An irregular ventricular rhythm may be caused by changing degrees of AV nodal block (see Figures 1A and and 3), 3), including Wenckebach cycles. It should be emphasised that ECG diagnosis is based on atrial deflections and not on ventricular (QRS) rate and rhythm. Flutter wave morphology can be determined by activation outside the re-entry circuit, which would explain the often-difficult correlation between mechanism and ECG pattern. Conversely, a typical flutter ECG may be generated by atypical re-entry circuits, independent of the CTI, including LA circuits. In these cases ECG patterns are often atypical. (B) A 2:1 atrioventricular block with slower ventricular rate and narrow QRS allows recognition of slow but typical flutter waves.ĬTI-dependent MRT is also frequent in patients with previous surgical atriotomies or atrial baffle procedures, or after LA ablation for the treatment of AF. (A) Slow flutter (170 BPM) with 1:1 atrioventricular conduction and wide QRS complex (right bundle branch block and superior axis) in a patient treated with flecainide for paroxysmal atrial fibrillation. One to One AV Conduction in Flutter Slowed by Flecainide This reverse typical flutter is much less common clinically than the counter clockwise form, but the clinical manifestations are indistinguishable. superoinferior in the septal wall and inferosuperior in the anterolateral wall – with the same zones of block in the posterior RA and obligatory passage through the CTI (see Figure 3). For further explanation see text.Įither spontaneously or after programmed stimulation, re-entry may occur in the opposite (clockwise) direction – i.e. CS = coronary sinus ostium CTI = cavotricuspid isthmus PV = left pulmonary veins ostia. The circular arrow shows typical counter clockwise re-entrant activation. The terminal crest (TC) is shown as a vertically-dashed area reaching from the superior vena cava (SVC) to the inferior vena cava (IVC). Mitral and tricuspid rings are enlarged in order to show the posterior walls. The schema on the right displays the atria in a left anterior oblique view. Modern electrophysiology (EP) has confirmed the re-entrant mechanism of typical flutter, and has opened wide the spectrum of mechanisms of macro-re-entrant tachycardias (MRTs), prompting a new, more open view of clinical ECG-based classification (see Figure 1A and and 1B 1B).Ītrial activity in leads II and III is a continuous undulation with a sharp negative deflection (‘saw-tooth pattern’). This was not a significant consideration when digitalis and very few antiarrhythmic drugs (AADs) were the only therapeutic armamentarium, but determining the mechanism involved in flutter has become crucial for the design and application of catheter and surgical ablation techniques. Later human studies left the door open for a focal mechanism. Early studies suggested that flutter had a re-entrant mechanism but others attributed flutter to focal discharge. Slower tachycardias displaying discrete P waves, separated by isoelectric baselines, were called ‘atrial tachycardia’. On the ECG, flutter was a regular continuous undulation between QRS complexes at a cycle length (CL) of ≤250 ms (≥240 bpm). The term ‘flutter’ was coined to designate the visual and tactile rapid, regular atrial contraction induced by faradic stimulation in animal hearts, in contrast with irregular, vermiform contraction in atrial fibrillation (AF). In patients subjected to cardiac surgery or catheter ablation for the treatment of atrial fibrillation or showing atypical ECG patterns, macro-re-entrant and focal tachycardia mechanisms can be very complex and electrophysiological studies are necessary to guide ablation treatment in poorly tolerated cases. Secondary prevention, based on the treatment of associated atrial fibrillation risk factors, is emerging as a therapeutic option. In patients without a history of heart disease, cardiac surgery or catheter ablation, typical flutter ECG remains predictive of a right atrial re-entry circuit dependent on the inferior vena cava-tricuspid isthmus that can be very effectively treated by ablation, although late incidence of atrial fibrillation remains a problem. Electrophysiological studies have defined multiple mechanisms of tachycardia, both re-entrant and focal, with varying ECG morphologies and rates, authenticated by the results of catheter ablation of the focal triggers or critical isthmuses of re-entry circuits. Clinical electrophysiology has made the traditional classification of rapid atrial rhythms into flutter and tachycardia of little clinical use.
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