Atrial flutter

Atrial flutter generally results from structural or functional conduction abnormalities of the atria. Structural abnormalities include atrial dilation due to a number of processes (see Risk factors under the Epidemiology section); incisional scars from prior atrial surgery, particularly for congenital heart disease; prior atrial ablation sites; and idiopathic fibrosis within the atrium. In addition, it can be precipitated by toxic and metabolic conditions such as thyrotoxicosis, alcoholism, or pericarditis. Patients taking anti-arrhythmics for chronic suppression of atrial fibrillation may convert to atrial flutter, noted most commonly with Vaughan Williams class Ic drugs (flecainide and propafenone) and amiodarone.[5][7][8] Occasionally, it can be congenital.[9]

The typical form of atrial flutter is a prototypic macro re-entrant arrhythmia, in which the re-entrant wavefront travels up the interatrial septum and down the right atrial free wall ('typical' form) or vice versa ('reverse typical' form). The lateral anatomical boundaries are critical to the development and maintenance of the circuit. One of these boundaries is the tricuspid valve annulus and is fixed or anatomical. The other is generally a functional line of block between the venae cavae.[10] Atypical flutters are seen when the cavotricuspid isthmus is not part of the circuit, and are characterised by a continuously undulating pattern by ECG that does not fit strict criteria for the typical and reverse typical forms of atrial flutter. This is a limitation in the mechanistic/anatomical classification scheme, as the exact mechanism can be determined only by electrophysiological mapping studies and not from the ECG alone. Clinical presentations and electrophysiological features of atypical atrial flutter and other types of atrial tachycardia can overlap.[3][Figure caption and citation for the preceding image starts]: Left panel: atrial activation in typical atrial flutter (AFL). Right panel: activation in reverse typical AFL. The atria are represented schematically in a left anterior oblique view, from the tricuspid (left) and mitral rings. The endocardium is shaded and the openings of the superior (SVC) and inferior vena cava (IVC), coronary sinus (CS), and pulmonary veins (PV) are shown. The direction of activation is shown by arrows. Dashed areas mark approximate location of zones of slow conduction and block. Lettering on the right-hand panel marks the low (LPS), mid (MPS), and high (HPS) posteroseptal wall, respectivelyFrom: Waldo AL. Heart. 2000;84:227-227; used with permission [Citation ends].

Atrial flutter is traditionally defined according to the ECG appearance, which shows continuous regular electrical activity, most commonly a saw-tooth pattern.[5]

It is a macro re-entrant atrial tachycardia with constant P wave/flutter morphology with an atrial rate usually >250 beats per minute (bpm).[5] It is distinguishable from focal atrial tachycardia, which has discrete P waves with an intervening isoelectric segment. Focal atrial tachycardia is caused mechanistically by micro re-entry or increased automaticity and generally has atrial rates in the range of 100 to 250 bpm.[2]

Cavotricuspid isthmus-dependent (typical atrial flutter):[5]

Anticlockwise atrial flutter with ECG flutter waves characterised by:[2][5]
- Negative deflection in leads II, III, aVF
- Positive deflection in lead V1
Clockwise atrial flutter (reverse typical atrial flutter) with ECG flutter waves characterised by:
- Positive deflection in leads II, III, aVF
- Negative deflection in lead V1.

Non-cavotricuspid isthmus-dependent (atypical atrial flutter):[2]

Re-entry that does not depend upon conduction through the cavotricuspid isthmus
Circuit is typically defined by atrial scars due to prior heart surgery, ablations, or idiopathic causes
Location determines ablation approach and risks
Multiple sites of re-entry may be present
Can occur in both the left and right atria.

Pathophysiology

Classification