial rate during flutter is slightly slower than the typical 300 bpm. This slowing can be an undesirable effect of anti-arrhythmic medication.
There is some confusion around the use of the terms atrial flutter and atrial tachycardia. Flutter is a term based primarily on the ECG appearance. As atrial tachycardia describes a fast rhythm arising exclusively in the atria then atrial flutter represents a subset of atrial tachycardias. However the term atrial tachycardia is usually reserved for slower tachycardias. Atrial flutter can be described in electrophysiological terms as a form of macro-reentrant atrial tachycardia.
The Electrophysiology of Atrial Flutter
Typical atrial flutter is a rhythm of the right atrium (RA). It is a re-entry circuit around the tricuspid valve and occurs because the RA is really two bits stuck together – the posterior smooth-walled venous portion and the anterior trabeculated muscular portion. The join between the two - the crista terminalis (CT) forms a region of conduction block which protects the flutter circuit. The anterior part of the RA looks like a ring – the perfect structure for the generation of a re-entrant wave (like a stadium for a Mexican wave). During flutter the impulse moves round this circuit about 300 times a minute. The wave is prevented from “catching up with itself” because of very slow conduction in one main area – the gap between the IVC and the tricuspid valve. An isthmus is a narrow channel between two obstacles and this region is known as the cavo tricuspid isthmus (CTI) and is critical for flutter to sustain. An ablation line can be burnt across this isthmus blocking the wave of excitation and curing the patient of flutter (see ablation of flutter). In the most common form, this circuit is activated in the anti-clockwise direction.
The impulse propagates down the lateral RA wall and then is channelled through the CTI. The impulse reaches the mouth of the coronary sinus (CS) then moves up the septum and across the roof of the RA to complete the circuit. The left atrium (LA) and the posterior RA are not part of the circuit and are activated passively by the impulse as it breaks from near the CS. The wave that activates the posterior RA could short circuit the tachycardia, causing it to terminate but is prevented from doing so by the crista terminalis and its extension the Eustachian ridge.
This rhythm is known as counter or anti-clockwise cavo tricuspid isthmus dependent flutter or isthmus dependent flutter for short. It is this rhythm that has the typical saw-tooth appearance on the ECG. The circuit can occur in the opposite direction, but this arrhythmia – clockwise isthmus dependent flutter is much less common and the ECG looks somewhat different (see fig 2) with the saw-tooth pattern inverted. It is however treated in the same way – by ablating the CTI. Conditions which increase the size of the RA and/or cause slowing of conduction promote atrial flutter.
Less Common Flutters
The typical ECG pattern of saw-tooth waves is caused by anticlockwise cavo-tricuspid dependent flutter. However there are other rapid macro re-entrant atrial tachycardias which produce a” fluttery appearance on the ECG. These may be described as atypical flutter. Atypical flutter is a term based on the ECG appearance and the use of the terms typical and atypical often causes confusion. Following an EP it is possible to be more precise with the name used to describe the flutter. Sometimes it turns out simply to be the same circuit in the opposite direction - clockwise isthmus dependent flutter (fig 2).
In other patients the EP study reveals that the cavo-tricuspid isthmus is not critical for the maintenance of the arrhythmia. Such rhythms are termed non-isthmus dependent flutter and it is often considerably slower than typical flutter. The ECG often lacks the asymmetrical saw-tooth appearance. Patients presenting with this type of tachycardia have often had previous heart surgery or extensive ablation for AF. Operations which can cause non-isthmus dependent flutter include repair of congenital heart disease (particularly ASD repair) and MV repair/replacement. The circuit in these patients may be created by scar tissue from incisions made during the operation and is often referred to as scar related flutter or incisional re-entry. Ablation for AF, particularly linear ablation, can also create regions of scar which predispose patients to non-isthmus dependent flutter. These rhythms can still be ablated but the procedure is somewhat more difficult than for isthmus dependent flutter because the location of the critical isthmus is not known beforehand and varies between patients. The location of the isthmus must be worked out from the sequence of intracardiac signals, the response to pacing manoeuvres (entrainment) and the location of regions of scar tissue and anatomical areas of block such as the mitral valve and the mouths of the pulmonary veins. 3D mapping technology (such as CARTO, Navx or ensite balloon) is often used to help the electrophysiologist to put together all this information in a more easily digestible form..
Congenital heart disease and heart surgery also predispose patients to typical isthmus dependent flutter as well as the less common forms because they tends to promote right atrial enlargement and slowing of conduction. In fact typical isthmus dependent flutter is more common in these patients than the less typical forms but sometimes looks different on the ECG because of the changes in the heart’s orientation and sizes of the atria. Intra-cardiac recordings may be required to establish the mechanism of flutter in such patients.
Ablation of Atrial Flutters
Atrial flutter does not respond well to drug therapy and ablation has become the first-line therapy for recurrent typical atrial flutter. It has a high success rate with low recurrence and low associated risks. To ablate a re-entrant rhythm one must destroy a critical isthmus through which the impulse must pass. In AVRT for example, the wave must pass through the accessory pathway and this can often be destroyed with a single lesion curing the tachycardia. In isthmus dependent flutter the impulse must pass between the tricuspid valve and the mouth of the IVC. This is larger region which must be tackled by applying a number of ablation lesions in a line to create complete conduction block. The line is “drawn” medially, away from the septum to minimize risk of AV node damage.
If the ECG has the appearance of typical flutter the CTI is targeted for ablation. If the patient is in flutter the tachycardia will terminate during ablation. This is not the end of the procedure however as flutter will terminate before complete, lasting block is achieved. To determine when the CTI is blocked electrophysiologists look for an increase in trans-isthmus conduction time. This can be seen dynamically by a sudden change in the pattern of activation on a multi-polar catheter placed around the tricuspid valve (in the flutter circuit).
The atria are being paced via the coronary sinus. In the first two beats activation spreads in two directions around the tricuspid valve resulting in a fused chevron appearance in the multipolar catheter (labelled halo). On the achievement of block the paced impulse can no longer spread through the CTI and now the halo catheter can only be activated in one direction so the sequence of activation changes to a diagonal line. On the ablation catheter (MapD) there is simultaneously the splitting of two atrial potentials one from each side of the ablation line. In the first two beats the impulse just “squeezes” through a gap in the line, on the last two the second component is created by the wave passing all the way around the tricuspid valve the other way.
Ablation Catheters for Flutter
When flutter ablation was first performed it was long and difficult procedure because of the need to create a continuous lesion. Flutter ablation is now routine and usually fairly quick partly through better understanding of the technique but also because of improvements in catheter design. There are a now two ablation catheters that can create bigger lesions than the original 4mm tip ablation catheters and these bigger lesions can facilitate the achievement of block in the cavo-tricuspid isthmus. A saline-irrigated ablation catheter cools the tip electrode allowing greater power delivery before maximal temperature is achieved. An 8 mm electrode catheter works in a similar way because the large electrode tip is cooled more by circulating blood than a 4mm tip allowing greater power delivery. These catheters can create conduction block in the isthmus with a smaller number of energy applications.
