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Supraventricular Arrhythmias, Part II: Atrial Flutter and Atrial Fibrillation


This chapter discusses two of the most common and clinically important tachycardias: atrial flutter and atrial fibrillation (AF), schematized in Fig. 15.1 . Up to this point, we have focused primarily on those supraventricular tachycardias (SVTs) characterized by (1) organized atrial activity manifested by discrete P waves (when not hidden in the QRS), usually associated with (2) 1:1 atrioventricular (AV) conduction. a

a The term 1:1 AV conduction means that there is one atrial wave for every QRS complex, except in some cases of atrial tachycardia with AV conduction block. Note also that in paroxysmal supraventricular tachycardia due to AV nodal reentry (AVNRT), retrograde P waves are present but often hidden in the QRS ( Chapter 14 ).

In contrast, AF and atrial flutter are two distinct but interrelated SVTs both characterized by very rapid atrial rates that usually greatly exceed the ventricular rate (QRS response) ( Figs. 15.2–15.12 ). b

b Some authors consider atrial fibrillation separately from the group of SVTs.

This finding indicates that some degree of physiologic (functional) AV block c

c Functional AV block (often 2:1) refers to physiologic limitations of the AV node in conducting excessively rapid stimuli due to its inherent refractoriness . In contrast, organic AV block (see Chapter 17 ) refers to impaired conduction in the AV node area associated with intrinsic (e.g., disease processes, excess vagal tone) or extrinsic (e.g., drugs) factors that may impair conduction.

is present. Furthermore, both tachyarrhythmias involve reentrant mechanisms in which electrical impulses rapidly and continuously spin around, “chasing their tails” in the atrial muscle (see Fig. 15.1 ). The rapid atrial rate combined with reentrant activity generates continuous atrial activity, manifest as F (flutter) or f (fibrillatory) waves, rather than discrete P waves.

Fig. 15.1
Schematic comparing mechanisms of atrial flutter ( left panel ) and atrial fibrillation (AF; right panel ). Atrial flutter is typically caused by a large reentrant wave circulating in the right atrium and initiated by a premature atrial complex (indicated by a star ). With the most common type of atrial flutter, the large (macroreentrant) wave spreads in a counterclockwise direction, involving the area near the tricuspid valve (TV) and inferior vena cava (IVC), the cavo-tricuspid isthmus. (Note that the impulse is blocked in the clockwise direction.) In contrast, AF is sustained by multiple microreentrant wavelets in a process usually initiated by abnormal impulse formation (automaticity) in the left atrial area of the pulmonary veins (PVs; only one PV labeled). AV, Atrioventricular junction; LV, left ventricle; MV, mitral valve; RV, right ventricle.

Fig. 15.2
(A) Typical counterclockwise atrial flutter most commonly involves a reentrant (“merry-go-round”-like) circuit in the right atrium, proceeding in a highly consistent, counterclockwise pathway involving the cavo-tricuspid isthmus. The cycle length (rotation time) is about 200 msec, corresponding to an atrial rate of 300 beats/min. Note that the “sawtooth” flutter (F) waves ( arrows ) appear negative in the inferior leads (II, III, and aVF) and V 6 but positive in V 1 . In the absence of drugs or atrioventricular node disease, the ventricular response is often exactly half the atrial rate (i.e., 150 beats/min). (B) With the clockwise variant of typical atrial flutter, the F waves are positive in the inferior leads and V 6 and negative in V 1 . These variants have the same clinical implications. (C) Atypical atrial flutter variant appearing postablation and probably arising in left atrium. Group beating (periodic pattern) and a premature ventricular complex are incidentally present but do not relate to the mechanism of atypical flutter. Differentiating isthmus-dependent (typical) and non–isthmus-dependent types of AF may be difficult or impossible from the surface ECG, requiring intracardiac recordings.

However, clinicians should bear in mind that the classic “sawtooth” flutter waves or oscillatory waves of fibrillation are not always clearly apparent. Not surprisingly, both atrial flutter and AF are often mistaken for other supraventricular arrhythmias when these F and f waves, respectively, are confused with true P waves associated, for example, with sinus tachycardia with frequent atrial ectopy or with (nonsinus) atrial tachycardias. These and other common mistakes in electrocardiogram (ECG) reading, which also occur with computerized (electronic) interpretations, are summarized in Chapter 24 .

Atrial Flutter: ECG Considerations

Atrial flutter is a reentrant arrhythmia (see Fig. 15.1 ) with a circuit traversing large portions of the atria. Hence, flutter is sometimes considered under the heading of macroreentrant atrial tachyarrhythmias. The boundaries of the flutter circuit are composed of anatomic barriers. Tricuspid and mitral valves, ostia of the pulmonary veins and vena cava, atrial scar tissue after heart surgery, or ablation procedures can all serve as such boundaries.

Based on the anatomic pathway of its reentrant circuit, atrial flutter can be most usefully classified as “typical” or “atypical.” The circuit of “typical” atrial flutter involves a path around the right atrium with its lower part passing through the narrow region between the inferior vena cava and the tricuspid valve annulus (cavo-tricuspid isthmus ). Hence, another term for typical atrial flutter is isthmus-dependent flutter. As in the case of the paroxysmal supraventricular tachycardias (PSVTs), a premature atrial complex (PAC) most often initiates atrial flutter.

Typical atrial flutter can be further classified based on the direction (counterclockwise or clockwise) that the reentrant wave traverses the right atrium. The most common form of typical atrial flutter involves a counterclockwise loop, with the impulse going up the interatrial septum and down the right atrial lateral wall ( Fig. 15.2A and B ), also activating the left atrium.

The typical atrial flutter activation front follows a consistent, repetitive path, producing a stable atrial rate (usually around 300 cycles/min; range 240-350 cycles/min). Furthermore, the flutter (F) waves (1) occur at very regular (predictable) intervals and (2) are identical in appearance in any single lead recording.

In contrast, non–isthmus-dependent (atypical) variants of atrial flutter ( Fig. 15.2C ) usually revolve around scar tissue within the left or right atrium, resulting from surgery, catheter ablation, or an idiopathic (undefined) process. In typical atrial flutter patterns, you can predict the direction of the reentrant circuit from the ECG. With counterclockwise atrial flutter, the asymmetric F waves appear negative in the inferior leads, positive in lead V 1 , and negative in the left precordial leads producing the classic “sawtooth” pattern in leads II, III, and aVF usually with a very regular ventricular (QRS) rate of about 150/min (due to functional 2:1 AV block) ( Fig. 15.2A ). The asymmetric morphology of these waves reflects their slowly downsloping phase followed by a shorter, more rapid upward deflection. This sawtooth asymmetry is probably related to differences in conduction velocity within the flutter-left atrial circuit.

Less often, the atrial activation proceeds in the opposite direction, producing clockwise flutter. The polarity of the F waves will then be reversed: positive in leads II, III, and aVF and negative in lead V 1 ( Fig. 15.2B ). Clockwise and counterclockwise flutter can occur in the same patient. Because both are usually isthmus-dependent, d

d The cavo-tricuspid isthmus is the most common area around which atrial flutter develops. However, it can develop around other atrial obstacles such as scars formed after cardiac surgery or areas of fibrosis following pericarditis or after ablation procedures in the left atrium to treat atrial fibrillation.

ablation in this critical area will reliably eliminate these reentrant circuits. Flutter wave morphology/polarity in atypical forms of flutter can be variable and their sites of origin and rotation are as reliably deducible from the surface ECG.

This chapter focuses on typical (cavo-tricuspid isthmus) atrial flutter. Readers wishing to learn more about atypical flutter variants ( Fig. 15.2C ) are referred to the Bibliography and the specialized and evolving literature on this advanced topic.

The atrial rate during typical atrial flutter, as noted, is around 300 cycles/min (range of about 240-330 cycles/min). Slower atrial rates, closer to 200 cycles/min or less, can be caused by drugs such as flecainide and factors such as aging, atrial dilation/atrial fibrosis, and other factors that slow atrial conduction velocity (prolong atrial cycle length). Fortunately, because of its inherent refractoriness, the AV node cannot usually conduct electrical signals at rates around 300 cycles/min to the ventricles—although a bypass tract in the Wolff–Parkinson–White (WPW) syndrome (see Chapter 18 ) may be able to conduct 1:1 at these rates. Thus with atrial flutter, physiologic AV block develops (commonly with a 2:1 A/V ratio) ( Figs. 15.2 and 15.3 ). In the presence of enhanced vagal tone, intrinsic AV nodal disease, or AV nodal blocking drugs (e.g., beta blockers, digoxin, and certain calcium channel blockers), higher degrees of AV block can be seen, for example, producing 4:1 conduction ratio ( Figs. 15.3 and 15.4 ).

Fig. 15.3, (A) Note the variable appearance of flutter waves in different leads. In lead I, the waves are barely apparent, leads II and III show the classic “sawtooth” appearance. The ventricular rate is about 160 beats/min, and the flutter rate is about 320 beats/min; thus 2:1 AV conduction is present. (B) Carotid sinus massage produces marked slowing of the ventricular rate by increasing vagal tone. R, R waves; ( R ), partially hidden R wave.

Fig. 15.4, Atrial flutter from different patients (A through E) showing variable patterns of atrioventricular (AV) conduction (block). As shown, the block may alternate between two values. In other cases it is more variable.

Often the AV nodal conduction shows more complex patterns and the degree of AV block varies in a periodic way, producing F wave/QRS ratios with repeating patterns ( Fig. 15.4 ) of RR intervals ( group beating ). This phenomenon is attributed to multiple levels of block within the conduction system. Variable AV block may also be caused by other mechanisms (e.g., AV Wenckebach), producing noninteger ratios of F waves to QRS complexes ( Fig. 15.5 ).

Fig. 15.5, With atrial flutter, the ventricular response may be variable but not always a simple ratio (1/2; 1/3; 1/4) of the atrial rate. Even in these cases, the response usually shows some underlying patterns, in contrast to the random appearing ventricular rate in atrial fibrillation.

Atrial flutter with 1:1 AV conduction ( Fig. 15.6 ), although uncommon, constitutes a medical emergency because of the very rapid ventricular rate, and it is most likely in four specific settings:

  • 1.

    In high catecholamine states (strenuous physical activity, infection, high fever, shock, etc.)

  • 2.

    With certain antiarrhythmic medications, such as flecainide, which slow conduction through atrial tissue and therefore slow the flutter rate sufficiently (e.g., 300-220 beats/min or less) such that the AV node is capable of conducting each of the F waves (1:1 conduction)

  • 3.

    In the presence of a bypass tract (WPW preexcitation syndrome) capable of rapid conduction (shorter refractory period than that of the AV node)

  • 4.

    In some cases of atypical atrial flutter, which usually have relatively slower atrial rates than typical variants

Fig. 15.6, Atrial flutter with 2:1 atrioventricular (AV) conduction (A) compared with 1:1 (one-to-one) AV conduction (B) in the same patient. In the latter case, the flutter waves are hard to locate. Owing to the very rapid ventricular response (about 300 beats/min), atrial flutter with 1:1 conduction is a medical emergency, often necessitating direct current (DC) cardioversion.

Because of the dangerously rapid ventricular rate, atrial flutter with sustained 1:1 AV conduction requires consideration of immediate synchronized electrical cardioversion (see below).

Atrial Fibrillation (AF): ECG Considerations

Unlike atrial flutter, the reentrant waves of AF cannot be localized to any consistent, stable circuit in the atria. Most cases of AF are thought to originate initially in the areas of pulmonary vein–left atrial junctions, involving the emergence of rapidly firing ectopic foci. With time, more and more of the atrial tissue becomes involved in the active maintenance of the arrhythmia, associated with the simultaneous formation of multiple unstable small (micro)-reentrant circuits (see Fig. 15.1 ). Therefore atrial electrical activity on the ECG appears as irregular f (fibrillatory) wavelets, varying continuously in amplitude, polarity (reversing from positive or negative orientation in the same lead), and frequency (changing cycle length, measured as the very brief interval from one f wave to the next).

Milder degrees of atrial activity “disorganization” or drugs that slow atrial activation may produce coarse AF with high amplitude f waves resembling atrial flutter ( Fig. 15.7 ). Advanced rheumatic mitral stenosis may also be associated with coarse AF.

Fig. 15.7, Atrial flutter with variable block (A) and coarse atrial fibrillation (B) are often confused. Notice that with atrial fibrillation the ventricular rate is completely erratic and the atrial waves are not identical from segment to segment, as they are with atrial flutter.

Key Point

Usually, the single best lead to identify the diagnostic irregular atrial activity of AF is lead V 1 , where characteristic f waves are likely to be most clearly seen ( Fig. 15.8 ).

Fig. 15.8, Atrial fibrillation (not flutter) is present with a slow ventricular response. The fibrillatory waves are best seen in lead V 1 . There is an atypical left bundle branch block pattern (see Chapter 8 ). The rsR′ in lateral leads (e.g., V 6 here) is highly suggestive of prior myocardial infarction (MI). A QR (or rsR′) complex is also present in leads I and aVL, also consistent with underlying MI. Left axis deviation and a long QT interval are noted as well. The patient had chronic heart failure due to severe coronary artery disease with prior “silent” MIs. The slow ventricular response raises the question of drug effect or excess (e.g., digoxin) or intrinsic atrioventricular (AV) node disease (see 17 , 20 ).

Severe atrial abnormalities (due to atrial dilation, fibrosis, or longstanding fibrillation or drugs such as digoxin) often result in fine AF with almost isoelectric (flat), very fast fibrillatory waves that can be confused with atrial asystole. Sometimes both fine and coarse f waves can appear in the same ECG.

Atrial Fibrillation and AV Nodal Conduction

In AF, the AV node is bombarded with highly disorganized impulses of different amplitude and frequency with atrial rates of up to 400 to 600 beats/min. Most of the signals are blocked in the AV node and only a fraction conduct to the ventricles (see Figs. 15.7B and 15.8 ). Still, in the absence of AV nodal disease or certain drugs, the ventricular heart rate in AF is much higher than with sinus rhythm. Usually, the mean QRS rate in untreated AF at rest is over 100 beats/min at rest, with often abrupt, inappropriate increases during even mild exercise.

Because of random penetration of the impulses through the AV node, the RR intervals in AF are haphazardly irregular. However, when the ventricular rate gets very fast, this RR irregularity may become more difficult to appreciate; sometimes the rhythm appears regular ( pseudoregularization ) and may be confused with other tachyarrhythmias such as PSVT ( Figs. 15.9 and 15.10 ).

Fig. 15.9, This patient with atrial fibrillation with a rapid ventricular response at rest had hyperthyroidism. (Note: the commonly used term rapid atrial fibrillation is actually a misnomer because “rapid” is intended to refer to the ventricular rate rather than the atrial rate. The same is true for the term slow atrial fibrillation.) Note also that the atrial fibrillation waves here have a “coarse” appearance, which might lead to confusion with true (discrete) P waves or with atrial flutter.

Fig. 15.10, Atrial fibrillation with a rapid ventricular response. At rapid rates, the RR interval variability may be more subtle, leading to a mistaken diagnosis of paroxysmal supraventricular tachycardia (PSVT) or even sinus tachycardia. See also Fig. 15.9 .

Atrial Fibrillation with a Regularized Ventricular Response

There are three major settings where AF may occur with a regularized ventricular response, in contrast to the highly irregular cadence usually associated with this arrhythmia:

  • 1.

    With complete heart block, in which case the ECG will usually show a very slow regular QRS escape rhythm, usually 40 to 50 beats/min or less ( Fig. 15.11 )

    Fig. 15.11, Complete atrioventricular (AV) heart block (see Chapter 16 ) can occur with underlying atrial fibrillation (or flutter); the ventricular response will be very slow, usually 50 beats/min or less, and regular. In this case the narrow QRS complex indicates that the escape rhythm is in the nodal area. Such patients usually require both permanent pacing and anticoagulation.

  • 2.

    During sustained ventricular pacing (see Chapter 22 )

  • 3.

    With certain cases of digoxin toxicity ( Chapter 20 )

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