Chapter 15 Supraventricular Arrhythmias, Part II Atrial Flutter and Atrial Fibrillation
The supraventricular (common narrow complex) tachycardias discussed so far have organized atrial activity (manifest by discrete P waves) and, with some notable exceptions, 1:1 atrioventricular (AV) conduction.∗ Atrial fibrillation (AF) and atrial flutter (AFL) are two related (and sometimes missed or mistaken) arrhythmias with very rapid atrial rates that greatly exceed the ventricular rate (Fig. 15-1). This finding implies that some degree of physiologic (functional) AV block† is almost always present. Furthermore, both arrhythmias involve reentrant mechanisms with impulses rapidly and continuously spinning around, “chasing their tails,” in the atrial muscle itself (see Fig. 15-1). Therefore, instead of true P waves, one sees continuous F (flutter) or f (fibrillatory) waves.
Figure 15-1 Diagram comparing mechanisms of atrial flutter and atrial fibrillation (AF). Atrial flutter is typically due to a large reentrant wave, originating in the right atrium by a premature atrial complex. With the common type of typical atrial flutter, the wave spreads in counterclockwise direction, involving the area near the tricuspid valve and inferior vena cava (cavo-tricuspid isthmus). In contrast, AF is sustained by multiple reentrant wavelets, not a single one, and often initiated by increased impulse formation in the area of the pulmonary veins in the left atrium. LV, left ventricle; RV, right ventricle, SA, sinoatrial.
The reentrant circuit of “typical” atrial flutter revolves around the tricuspid valve in the right atrium. Like reentrant supraventricular arrhythmias in general, it is initiated by a premature atrial complex (PAC) that blocks in one direction, while propagating in another. The signal then keeps circling in the same trajectory over and over again. In atrial flutter the typical frequency is about 300 cycles per minute (which is determined by the atrial size and conduction velocity) producing identical F waves.
The “bottleneck” where the signal usually blocks is the relatively narrow area between the tricuspid valve and inferior vena cava at the bottom of the right atrium (cavo-tricuspid isthmus). Conduction of the initiating PAC is blocked from propagating from the middle area of the right atrium to its lateral wall through this narrow isthmus. However, the electrical signal can propagate through the rest of the atrium and reach the isthmus from the other side. By this time the isthmus tissue has already recovered electrically and is ready to conduct. The signal goes through the isthmus in a counterclockwise direction, and the large (macro-) reentrant cycle starts again.
The classic “sawtooth” pattern of F waves that are predominantly negative in leads II, III, and aVF and positive in V1 with a very regular ventricular (QRS) rate of about 150/min (functional 2:1 AV block) is suggestive of the counterclockwise (common) type of typical right atrial flutter (Fig. 15-2A). Less frequently the same circuit gets initiated 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 V1 (Fig. 15-2B). Clockwise and counterclockwise flutter can occur in the same patient and both are usually isthmus-dependent.‡ Clinically, the development of atrial flutter most often indicates the presence of underlying structural/electrical atrial disease.
Figure 15-2 A, Typical atrial flutter most commonly involves a reentrant (“merry-go-round”-like) circuit in the right atrium, proceeding in a highly consistent, counterclockwise pathway. The cycle length (rotation time) is about 200 msec, corresponding to an atrial rate of 300/min. Note that the “sawtooth” flutter (F) waves (arrows) are negative in the inferior leads (II, III, and aVF) and V6, but positive in V1. 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, the flutter (F) waves are positive in the inferior leads and V6, and negative in V1. These variants have the same clinical implications.
The atrial rate during typical atrial flutter, as noted, is around 300 cycles/min (range usually between about 240 to 330 cycles/min). Slower rates can be due to drugs that slow atrial conduction. Fortunately, the AV node cannot conduct electrical signals at that rate to the ventricles—although a bypass tract in the Wolff-Parkinson-White (WPW) syndrome (see Chapter 12) can! Thus, with atrial flutter, physiologic AV block develops (usually with a 2:1 A/V ratio) (Figs. 15-2 and 15-3). In the presence of high vagal tone, AV nodal disease, or AV nodal blocking drugs (e.g., beta blockers, digoxin, and certain calcium channel antagonists) higher degrees of AV block can be seen, for example with a 4:1 conduction ratio (Figs. 15-3 and 15-4).
Figure 15-3 A, Notice the variable appearance of flutter waves in different leads. In lead I, the waves are barely apparent, whereas in leads II and III, the classic “sawtooth” waves appear. 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.
Often the AV nodal conduction shows more complex patterns and the degree of AV block varies in a periodic way, producing flutter/QRS ratios with repeating patterns (Fig. 15-4) of RR intervals (group beating). This phenomenon is believed to be due to multiple levels of block within the conduction system. Variable AV block may be due to other mechanisms (e.g., AV Wenckebach) and produce noninteger ratios of F waves to QRS complexes (Fig. 15-5).
Figure 15-4 Atrial flutter from different patients (A through E) showing variable patterns of conduction (block). As shown, the block may alternate between two values. In other cases it is more variable.
Figure 15-5 With atrial flutter, the ventricular response may be variable, but not always a simple fraction (½, ⅓, ¼) 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.
• With certain antiarrhythmic medications (such as flecainide) that slow down the flutter rate (for example, from 300 to 250/min or less) to the point where 1:1 conduction through AV node becomes possible
Figure 15-6 Atrial flutter with 2:1 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 is a medical emergency, often necessitating direct current (DC) cardioversion (see later discussion).
Atrial flutter with sustained 1:1 AV conduction represents an emergency situation, requiring consideration of immediate synchronized electrical cardioversion because of the dangerously rapid ventricular rate.
Unlike atrial flutter, the reentrant waves of atrial fibrillation (AF) cannot be localized to any repetitive and stable circuit in the atria. Most cases of AF are thought to originate in the area of pulmonary vein–left atrial junctions. 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 reentrant circuits throughout the atria (see Fig 15-1).
Atrial electrical activity on the ECG appears as irregular f (fibrillatory) waves, varying continuously in amplitude, polarity (reversing from positive or negative orientation in same lead), and frequency (changing cycle length, measured as the very brief interval from one f wave to the next).
Figure 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.