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Electrocardiographic and electrophysiologic features of atrial flutter

Electrocardiographic and electrophysiologic features of atrial flutter
Literature review current through: Jan 2024.
This topic last updated: Mar 31, 2023.

INTRODUCTION — Atrial flutter (AFL) is an abnormal cardiac rhythm characterized by rapid, regular atrial depolarizations at a typical atrial rate of 250 to 350 beats per minute. There is frequently 2:1 conduction across the atrioventricular (AV) node, meaning that every other atrial depolarization reaches the ventricles. As a result, the ventricular rate is usually one-half the AFL rate in the absence of AV node dysfunction. AFL is classified as typical or atypical based on whether the flutter circuit traverses the cavotricuspid isthmus in the right atrium [1].

Other topic reviews discuss the clinical aspects of AFL. (See "Overview of atrial flutter" and "Restoration of sinus rhythm in atrial flutter" and "Control of ventricular rate in atrial flutter" and "Atrial flutter: Maintenance of sinus rhythm" and "Embolic risk and the role of anticoagulation in atrial flutter" and "Atrial fibrillation and flutter after cardiac surgery".)

CLASSIFICATION — The first classification scheme in 1970 defined atrial flutter (AFL) as "common" or "atypical," depending on whether the flutter wave had a negative sawtooth pattern in the inferior leads [2]. A few years later, the terms types I and II were created to describe flutter [1]. Type I AFL was classified as a macroreentrant atrial tachycardia while type II AFL was considered unclassified because the mechanisms were not fully understood.

A 2001 working group from Europe and North America tried to reconcile new data from electrophysiology studies and activation mapping [3]. Flutter was defined as a regular tachycardia ≥240 beats/min with no isoelectric baseline between atrial deflections. Typical and reversal typical flutter were characterized, as described below, and all other flutters were atypical.

An American College of Cardiology, American Heart Association, and Heart Rhythm Society guideline on the management of supraventricular tachycardia reaffirmed the classification of AFL into cavo-tricuspid-isthmus (CTI)-dependent ("typical") versus non-CTI dependent ("atypical") [4] and this is the methodology currently used.

Typical AFL is a macroreentrant atrial tachycardia, with the inferior border of the circuit traversing the isthmus of tissue between the inferior vena cava and tricuspid annulus as a necessary component. AFL involving this cavotricuspid isthmus is referred to as "typical" or "isthmus-dependent" flutter.

In the most common form of CTI-dependent flutter, the reentrant circuit rotates around the tricuspid annulus in a counterclockwise direction when the heart is viewed in a left anterior oblique projection, traversing up the septum and down the lateral wall. This is the arrhythmia associated with the classic electrocardiogram finding of sawtooth flutter waves in the inferior leads. (See 'Electrocardiographic features' below.)

Less often, the reentrant circuit rotates in the opposite direction. This arrhythmia is called "clockwise" or "reverse" typical flutter.

Atypical AFL is an intraatrial reentrant tachycardia or AFL that does not involve the CTI. It may be a lesion macroreentrant tachycardia, upper loop flutter, intra-isthmus reentry, non-atriotomy-related right atrial flutter, left atrial macroreentry, post-Maze or atrial fibrillation ablation left atrial flutters, or mitral annular flutter [5]. It is frequently seen in those who have had prior cardiac surgery, prior intracardiac ablation, congenital heart disease, or cardiomyopathy but may also be idiopathic. Atypical flutter may be in the right or left atrium and usually revolves around a prior incisional or idiopathic scar, ablation lesion set, or other fixed anatomic barriers. If there has been an incomplete ablation line from a prior procedure, this can increase the chances of an atypical flutter. Many patients with congenital heart disease, especially with more complex disease or surgical repairs, will present with atypical flutter, known as intraatrial reentrant tachycardia [6]. Some patients with idiopathic atrial fibrosis will also present with scar-based atypical flutters.

ELECTROPHYSIOLOGIC FEATURES — Electrophysiologic studies, using entrainment mapping and electroanatomic mapping, have been used to define the atrial flutter (AFL) circuit in the electrophysiology laboratory and at surgery [7-11].

The principal electrophysiologic features of AFL are:

Reentry

Excitable gap

Transient entrainment and termination by rapid atrial pacing

Electrophysiologically, AFL is a reentrant arrhythmia in that it excites an area of the atrium and then travels sufficiently slowly in a pathway that is long enough such that the initially excited area recovers its excitability and is reactivated [7-9,12-15]. Either a single premature extrastimulus or rapid atrial pacing can initiate AFL and, because there is an excitable gap, terminate the arrhythmia [13-15]. The excitable gap is the portion of a reentrant circuit that has recovered its excitability and can again be depolarized, allowing for entrainment with overdrive pacing during AFL [13,14,16]. (See "Reentry and the development of cardiac arrhythmias", section on 'Definition and characteristics'.)

Typical AFL commonly starts after a transitional rhythm of variable duration, usually atrial fibrillation [17,18]. It has been postulated that a fundamental feature that determines whether an atrial arrhythmia becomes sustained typical AFL or atrial fibrillation is the development of a line of functional refractoriness or block between the vena cavae [18]. In spontaneous typical AFL, the critical line of functional block between the vena cavae may be created by transient atrial fibrillation. This line of block results in unidirectional block and stable AFL follows. According to this theory, if the line of functional block is not created, atrial fibrillation persists or the rhythm reverts back to sinus.

Another view, based in part on a small electrophysiologic study of 10 patients, emphasizes the anatomic barriers as well as the properties of conduction and refractoriness during atrial fibrillation to explain the usual pattern observed with typical AFL [19]. In the electrophysiology laboratory, premature electrical stimulation may function in a manner similar to the transitional atrial fibrillation in forming the critical functional line of block between the vena cavae [18].

An additional determinant of whether the transitional atrial tachyarrhythmia becomes AFL or atrial fibrillation may be the cycle length of the flutter [18]. If the cycle length is critically short, it will create fibrillatory conduction and atrial fibrillation.

Lastly, the electrical properties of the isthmus may also be a factor in the tendency for AFL to disorganize into atrial fibrillation in some patients [20].

Similar to what has been reported in atrial fibrillation, AFL results in electrical remodeling of the atrial myocardium, perhaps accounting for the observation that untreated AFL can eventually lead to atrial fibrillation [21]. In contrast to the normal situation in which the atrial refractory period shortens with an increase in rate and prolongs when the rate decreases, the refractory period fails to lengthen appropriately at slow rates (eg, with return to sinus rhythm) in patients with AFL present for a mean of 8.5 months (range 1 to 32 months) [22]. This abnormality persists for at least 30 minutes after cardioversion to sinus rhythm; the duration of AFL has no significant impact upon the magnitude of these electrophysiologic changes. Those with a history of AFL, but not fibrillation, have significant changes in the electrophysiologic properties of the right atrium, even when they are in normal sinus rhythm. The right atrium is more likely to be enlarged, have lower voltage suggesting scar, longer P wave duration, and slowed conduction velocity most prominent in the lower right atrium, and sinus node dysfunction [23].

The duration of AFL does impact the time course of electrical remodeling recovery after arrhythmia termination. As an example, one study of 25 patients with paroxysmal or chronic flutter (average duration 17 months) found that, in those with paroxysmal AFL, the refractory period shortened after a 5- to 10-minute period of flutter and reversed within five minutes of restoration of sinus rhythm; atrial fibrillation developed in some patients when the refractory period was at its nadir [24]. In patients with chronic AFL, the atrial refractory period increased during the first three weeks after resumption of sinus rhythm.

Typical flutters — A large macroreentrant circuit in the right atrium is involved in typical AFL.

If one begins the cycle at the end of the negative deflection of the F wave in lead II, the impulse at that point exists in the low right atrial septum between the inferior vena cava (IVC) and the tricuspid valve.

In counterclockwise typical flutter, the impulse then travels anteriorly through the region of the low septum, ascends superiorly and anteriorly up the septal and posterior walls of the right atrium, and returns or descends over the anterior and lateral free wall (figure 1) [25]. This circuit is then completed through the region between the tricuspid valve and IVC (counterclockwise reentry). A reverse direction of rotation (clockwise reentry, ascending the anterior wall, and descending the posterior and septal walls) is seen in reverse typical AFL [3,25].

The crista terminalis (and its continuation as the eustachian ridge) and IVC often form the posterior barrier, while the tricuspid annulus constitutes the anterior barrier of the circuit (figure 1) [11,26]. This has potential clinical implications, since this region can be a target for ablation therapy in patients with refractory AFL [26,27]. (See "Atrial flutter: Maintenance of sinus rhythm", section on 'RF catheter ablation'.)

The presence of slow conduction in the cavotricuspid isthmus has been confirmed by noncontact mapping [28]. The cavotricuspid isthmus is a part of the circuit most vulnerable to interval-dependent conduction delay [16] and termination of AFL with ibutilide, propafenone, or amiodarone is due in part to failure of impulse conduction through this tissue [22]. (See "Overview of catheter ablation of cardiac arrhythmias", section on 'Noncontact mapping'.)

The typical AFL circuit has been thought to run anterior to the superior vena cava (SVC) in most patients [29]. However, a study of 15 patients with typical flutter using noncontact and entrainment mapping showed that the posterior wall was a part of the circuit in seven patients [30]. In a study of 50 patients using entrainment mapping, between one-quarter to one-third did not use the atrial roof anterior to the SVC as part of the circuit [31]. These studies imply that the crista terminalis is not always a fixed barrier to conduction and the circuit can be posterior to the SVC.

Partial isthmus atrial flutter is a type of typical flutter where a wavefront goes between the IVC and coronary sinus ostium after conducting through the posterior cavo-tricuspid-isthmus (CTI). This wavefront then conducts around the CS ostium and up the septum, but also goes retrograde back into the anterior CTI. For this circuit to occur, there must either be a pectinate muscle that breaks the CTI into an anterior and posterior portion [32] or rapid conduction through the eustachian ridge [26].

Intra-isthmus reentry is usually seen in those with prior CTI ablation [33]. The circuit is contained entirely within the CTI and may be in the septal, medial, or anterior portions, with areas of long fractionated potentials the best target for ablation [33].

The circuit for lower loop reentry circles around the IVC, on the septal side usually between the IVC and coronary sinus ostium [34]. It exits out on the low lateral wall, with wavefront one conducting up the lateral wall and wavefront two going through the CTI, anterior to the coronary sinus ostium, and up the septal wall in a manner similar to counterclockwise typical flutter. The two wave fronts collide somewhere in the lateral right atrium or septum, but the dominant circuit still encircles the IVC. Lower loop reentry frequently morphs into counterclockwise AFL and may be associated with an atrial myopathy [5].

Atypical right atrial flutters

Lesion macroreentrant tachycardia — An atriotomy scar or suture line can act as an obstacle to conduction and create reentry. There may also be atrial septal defect patches that can lead to an atypical flutter circuit. In addition, scar from congenital heart disease lesions such as after an atrial level switch surgery (Mustard or Senning repairs) for transposition of the great arteries or after a Fontan repair may lead to atypical flutters. (See "Management of complications in patients with Fontan circulation", section on 'Arrhythmias'.)

Atriotomy scar-related atypical flutters are the most common of this type, where the scar is vertical along the lateral right atrium. The anterior right atrial wall may have ascending or descending activation depending on whether the circuit is clockwise or counterclockwise, while the septum may have more variable conduction [3]. The circuit wraps around the incision, with the upper turnaround point between the scar and SVC and the lower turnaround point between the scar and IVC. Alternatively, one of the turnaround points may be through an area of conduction within the scar. As is true for all flutters, entrainment and activation mapping are helpful for defining the circuit. The atriotomy region will have double potentials and low voltage to denote its location. During flutter, the double potentials are more widely spaced in the center of the scar and usually become one single fractionated electrogram at the turnaround points.

Typical flutter may be seen after ablation of this atypical flutter, if a prior cavotricuspid isthmus ablation has not previously been completed.

Nonatriotomy-related right atrial flutter — For unexplained reasons, some patients will have areas of low voltage in the right atrium. This may lead to a scar similar to an atriotomy lesion, even though there has been no cardiac incision. This leads to a flutter wrapping around the scar, though may also be a figure-8 reentry if there is conduction through the low voltage area [32]. Ablation from the lower border of the scar to the IVC frequently terminates the arrhythmia.

Upper loop reentry — This circuit crosses through a conduction gap in the crista terminalis in the upper right atrium, which is where the successful site of ablation can be [35]. It can be clockwise or counterclockwise, with activation going up or down the anterior right atrial free wall. At least one patient also demonstrated successful ablation in the region between the fossa ovalis and IVC [32], indicating that this tachycardia circuit may not be as clearly defined as previously thought.

Atypical left atrial flutters

Post-Maze or atrial fibrillation ablation left atrial flutters — These tachycardias are most frequently due to incomplete ablation lines from either a transvenous catheter ablation or a surgical Maze procedure. They may also be related to left atrial fibrosis seen in those with a history of atrial arrhythmias. They are usually seen in the anterior wall, through the roof, or on the septum. Mapping can often be difficult due to low voltages. (See "Atrial fibrillation: Surgical ablation", section on 'Maze procedure'.)

Mitral annular flutter wraps around the mitral valve clockwise or counterclockwise [36,37]. Entrainment from a catheter in the coronary sinus will frequently demonstrate concealed entrainment on all poles for mitral annular flutter, but not for other left atrial flutters. It can be difficult to terminate and often needs ablation within the coronary sinus or vein of Marshall to achieve a line of block [38]. Even in the presence of apparent complete block, there may still be recurrence of mitral flutter as there may only be significant conduction slowing rather than block [39].

Left atrial macroreentry — Less commonly, atypical flutters can occur in those with no prior ablation or surgery in the left atrium. They may be located on the anterior or posterior wall and are bounded by an anatomic obstacle like the mitral annulus [40]. They may be a single circuit or double loop and are associated with low voltage signals with areas of fractionated signals [41].

Atrioventricular node and the ventricular response — The electrophysiologic events in AFL can be viewed as an input (the F waves) and an output (QRS complexes) that is processed through a regulator or black box (the atrioventricular [AV] node). The electrophysiologic characteristics of the AV node, which is a "slow response" tissue in comparison to the atria, primarily determine the ventricular response. (See "The electrocardiogram in atrial fibrillation".)

As noted below (see 'Electrophysiologic features' above), the ventricular response in AFL is generally one-half the atrial input, resulting in a ventricular rate of about 150 beats/min. 3:1 and 4:1 input/output ratios are also relatively common, leading to ventricular rates of about 100 and 75 beats/min, respectively. Thus, AFL should be considered whenever the electrocardiogram shows a heart rate of 150, 100, and 75 beats/min.

Rarely, the input/output ratio is 1:1, resulting in a ventricular response of nearly 300 beats/min. This may occur in states characterized by marked catecholamine excess and in the presence of AV bypass tracts with preexcitation (waveform 1). A 1:1 response is more commonly seen when the atrial rate is slowed and AV nodal conduction is enhanced, leading to ventricular rates of 220 to 250 beats/min. This combination can be induced by class IA or IC antiarrhythmic drugs (table 1) due to:

Slowing of the conduction velocity in the reentrant circuit and therefore the flutter rate by inhibition of sodium channels.

Increasing AV nodal conduction by their vagolytic effects.

These characteristics have implications for management. (See "Control of ventricular rate in atrial flutter".)

Partial or complete block in the AV node or in the specialized infranodal conduction system (His bundle, bundle branches and fascicles, and terminal Purkinje fibers) may lead to escape or accelerated rhythms from within the AV node or below to assume control of the ventricles. The ventricular rate in this setting may be normal, faster, or slower than is normal for these lower pacemakers.

The diagnosis of complete heart block may be missed if F waves are not carefully matched with R waves or when the lower escape rate approaches an arithmetic divisor of the flutter rate. As is true for atrial fibrillation, there may be a Wenckebach type of exit block around such an escape site, resulting in group beating.

ELECTROCARDIOGRAPHIC FEATURES — The electrocardiographic features of typical atrial flutter (AFL) in the presence of normal atrioventricular (AV) nodal conduction are (waveform 2):

P waves are absent.

For counterclockwise typical AFL, biphasic "sawtooth" flutter waves (F waves) are present at a rate of about 300 beats/min, with the range being 240 to 340 beats/min [1].

The F waves are fairly regular on the surface electrocardiogram with constant amplitude, duration, morphology, and reproducibility throughout the cardiac cycles. There can be very subtle variability, however, as spectral analysis has detected an underlying periodic pattern modulated by an interplay between the autonomic nervous system, respiratory system, and ventricular rate [42].

The F waves usually do not have an isoelectric interval between them (ie, the F waves blend into one another) unless the rate of the AFL is slow.

In counterclockwise typical AFL, the F waves have an axis of around 90º and are prominently negative in the inferior leads (II, III, aVF). The F waves often have an initial slowly downsloping segment followed by a sharp negative deflection, then a sharp positive deflection that may have a positive overshoot leading into the next downward deflection (waveform 2). With 2:1 flutter, there is commonly a negative deflection superimposed on the ST segment, giving the appearance of ST depression related to myocardial ischemia.

In clockwise typical AFL (reverse typical AFL), the F waves are usually positive in the inferior leads due to an opposite direction of atrial activation, but there is significant heterogeneity in the F wave morphology [3]. The F wave may even have a sine wave pattern. The deflection in V1 is often broad and negative (waveform 3) (panel B).

The ventricular response (R-R intervals) is usually one-half the rate of the atrial input (ie, 2:1 AV nodal conduction with a ventricular response of about 150 beats/min). This finding is sufficiently common and the diagnosis of AFL should be considered whenever the ventricular rate is about 150 beats/min. AV block greater than 2:1 in the absence of drugs that slow the ventricular response suggests AV nodal disease and the possibility of associated sinus node disease, which may be part of the tachy-brady syndrome.

A 1:1 AV response suggests accessory bypass tracts, sympathetic excess, parasympathetic withdrawal, or class IC antiarrhythmic agents. Even ratios of input to output (eg, 2:1, 4:1) are more common than odd numbers (eg, 3:1, 5:1). Odd ratios and shifting ratios (eg, alteration of 2:1 with 4:1) probably reflect bilevel block in the AV node.

The QRS complex is narrow unless there is functional aberration, preexisting bundle branch or fascicular block, preexcitation, or ventricular pacing.

The electrocardiographic features of atypical AFL are:

P waves are absent.

F waves are regular, but in contrast to typical AFL, there may be an isoelectric appearance between F waves if there is an area of significantly slowed conduction.

There is no clear F wave morphology to identify the location consistently, as atypical flutters are often associated with atrial scar that can alter conduction velocity and direction. That said, some patterns described below may be seen.

Lower loop reentry typically has negative F waves in the inferior leads (waveform 4). Upper loop reentry has positive F waves in the inferior leads and negative, flat, or barely positive F waves in lead I [43].

Intra-isthmus reentry will appear like typical counterclockwise AFL.

If there is a negative F wave in V1, the flutter is usually in the right atrium (waveform 5).

Left atrial flutters have variable morphologies, but may have a positive F wave in V1 or may be isoelectric (waveform 6) [5]. It is often positive in the inferior leads, but not always (waveform 7).

Counterclockwise mitral annular flutter is positive in V1-6 and the inferior leads and negative in aVL [44]. Clockwise mitral annular flutter is positive in the right precordial leads but usually negative and then positive in the lateral precordial leads (waveform 8). It is negative in the inferior leads and positive in I and aVL.

Morphology of the QRS complex — Activation through the AV node and infranodal conduction system is normal in AFL, so the QRS complex is narrow unless:

A preexisting conduction defect is present.

Functional block occurs in a portion of the infranodal conduction system, leading to a bundle branch or fascicular block. The refractory period of the bundle branches and fascicles is determined by the preceding cycle length. A long preceding cycle lengthens the refractory period in these structures, so a premature beat is more likely to be functionally blocked after a long cycle, known as Ashman's phenomenon.

Preexcitation through an AV bypass tract is present.

Ventricular pacing is present.

Pitfalls — The electrocardiographic criteria listed above are usually sufficient to make the proper diagnosis; there are, however, potential pitfalls:

One of the F waves may be obscured by the QRS complex or the ST-T wave (waveform 9) in patients with 2:1 AV nodal conduction. In this setting, AFL may be misdiagnosed as a sinus tachycardia or a paroxysmal supraventricular tachycardia with downsloping ST depression.

In clockwise, typical flutter, the F waves may be positive, and if every other F wave is obscured, it may be mistaken for a long RP tachycardia such as sinus tachycardia, ectopic atrial tachycardia, atypical AV nodal reentrant tachycardia, or AV reciprocating tachycardia.

The atrial electrical potential may be small and the F waves may be difficult to see in the standard leads. Sometimes it may be necessary to increase the gain of the electrocardiogram to see the F waves more clearly (ie, 20 mm/mV).

Atrial fibrillation, especially with coarse fibrillatory waves in lead V1, is often misdiagnosed as AFL [45]. Examination of a rhythm strip will often show that the atrial fibrillatory rate and morphology change over a period of time. We discourage using the term AFL-fibrillation, since the rhythm more closely resembles atrial fibrillation in its response to drugs that slow AV nodal conduction and in the higher energy requirement for direct current cardioversion.

Sometimes the negative F wave merges with the beginning or end of the QRS complex, suggesting a pathologic Q wave in the first case and a conduction delay in the second. Likewise, the F wave may appear to cause pathologic ST-segment depression.

The F wave morphology may appear atypical in those with congenital heart disease, atrial fibrosis, following cardiac surgery, or after left atrial ablation for atrial fibrillation even though the rhythm is typical flutter [46,47]. Prior extensive ablation in the left atrium may alter the morphology of F waves in typical AFL, due to reductions in left atrial potentials and changes in the atrial activation sequence. This was illustrated in a series of 15 patients who had undergone circumferential left atrial ablation for the treatment of atrial fibrillation and later developed typical AFL (12 counterclockwise, 3 clockwise) [47]. In 9 of 15 cases, the F waves were upright in the inferior leads, including 7 of 12 of typical counterclockwise flutter.

Electrocardiography and telemetry artifacts caused by tremor [48] or electromagnetic interference [49,50] may suggest the occurrence of AFL, but this “pseudo-atrial flutter” will be revealed when the tremor or interference ceases.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of atrial flutter (AFL) includes a number of supraventricular tachyarrhythmias. (See "Focal atrial tachycardia" and "Intraatrial reentrant tachycardia" and "Sinoatrial nodal reentrant tachycardia (SANRT)" and "Cardiac arrhythmias due to digoxin toxicity" and "Multifocal atrial tachycardia" and "Atrioventricular nodal reentrant tachycardia" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Types of narrow QRS complex tachycardia'.)

As noted above, obscured atrial activity or F waves that resemble normal or inverted P waves may suggest sinus tachycardia, paroxysmal supraventricular tachycardia, or atrial fibrillation.

There are four major ways to help establish the correct diagnosis:

An earlier electrocardiogram, if available, may allow comparison of the F or presumed P wave with the previous P wave morphology.

Scrutiny of the ST-segment and T waves may show a bump or irregularity caused by a second flutter wave.

Decreasing atrioventricular (AV) nodal conduction physiologically with a vagotonic maneuver (such as the Valsalva maneuver or carotid sinus massage) or with a rapidly acting drug (such as adenosine, verapamil, or esmolol) will increase the AV nodal block and reveal the atrial F waves (waveform 9).

Recording from an atrial catheter, atrial pacing wire, or an esophageal electrode will also demonstrate the regular atrial activity (waveform 10).

Even with these maneuvers, ectopic atrial tachycardia and other supraventricular tachycardias with 2:1 block may remain in the differential diagnosis. Furthermore, two types of arrhythmia can occur in the same patient, as a supraventricular tachycardia can initiate AFL or atrial fibrillation.

An example of this difficulty occurs when AFL has a slow ventricular response that overlaps with the rate seen in other supraventricular tachycardias. If, for example, the patient is taking digitalis for flutter, then an atrial tachycardia with a 2:1 AV response that reflects a high degree of digitalis toxicity must be excluded. Treatment of these two disorders is clearly different, and atrial morphology may be of little help in identifying the underlying arrhythmia. In this setting, establishment of the correct diagnosis may depend upon the clinical history, plasma digoxin levels, and the response following cessation of digoxin therapy.

As noted above, complete heart block may be difficult to recognize in the presence of AFL. The presence of F waves and a regular rate of the lower pacemaker may lead to the appearance of an uncomplicated AFL.

MANAGEMENT — The control of ventricular rate and the approach to anticoagulant therapy for patient with atrial flutter is discussed elsewhere. (See "Overview of atrial flutter" and "Embolic risk and the role of anticoagulation in atrial flutter".)

Cardioversion in patients with atrial flutter is discussed separately. (See "Restoration of sinus rhythm in atrial flutter".)

The approach to the maintenance of sinus rhythm and the impact of electrophysiologic type is discussed separately. (See "Atrial flutter: Maintenance of sinus rhythm" and "Atrial flutter: Maintenance of sinus rhythm", section on 'RF catheter ablation'.)

SUMMARY — Atrial flutter (AFL) is a supraventricular tachycardia with regular flutter waves and usually an absent isoelectric interval. The rhythm is due to macroreentry, has an excitable gap, and can be transiently entrained and terminated by rapid atrial pacing. Electrocardiographic characteristics include:

Biphasic, sawtooth F waves, best seen in the inferior electrocardiogram leads (II, III, aVF), at about 300 beats/min are the classic finding for typical, counterclockwise AFL.

The ventricular response is a multiple of the atrial rate, though most frequently is 2:1 with a ventricular rate of 150 beats/min.

Flutter waves may sometimes be obscured in the QRS complex in 2:1 conduction.

Typical AFL most frequently rotates counterclockwise posterior to the tricuspid valve and uses the critical region of the cavotricuspid isthmus within the circuit. Clockwise, typical AFL uses the same circuit, but rotates in the opposite direction.

Atypical AFL is any flutter that does not involve the cavotricuspid isthmus. The flutter wave morphology does not have a characteristic pattern to localize the flutter circuit.

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Topic 1061 Version 28.0

References

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