Typical atrial flutter (Aflutter) is characterized by a macroreentrant RA circuit that runs in a frontal, right-to-left plane, the base of which is a narrow isthmus bordered by the IVC and crista terminalis posteriorly and the tricuspid annulus anteriorly (cavotricuspid isthmus, CTI) (see figures in Chapter 15). The crista terminalis, a fibrous band that separates the anterior and posterior parts of the RA, constitutes the electrical barrier in front of which the Aflutter circuit is sustained.1 The typical Aflutter circuit is counterclockwise in > 90% of the cases, and clockwise in the remaining cases, where it is also called reverse typical Aflutter (Figure 11.1). Atypical Aflutter is characterized by a macroreentrant circuit not involving the isthmus. It may involve the left atrium, a right atrial scar, or less commonly a left atrial scar from a prior cardiac surgery (e.g., congenital heart disease surgery, atrial cannulation or incision), or a left atrial scar from pulmonary vein isolation. In these cases, the scar serves as the barrier that allows Aflutter to become sustained. The circuit is smaller than the isthmus-dependent Aflutter, which means the reentrant loop is crossed more quickly, leading to a faster flutter rate and smaller flutter waves on the ECG. Note that CTI-dependent flutter is also common in these patients, and both CTI- and non-CTI-dependent macroreentrant circuits often coexist in the same patient. In order to be sustained, the Aflutter must travel slowly across the CTI, such that the initially excited area recovers its excitability by the time it is reached again, and gets reactivated. This large area of excitability is called the excitable gap. This excitable gap allows a premature stimulus or atrial pacing to initiate Aflutter, but also to terminate it. That is how overdrive atrial pacing can penetrate the Aflutter circuit and break it.2 The excitable gap is larger in patients with a large RA. A small circuit with a small excitable gap eventually leads to collision of impulses inside the circuit and non-sustainability of Aflutter. Aflutter may, thus, be spontaneously initiated by a PAC. It may also be initiated by transient AF. In the presence of the electrical barrier that acts as a line of conduction block, the microreentrant circuits of AF may eventually organize on one side of this block into a stable Aflutter. AF is often easier to rate-control than Aflutter. The high atrial rate of AF leads to partial (concealed) conduction of some atrial beats across the AV node, which makes it refractory to subsequent beats that would otherwise be conducted. The slower atrial rate in Aflutter allows the AV nodal conduction of a higher number of atrial beats (less concealed conduction). On the other hand, Aflutter may trigger AF. Sustained Aflutter results in electrical and anatomical remodeling of the atrial tissue. For instance, the atrial refractory period progressively shortens with Aflutter, and only returns to baseline slowly after conversion of Aflutter. The longer the duration of Aflutter, the slower the recovery of the atrial refractory period. This atrial remodeling may lead to AF. Drugs that slow the conduction across the CTI increase the excitable gap and allow Aflutter to perpetuate rather than terminate. Therefore, class I drugs (especially Ic) are not helpful for Aflutter therapy. Even worse, by slowing the reentrant circuit, they slow the atrial rate, which allows more atrial impulses to be conducted through the AV node. They convert 2:1 Aflutter into 1:1 Aflutter. They may also organize AF into 1:1 Aflutter. While used as a “pill in the pocket” for acute AF conversion, class Ic antiarrhythmics are generally avoided in Aflutter. Aflutter tends to be an unstable rhythm, in the sense that it often converts to sinus rhythm or degenerates into AF. However, persistent or permanent Aflutter may be seen. Tachycardia-induced cardiomyopathy may be seen with a slow 2:1 Aflutter that does not attract medical attention early on. Aflutter may be secondary to LA enlargement/left heart disease. LA disease serves as a substrate for PACs, AF, or atrial runs that enter the RA and initiate the macroreentrant circuit. Aflutter may also be secondary to RA enlargement, which is often secondary to left heart disease or pulmonary disease. Most patients with left HF develop, at some point, an increase in RA pressure and a degree of RA structural abnormality that elicits Aflutter. Therefore, while right atrial pathology is notoriously an underlying disease (the circuit being a right atrial circuit), left heart disease, through both of the mechanisms explained above, is often the underlying provoker of Aflutter reentry (e.g., hypertension, CAD, valvular disease, any left HF, diabetes). Aflutter is more commonly seen in men, and in tall patients. These patients have a larger RA and thus a larger excitable gap, which allows the macroreentrant circuit to be sustained. A large proportion of Aflutter episodes (up to 60%) are triggered by an acute, possibly reversible predisposing event, such as surgery (especially cardiac or thoracic surgery) or acute medical or pulmonary illness (e.g., pneumonia, PE, COPD exacerbation, acute MI).3 The remaining patients have underlying cardiac or pulmonary disease (HF is most common, COPD is second most common). Lone Aflutter, i.e., Aflutter without any comorbidity, is less common than lone AF. In one study of patients over 50 years old, only 2% of Aflutter cases were lone;3 however, in other studies of patients undergoing Aflutter ablation, up to 40% of Aflutter cases did not have any underlying structural heart disease.4,5 The ECG is characterized by regular sawtooth atrial waves (called flutter waves). Look in leads II, III, aVF, and V1 (Figures 11.1–11.4). Flutter waves are negative in leads II, III, and aVF due to the retrograde activation of the left atrium and are positive in lead V1. In leads II, III, and aVF, the flutter waves do not return to an isoelectric baseline between the deflections, which gives the sawtooth morphology. In V1, the positive waves may return to the isoelectric baseline; in fact, since lead V1 overlies the RA, it mainly “sees” the local RA activity. In clockwise Aflutter, flutter waves are negative in V1 and positive in the inferior leads. The typical Aflutter rate is 240–350 per minute. A rate as low as 200 may be consistent with a slow Aflutter and is seen in the case of RA enlargement, wherein the Aflutter circuit is longer, or if drug therapy with class I antiarrhythmic agents or amiodarone is used (slows the conduction across the loop). The atypical Aflutter is usually faster (atrial rate of 350–450), with smaller flutter waves that return to the baseline between waves; the morphology of the flutter waves is similar to the morphology of P waves in atrial tachycardia, and depends on the site of origin of the Aflutter (RA, LA, low atrial). Aflutter is usually conducted in a 2:1 fashion (two flutter waves for one QRS: ventricular rate ~150 bpm). Conduction may be 4:1 in case of AV nodal disease or rate-slowing drug therapy. Odd conduction ratios (3:1, 5:1) are uncommon, except in the context of variable conduction. Variable conduction (e.g., 2:1, 4:1, and 3:1) usually leads to a regularly irregular rhythm, wherein identical R–R intervals are repeated cyclically. Variable conduction usually represents multilevel block in the AV node (Figure 11.5). A conduction ratio less than 4:1 suggests a high-grade AV block with a junctional escape rhythm, especially if the QRS complexes are regular and fall erratically over the flutter waves without a constant P–QRS relationship. Figure 11.1 Flutter circuit with illustration of the net atrial vectors of depolarization (gray arrows) seen by the specific lead and the subsequent morphology of the flutter waves. The gray star indicates the starting point of the depolarization vector for illustration purposes. In typical counterclockwise flutter, the negative flutter wave is close to the QRS. Lead V1 overlies the RA and mainly sees the local current in the RA, hence the positive deflection in V1, with possible return to isoelectric baseline between deflections. Figure 11.2 Aflutter with flutter waves rate (F wave) ~300 per minute and 2:1 conduction. It is a typical counterclockwise Aflutter, with negative flutter waves in lead II. At first glance, it seems there is ST elevation where the asterisks (*) are placed. This is, in fact, the upslope of the flutter waves. Bottom image. One way of diagnosing Aflutter is to imagine that QRS is removed, and then see what the atrial waveform looks like. A typical sawtooth pattern is subsequently seen. Acutely, Aflutter is managed like AF (rate control, anticoagulation). Approximately 55% of Aflutter episodes convert spontaneously, especially in the first 24–48 hours. If not: When Aflutter occurs in the context of an acute disease process (pneumonia, COPD exacerbation, the first 3 months after cardiac surgery) and in the absence of severe underlying heart or lung disease or further Aflutter episodes, catheter ablation is not necessary, as Aflutter is unlikely to recur later;6 DC cardioversion is performed if Aflutter does not revert spontaneously. In the remaining patients, catheter ablation of the CTI is first-line therapy; this has a curative rate > 90%, and may be performed in the acute setting, while Aflutter is ongoing. There is no need for antiarrhythmic therapy or long-term anticoagulation after radiofrequency ablation, unless the patient has AF associated with Aflutter. Catheter ablation may be reattempted, with a high success rate, in case of recurrence. Class III antiarrhythmic drugs may be used in patients who refuse ablation, while class Ic drugs are preferably avoided. For an overview of Aflutter ablation, see Chapter 15. Non-ablated paroxysmal or persistent Aflutter mandates chronic anticoagulation (according to CHA2DS2-VAS score), except when it occurs transiently in the context of a clear acute disease process and in the absence of severe underlying heart or lung disease. After curative catheter ablation, and in the absence of concomitant AF, anticoagulation is required for 4 weeks only. Figure 11.3 Typical counterclockwise Aflutter with variable conduction: 5:1, 4:1, 3:1, 2:1. The rhythm is overall irregular, but there is some repetition of the same R–R intervals. The interval between the 1st and 2nd, the 3rd and 4th, and the 7th and 8th R–R are equal. Typical sawtooth Aflutter waves are seen in lead II. In V1, there are upright P waves with an isoelectric baseline. Figure 11.4 Another typical counterclockwise 2:1 Aflutter. See how F is negative in lead II, and positive in lead V1, without return to baseline. Aflutter is seen in 25–35% of AF patients. In some cases, Aflutter waves abut remodeled LA areas with dispersed repolarization, degenerating into multiple small reentries and wavelets (= AF). In others, AF becomes organized along the CTI and triggers Aflutter. In patients whose predominant rhythm is Aflutter, i.e., Aflutter episodes are more often documented on ECGs and Holter monitoring than AF, Aflutter ablation may prevent AF. In general, AF occurs in ~25% of Aflutter cases at 1–3 years after CTI ablation, more so if LV dysfunction is present or if AF episodes were documented before Aflutter ablation.4,5 If only Aflutter is documented, the occurrence of AF after CTI ablation is only 8% at 20 ± 14 months. Conversely, for those with a predominant Aflutter but a history of AF, the recurrence rate of AF is 38%, whereas for those with a predominant AF, the recurrence rate of AF is 86%.5 Thus, Aflutter ablation markedly reduces AF occurrence over the long term only when Aflutter is the dominant arrhythmia. Occasionally, AF may organize into Aflutter when treated with class Ic drugs (class Ic Aflutter) or with amiodarone. In this subgroup, CTI ablation with continuation of the Ic drug often results in control of both AF and Aflutter. Atrial tachycardia (AT) may be initiated by three different mechanisms: microreentry, automaticity, and triggered activity. The frequency of each of these mechanisms varies according to different studies, with each mechanism probably accounting for a third of atrial tachycardias.7–9 One study suggested that > 80% of ATs are due to triggered activity. The automatic mechanism is rare in older patients, because automaticity decreases with age. Reentry and triggered activity can be induced and terminated with programmed electrical stimulation. During EP testing of an ongoing AT, pacing at a slightly faster rate (interval 20–50 ms shorter), called entrainment or incremental pacing, should be performed from the presumed site of origin of the arrhythmia, i.e., site of earliest atrial activation. If pacing does not break the arrhythmia, look at the post-pacing interval: a post-pacing interval that is equal to the tachycardia cycle length usually implies that pacing was performed from the actual reentrant focus, and that the mechanism is reentry; the A-wave morphology during pacing is similar to the tachycardia. If the atrium was entrained from outside the reentrant focus, the post-pacing interval will be equal to the tachycardia cycle length plus the distance between the pacing focus and reentry focus. On the other hand, automatic AT cannot be initiated or terminated with pacing or premature stimuli. An automatic focus is overdrive-suppressed during pacing, but “wakes up” after pacing cessation and may be a bit late and slow initially (long post-pacing interval).8 Figure 11.5 Rhythm in lead V1 (above) and lead II (below) with a ladder diagram showing how variable AV block occurs. Two levels of second-degree block are present in the AV junction: 2:1 block high in the AV junction and 3:2 type I block low in the AV junction. Flutter waves are indicated by vertical lines in the atrial (A) portion of the diagram. Every other flutter wave is blocked high, at level 1. Of those impulses making it through level 1, one-third are blocked at level 2, and two-thirds are conducted to the ventricles (V). Overall, this translates into an alternation of 2:1 and 4:1 conduction. The QRS complexes following the short R–R intervals are wide because of a functional block in the right bundle branch (Ashman type of aberrancy). Reproduced with permission of Baylor University Medical Center from Glancy DL, Hanna EB. Bigeminal rhythm IV. Proc (Baylor Univ Med Ctr) 2010; 23: 311–12. Figure 11.6 Coarse fibrillatory AF waves that simulate Aflutter in lead V1. Note their lack of consistent morphology and timing, and the lack of flutter waves in lead II. The surface ECG may help differentiate automaticity from reentry. In reentry, the PAC that initiates the arrhythmia may have a different P-wave morphology than the arrhythmia. In automatic tachycardia, the P wave that initiates the arrhythmia has a similar morphology to the P wave of the arrhythmia. An automatic mechanism tends to have a warm-up and warm-down phenomenon, but this is not very sensitive or specific. Through its inhibition of cAMP generation, adenosine terminates atrial tachycardia secondary to triggered activity, and may transiently suppress atrial tachycardia secondary to automaticity by hyperpolarizing the myocardium. It has a variable effect on reentrant atrial tachycardias (some studies suggest no effect,7 while others suggest a high rate of termination10). Transient atrial tachycardias, lasting < 30 seconds, are very common in patients with or without underlying heart disease, particularly older patients, and are benign and usually asymptomatic.11 More sustained atrial tachycardia is often symptomatic and may be paroxysmal or persistent (= incessant), with a risk of tachycardia-mediated cardiomyopathy (whether persistent or off-and-on paroxysmal).12 Approximately 40% of patients with sustained AT have an underlying cardiovascular disease, particularly in the case of reentrant AT. In fact, reentrant AT in older patients is frequently associated with AF or Aflutter, and AT may initiate AF or Aflutter. Automatic AT and triggered-activity AT are mostly seen in patients < 60–70 years of age who often do not have structural heart disease.8 The relative frequency of reentry increases and automaticity decreases beyond the age of 65. AT, particularly automatic AT, may be related to acute metabolic abnormalities or acute illness (hypoxia, sepsis). Atrial tachycardia with block (2:1 or, less often, 3:1 or Wenckebach) is usually due to digoxin toxicity or hypokalemia.
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Atrial Flutter and Atrial Tachycardia
I. Atrial flutter
A. Definition
B. Electrophysiological features
C. Underlying pathology and anatomical substrate
D. ECG
E. Management of atrial flutter
1. Acute treatment
2. Chronic treatment
3. The association between Aflutter and AF
II. Focal atrial tachycardia
A. Electrophysiological mechanisms
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